Goodheart’s Photoguide to Common Skin Disorders: Diagnosis and Management [3 ed.] 9780781771436, 0781771439, 2008024074

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G ood h eart’s Ph otogu id e

to Com m on Skin Disord ers Diagnosis and Managem ent

THIRD EDITION

G oodh eart’s Ph otoguide

to Com m on Skin Disorders Diagnosis and Managem ent

Herbert P. Goodheart, M.D. Assistant Clinical Professor Department of Dermatology Mount Sinai School of Medicine New York, New York

Acquisitions Editor: Sonya Seigafuse Managing Editor: Kerry Barrett Developmental Editor: Martha Cushman Production Editor: Bridgett Dougherty Senior Manufacturing Manager: Benjamin Rivera Design Coordinator: Risa Chow Compositor: Aptara® © 2009 by LIPPINCOTT WILLIAMS & WILKINS 530 Walnut Street Philadelphia, PA 19106 USA LWW.com All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this book prepared by individuals as part of their official duties as U.S. government employees are not covered by the above-mentioned copyright. Printed in China Library of Congress Cataloging-in-Publication Data Goodheart, Herbert P. Goodheart's photoguide to common skin disorders : diagnosis and management / Herbert P. Goodheart. — 3rd ed. p. ; cm. Includes index. ISBN-13: 978-0-7817-7143-6 ISBN-10: 0-7817-7143-9 1. Skin—Diseases—Handbooks, manuals, etc. 2. Skin—Diseases—Atlases. I. Title. II. Title: Photoguide to common skin disorders. [DNLM: 1. Skin Diseases—diagnosis—Atlases. 2. Skin Diseases—therapy—Atlases. WR 17 G652g 2008] RL74.G66 2008 616.50022'2—dc22 2008024074 Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editor, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of this information in a particular situation remains the professional responsibility of the practitioner. The authors, editor, and publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accordance with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any change in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new or infrequently employed drug. Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA) clearance for limited use in restricted research settings. It is the responsibility of the health care provider to ascertain the FDA status of each drug or device planned for use in their clinical practice. 10 9 8 7 6 5 4 3 2 1

To my family, who have provided immense support and encouragement throughout. What the mind does not know, the eyes cannot see. ANCIENT PROVERB

Contents Contributors ix Foreword by Warren R. Heymann Preface xiii Acknowledgments xvii

xi

INTRODUCTION

Illustrated Glossary of Basic Skin Lesions 2 Topical Therapy 13

PART ONE

Common Skin Conditions: Diagnosis and Management 21 1 Acne and Related Disorders 23 2 Eczema 49 3 Psoriasis 89 4 Inflammatory Eruptions of Unknown Cause 114 5 Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa 6 Superficial Viral Infections 140 7 Superficial Fungal Infections 168 8 Viral Exanthems 194

126

Kenneth Howe

9 Bacterial Exanthems

208 Kenneth Howe and Herbert P. Goodheart

10 Hair and Scalp Disorders Resulting in Hair Loss 215 Herbert P. Goodheart and Hendrik Uyttendaele

11 12 13 14 15 16 17 18 19

Hirsutism 237 Disorders of the Mouth, Lips, and Tongue Diseases and Abnormalities of Nails 260 Pigmentary Disorders 275 Pruritus: The “Itchy” Patient 290 Xerosis: The “Dry” Patient 294 Drug Eruptions 298 Diseases of Vasculature 304 Sexually Transmitted Diseases 331

244

Mary Ruth Buchness and Herbert P. Goodheart

20 Bites, Stings, and Infestations 351 21 Benign Skin Neoplasms 374 22 Premalignant and Malignant Skin Neoplasms

405

vii

PART TW O

Systemic Conditions and the Skin 441 23 Skin and Hair During Pregnancy 443 24 Cutaneous Manifestations of HIV Infection

450

Mary Ruth Buchness

25 Cutaneous Manifestations of Systemic Disease

470

Herbert P. Goodheart and Peter G. Burk

PART TH REE

Dermatologic Procedures 509 26 Diagnostic and Therapeutic Procedures

511

PART FOUR

Dermatologic Disorders in Special Populations 531 27 Special Considerations in the Skin of Pediatric and Elderly Patients 533 Appendix A: Brand Names of Dermatologic Medications in Various Countries

535

The following patient handouts can be found online, on the solution Web site Acne Acne: How to Apply Duac Gel, BenzaClin Gel, and Benzamycin Gel Acne: How to Apply Topical Retinoids Alopecia Areata Athlete’s Foot (Tinea Pedis) Atopic Dermatitis Atypical Nevus (Mole) Basal Cell Carcinoma Burow’s Solution Contact Dermatitis Dry Skin (Xerosis) Fungal Nails (Onychomycosis) Genital Warts Granuloma Annulare Hair Loss (Androgenic Alopecia) Hand Eczema Head Lice Herpes Simplex Herpes Zoster (Shingles) Hives (Urticaria) Keratosis Pilaris (Rough Bumpy Skin) Lichen Planus Lyme Disease Subject Index 537

viii

Contents

Lyme Disease: Prevention Malignant Melanoma Melasma Molluscum Contagiosum Pityriasis Rosea Poison Ivy and Poison Oak (Rhus Dermatitis) Pseudofolliculitis Barbae (Razor Bumps) Psoriasis Rosacea Scabies Scalp Psoriasis: Scale Removal Seborrheic Dermatitis of the Face Seborrheic Dermatitis of the Scalp and Dandruff Short-Term Cortisone Therapy Soak and Smear Instruction Sheet Solar Keratosis (Actinic Keratosis) Squamous Cell Carcinoma Sun Protection Advice Tinea Capitis Tinea Cruris (Jock Itch) Tinea Versicolor Vitiligo Warts

Contributors Mary Ruth Buchness, M.D. Associate Professor of Medicine New York Medical College Valhalla, New York Attending Physician Department of Medicine St. Vincent’s Catholic Medical Center New York, New York Herbert P. Goodheart, M.D. Assistant Clinical Professor Department of Dermatology Mount Sinai School of Medicine New York, New York Peter G. Burk, M.D. Clinical Associate Professor of Medicine (Dermatology) Albert Einstein College of Medicine Attending Physician Dermatology Service Montefiore Medical Center Bronx, New York Kenneth Howe, M.D. Assistant Clinical Professor Department of Dermatology Beth Israel Medical Center New York, New York Hendrik Uyttendaele, M.D. Instructor in Clinical Dermatology Department of Dermatology Columbia Presbyterian Medical Center Assistant Attending Physician New York Presbyterian Hospital New York, New York

ix

Foreword As a second-year medical student, I recall studying cardiology one evening when my brother Andrew asked me to look at a rash that developed on his trunk. I did not have a clue as to how to make any dermatologic diagnosis. So, after Andrew accused my father of wasting tuition money on my evidently inadequate education, I thought it proper to register for a dermatology elective in my fourth year. I reasoned that, regardless of whatever field I would ultimately choose, I would inevitably be confronted with some cutaneous dilemmas. It was with tremendous fortune that I subsequently trained at the Albert Einstein College of Medicine in the Bronx, New York, under the tutelage of Michael Fisher, M.D., the former head of the illustrious division of dermatology. It was during my training that I befriended the attending physician, Dr. Herb Goodheart. Herb always provided special insights, wisdom, and compassion in the evaluation of even the most rudimentary dermatologic disorders. He is a stellar teacher and dermatologist, who has compiled his years of perspicacity into this guide to dermatology. As we begin the twenty-first century, the landscape of American medicine and dermatology is changing at an accelerating pace. Even though we can now comprehend many skin disorders at a molecular level and have advanced our therapeutic realm to include laser technology and immunobiology, the cornerstone of all dermatologic endeavors will always be careful clinical observation. As venues of practice shift toward a greater proportion of primary dermatologic care being delivered by nondermatologists, resources for these providers must be accessible, comprehensible, and practical. Dr. Goodheart’s guide to dermatology is divided into common disorders, the interrelationship between the skin and systemic diseases, basic and advanced dermatologic procedures, and a very useful appendix that provides patient handout material in both English and Spanish. Importantly, it combines features of an atlas with Herb’s pithy perspectives, as though he is standing over your shoulder in the dermatology clinic. Those who use this guide will come to appreciate many of the finer points and opinions that Dr. Goodheart provides and even more so when becoming more facile with the discipline. Use this guide as a primer, an atlas, a consultant, and as a supplement to more in-depth dermatology texts and medical literature. Your dermatologic knowledge base will flourish, your appreciation of the field will blossom, and most importantly, your patients will benefit from your expertise. Warren R. Heymann, M.D. Head, Division of Dermatology UMDNJ—Robert Wood Johnson School of Medicine at Camden Newark, New Jersey

xi

Preface to the Second Edition In dermatology, the naked eye is our primary tool, and because virtually every skin disorder is visible, the photographic image is an essential teaching aid. Despite the commonplace occurrence of skin disorders, making a correct dermatologic diagnosis is a customary stumbling block for many health care professionals. It is rather unusual to find a nondermatologist who is comfortable diagnosing or managing most skin problems; in fact, many admit to using the therapeutic approach of “trial and error.” Medical schools simply do not emphasize the teaching of dermatology. Skin diseases are generally considered less life threatening and are a lower priority than most of the conditions seen in teaching hospitals. Frequently, this can result in mistreatment, a delay in appropriate treatment, or a referral to a dermatologist. This book is intended to be an accessible reference for nondermatologists such as family physicians, physician assistants, nurse practitioners, and medical students, who are often on the frontline in treating skin problems. Its focus has been limited intentionally to the diagnosis and management of the most common skin problems encountered in an outpatient setting. Wherever possible, “look-alike” photos are juxtaposed with photos of primary dermatoses to help the reader make the differential diagnosis.

xiii

Preface to the Third Edition Many changes have occurred in the 10 years since the first edition, A Photoguide of Common Skin Disorders, was published. This third edition has been expanded and extensively rewritten to reflect these changes. The treatment sections have been updated and offer more therapeutic options that also will serve as a resource for those in dermatology residency training. The photographs, which are fundamental to this text, have been enlarged to achieve greater clarity and detail. New to this edition is an online Solution site that allows the reader to access the entire contents of the book plus additional material such as patient handouts in English and Spanish. The handouts can be downloaded as PDF files and given to patients to read. They also can serve as an ongoing source of information for health care providers who use this book. Also included online is an image bank that allows the user to download and save the images found on the site as .pdf or .jpg files for teaching and lecturing purposes. International readers should benefit from Appendix A, where Canada and India now appear on the list, allowing the reader to recognize dermatologic agents that often have different brand names in their respective countries. The addition of Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients,” covers many disorders that are not discussed in the preceding chapters. The thumbnail images that appear in this chapter can be viewed in a larger size online. It is hoped that these changes will make this edition even more useful to those responsible for diagnosing and managing the common problems that account for the vast majority of dermatologic complaints. Herbert P. Goodheart, M.D.

xv

Acknowledgm ents I owe a great deal of gratitude to many for making the writing of this third edition a truly satisfying and enjoyable experience. I am immensely pleased with the superb job that my publisher, Lippincott Williams & Wilkins, has done in producing this edition. Beginning with Sonya Seigafuse, who had the foresight and determination to take on the project, I am deeply indebted. Sonya was the catalyst for this book. Martha Cushman, my editor par excellence, practically worked side by side with me in pulling the project together; my heartfelt appreciation goes to her. She has been a terrific partner. Another key player was Kerry Barrett, whose attention to detail and availability to answer a multitude of questions brought this complicated project to completion. Special credit also goes to Brett MacNaughton, who kept track of the illustrations and the multitude of disconnected digital and 35-mm images, and to Risa Clow, whose creative layout and design suggestions always respected the content of the material. Muchas gracias to Rebeca Barroso, who supplied the Spanish translations of the patient handouts. Many helped with the foreign brand names of drugs, including Danille Luquin (French), Hans J. Kammler (French and German), and Terry Marshall (British)—merci, danke, and thanks. My appreciation also goes to Ashit Mahar and Ben Barankin, who added India and Canada, respectively, to the list of brand names of drugs. Thanks go to Joe Eastern, M.D., my colleague, whose critical judgment and comments concerning the accuracy of the material have been invaluable. I also wish to thank Ross Levy, M.D., my friend, whose advice about wound healing has been a great addition; his hands and surgical skills are featured more than once in this book. I also would like to express thanks to the people at Aptara, particularly Stephanie Lentz, who helped me finalize the manuscript and whose patience and enthusiasm saved me from many errors. My gratitude also goes to Jenny Ceccotti, General Manager of Aptara, Tom Chronister, who made sure the images were as clear as possible, and Max Leckrone, who assisted with the final editing. Thanks go to my colleagues at Derm-Chat/Derm-Rx, who kept me up to date on the latest diagnostic and therapeutic issues in dermatology: Art Huntley at UC Davis, who founded and maintains this valuable online resource, as well as “heavy posters” Joe Eastern, Orin Goldblum, Diane Thaler, Ashit Mahwar, Otto Bastos, Bob Rudolph, Sahar Ghannam, Larry Finkel, Bill Danby, Sate Hamza, Noah Scheinfeld, Steve Feldman, Bernie Recht, Barry Ginsberg, Bill Smith, Pierre Jaffe, Omid Zargari, Becky Bushong, Ed Zabawski, Jerry Litt, Skee Smith, Jo Bohanon-Grant, Ben Treen, Norman Winkler, Chuck Fishman, Susan Bushelman, Robin Berger, Maida Burrow, Stu Kittay, Diane Davidson, Chuck Miller, Norm Guzick, Joel Schlessinger, Jane Chew, Mauricio Goihman, Pat Condry, Kevin Smith, Steve Stone, Gail Drayton, Steve Emmet, Linda Spencer, and many others who are too numerous to mention, who have been my “online classmates.”

xvii

I N T RO D U C T I O N

Illustrated Glossary of Basic Skin Lesion s Topical Th erapy

Illu st ra t ed Glo ssa r y o f Ba sic Sk in Lesio n s LESIONS Prim ary Lesion s

Macule. Freckles (ephelides). Macules are small, flat, nonpalpable changes in skin color (you cannot feel macules and, if you close your eyes, they “disappear”). They occur in various shapes and sizes. Examples include tattoos, flat nevi, postinflammatory hyperpigmentation, postinflammatory hypopigmentation, erythema, purpura, and freckles. Patches are large macules. Examples include melasma and vitiligo. There is some confusion regarding patches; some dermatologists refer to a patch as a large macule, whereas others refer to patches as macules with overlying fine scale (e.g., the scaly patches seen in pityriasis rosea and tinea versicolor). Patch. Vitiligo.

Papules are small, solid lesions that are generally 1 cm or less in diameter. Examples include, molluscum contagiosum, warts, and palpable nevi (moles). Papule. Multiple nevi

2

Introduction

Note: “Maculopapule” is a contradiction in terms, and the use of this term should be abandoned (an eruption may be described as being macular and papular, rather than “maculopapular”).

Nodules are firm, solid palpable lesions that are generally 1 cm or more in diameter. They may be seen as elevated lesions or can be palpated without any elevation of the skin. Examples include erythema nodosum, lipoma, rheumatoid nodules, basal cell carcinoma, and keloid.

Nodule. Keloid

Vesicles (small blisters) are clear, fluid-filled lesions generally 1 cm or less in diameter. Examples include herpes simplex, acute vesicular tinea pedis, and early chickenpox. Vesicle. Chickenpox.

Bullae (large blisters) are clear, fluid-filled lesions generally 1 cm or more in diameter. Examples include second-degree burns, herpes zoster, and insect bite reactions.

Bulla. Bullous insect bite reaction.

Introd uction

3

Pustules are superficial lesions that contain purulent, cloudy material. Examples include evolving chickenpox, folliculitis, and pustular acne. Pustule. Folliculitis barbae.

Plaque. Psoriasis vulgaris.

Atrophic plaque. Atrophy caused by intralesional cortisone injections.

4

Introduction

Plaques are solid, elevated, or depressed (atrophic) flattopped, plateaulike lesions that cover a fairly large area; they may arise from papules that coalesce or arise de novo. Examples include chronic eczematous dermatitis and psoriasis.

Atrophic plaques include discoid lupus erythematosus, morphea (localized scleroderma), and steroid atrophy.

Wheals are raised flesh-colored or erythematous papules or plaques that are transient lesions. They generally last less than 24 hours, during which time they may change shape and size. Examples include urticaria (hives) and angioedema. Wheal. Urticaria.

Cysts are walled-off lesions containing fluid or semisolid material. (They feel like an eyeball when you palpate them.) Examples include pilar and epidermoid cysts.

A

B Cyst. Epidermoid cyst.

Introd uction

5

Secon d ary (Mod ified ) Lesion s Secondary lesions are those primary lesions that have evolved naturally or have been manipulated by the patient.

Scale. Dandruff.

Crust. Bullous impetigo.

6

Introduction

Scales (desquamation) comprise the outer layer of epidermis. The outer epidermis normally desquamates or sheds imperceptibly on a daily basis. In many dermatologic conditions, when this shedding becomes visible, it is abnormal and is called “desquamation” or “scale.” Common examples of conditions that produce scale are psoriasis, ichthyosis, and dandruff.

Crusts (scabs) are formed from blood, serum, or other dried exudate. “Honey-colored crusts” (impetiginization) are often a sign of superficial bacterial infection. Examples include excoriated or infected insect bites and evolving bullous lesions of impetigo.

Erosions are shallow losses of tissue involving only the epidermis (“topsoil”). They often result from blisters and pustules and usually heal without scarring. Examples include the secondary lesions of herpes simplex, herpes zoster, and lesions of aphthous stomatitis.

Erosion. Aphthous stomatitis (“canker sore”).

Ulcer. Vasculitis.

Ulcers are defects deeper than erosions. Ulcers involve the dermis or deeper layers and usually heal with scarring. Examples include pyoderma gangrenosum, venous stasis ulcers, and vasculitis.

Introd uction

7

Fissure. Atopic dermatitis of lips (atopic cheilitis). Fissures are linear ulcers or cracks in the skin. They are often painful. Examples of conditions in which they may be seen include eczematous dermatitis of the fingers, angular stomatitis (perlèche), and eczema of the lips.

Excoriation. Punctate and linear lesions from scratching.

Excoriations are linear or punctate erosions or excavations induced by scratching, picking, or digging. Examples include insect bites, cat scratches, and self-induced lesions.

REACTION PATTERNS, SH APES, AND CONFIGURATIONS Diseased skin has a limited number of clinical manifestations. Many skin disorders tend to occur in characteristic shapes, distributions, arrangements, and reaction patterns that often serve as diagnostic clues.

Reaction Pattern s

Papulosquamous reaction pattern. Pityriasis rosea. 8

Introduction

The convention of describing skin disorders in terms of certain reaction patterns is often inexact, and there is a great deal of overlap. However, using these patterns to describe individual

skin lesions or eruptions often helps greatly in formulating a differential diagnosis. Papulosquamous reaction patterns refer to eruptions in which the primary lesions consist of macules, papules, or plaques with scale. Thus, a papulosquamous reaction pattern suggests a diagnosis from a list that includes the following differential diagnoses: psoriasis, tinea corporis, tinea versicolor, lichen planus, parapsoriasis, mycosis fungoides, and pityriasis rosea. Eczematous reaction patterns are a little more difficult than papulosquamous patterns to describe (see Chapter 2, “Eczema”), because they may have various presentations and, at times, may be impossible to distinguish from papulosquamous patterns.

Acute eczematous reaction pattern. Poison ivy.

• Acute and subacute eczema. Examples include erythematous “juicy” papules or plaques and/or weeping vesicobullous lesions. A classic example is an acute contact dermatitis such as poison ivy. • Chronic eczema. The hallmark lesion of chronic eczematous dermatitis caused by repeated scratching is known as lichenification, a plaque with an exaggeration of the normal skin markings that looks like the bark of a tree. Typical examples include the lesions seen in long-standing atopic dermatitis and lichen simplex chronicus.

Chronic eczematous reaction pattern. Atopic dermatitis with lichenification. Vesicobullous reaction patterns consist of fluid-filled blisters. Examples include second-degree burns, herpes simplex, and herpes zoster infections.

Vesicobullous reaction pattern. Herpes zoster.

Introd uction

9

Dermal reaction patterns are lesions or eruptions that are confined to the dermis. Examples include granuloma annulare and cutaneous sarcoidosis. Subcutaneous reaction patterns are characterized by lesions or eruptions that are confined to the cutis (subcutaneous tissue). Examples include erythema nodosum and lipomas. Vascular reaction patterns refer to erythema or edema resulting from changes in the vasculature, such as vasodilatation and vasculitis. Examples include first-degree burns, viral exanthem, urticaria, erythema multiforme, vasculitis, and drug rashes. Dermal reaction pattern. Cutaneous sarcoidosis.

Subcutaneous reaction pattern. Multiple lipomas.

Vascular reaction pattern. Drug rash.

10

Introduction

Sh ap e of Lesion s

Annular and arciform are terms used to describe lesions that are ring-shaped or semiannular. Examples include urticaria, granuloma annulare, and tinea corporis (ringworm).

Annular lesion. Tinea corporis.

Nummular is a term that describes coin-shaped lesions. Examples include lesions seen in discoid lupus erythematosus, psoriasis, and nummular eczema. Nummular lesions. Coin-shaped lesions of nummular eczema.

Linear lesions may result from exogenous agents, excoriations, and congenital growths. Examples include lesions of poison ivy and dermatographism.

Linear lesion. Dermatographism.

Introduction

11

Con figu ration of Lesion s The arrangement (configuration) of lesions is the interrelationship of multiple lesions.

Grouped lesions are noted in herpetiform and zosteriform vesicles or bullae. Examples are seen in insect bite reactions, herpes zoster, and herpes simplex. Grouped lesions. Herpes simplex. Grouped vesicles.

Follicular lesions. Follicular eczema. Note the gridlike pattern of tiny papules.

12

Introduction

Follicular arrangement of lesions involves hair follicles. Lesions are often papular or pustular, at times with a visible central emerging hair. Lesions are spaced at fairly equal distances in a gridlike pattern. Examples are seen in keratosis pilaris and folliculitis.

To p ica l Th era p y OVERVIEW Topical therapy, the mainstay in the treatment of many dermatologic conditions, has traditionally been the bailiwick of dermatologists. Thus, it is no surprise that an understanding of the appropriate use and abuse of these agents has been either neglected or misunderstood by other health care professionals. The following is an attempt to provide a practical overview of topical therapy. The primary focus is on the use of topical steroids; other topical agents such as antibiotics and antifungals will be discussed in other sections of the book. (Topical antibiotics used for acne are listed in Chapter 1. Topical antibiotics for other cutaneous infections such as impetigo are described in Chapter 5.)

GENERAL PRINCIPLES BASICS • Topical therapy is generally safer than systemic therapy. • Creams are generally more popular with patients than ointments because they are less greasy and messy; however, they are usually less potent and more drying. • In addition to their enhanced potency, ointments are more moisturizing than creams, gels, and foams. • Gels and foams are greaseless; they spread more easily and are very practical for acne and for application to hairy areas of the body. They also dry on contact, leaving a thin, invisible film. • Solutions tend to be drying but cover large areas more easily than other preparations. • Lotions are moisturizing to some extent; however, those that contain propylene glycol may have drying effects. They are also easy to apply and can be used on any skin type. • Although foams may be somewhat drying, they are easy to spread, particularly on hairy areas such as the scalp as well as on the chests and backs of hirsute males. However, foams are expensive. Emollient (nonalcohol-based) foams have recently become available. • Patients’ choice should be taken into account because compliance is often related to patients’ personal preference for a vehicle. • The amount of a topical preparation applied does not affect its penetration or potency. The thicker the application, the greater the wastage—only the thin layer that is in intimate contact with the skin is absorbed; the remainder is rubbed off. More is not always better! • Once- or twice-daily applications are usually sufficient for most preparations (sunscreens and some moisturizers are generally applied more frequently).

Ve h icle s • The active drug is combined with a vehicle, or base. The vehicles vary in their ability to “deliver” to the target site in the skin.

• The rate of penetration and of absorption of a topical preparation into the skin depends on how occlusive its vehicle is (discussion to follow) and on how readily the vehicle releases the active chemical. • The vehicle should be cosmetically acceptable and nonsensitizing.

We t Dre ssin g s • There is some validity to the old adage: “If it’s dry, wet it; if it’s wet, dry it.” • Wet dressings help dry wounds, and they aid in the débridement of wounds by removing debris (e.g., serum, crusts). They also have a nonspecific antifungal and antibacterial effect, especially when chemicals such as aluminum sulfate, silver nitrate, acetic acid (vinegar is dilute acetic acid), and potassium permanganate are added. • For example, the application of Burow’s solution (aluminum sulfate and calcium acetate) helps dry out lesions that are weeping and oozing (e.g., poison ivy, tinea pedis, herpes simplex, herpes zoster) or impetiginized (e.g., impetigo, infected stasis ulcers). It is available without a prescription. • However, white vinegar in water, or even, plain unsterilized tap water may serve as less expensive, readily available— although probably less effective—alternatives, if Burow’s solution cannot be obtained. SEE PATIENT HANDOUT, “Buro w’s So lut io n ” ON THE SOLUTION SITE

TOPICAL STEROIDS See TABLES I.1 and I.2 MECHANISM OF ACTION Topical steroids have two basic mechanisms of action: antiinflammatory and antimitotic. • Anti-inflammatory properties are of particular importance when they are used to treat eczematous and other primarily inflammatory conditions. • Antimitotic properties of topical steroids help to reduce the buildup of scale, as in the treatment of psoriasis, a condition that is both inflammatory and hyperproliferative (rapid cell division). GENERAL CONSIDERATIONS • Topical steroids are used to treat most inflammatory dermatoses. They are the cornerstone of therapy in dermatology, and, when used properly, they are quite safe. • The unwanted effects of topical steroids are directly related to their potencies. • When possible, the lowest-potency steroid should be used for the shortest possible time. Conversely, one should avoid Introduction

13

•

•

•

•

using a preparation that is not potent enough to treat a particular condition. For severe dermatoses, a very potent steroid may be used to initiate therapy, and a less potent preparation may be used afterward for maintenance (“downward titration”). Occlusion, which involves placing medications under occlusive dressings produces increased hydration of the stratum corneum. Hydration increases penetration, which, in turn, increases efficacy and potency. Tachyphylaxis (tolerance) occurs when the medication loses its efficacy with continued use. It is most often seen in the treatment of psoriasis and other chronic conditions when very strong topical steroids are used continuously for prolonged periods. To help minimize tachyphylaxis, a high-potency preparation is applied until a dermatosis clears (“strong, but not long”), and a lower-potency topical steroid is prescribed for intermittent flares should they occur.

Po t e n cie s • Fluorinated topical steroids are generally more potent than other topical steroids. For example, triamcinolone acetonide, which contains a fluoride ion, is 100 times more potent than nonfluorinated hydrocortisone. • When treating children and elderly patients, clinicians should take extra measures to avoid the use of potent fluorinated compounds, when possible. • Even without an added fluoride ion, certain molecular structural changes can increase potency in corticosteroids. For example, hydrocortisone valerate, which contains no fluoride ion, is almost as potent as triamcinolone acetonide. • Only nonfluorinated, mild topical steroids should be applied to the face and, ideally, only for short periods of time, to avoid atrophy and steroid-induced rosacea. (However, this rule can be broken. For example, for the treatment of severe acute contact dermatitis of the face, a superpotent topical steroid used briefly may be preferable to a mild, ineffective topical steroid or a systemic steroid.) • Thin eyelid skin requires the least potent preparations for the shortest periods of time. The intertriginous (skin touching skin) areas similarly respond to lower potencies because the apposition of skin surfaces acts like an occlusive dressing. The axillae and inguinal creases are particularly prone to higher absorption and resultant steroid atrophy (see FIG I.3). • Every potency class has a generic preparation that is generally more economical than the trade-name preparation; however, there is some concern about the bioequivalence between trade and generic formulations. De live ry (Pe rcut an e o us Pe n e t rat io n ) Topical steroids and other topical preparations are ineffective unless they are absorbed into the skin. Percutaneous penetration varies among individual patients, and it can be manipulated by hydrating the skin, occlusive dressings, changing the drug, the vehicle, the length of exposure, or the anatomic surface area to which the drug is applied. It also depends on 14

Introduction

whether the skin is inflamed and therefore less of a barrier to penetration (e.g., eczematous skin). • The barrier to cutaneous penetration resides in the stratum corneum. The thicker the stratum corneum—as on the palms, soles, elbows, and knees—the more difficult it is for the topical agent to penetrate the skin. The ability to penetrate varies by anatomic site as follows: Mucous membranes Torso Extremities

Scrotum Eyelids Palms and soles

Face

• Because the stratum corneum serves as a “reservoir”—a storehouse of medication—it continues to release the topical steroid into the skin after application. Consequently, once-daily application is often sufficient to manage many inflammatory dermatoses. The following are methods of decreasing the epidermal barrier to penetration: • Soaking. Soaking an affected area in water before the application of a topical agent allows water to hydrate the stratum corneum and thus allows the topical steroid to penetrate more deeply into inflammatory foci. The wrinkling

that develops after a hand or foot is immersed in water for a prolonged period results from the skin’s increasing its surface area to accommodate the water it absorbs (FIG. I.1). • Smearing. After soaking, the application (“smearing”) of a topical steroid (particularly an ointment-based preparation) to wet skin traps the absorbed water, which cannot easily evaporate through the greasy, occlusive barrier. • Occlusion. A “nonbreathing” polyethylene wrap such as Saran Wrap or Handi-Wrap, held in place by tape, a bandage, a sock, or an elastic bandage, can provide occlusion to an area where topical steroids have been applied (FIG. I.2). The wrap may be left on while the patient sleeps or worn for several hours while the patient is awake. Specific areas may be occluded as follows: • A plastic shower cap can be used when the scalp is treated with a topical steroid. • Cordran tape, which is impregnated with the steroid flurandrenolide, is helpful for occlusive therapy when relatively small areas are treated. However, it is expensive and can be uncomfortable when it is removed from hairy areas. • Rubber or vinyl gloves or finger cots may be used for the hands and fingers. • Small plastic bags (e.g., Baggies) may be used for the feet. • Occlusive garments (“sauna suits”) can be worn when extensive areas are involved.

I.1 Hydration. These fingers have been immersed in water for a prolonged period to increase the penetration of a topical drug. The corrugated appearance is the result of water absorption.

SEE PATIENT HANDOUT, “Soak an d Sm ear In struct ion Sh eet” ON THE SOLUTION SITE

A Cre am , an Oin t m e n t , a Ge l, o r a Lo t io n ? • Creams are often preferred by patients for aesthetic reasons. However, their water content makes them more drying than ointments (oil-in-water preparations). • Generally, ointments are more potent than are creams or lotions, but their inherent greasiness often makes them cosmetically unacceptable. Ointments are helpful for dry skin conditions because of their occlusive properties. They are also more lubricating and tend to be less irritating and less sensitizing. • Lotions, gels, aerosols, foams, and solutions are useful on hairy areas. • They are easier than other preparations to apply to large areas but may cause stinging and/or drying.

I.2 Occlusion. A topical steroid cream has been applied, and a “nonbreathing” polyethylene wrap is used to cover it.

Introduction

15

Po t e n t ial Sid e Effe ct s Possible adverse reactions to topical steroids are as follows:

I.3 Skin atrophy. Inguinal striae. Linear atrophic scars may develop after repeated use of a potent topical steroid, particularly in an intertriginous (naturally occluded) area.

• Skin atrophy. Epidermal atrophy is a local reaction demonstrated by shiny, thinned skin and telangiectasias. It generally reverses when topical drugs are discontinued. Striae (linear atrophic scars) may occur after repeated use of a potent topical steroid in one area. These permanent scars are seen most often in intertriginous areas, such as the axillae and groin, where the skin is generally thin, moist, and naturally occluded (FIG. I.3). • Acneform eruptions of the face (FIG. I.4). Lesions resembling acne vulgaris, rosacea, and perioral dermatitis may result from the regular use of topical fluorinated steroids on the face. These eruptions manifest as persistent erythema, papules, pustules, and telangiectasia. The condition often flares once the steroid is withdrawn (“rebound rosacea”). • Tinea incognito, a superficial fungal infection. This condition may be misdiagnosed because its clinical signs may be obscured by the use of topical steroids, which reduce inflammation and itching without killing the fungus. Less common side effects include:

I.4 Perioral dermatitis resembling rosacea. This reaction was caused by long-term use of a potent fluorinated topical steroid.

16

Introduction

• Hypersensitivity reactions. Allergic contact dermatitis to the steroid molecule may occur and may easily be overlooked. The hypersensitivity can be evoked by the steroid, the vehicle, or both, and it is often not suspected clinically. A clue to its presence is a lack of the expected anti-inflammatory effect of the topical steroid. • Purpura. This condition may be noted after prolonged topical steroid use, particularly in elderly patients. • Other local effects. These include hypopigmentation, excess facial hair growth, and delayed wound healing. • Systemic effects, which may result from extensive use of and occlusion with potent topical steroids. Fortunately, these events rarely occur; in fact, hypothalamic-pituitaryadrenal axis suppression is quickly reversible and is unlikely to cause the same side effects as systemic steroid use. Infants, particularly those born prematurely, are more likely to have a greater risk of systemic side effects because of their increased body surface compared to body mass as well as their less efficient cutaneous permeability barriers.

POINTS TO REMEMBER TREATMENT NOTE • Many topical steroids are available. However, all agents in the same class have roughly the same potency; they differ primarily in vehicle and price.

HELPFUL HINTS • Large amounts of triamcinolone cream and ointment may be purchased in 240-g (1-lb) jars, at considerable savings. • Become familiar with only one or two agents from each potency class; that should be enough to treat most skin conditions that are responsive to topical steroids. • Prolonged application of combination topical antifungal/corticosteroid preparations such as Lotrisone and Mycolog II that contain potent topical steroids can result in striae, particularly when used in skinfold sites.

• Intertriginous areas such as the axillae, as well as inguinal creases, are physically occluded, so less potent preparations are used in these sites to avoid atrophy. • When treating children and the elderly, avoid the use of potent fluorinated compounds, when possible. • Soaking and occlusion increase penetration and potency; they also can make a low potency agent as strong—in efficacy and side effects—as a mid- to highpotency agent. • How much cream, ointment, or lotion should one apply? Application should be thin, not thick—a little works as well as a lot. • Higher potency steroids bring more rapid clearing and limit the overall exposure to the preparation. In contrast, prolonged application of low-potency agents takes much longer to produce comparable effects.

TOPICAL IMMUNOMODULATORS (CALCINEURIN INH IBITORS)* These topical nonsteroidals inhibit the activity of T-lymphocytes, which produce the cascade of cytokines that increase inflammation and thus have the potential to be “topical steroid-sparing agents.” They are approved only for the treatment of eczema and are best used in areas of high risk where skin thinning (atrophy) tends to occur—the face, eyelids, groin, and axillae, as well as the upper chest. Both Protopic and Elidel have been used as effective “off-label” treatments for the management of other dermatoses such as seborrheic dermatitis, oral lichen planus, inverse psoriasis, discoid lupus erythematosus, as well as various other dermatoses. • Protopic ointment in a 0.1% concentration has been approved for treatment in adults. A lower 0.03% concentration is designated for treatment in children. • Elidel cream (pimecrolimus) is available in a 1% formulation.

*The long-term safety of these two agents has been brought into question and has resulted in a “black box” warning by the Food and Drug Administration. Animal studies using high doses of these drugs have suggested an increased rate of malignancy; however, the risk of malignancy in humans has not been established. Currently, these drugs are indicated for short-term or intermittent treatment of atopic dermatitis and are considered as second-line therapy when conventional therapies are inadvisable, ineffective, or not tolerated. Introduction

17

TABLE I.1 TOPICAL STEROIDS (“THE SHORT LIST”) a CLASS/POTENCY

GENERIC NAME

BRAND NAMES

Class I: Superpotent

Clobetasol propionate cream/gel/ointment/ foam, lotion 0.05% Diflorasone diacetate ointment 0.05% Halobetasol propionate cream/ointment 0.05% Flurandrenolide

Temovate, Olux foam, Clobex lotion, spray, Cormax scalp solution Psorcon Ultravate Cordran tape (small roll, large roll)

Class II: Very high potency

Desoximetasone cream/ointment 0.25%, gel 0.05% Fluocinonide cream/ointment/solution/gel 0.05%

Topicort

Fluticasone ointment 0.005%

Cutivate

Class III: High potency

Lidex

Class IV: Medium-high potency Triamcinolone acetonide ointment 0.1% Hydrocortisone valerate ointment 0.2%

Kenalog Westcort

Class V: Medium potency

Hydrocortisone valerate cream 0.2% Triamcinolone acetonide cream 0.1% Desonide ointment 0.05%

Westcort Kenalog DesOwen

Class VI: Low potency

Desonide cream 0.05%

DesOwen

Class VII: Very low potency

Hydrocortisone cream/ointment/lotion 0.5%, 1.0%, 2.5%b

Hytone, Cortizone 10 and many other brands

a

Most preparations are available in tubes of 15, 30, or 60 g; lotions and solutions are available in bottles of 20 to 60 mL. Prescription 2.5% hydrocortisone is hardly more potent than 1% hydrocortisone. The agents listed should provide more than enough treatment options for the conditions discussed in this book.

b

TABLE I.2 CLASSIFICATION, STRENGTH, AND VEHICLE OF SOME COMMONLY USED TOPICAL CORTICOSTEROIDS (“THE LONG LIST”) GENERIC NAME Class I: Superpotent Betamethasone dipropionate gel/ointment/lotion 0.05% Clobetasol propionate cream/ointment/gel/lotion/foam 0.05%

BRAND NAME(S)

Diflorasone diacetate ointment/lotion/gel 0.05% Halobetasol propionate cream/ointment 0.05% Flurandrenolide Fluocinonide cream 0.1%

Diprolene Temovate, Olux foam, Clobex lotion, spray, Cormax scalp solution Psorcon Ultravate Cordran tape Vanos

Class II: Very high potency Amcinonide ointment 0.1% Betamethasone dipropionate ointment 0.05% Desoximetasone cream/ointment 0.25%/gel 0.05% Diflorasone diacetate cream 0.05% Betamethasone dipropionate cream 0.05% Fluocinonide cream/ointment/gel 0.05% Halcinonide cream/ointment/solution 0.1% Mometasone furoate ointment 0.1%

Cyclocort Diprosone Topicort Psorcon Diprolene AF Lidex Halog Elocon (continued)

18

Introduction

TABLE I.2 CLASSIFICATION, STRENGTH, AND VEHICLE OF SOME COMMONLY USED TOPICAL CORTICOSTEROIDS (“THE LONG LIST”) (Continued) GENERIC NAME

BRAND NAME

Class III: High potency Amcinonide cream/lotion 0.1% Betamethasone dipropionate cream/lotion 0.05% Betamethasone valerate ointment 0.1% Diflorasone diacetate cream 0.05% Fluticasone propionate ointment 0.005% Triamcinolone acetate ointment 0.1%, cream 0.5%

Cyclocort Diprosone Valisone Florone, Maxiflor Cutivate Aristocort A

Class IV: Medium-high potency Betamethasone valerate foam 0.12% Desoximetasone cream 0.05% Fluocinolone acetonide cream 0.2% Fluocinolone acetonide ointment 0.025% Hydrocortisone valerate ointment 0.2% Mometasone furoate cream 0.1% Triamcinolone acetonide ointment 0.1% Hydrocortisone probutate 0.1%

Luxiq Foam Topicort LP Synalar-HP Synalar Westcort Elocon Kenalog, Aristocort Pandel

Class V: Medium potency Betamethasone valerate cream/lotion 0.1% Desonide ointment 0.05% Fluticasone propionate 0.1% cream Fluocinolone acetonide cream 0.025% Flurandrenolide cream 0.05% Hydrocortisone butyrate cream/ointment/solution 0.1% Hydrocortisone valerate cream 0.2% Prednicarbate 0.1% Triamcinolone acetonide cream/lotion 0.1% Triamcinolone acetonide cream 0.025%

Valisone DesOwen, Tridesilon Cutivate Synalar, Synemol Cordran SP Locoid Westcort Dermatop-E Kenalog Aristocort

Class VI: Low potency Alclometasone dipropionate cream/ointment 0.05% Betamethasone 17-valerate lotion 0.1% Desonide cream/lotion 0.05% Desonide cream 0.05% Fluocinolone acetonide cream/solution 0.01% Fluocinolone acetonide 0.01% Mometasone furoate cream/ointment 0.1%

Aclovate Valisone DesOwen Tridesilon Synalar Capex shampoo, Derma-Smoothe Elocon

Class VII: Very low potency Hydrocortisone cream/ointment/lotion 0.5%, 1.0%, 2.5%

Hytone, Cortaid, Cortizone-10, Cortizone 5 Creme

Introduction

19

P ART O N E

Com m on Skin Con dition s: Diagn osis an d Man agem en t

C H AP T ER

Acne and Related Disorders

1 OVERVIEW Acne, the most common skin disorder in the United States, is an embarrassing problem for many teenagers, but it is not limited to that age group. It may develop before puberty in either sex, or it may first be seen in adults, particularly in women. Acne is a condition that involves the pilosebaceous apparatus of the skin. Acne vulgaris, or common acne (referred to herein as adolescent acne), begins in the teen or preteen years. In general, it becomes less active as adolescence ends but may continue into adulthood. Acne that initially occurs in adulthood is designated postadolescent acne or adult-onset acne. Despite the clinical similarities and occasional overlapping of adolescent and postadolescent acne, the pathogenesis and treatment of each are somewhat different. Acnelike disorders, such as neonatal acne, drug-induced acne, rosacea, and other so-called acneiform conditions, are also considered separate entities because of differences in pathogenesis. That being said, no clear lines separate the various types of acne; much of acne’s features overlap and lie along a continuum. However, readers may find the following classifications useful for diagnostic and therapeutic purposes.

CLASSIFICATION OF ACNE Adolescent Acne (Acne Vulga ris) • Preteen acne and adolescent acne, which m ay persist into adulthood Posta dolescent Acne • Fem ale adult-onset acne, acne excoriée des jeunes filles • Male adult-onset acne Acnelike Disorders • Rosacea • Perioral derm atitis • Neonatal acne • Drug-induced acne • Endocrinopathic acne • Physically induced and occupational acne • Folliculitis (see Chapter 5, “Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa”) • Hidradenitis suppurativa (see Chapter 5, “Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa”) • Pseudofolliculitis barbae (see Chapter 10, “Hair and Scalp Disorders Resulting in Hair Loss”) • Acne keloidalis (see Chapter 10, “Hair and Scalp Disorders Resulting in Hair Loss”)

23

Ad o lescen t Acn e BASICS ACNE MYTHS VERSUS FACTS Myt h : Blackheads are caused by dirt. Fact : They are black because of oxidized m elanin. Blackheads, or open com edones, are collections of sebum and keratin that form within follicular openings and that, when exposed to air, becom e oxidized and turn black. Myt h : Acne should disappear by the end of adolescence. Fact : Som e wom en have acne that persists well past adolescence. Others have an initial episode in their 20s or 30s. Myt h : Acne is caused or worsened by certain foods, such as chocolate, sweets, and greasy junk food. Fact : Despite occasional personal anecdotes and persistent cultural m yths, acne is probably not significantly influenced by diet. Myt h : A dirty face exacerbates acne; therefore, scrubbing the face daily helps clear it up. Fact : Scrubbing and rubbing a face that has acne, particularly inflam m atory acne, will only serve to irritate and redden an already inflam ed com plexion. Instead, the face should be washed daily with a gentle cleanser.

Teenage acne has a strong tendency to be hereditary and is less likely to be seen in Asians and dark-skinned people. Lesions begin during puberty when androgenic hormones cause abnormal follicular keratinization, which then blocks the sebaceous duct. This blockage results in a microcomedo (the microscopic primary lesion of adolescent acne). The microcomedo enlarges to become the visible comedo: the noninflammatory blackhead or whitehead. Alternatively, the microcomedo may become an inflammatory lesion, such as a papule or pustule. The development of inflammatory lesions theoretically occurs as follows: Androgenic hormones stimulate sebaceous glands to increase in size and function and thus to produce more sebum. The skin becomes oilier and the microcomedo becomes more hospitable to the anaerobe Propionibacterium acnes. Then P. acnes produces lipases that digest the lipids into fatty acids, causing a rupture of the microcomedo that incites an inflammatory cell response (ILLUS. 1.1–1.4) will be helpful.

Myt h : Frequent facials are beneficial. Fact : Professional facials and at-hom e scrubs, astringents, and m asks are generally not recom m ended because they tend to aggravate acne.

Oily skin

Androgen stimulation

Increased oil production Growth of sebaceous gland

I1.1 Androgenic stimulation. The sebaceous gland overreacts to androgen stimulation 24

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

Oily skin

Pore

Papule

Oil bottleneck

Bacteria White blood cell

A Enlarged sebaceous gland Oil trapped in hair canal

Pustule Bacteria

B I1.2 Follicular occlusion. Pores become clogged and the follicular canal narrows.

Nodule

Open comedo

C I1.4 Inflammatory acne. The microcomedo becomes an inflammatory papule (A), pustule (B), or nodule (C).

A Microcomedo

The canal swells Closed comedo

B I1.3 Comedogenesis. The microcomedo forms and becomes either an open (A) or closed comedo (B).

Chap ter 1 • Acne and Related Disorders

25

DESCRIPTION OF LESIONS Acne lesions are designated as inflammatory or noninflammatory (comedonal), or a combination of the two.

In flam m at o ry Le sio n s See FIGURES 1.1–1.3

1.1

Inflammatory acne. Papules.

• Papules: Superficial red “pimples” that may have crusted, scabbed surfaces caused by dried pustules or by picking or squeezing. • Pustules: Superficial raised lesions containing purulent material, generally found in the company of papules. • Macules: The remains of formerly palpable inflammatory lesions that are in the process of healing from therapy or spontaneous resolution. They are flat, red or sometimes purple (violaceous) blemishes that slowly heal and may occasionally form a depressed, atrophic scar. • “Acne cysts” (nodules): Large, deep papules or pustules. Acne “cysts” are not really cysts. True cysts are neoplasms that have an epithelial lining. Acne “cysts” do not have an epithelial lining; they are composed of poorly organized conglomerations of inflammatory material.

No n in flam m at o ry (Co m e d o n al) Le sio n s A comedo is a collection of sebum and keratin that forms within follicular ostia (pores) (FIG. 1.4). • Open comedones (blackheads) have large ostia that are black as a result of oxidized melanin. • Closed comedones (whiteheads) have small ostia. • Follicular prominence. These blackheadlike, dilated pores are frequently seen on the nose and cheeks in acne patients (FIG. 1.5).

A

Se ve rit y Acne may be further classified as mild, moderate, or severe.

B 1.2 A an d B Inflammatory acne. A: Papules and pustules. B: Macules. The same patient after 6 weeks of treatment. These reddish purple (violaceous) blemishes are frequently evidence of improvement following treatment.

26

• Mild acne consists of comedones and/or occasional papules and pustules. • Moderate acne is more inflammatory, with relatively superficial papules and/or pustules (papulopustular acne); comedones may also be present. Lesions may heal with scars. • Severe acne (“cystic” or nodular acne, acne conglobata) has a greater degree, depth, and number of inflammatory lesions: papules, pustules, nodules, “cysts,” and possibly abscesses. Sinus tracts, significant scarring, and keloid formation may also be evident (FIG. 1.6).

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

A

1.5 Follicular prominence. These blackheadlike, dilated ostia (pores) are frequently seen on the nose and cheeks in acne patients.

B 1.3 A an d B A: Inflammatory acne. Nodules. Severe “cystic” acne. B: The patient 6 months later after treatment with isotretinoin (Accutane).

1.6 Acne scars. Hypertrophic scars are seen on the shoulder of this patient.

1.4 Noninflammatory acne. Open and closed comedones, as well as inflammatory lesions are evident.

Chap ter 1 • Acne and Related Disorders

27

DISTRIBUTION OF LESIONS • Acne most commonly erupts in areas of maximal sebaceous gland activity: the face, neck, chest, shoulders, back, and upper arms. CLINICAL MANIFESTATIONS AND SEQUELAE

1.7 Severe, “cystic” acne. This patient’s severe acne shows early signs of significant scarring. Involvement of the chest and back predict that this patient will have a poorer prognosis and will be more difficult to treat.

• The more severe inflammatory lesions of acne are prone to heal with atrophic or pitted (“ice-pick”) scars on the face, and hypertrophic scars or keloids on the trunk (FIG. 1.7). • Postinflammatory hyperpigmentation may occur, particularly in patients with darker skin (FIG. 1.8). • The negative psychologic effects of acne (e.g., lowered selfesteem) and its impact on limiting employment opportunities and social functioning are among the overriding concerns of individuals who have moderate to severe acne. DIAGNOSIS • Adolescent acne is easy for both the patient and practitioner to recognize. • However, specific underlying causes of acne (e.g., hyperandrogenism ) should be considered in certain female patients (see following).

1.8 Postinflammatory hyperpigmentation. Resolving acne lesions often leave dark macules such as those seen in this African-American patient.

28

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

DIFFERENTIAL DIAGNOSIS

Ke rat o sis Pilaris (See Chapter 2, “Eczema, Atopic Dermatitis.” • Keratosis pilaris consists of small, follicular, horny spines. The tiny papules may resemble acne when they are inflamed. • The lesions of keratosis pilaris are most often seen on upper outer arms (FIG. 1.9), back, thighs, and lateral face.

1.9 Keratosis pilaris. Acnelike papules located in a typical location.

MANAGEMENT

Go als The three main therapeutic goals are: • To prevent scarring • To help improve the patient’s appearance • To make every effort to control acne with topical therapy alone Ge n e ral Prin cip le s • Treatment of acne should be individualized and frequently involves a trial-and-error approach that begins with those agents that are known to be most effective, least expensive, and have the fewest side effects. • Acne is a multifactorial disease; therefore, appropriate therapy often involves the use of more than one agent, each of which targets a different pathogenic factor. • Mild acne can often be managed successfully with overthe-counter (OTC) remedies. • Oral medications should be tapered as soon as control is achieved.

• In children, the lateral sides of the cheeks are frequently involved. These findings are commonly mistaken for acne (FIG. 1.10).

Fo lliculit is See Chapter 5, “Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa.” Ro sace a an d Pe rio ral De rm at it is See the following section for discussion of these conditions.

1.10 Keratosis pilaris. Often mistaken for acne, these rough-textured acnelike lesions are noted on the lateral face of this child.

• A patient should be advised not to squeeze or pick lesions.

To p ical Th e rap ie s Notwithstanding the testimonials seen on late-night television infomercials for acne preparations, no “one size fits all” treatment for acne exists. In fact, the active ingredients in these advertised preparations can be obtained less expensively in many OTC products. Ben zo yl Pero x id e

See TABLE 1.1. • In addition to being potent antibacterial agents, benzoyl peroxide preparations improve both inflammatory and noninflammatory lesions (comedones). • They dry and peel the skin, and they help clear blocked follicles. • Benzoyl peroxide may be used alone to treat mild acne, but for more severe cases, it should be used in conjunction with topical retinoids, as well as topical or systemic antibiotics. continued on page 30

Chap ter 1 • Acne and Related Disorders

29

MANAGEMENT Continued

Tab le 1.1 BENZOYL PEROXIDE– CONTAINING PREPARATIONS OVER-THE-COUNTER PREPARATIONS Oxy-5, Oxy-10 Clear by Design Clearasil 10%

5%, 10% benzoyl peroxide 2.5% benzoyl peroxide gel 10% benzoyl peroxide lotion

PRESCRIPTION FORMULATIONS Desquam-Xerosis

5%, 10% benzoyl peroxide gel (water based) 2.5%, 5%, 10% benzoyl peroxide gel (water based) 4%, 8% benzoyl peroxide gel (water based) 3%, 6%, 10% benzoyl peroxide gel (water based)

Desquam-E Bevoxyl Triaz pads

• Benzoyl peroxide is an ingredient of many brand-name OTC products, such as Clearasil, Oxy 5, and Oxy 10, as well as less expensive generics. It is available in waterand alcohol-based vehicles, soaps, medicated pads, and washes. • Lower-strength (e.g., 2.5%) preparations are less irritating and probably as effective as the 5% and 10% concentrations. • The addition of zinc to benzoyl peroxide in several newer products, such as Triaz, may enhance efficacy. • Benzoyl peroxide is also available in combination with erythromycin (Benzamycin) and clindamycin (BenzaClin and Duac). How to Use Benzoyl Peroxide

• Beginning with a lower strength preparation, benzoyl peroxide is applied sparingly once or twice daily, in a thin layer on acne-prone areas. • Irritation and burning are not uncommon but usually resolve in 2 to 3 weeks.

ADVANTAGES

DISADVANTAGES

To p ica l Ret in o id s

Available over the counter No reported bacterial resistance Available in many formulations, including cream and liquid (waterbased gels less irritating than alcohol-based preparations)

Often irritating (causes stinging, redness, and scaling) Contact sensitivity may occasionally occur May bleach clothing and bed linen

See TABLE 1.2. • Topical retinoids are primarily comedolytic (i.e., they treat comedones); they also have potent anti-inflammatory effects. • In addition, retinoids facilitate the penetration of, and may be used in combination with, other topical antiacne agents such as benzoyl peroxide. • These agents help “plump up” the skin and make enlarged pores (follicular prominence) less obvious. • All retinoids may produce sun sensitivity. • They should not be used during pregnancy or breastfeeding (although no studies have shown them to be harmful to the fetus).

Tab le 1.2 TOPICAL RETINOIDS BRAND NAME

GENERIC NAME

ADVANTAGES/ DISADVANTAGES

Retin-A cream, gel

Tretinoin

Retin-A Micro topical gel Avita cream, gel

Tretinoin

Available in various strengths and less expensive generic formulations Often irritating Less irritating than other forms of Retin-A Less irritating than Retin-A One strength Less irritating than Retin-A; causes less sun sensitivity than Retin-A One strength Possibly more effective and faster acting than Retin-A; two strengths Irritating; expensive

Tretinoin

Differin cream, gel, solution, pledgets

Adapalene

Tazorac dream, gel

Tazarotene

STRENGTHS

SIZES

Creams: 0.025%, 0.05%, 0.1% Gels: 0.01%, 0.025% 0.04%, 0.1%

20, 45 g

0.025%

20, 45 g, 50-g pump dispenser 20, 45 g

0.1%, 0.3%

15, 45 g 30 ml, #60

0.05%, 0.1%

30, 100 g

continued on page 31

30

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

MANAGEMENT Continued

Tab le 1.3 TOPICAL ANTIBIOTICSa BRAND NAME

GENERIC NAME

ADVANTAGES/DISADVANTAGES

SIZES

A/T/S solution, gel

Erythromycin 2%

60 ml, 30 g

Akne-Mycin ointment

Erythromycin 2%

Cleocin T solution, gel, lotion

Clindamycin 1%

Evoclin foam Theramycin Z

Clindamycin 1% Erythromycin 2%/ zinc acetate Clindamycin 1.2%/ tretinoin 0.25% gel

Effective for postadolescent acne, rosacea; irritation is infrequent Often used in conjunction with benzoyl peroxide and/or retinoids Least irritating topical antibiotic; excellent for atopic skin Somewhat messy to apply Effective for postadolescent acne, rosacea Lotion is less irritating than solution and gel Easy to apply to large and hairy areas Contains zinc

Ziana

a

New combination drug

25 g

30, 60 ml 50, 100 g 50, 100 g 60 ml 30, 60 g

Bacterial resistance is possible with all of these agents.

How To Use Topical Retinoids

• Topical retinoids are applied once daily, usually at bedtime. • Beginning with lower-strength preparations, such as tretinoin 0.025%, adapalene cream 0.1%, or tazarotene cream 0.05%, they are applied sparingly in a thin layer over the acne-prone areas. In time, higher concentrations can be applied. • Patients who exhibit sensitivity may use it every other day, or less frequently, until they develop a tolerance to it. • The area of application should first be washed and thoroughly dried. • Side effects may include erythema, dryness, and peeling. These usually resolve after 3 weeks. • Use of a sunscreen should be advised, because tretinoin and adapalene may cause photosensitivity in some patients.

• In addition to their antibacterial action, these drugs have an anti-inflammatory action that helps clear inflammatory acne lesions (papules and pustules). • Topical clindamycin and erythromycin are considered equally effective. • Drug resistance has been reported with these antibiotics. How To Use Topical Antibiotics

• These agents are applied once or twice daily, in a thin layer across the acne-prone areas. • Irritation and burning are uncommon and may be avoided by using an ointment-based erythromycin such as AkneMycin or clindamycin (Cleocin) in a lotion preparation. • Topical antibiotics are available in a variety of vehicles, including creams, lotions, ointments, gels, and solutions.

To p ica l An t ib io t ics

Co m b in a t io n o f To p ica l An t ib io t ic a n d Ben zo yl Pero x id e

See TABLE 1.3.

See TABLE 1.4.

• Preparations that contain the topical antibiotics clindamycin and erythromycin are active against P. acnes.

• Benzamycin, BenzaClin, and Duac gels are the most commonly prescribed formulations.

Tab le 1.4 COMBINATION TOPICAL ANTIBIOTIC AND BENZOYL PEROXIDE AGENTSa

a

BRAND NAME GENERIC NAME

ADVANTAGES/DISADVANTAGES

SIZES

Benzamycin gel

Erythromycin 3%/benzoyl peroxide 5%

23.3, 46.6 g

BenzaClin gel Duac gel

Clindamycin 1%/benzoyl peroxide 5% Clindamycin 1%/benzoyl peroxide 5%

Less expensive than comparable products Refrigeration necessary No refrigeration necessary; 50-g pump dispenser No refrigeration necessary

25, 50 g 45 g

No bacterial resistance is reported with these agents. continued on page 32

Chap ter 1 • Acne and Related Disorders

31

MANAGEMENT Continued • The combination of erythromycin and clindamycin with benzoyl peroxide helps prevent bacterial resistance furthermore, there appears to be a synergistic effect (the combination appears to be more effective than either drug used alone) when clindamycin and erythromycin are combined with benzoyl peroxide. How To Use Com bination of Topical Antibiotics and Benzoyl Peroxide

• These agents are applied sparingly once daily to acneprone areas. • The same cautions apply as for benzoyl peroxide. Dryness, erythema, and pruritus are the most common side effects. Alt er n a t ive To p ica l Prescrip t io n Dr u gs

• These include azelaic acid (Azelex 20%), as well as older preparations that contain sulfur and sodium sulfacetamide such as Sulfacet-R lotion, Novacet lotion, and Klaron lotion. • These medications are used as alternatives or adjuncts to retinoids, benzoyl peroxide, and topical clindamycin and erythromycin. They are second-line therapy for acne and are also used in the treatment of rosacea (see following). To p ica l No n p rescrip t io n Agen t s Alpha- and Beta-Hydroxy Acids

• Many OTC products contain ingredients that have been used for acne for many generations without great success. • However, for children just beginning to develop acne or for patients with very mild acne, gentle topical peeling agents such as salicylic acid or glycolic acid, or antiinflammatory agents that contain resorcinol or sulfur, may be helpful.

to topical therapy. Furthermore, significant acne on the chest and back often requires systemic therapy because truncal acne does not respond to topical therapy as readily as does facial acne. In comparison with topical therapy, systemic therapy has a more rapid onset of improvement, which may enhance patient compliance. However, whenever systemic drugs are administered, the potential dangers—including side effects, drug allergy/intolerance, drug interactions, and fetal exposure in women who are or may become pregnant—must be carefully considered. A risk-benefit calculation is particularly important whenever treating a benign condition, such as acne. Systemic agents for acne include the following: • Oral antibiotics, most often tetracycline derivatives, are prescribed. • The oral retinoid 13-cis-retinoic acid (Accutane) is reserved for more severe, recalcitrant disease. • In female patients, hormonal agents, such as oral contraceptives, and antiandrogenic drugs, such as spironolactone, may be prescribed in carefully selected situations.

Oral An t ib io t ics See TABLE 1.6 at end of chapter Tet ra cyclin es

The tetracycline derivatives are the mainstay of oral acne therapy. They are the first-line antibiotic drugs of choice in the management of moderate to severe acne. As with the topical antibiotics, tetracycline derivatives inhibit the growth of P. acnes, which decreases free fatty acid production and pustule formation. In addition, they have a significant anti-inflammatory action as a result of their inhibition of the chemotactic response of neutrophils.

Multiingredient and Other Over-the-Counter Products

• Numerous products contain various combinations of resorcinol, aloe, glycolic acid, sulfur, and salicylic acid. • Herbal remedies that contain aloe and benzoyl peroxide are available. • Such products are difficult to evaluate clinically. Retinols

• Although retinols were originally marketed to fight aging skin, they are currently being touted for use in treating acne. • Their efficacy in acne has not been scientifically tested.

Syst e m ic Th e rap ie s Patients who have moderate to severe acne that is unresponsive to topical treatment alone, or acne that tends to scar, are generally prescribed systemic therapy, in addition

Side Effects

• The use of any of the tetracyclines during a child’s tooth development (before 10 years of age) may cause a permanent discoloration of the teeth. • There are risks to the teeth and bones of unborn fetuses and nursing children. • Tetracyclines may temporarily stain the teeth of older patients, particularly those with orthodontic braces. While taking any one of the tetracyclines, a patient should be advised to practice good dental hygiene, including flossing. These drugs may also cause gastrointestinal irritation, phototoxic reactions, and candidal vulvovaginitis. • In addition, the tetracyclines have been implicated in the development of benign intracranial hypertension continued on page 33

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MANAGEMENT Continued (pseudotumor cerebri), particularly when taken concurrently with isotretinoin (Accutane).

Te t racyclin e s: An o t h e r Co n ce rn Because patients frequently take tetracyclines on a longterm basis (in some instances for years), there is understandably a concern about their consequences. Studies have indicated that routine laboratory supervision of healthy young people receiving long-term tetracycline therapy is not necessary. However, when treatment extends for more than 1 to 2 years, some dermatologists recommend periodically monitoring via appropriate blood tests. This is particularly important if the patient has a history of liver, kidney, or autoimmune disease.

drome that is antinuclear antibody positive. This syndrome, which occurs most often in young women, usually develops late in the course of therapy. The symptoms consist of swollen glands, rash, fever, and joint pains and generally disappear following discontinuation of the drug.

An extended-release formulation of minocycline tablets, Solodyn, is available and prescribed in a weight-based dosage of 1 mg/kg daily. The tablets are supplied in 45-, 90-, and 135-mg strengths (see TABLE 1.5). It has been shown to have anti-inflammatory effects without acting on P acnes, the bacteria involved in causing acne. This approach is intended to prevent bacterial resistance.

Plain Tetracycline

Doxycycline

• Tetracycline is given in dosages ranging from 250 to 500 mg twice a day. • The dosage may be tapered as inflammatory lesions diminish (usually after 6 to 8 weeks), but this will vary depending on an individual patient’s response. • Tetracycline is taken on an empty stomach (1 hour before or 2 hours after a meal). • Esophageal irritation may be avoided by taking the drug with a full glass of water. • Dairy products such as milk or divalent cations that contain iron, magnesium, zinc, or calcium may interfere with tetracycline’s absorption from the stomach. Therefore, the drug should not be taken with these compounds.

• Doxycycline is given in doses ranging from 50 mg twice a day, 75 mg once or twice a day, or 100 mg once or twice a day. • Doxycycline is absorbed well and may be taken with food. • Its main disadvantage is its phototoxic potential—the highest of the tetracyclines. Patients should be advised regarding sun protection. • Vestibular dysfunction, hyperpigmentation, and the lupuslike syndrome associated with minocycline have not been reported. • Benign intracranial hypertension may occur.

Minocycline

• Doses are 50 mg twice a day, 75 mg once or twice a day, or 100 mg once or twice a day. • Minocycline is more expensive but more effective than plain tetracycline for treating inflammatory acne. • The drug’s excellent absorption allows it to be taken with food. • It causes few, if any, phototoxic problems. • Minocycline appears to be less likely to induce candidal vulvovaginitis than plain tetracycline. However, it is more likely to cause such side effects as nausea, vomiting, and, in high doses (those that approach 200 mg/day), dizziness owing to vestibular dysfunction. The dizziness usually diminishes after a few days or when the dosage is lowered. • Less commonly, long-term treatment may cause a reversible bluish hyperpigmentation of the gums and/or skin. • In rare cases, minocycline is associated with benign intracranial hypertension, hepatitis, and a lupuslike syn-

Seco n d -Lin e Ora l An t ib io t ics Erythrom ycin

• Erythromycin derivatives may be useful as second-line alternative when a tetracycline fails or is not tolerated, or when the patient is younger than 10 years of age or pregnant. • Erythromycin is generally less effective than tetracycline. • Gastrointestinal upset is common. An enterically coated erythromycin product such as E-Mycin is less likely to cause gastrointestinal symptoms. • Multiple drug interactions may occur (e.g., erythromycin may elevate digoxin, theophylline, and cyclosporine levels). Reports of P acnes resistance to erythromycin, which may be the cause of some treatment failures, are also increasing. • As with the tetracyclines, candidal vulvovaginitis may occur. Am oxicillin

• This penicillin derivative is another safer alternative to a tetracycline that can be used during pregnancy. continued on page 34

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MANAGEMENT Continued Azithrom ycin (Zithrom ax)

• The use of azithromycin in a 4- or 5-day pulse therapy regimen has recently gained some interest. Pulse (also called intermittent) therapy refers to taking the drug for several days per week or for 1 week per month, discontinuing it, and then starting it again. For example, the drug could be taken for just 1 week prior to premenstrual flares. Pulsing routines have been suggested to reduce the cost of this expensive drug. • Azithromycin has no serious side effects; however, as with all of the antibiotics, buildup of bacterial resistance is a concern. Clindam ycin

• Clindamycin is a very effective antibiotic; however, its resistance pattern is similar to that of erythromycin. • Clindamycin also has the potential serious side effect of pseudomembranous colitis.

severe nodular acne who are unresponsive to conventional therapy. The original brand names for oral isotretinoin were Accutane in the United States and Roaccutane in rest of the world. In addition to Accutane and Roaccutane, the drug is now sold under several generic brand names in the United States, including Amnesteem, Claravis, and Sotret Isotretinoin treats acne by: • Dramatically reducing the size and output of sebaceous glands. It limits the amount of sebum and thus the food supply of P. acnes. • Shedding dead skin cells more normally (stabilizes keratinization), the process through which keratinocytes (epidermal cells) produce the protein keratin. Consequently, the keratinocytes are less likely to clog pores (comedogenesis).

Isotretinoin can cause severe birth defects if taken by a pregnant woman or a woman who becomes pregnant while taking the drug, even for a short time. Teratogenic birth defects include skull abnormalities, heart defects, deafness, cleft palate, and central nervous system defects. Because the drug remains in the body for a long time, it can cause birth defects for 1 month after a woman has stopped taking it. It also carries an increased risk of miscarriage when used during pregnancy or up to 1 month prior to pregnancy.

Cephalosporins

The new-generation cephalosporin antibiotics appear to have good efficacy against acne. Again, bacterial resistance is a concern.

Trim e t h o p rim -Sulfam e t h o xazo le • Oral sulfonamides such as trimethoprim-sulfamethoxazole (TMZ) are very effective as antiacne agents. They are reserved for unusually stubborn cases of severe acne that do not respond to any of the other antibiotics listed here. They are sometimes used in situations in which oral isotretinoin (Accutane) is not indicated. • TMZ has been associated with severe side effects and may precipitate severe allergic reactions. • The development of resistance is also an issue. Ho rm o n al Tre at m e n t Oral contraceptives or systemic antiandrogens (such as spironolactone) are used in women in whom hormonal treatment may be an effective alternative or adjuvant to antibiotics and oral retinoids. Hormonal treatment is an option when conventional topical and systemic therapies are ineffective or when an endocrine abnormality is discovered. (For a more detailed discussion, see the next section; see also Chapter 11, “Hirsutism.”) Oral Re t in o id s (Accut an e ) Commonly referred to as Accutane, isotretinoin (13cis-retinoic acid) is an oral synthetic derivative of vitamin A that promotes long-term remissions in severe acne. The efficacy of isotretinoin in patients with previously unresponsive acne is often profound and long lasting. This powerful drug is reserved for patients with

Do sa ge

Oral isotretinoin is available as capsules in strengths of 10, 20, 30, and 40 mg. It is generally taken for 20 weeks; in Europe, the drug is given until a total dosage of 120 to 140 mg/kg is reached. Many prescribers require that women use oral contraceptives before starting treatment, during treatment, and for 1 month after isotretinoin treatment is completed. Sid e Effect s General

• Isotretinoin’s ability to shut down the oil production in the body accounts for some of its less serious side effects, such as cheilitis, conjunctivitis, dry skin, nose-bleeds, dry eyes, increased sensitivity to the sun, and itching. In general, these reactions are well tolerated because the drug is so effective that patients want to continue taking it despite any side effects. • Less commonly, a patient experiences musculoskeletal and joint pains. • Some patients have reported thinning hair during treatment. Rarely has this been a persistent or a permanent continued on page 35

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MANAGEMENT Continued problem—the hair generally grows back when treatment is discontinued. • Allergic reactions, decreased night vision, persistent headaches, benign intracranial hypertension, and hearing impairments, are rare findings. Skeletal hyperostosis is limited to those who take a high dosage, one much higher than is used to treat acne, and those undergoing longterm isoretinoin therapy. • Approximately 25% of patients experience serum triglyceride elevations, and 15% experience decreases in high-density lipoprotein levels. • Studies performed in men taking isotretinoin showed no significant effects on their sperm and no long-term damage to a man’s ability to have healthy children. Depression and Suicide

• Depression is unfortunately a common problem in the age group that needs isotretinoin most frequently— adolescents. Acne appears most often in patients between 12 and 24 years of age. The onset of depression also commonly occurs at about the same time. • In the United States, the Food and Drug Administration (FDA) has received reports of depression and suicide in patients who take isotretinoin, and there is concern about a possible link between the drug, psychiatric disorders and suicide. • Emotional problems in the adolescent population coupled with the stress of having severe acne makes it difficult to determine whether isotretinoin can trigger depression and suicide or whether successful treatment may thwart such problems. Because suicide is a major cause of death in teenagers, particularly in boys, it has been difficult to determine a causal relationship between isotretinoin and these events, and there is a great need for further study.

If a patient taking isotretinoin is showing signs of moodiness, depression, or psychosis, the drug should be discontinued!

The iPLEDGE Program

Isotretinoin’s toxicity during pregnancy has long been known, but past efforts to reduce birth defects, including stricter product labeling and a limited pregnancy testing system, failed to resolve the problem. Therefore, in 2005, the FDA established an isotretinoin federal registry program called iPLEDGE. The registry keeps tabs on all isotretinoin prescriptions in the United States. Manufacturers, wholesalers, pharmacists, prescribers, and patients are linked

through a centralized computer registry. The registry also connects to the laboratories that perform the required pregnancy testing in this system.

Procedures All iPLEDGE Patients Must Follow

Everyone in the United States who is prescribed the isotretinoin must register with iPLEDGE. After registration, a female patient of child-bearing potential must receive ongoing counseling and pregnancy testing each month while taking the drug. All patients, male or female, are allowed only a 30-day supply of isotretinoin at each office visit. These prescriptions are only valid for seven days after they are prescribed (unless the patient is a man or a woman who is unable to become pregnant).

Ot h e r Th e rap e ut ic Mo d alit ie s Co m ed o Ex t ra ct io n (Acn e Su rger y)

• This has been performed less commonly since the topical retinoids have become available. • Comedones may be removed more easily if the patient is pre-treated with a topical retinoid for 3 to 4 weeks before comedo removal. In t ra lesio n a l Co rt ico st ero id In ject io n

• Intralesional injections of glucocorticosteroids, introduced with a syringe and a 30-guage needle, can reduce the inflammatory response and decrease the size of nodular inflammatory lesions. • The recommended dose of a triamcinolone acetate suspension is given in a concentration of 2.5 mg/mL to avoid local steroid atrophy. For patients with severe disease and considerable scarring, the concentration can be increased to 5 or 10 mg/mL. • If too strong a concentration of cortisone is used, atrophy, or depressed scars, may result at the injected sites. These atrophic “dents” usually resolve after several months, but they can be permanent. Similar atrophy may also have been the “normal” healing response of the inflamed lesion if it had not been injected. La sers, Ligh t s, a n d Ot h er New er Tech n o lo gies

Because of the concerns over the safety of isotretinoin, hormones, and long-term antibiotic use in the treatment of acne, lasers and other newer technologies will probably play an ever-larger role as future therapies for acne. Laser and light therapies offer a promising, noninvasive treatment alternative. They have shown evidence of continued on page 36

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35

MANAGEMENT Continued improving not only inflammatory acne but also acne scarring. Laser and light therapy seem to be most helpful when used in combination with traditional acne medication treatments. Potential acne treatments currently under consideration include: • Photodynamic therapy (PDT): This involves applying a solution of a photosensitizing agent, aminolevulinic acid (ALA), to the skin. The ALA accumulates in target cells— the sebaceous glands. The skin is then exposed to a highintensity light source. Light sources used in PDT include visible (nonlaser) or laser light. The P. acnes that reside in sebaceous glands produce porphyrins as a by-product of their metabolism. The light activates these porphyrins and thus kills the bacterial cells. • Intense pulsed light (IPL): These devices are similar to lasers, but they use a wider range of wavelengths as opposed to only a single beam of light. These wavelengths can be customized to reach the specific targets such as blood vessels and sebaceous glands. • Pulsed dye laser (PDL): Results for acne have so far been inconsistent. This laser is “tuned” to a specific wavelength of light. It produces a bright light that is

absorbed by blood vessels. This laser is also being used to improve the appearance of acne scars and is effective in removing the enlarged blood vessels associated with rosacea. • Pulsed light and heat energy (LHE) therapy: This treatment combines pulses of light and heat, which may target both P. acnes and sebaceous glands. • Diode laser: This laser uses infrared frequencies that are longer, invisible wavelengths. It appears to be effective not only on acne but on the acne scars as well. Offi ce-Ba sed Ch em ica l Peels

• Chemical peels have become popular as antiaging facial rejuvenation procedures; however, they are sometimes used to treat acne as well. In this procedure, a chemical acid solution is applied to the skin, causing the skin to peel off so that new skin can regenerate. • Chemical peels are probably not effective for the treatment of inflammatory lesions of acne. They seem to work best in the elimination of comedonal acne. • Deeper peels, with stronger concentrations of acids, are sometimes used to treat acne scars. • The two most commonly used chemicals for peels are the alpha-hydroxy acids and the beta-hydroxy acids.

POINTS TO REMEMBER • The patient should be informed that a significant therapeutic response may require 6 to 8 weeks. • Every effort should be made to try tapering oral medications as soon as acne is controlled. • If there is evidence of scarring, acne should be treated more aggressively (even mild acne can heal with significant scarring). • The two Hs—hormones and heredity—underlie teenage acne (one or both parents probably had acne), and not the proverbial poor diet and dirty face (the two Ds). A minority of dermatologists believe that there is a connection between certain dairy products and acne. • In the treatment of females of childbearing potential, isotretinoin should be used only for patients with severe, disfiguring, cystic acne.

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Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

HELPFUL HINTS • Compliance is often a problem for teenagers, who are notoriously poor at dealing with delayed gratification, so it is quite important to clearly explain the treatment regimen, make it simple, and give written instructions. The teenager—or more likely the parent— should be advised to call the health care provider with any questions or concerns. • Because topical retinoids may appear to make acne worse, BenzaClin, Duac, or Benzamycin gel may be used first with inflammatory lesions. Such lesions are usually the first to respond, and thus their quick disappearance can be helpful in obtaining compliance in teenagers. • For those patients who experience irritation and excessive dryness, topical retinoids may be applied for 2 to 3 minutes and then washed off. This short-contact treatment appears to work quite well and helps avoid irritation. The time of application can be gradually increased as tolerated. • “Rollercoasting” (i.e., titrating or fine-tuning the dosage of oral antibiotics such as tetracycline, minocycline, and doxycycline) may help minimize potential side effects such as vertigo and the total dosage of the medication. For example, a dosage schedule can begin as 50-mg minocycline capsules—two in the morning and one in the afternoon. This method may also lessen the total dosage, and help lower the cost of the medication. (In addition, because the highest recommended dosage is 200 mg per day, this dosage allows for a possible increase of an additional 50 mg per day after the patient’s next follow-up visit. However, if the acne shows marked improvement, the dosage can be lowered—to perhaps, 50 mg twice a day.) • For patients who experience premenstrual flares of acne, increasing the dosage 5 to 7 days before the next menstrual period and then lowering the dosage afterward can help reduce the amount of drug used.

FURTHER ACNE FACTS • In m ost people, acne tends to im prove tem porarily during the sum m er m onths. Exposure to the sun in sm all doses dim inishes acne, and tanning prom otes a blending of skin tones. • Fall and winter acne flareups are quite com m on and are often influenced by m ood swings. • Som e wom en m ay note im provem ent of acne during pregnancy or while taking birth control pills. Others m ay note a worsening of acne or no change at all. • Moderate to severe involvem ent of the chest and back predict that the patient will have a poorer prognosis and will be m ore difficult to treat. Severe, unrem itting, scarring acne is m ore prevalent am ong m en. • Because acne is a visible disease, acne patients m ay suffer from im paired self-im age, depression, anxiety, em ploym ent insecurities, social withdrawal, self-destructive behaviors, and even suicidal ideation. • Acne, hirsutism , and irregular periods m ay be associated with hyperandrogenism and/ or polycystic ovaries. • Som e drugs, including system ic steroids, lithium , epilepsy agents, and antituberculosis m edicines, can cause or exacerbate acne. • Stress seem s to worsen acne. College students at exam ination tim e, teenagers about to go to the prom , or som eone going for a first job interview often provide testim ony to this phenom enon. The question is: are these individuals sim ply m ore aware of the appearance of their skin at these critical tim es, or is the acne actually worse at these tim es because of stress? It is proposed that the release of excess am ounts of glucocorticoids and a resulting increase in sebaceous gland activity account for this worsening of acne. • In darkly pigm ented people, the severity of inflam m ation m ay be equivalent to that in fairer-skinned people, but it m ay not be as apparent. Consequently, African-Am erican patients are often as concerned about the acne-related pigm entary changes as they are about the acne itself.

SEE PATIENT HANDOUTS, “Acne: How to Ap p ly Topical Retinoid s” AND “Acne: How to Ap p ly: Duac Gel, BenzaClin Gel, Benzam ycin Gel” ON THE SOLUTION SITE

Chap ter 1 • Acne and Related Disorders

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Po st a d o lescen t Acn e

(Ad u lt -On set Acn e)

BASICS Dermatologists regularly hear the lament “acne, at my age!” expressed by women in whom acne suddenly appears or in whom acne has not resolved by 20 years of age. Adult-onset acne is overwhelmingly a condition of women. In fact, women often develop acne in their 20s and early 30s, sometimes for the first time in their lives. Although frustrating for those women who were spared acne during adolescence, adult-onset acne is often even more upsetting for those who had teenage acne and “grew out of it” only to discover the return of pimples when they reach 32 years of age. Some women continue to have acne into their 40s and 50s. In some cases, teenage acne that persists into adulthood is complicated by the appearance of adult-onset acne. The prevalence of female adult acne has increased significantly in the past several generations. Proposed hypotheses to explain this apparent increase include: • The entry of women into the workforce and its attendant stresses • The use of low-estrogen containing oral contraceptives • The proliferation of food additives and the injection of hormones and antibiotics into livestock • The increased use of cosmetics There is little question that acne is influenced by hormones. For example, many women report premenstrual or

38

(less commonly) midcycle flares of inflammatory acne. Pregnancy, oral contraceptives, and hormonal supplementation also appear to affect a woman’s complexion and cause fluctuations in acne. “Acne cosmetica” is the traditional name for acne that is supposedly caused by cosmetics. Indeed, some reactions to cosmetics can sometimes look like inflammatory acne; however, such “acne” is often the result of an irritating skin reaction. Acne with an onset in adult males has traditionally been an unusual finding; however, it has been seen increasingly in men and some women who participate in athletic activities. The reason for the recent increased prevalence of this type of acne is unknown. Causes are speculated to be one or all of the following: sweating, mechanical friction, anabolic steroids, and creatine-containing dietary body-building supplements. DESCRIPTION OF LESIONS Unless preexisting adolescent acne is a concurrent problem: • Postadolescent acne is relatively free of comedones and consists of evanescent, inflammatory red papules and/or pustules. • The lesions more closely resemble those seen in rosacea or perioral dermatitis. • In general, lesions tend to be few in number.

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

DISTRIBUTION OF LESIONS • In women, lesions occur on the face, most often in the perioral area, along the jawline, or on the chin—the lower part of the face. Also, the hairline, neck, and upper trunk may also be affected. The acne in this location is probably caused by an increase in the response of hair follicles to male hormones (androgen receptor sensitivity) (FIG. 1.11). • In men who develop adult-onset acne, lesions tend to be limited to the trunk. CLINICAL MANIFESTATIONS • Lesions tend to appear and reappear like clockwork according to a woman’s fluctuating levels of circulating hormones. They are more likely to recur premenstrually or at ovulation. They last for several days; sometimes they persist for a month or longer. In some women, lesions occur without any pattern. • No such fluctuation occurs in men. DIAGNOSIS • The diagnosis is made clinically. • However, in female patients whose acne is not responding to treatment, or for those who have other signs of hormonal excess such as male characteristics (e.g., facial hair) or irregular menstrual periods, hormonal tests are indicated. More often than not, these levels are normal, and it appears that these women may have an end-organ hypersensitivity to their endogenous androgens.

MANAGEMENT

To p ical Tre at m e n t • Skin care should be kept simple and gentle with the use of mild soaps. • Postadolescent acne in female patients may be treated with many of the same agents used for adolescent acne; however, treating adults who have acne can be more challenging because aging skin is often more sensitive than teenage skin and sometimes cannot tolerate the potentially drying, irritating effects of some topical acne medications. Syst e m ic Tre at m e n t Ora l An t ib io t ics

For more information on treatment of postadolescent acne with oral antibiotics, see the earlier discussion in TABLE 1.5. H o rm o n a l Trea t m en t

Indications include: • Normal serum androgens and intractable acne

1.11 Postadolescent acne. Characteristic location of erythematous acne papules along the jawline in a female adult .

DIFFERENTIAL DIAGNOSIS

Ro sace a an d Pe rio ral De rm at it is See also the following sections. • These conditions are seen primarily in adults. • They most often occur on the central third of the face (rosacea) or perioral area (perioral dermatitis). • In older women, and in some men, rosacea and acne often appear simultaneously, and there are no comedones.

• Ovarian or adrenal excess • An alternative to oral isotretinoin or antibiotics; in women of childbearing potential, oral contraceptives are often taken during a course of oral isotretinoin. • Relapse after taking a course of oral isotretinoin Ora l Co n t ra cep t ives

By suppressing gonadotropins, reducing ovarian androgen secretion, and increasing sex hormone–binding globulin levels, oral contraceptives decrease serum testosterone concentrations. Besides suppressing ovulation, the estrogens in birth control pills can help improve acne by blocking the androgenic stimulation of sebaceous glands by acting as androgen receptor blockers. Oral contraceptives such as Yasmin and YAZ have, in addition to an estrogen, a progestin, drospirenone, which is a very close chemical relative to spironolactone (see following). Hormonal treatments with oral contraceptives such as Ortho continued on page 40

Chap ter 1 • Acne and Related Disorders

39

MANAGEMENT Continued Tri-Cyclen, Ortho-Cyclen, Ortho-Cyclen Lo, Estrostep, Ortho-Cept, Alesse, Mircette, and Desogen are also relatively low in androgenic activity. Antibiotics and the “Pill”

A recent study has concluded that the antibiotics used to treat acne probably do not interfere with the efficacy of oral contraceptives. Nevertheless, patients taking oral antibiotics should be advised of this controversy so that they can decide to use an alternative or additional form of birth control. Ora l An t ia n d ro gen s

Before oral antiandrogens are prescribed, a hormonal and gynecologic evaluation is appropriate for a small number of acne patients, particularly for women who have treatment-resistant acne, a sudden onset of severe acne, virilizing signs or symptoms, irregular menstrual periods, or hirsutism. Oral antiandrogens (androgen receptor blockers) may also be considered for those women who are reluctant to take oral contraceptives for moral or religious reasons. Spironolactone (Aldactone) is the antiandrogen used most frequently to treat acne. It has potent antian-

drogenic effects and works by decreasing sebum production. Spironolactone is started at a low dosage of 25 to 50 mg per day and may be increased. It may take 3 months for any positive effects to become visible, but results may appear sooner. The dosage may need to be adjusted during the first 6 months of treatment. The most common side effect of spironolactone is an irregular menstrual cycle; however, if the patient is taking birth control pills, this is less likely to happen. It is recommended that an oral contraceptive be taken concurrently, because there is a risk of feminization of a male fetus if a woman becomes pregnant while taking an antiandrogen. Breast tenderness sometimes occurs. Flutamide (Eulexin) is another antiandrogen that is sometimes used in unmanageable female adult acne. It has the potential of causing severe liver damage, which greatly limits its use. Cyproterone is an acetate steroidal androgen receptor blocker. It acts as a competitive inhibitor of testosterone and dehydroepiandrosterone at the level of androgen receptors. A drug with the trade name Diane-35, an oral contraceptive that is very effective in the treatment of acne but not available in the United States, contains a combination of cyproterone acetate and ethinyl estradiol.

HELPFUL HINTS • A minimum of 3 to 6 months of therapy is required to evaluate the efficacy of oral contraceptives and antiandrogen agents in treating adult-onset acne. • Hormonal birth control methods such as the birth control patch and ring have an unpredictable effect on acne and can actually provoke acne. Depo-Provera, an injectable form of birth control containing synthetic progesterone, can also worsen or trigger acne at times. • Because it is very common for women to have premenstrual flares of acne, an increased dosage of oral antibiotics can be given 5 to 7 days before her next menstrual period (see earlier discussion of “rollercoasting”).

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Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

POINT TO REMEMBER • Every female patient with acne should be questioned about her menstrual history and virilizing symptoms.

Ro sa cea BASICS Rosacea is a common disorder that is frequently mistaken for acne. In fact, as recently as 20 years ago, rosacea was referred to as “acne rosacea.” Both conditions look alike, they often respond to the same treatments, and they may coexist. Rosacea arises later in life than acne, usually when patients are between 30 and 50 years of age. It occurs most commonly in fair-skinned people with an ethnic background from Great Britain (Scotland and Wales), Ireland, Germany, Scandinavia, and certain areas of Eastern Europe. Women are reportedly three times more likely to be affected than men. Rosacea is rare in all dark-skinned people, including Hispanic, African, and African-American populations. Although the precise cause of rosacea remains a mystery, it is believed that certain environmental factors contribute to its development and progression. Rosacea is not caused by drinking excessive amounts of alcohol—a serious misconception that has been around for ages and should be put to rest! Precipitating factors that may exacerbate rosacea include: • Sun exposure • Excessive washing of the face • Irritating cosmetics There is no convincing evidence that the following environmental factors have any long-term deleterious effects on rosacea: • Excess alcohol ingestion • Emotional stress • Spicy foods, smoking, or caffeine

Despite their similarities, acne vulgaris and rosacea seem to have quite different pathophysiologies. It has been suggested that the bacterium, Helicobacter pylori, which is found in the stomach, may cause or exacerbate rosacea; other investigators have implicated the Demodex species of mite that is often found in the hair follicle of patients with rosacea. However, evidence that either organism plays a central role in the pathogenesis of this disorder is lacking. Recent investigations have suggested that an excess of the protein cathelicidin plays a role in the inflammation of rosacea. DESCRIPTION OF LESIONS • Rosacea is a facial eruption that consists of acnelike erythematous papules, pustules, and telangiectasias. • It lacks the comedones (“blackheads” or “whiteheads”) that are seen in acne. • It does not appear to have any relationship to androgenic hormones. • In general, rosacea does not scar or present with nodules or cysts, unless the patient has concomitant acne. • When it first appears, rosacea may begin with erythema on the cheeks and forehead that later spreads to the nose and chin. This is referred to as “erythemotelangiectatic rosacea” (formerly known as prerosacea). Often, affected patients describe how they are inclined to flush and blush easily. • As rosacea progresses, telangiectasias, papules, and sometimes, pustules begin to arise against a background of erythema. The papules and pustules (papulopustular rosacea) tend to come and go in cycles, but the erythema and telangiectasias tend to remain.

Chap ter 1 • Acne and Related Disorders

41

DISTRIBUTION OF LESIONS • Lesions are most typically seen on the central third of the face-the forehead, nose, cheeks, and chin (the so-called “flush/blush” areas) (FIG. 1.12). • Lesions tend to be bilaterally symmetric, but they may occur on only one side of the patient’s face. CLINICAL MANIFESTATIONS

1.12 Rosacea. As seen here, rosacea involves inflammatory papules and pustules and telangiectasias that are located on the central third of the face.

• Rosacea is primarily a cosmetic problem; however, burning and flushing can be quite uncomfortable. • Patients may also have ocular involvement, which results most often in blepharoconjunctivitis. Episcleritis and keratoconjunctivitis sicca are rare complications. Ocular rosacea may precede the skin manifestations in up to 20% of people (FIG. 1.13). DIAGNOSIS • Rosacea is diagnosed clinically. • A biopsy may be necessary in atypical cases.

1.13 Ocular rosacea. Note the conjunctivitis as well as the typical facial papules of rosacea.

DIFFERENTIAL DIAGNOSIS Rosacea is different from acne vulgaris and adult-onset acne in several ways, although the three conditions are sometimes similar.

Ad ult Acn e • The microcomedo, the primary lesion of acne, arises in response to hormonal (androgenic) stimulation. • Lesions are influenced by a woman’s menstrual cycle. • Adult-onset acne tends to occur on the lower part of the face and tends to have a much wider distribution, such as on the chest and back.

Se b o rrh e ic De rm at it is See also Chapter 2, “Eczema.” • The presence of scale and erythema, without acnelike lesions (papules and pustules) • Appears on the nasolabial area, eyebrows, and scalp

Syst e m ic Lup us Eryt h e m at o sus (See Chapter 25, “Cutaneous Manifestations of Systemic Disease”) • “Butterfly” distribution of rash • Absence of papules and pustules • Presence of antinuclear antibodies and other manifestations of lupus

continued on page 43

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Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

DIFFERENTIAL DIAGNOSIS Continued

Sun -Dam ag e d Skin (De rm at o h e lio sis) • Rosacea is a condition that is regularly “overdiagnosed” by health care providers; sometimes these patients may simply have “rosy cheeks” (FIG. 1.14). In many instances, rosacea can be difficult to distinguish from weathered, sun-damaged skin that is seen in many fairskinned farmers, gardeners, sailors, or in people who have worked or spent long periods of their lives outdoors. • Such long-term sun exposure can also lead to persistent red faces and telangiectasias and can resemble rosacea. “Flush e r/ Blush e rs” • In a “flusher/blusher” redness occurs in different places than where it is commonly seen in rosacea. Symptoms tend to appear on the sides of the cheeks, the front and side of the neck, and the ears, rather than the central area of the face.

MANAGEMENT Patients should be advised to avoid significant environmental triggers and to apply a sunscreen prior to sun exposure.

To p ical Th e rap y Some of the topical medications used to treat acne are also very effective for rosacea; however, some precautions must be taken, because many people with rosacea have very sensitive skin. Consequently, standard acne medications such as topical retinoids and benzoyl peroxide can be drying and/or irritating, may sensitize the skin to the sun (retinoids), and can even exacerbate rosacea. If possible, long-term control of rosacea should be attempted with topical therapy alone, and oral antibiotics should be reserved for initial control and for breakthrough flares. The preparations described in this section can be used in combination with oral antibiotics as well as the other topical medications. It may take 6 to 8 weeks before significant improvement is noted.

1.14 Facial erythema. Frequently misdiagnosed as rosacea, this woman has “rosy cheeks” and telangiectasias.

considered to be as effective as metronidazole in the treatment of rosacea. • Application is twice a day. So d iu m Su lfa cet a m id e a n d Su lfu r

• Medications containing sodium sulfacetamide and sulfur are also effective for rosacea. Klaron and Sulfacet-R are preparations containing sodium sulfacetamide 10% and sulfur 5%. Brand names include Klaron, Plexion, Rosula, Rosac, Rosanil, Novacet, and Ovace. They are available as lotions, creams, and washes. • Some of these products contain a humectant and can be used in patients with rosacea who have dry, sensitive skin. Others have color tinting to help hide the redness of rosacea. These agents are generally applied twice a day to clean dry skin. When used in combination, they also appear to enhance the effectiveness of the other topical agents (azelaic acid and metronidazole) that are detailed in this section.

Syst e m ic Th e rap y See TABLE 1.6 at the end of this chapter

Met ro n id a zo les

• The “metros” are the most frequently prescribed firstline topical therapy for rosacea. • Noritate (metronidazole) 1% cream, and MetroGel 1% gel are applied once daily on rosacea-prone areas. Azela ic Acid

• Azelex cream and Finacea gel are 15% azelaic acid preparations. (Skinoren is available in Europe.) They are

Ora l An t ib io t ics

• The same systemic oral antibiotics used to treat acne also can be used to treat the papules and pustules of rosacea. Most cases can be treated and controlled with topical agents alone; however, if topical treatment is ineffective, an oral antibiotic is generally prescribed. continued on page 44

Chap ter 1 • Acne and Related Disorders

43

MANAGEMENT Continued

Tab le 1.5 TOPICAL AGENTS FOR ROSACEA AND PERIOROFICIAL DERMATITIS BRAND NAME

GENERIC NAME

ADVANTAGES/DISADVANTAGES

SIZES

Noritate cream

Metronidazole 1%

30 g

MetroGel, MetroCream Azelex, Finevin, Skinoren creams Finacea gel Rosac cream Sulfacet-R lotion

Metronidazole 1% Metronidazole 0.75% Azelaic acid 15%, 20% Azelaic acid 15% Sodium sulfacetamide 10%/sulfur 5% Sodium sulfacetamide 10%

Minimal irritation Once-daily application Once-daily application Twice-daily application May lighten skin; irritation is common May lighten skin; irritation is common Contains broad-spectrum sunscreen Tinted preparation may be a good camouflage in fair-skinned acne patients

• Tetracycline and tetracycline derivatives, such as minocycline and doxycycline, are the first-line oral drugs of choice in the management of moderate to severe rosacea. The mechanism of action of these drugs is more likely antiinflammatory than antibiotic, because no microorganisms have been definitively identified as a cause of rosacea or its variants. • In comparison with topical therapy, systemic therapy has a more rapid onset of action. With oral antibiotics, improvement of rosacea is usually noticeable in a week or two. The papules and pustules begin to flatten and disappear, and new ones stop appearing. The antibiotic is then tapered when this improvement persists (usually after 3 to 4 weeks).

60 g 45 g 30, 50 g 30 g 45 g 25 g

• If tetracycline is ineffective, minocycline (50 to 100 mg bid), doxycycline (50 to 100 mg twice a day), or erythromycin (250 mg twice to four times daily) may be tried. Oracea, an anti-inflammatory low-dose (subantimicrobial) doxycycline, is available as a 40-mg capsule that contains 30-mg immediate-release and 10-mg delayed-release beads. It is taken once daily. Alt er n a t ive An t ib io t ics

Azithromycin, clarithromycin, or amoxicillin are used as second-line alternatives when a tetracycline fails or is not tolerated.

Ot h e r Tre at m e n t Op t io n s Elect ro ca u t er y

Dosage

• Tetracycline is given in dosages ranging from 250 to 500 mg, taken twice daily. • It is tapered when the inflammation has improved (usually after 2 to 3 weeks).

44

• Electrocautery with a small needle is used to destroy small telangiectasias. Pu lse Dye La sers a n d In t en se Pu lsed Ligh t

• These light treatments are used to destroy larger telangiectatic vessels.

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

HELPFUL HINTS • Initial treatment with oral antibiotics typically delivers a rapid therapeutic response and helps confirm the diagnosis of rosacea. • It should be recognized that the “flat” telangiectasias and flushing erythema tend to persist and respond minimally, if at all, to antibiotic therapy. • Men who have difficulty shaving around the papules of rosacea should try using an electric razor rather than a blade to reduce abrasion. • The patient should be instructed to avoid irritating cosmetics, astringents, and exfoliating agents. Instead, water-based moisturizers and cosmetics and makeups or moisturizers with a sunscreen already added are recommended. • Sunscreens that contain zinc oxide or titanium dioxide-the barrier sunscreens-should be used, especially if other sunscreens irritate or worsen rosacea. • Cosmetic foundations can be applied to cover erythematous areas. Green-tinted foundations can hide the red. Other nonprescription products that may be used to cover up the redness are Dermablend and Covermark. They can be matched to a patient’s normal skin color. These products can be found at makeup counters in some department stores.

POINTS TO REMEMBER • Rosacea is a chronic condition with no known cure. • Acne and rosacea share similar clinical manifestations and overlapping management strategies, yet each has a distinctive course and prognosis; consequently, an attempt at making a specific diagnosis should be made. • If possible, long-term control of rosacea should be attempted with topical therapy alone, with oral antibiotics used only for breakthrough flares.

TRIGGERS OF ROSACEA Co m m o n fact o rs include: • Sun exp o sure • Excess alcoh ol in g est ion . Drinking habits have nothing to do with causing rosacea; however, it is accepted that the blushing and flushing of rosacea m ay flare up in the short term when som e people drink alcohol—especially red wine. However, it is questionable that the drinking of alcoholic beverages causes a long-term worsening of the condition. There is no convincing evidence that the following factors have any long-term harm ful effects on rosacea. However, they can increase the redness of the face tem porarily. • • • •

Sp icy fo o d s, sm o kin g , an d caffein e Co o kin g o ve r a h o t st o ve o r o ve n Em o t io n al st re ss Ph ysical exe rt ion

Chap ter 1 • Acne and Related Disorders

45

Ro sa cea Va ria n t s PERIORAL DERMATITIS This condition, which is also known as “periorificial dermatitis,” perioral dermatitis is a rosacea-like eruption seen primarily in young women and uncommonly in young boys and girls. It is usually found around the mouth, but it may be noted around the eyes and nose (which explains the more inclusive term, “periorificial”) (FIG. 1.15). As with rosacea, the etiology is unknown. Potent topical steroids and fluoridated toothpaste have occasionally been implicated, but there is no consistent evidence. Features that distinguish perioral dermatitis from rosacea include the following:

1.15 Perioral dermatitis. Multiple, small, acneiform papules can be seen on this young woman. Note the characteristic sparing around the lips.

• Perioral dermatitis appears in women between 15 and 40 years of age. • It manifests in small, erythematous papules or pustules without telangiectasia. • It characteristically circles the mouth and spares the vermilion border of the lips. • Occasionally, there is superimposed scaling. • Usually it does not recur after successful treatment. TOPICAL STEROID–INDUCED “ROSACEA” Rosacea induced by topical steroids is often clinically indistinguishable from ordinary rosacea, but a history of long-term, indiscriminate misuse of potent topical steroids on the face helps confirm the diagnosis. It is sometimes referred to as “steroid use/abuse/misuse/dermatitis” (FIG. 1.16).

1.16 Topical steroid-induced rosacea. This woman has been applying a potent topical steroid every day to her face for eight months.

46

• The topical steroids are often prescribed for other skin conditions and then overused by the unsuspecting person, who continues to apply them. • The condition typically worsens when the topical steroids are discontinued (an occurrence known as “rebound rosacea”). • In an unfortunate cycle, the steroid is sometimes reapplied to diminish the erythema, which only worsens the condition. • This condition is treated by stopping the offending topical steroid and by taking a tetracycline derivative for a few weeks or more to get over the “hump” of the rebound.

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

RHINOPHYMA Rhinophyma can be an unsightly manifestation of rosacea. This condition usually occurs in men over 40. It consists of knobby nasal papules that tend to become larger and swollen over time (FIGS. 1.17 and 1.18). It is quite uncommon and is rarely seen in women. The usual treatments described in this chapter for rosacea are not effective for rhinophyma. Recontouring procedures with a scalpel or a carbon dioxide laser have been used successfully to remove (“sculpt”) the excess nose tissue, resulting in a more normal shape and appearance. This may also be accomplished by electrocautery and dermabrasion.

1.17 Rhinophyma. This man’s enlarged nose is caused by marked sebaceous hyperplasia.

1.18 Rhinophyma. Ghirlandaio’s portrait of an old man with his grandson (showing a tender human relationship, despite the appearance of his nose).

Chap ter 1 • Acne and Related Disorders

47

Acn e: Ot h er Typ es SYSTEMIC DRUG-INDUCED (OR DRUG-EXACERBATED) ACNE Several drugs are known to provoke acneiform reactions. • Oral corticosteroids and adrenocorticotropic hormone produce acnelike lesions that are usually more monomorphic and symmetric in distribution than those seen in adolescent and postadolescent acne. Lesions are located primarily on the trunk. The precise mechanism is uncertain. • Lithium may exacerbate acne. • Androgens. including anabolic steroids and gonadotrophins, may precipitate acne, especially in athletes who take such drugs. • Antiepileptic drugs, especially phenytoin, have been held responsible for causing or exacerbating acne; however, modern anticonvulsants do not appear to have acne as a potential side effect. • Patients taking isoniazid, especially those who slowly inactivate the drug, appear to be prone to develop acne. • The management of drug-induced or drug-exacerbated acne includes the following choices: discontinuation of the causative drug, decreasing the dosage, or substituting the drug with another agent. Treatment of acne is described earlier in this chapter. NEONATAL ACNE • This self-limiting form of acne is seen mainly in male infants; it occurs from the stimulation of maternal androgens. • Because it is self-limiting, it requires no treatment. (See Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients.”)

ENDOCRINOPATHIC ACNE • The presence of acne, coupled with other signs or symptoms, may indicate an endocrinopathy. • Hormonal disorders that can produce excessive androgens, as well as those that can manifest with elevated cortisol levels can be responsible for producing or aggravating preexisting acne (see Chapter 11, “Hirsutism”). AGENT ORANGE AND DIOXINS (CHLORACNE) • Agent Orange, an herbicide, was used during the war in Vietnam. This herbicide contains dioxins (halogenated aromatic hydrocarbons), a group of chemicals known to increase the likelihood of cancer. Some veterans reported a variety of health problems and concerns attributed to exposure to this agent. The first disease associated with dioxins was the extreme skin disease chloracne, which causes acnelike pustules on the body that can and do last for several years and result in significant scarring. • The chloracne develops a few months after swallowing, inhaling or touching the dioxin. Most cases are caused by occupational exposure, but chloracne can also develop after accidental environmental poisoning. HIDRADENITIS SUPPURATIVA (ACNE INVERSA) (See Chapter 5, “Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa.” • This is an acnelike condition.

Tab le 1.6 SYSTEMIC ANTIBIOTICS FOR ACNE, ROSACEA, AND RELATED DISORDERS

ACNE EXCORIÉE DES JEUNES FILLES This type of acne is routinely picked at by the patient, who almost invariably is female (FIG. 1.19).

BRAND NAME

GENERIC NAME

DELIVERY

• Many of these patients deny that they manipulate their skin, but it is rather obvious because there are no primary lesions present; all have crusts. • Some of these patients may benefit from selective serotonin receptor inhibitors and psychotherapy.

Tetracycline Generic Doxycycline Generic

Tetracycline

Capsules

Doxycycline

Adoxa

Doxycycline hyclate Doxycycline (subantimicrobial) Minocycline

Capsules, tablets, liquid Tablets

Oracea

Minocycline Generic Solodyn

1.19 Acne excoriée des jeunes filles. This type of acne has obviously been picked at by the patient.

Minocycline

Minocin

Minocycline

Dynacin

Minocycline

Capsules

Tablets Extendedrelease tablets Capsules, oral suspension Capsules, tablets

COMMON STARTING DOSE 250 or 500 mg twice a day 50, 75, 100 mg twice a day 75 or 100 mg twice a day 40 mg per day

50, 75, or 100 mg twice a day 1 mg/kg per day 45, 90, 135 mg once daily 50 or 100 mg twice a day 50 or 100 mg twice a day

C H AP T ER

Eczem a

2 OVERVIEW Despite being the most common inflammatory skin condition, eczema is the most confusing skin ailment for both patients and their nondermatologic health care providers. Eczema is very difficult to define. United States Supreme Court Justice Potter Stewart once said that he could not define pornography, but he knew it when he saw it. Such is the case with eczema, a condition that is best understood through repeated viewing. The word eczema was coined by the Ancient Greeks to mean “a boiling out or over.” Conceivably, Greeks viewed certain rashes as boiling out or erupting from under the skin. As a case in point, the acute eczematous eruption of poison ivy often manifests with a fiery red color and a linear, blistered appearance, suggesting an acute boiling, bubbling, second-degree burn. Terminologic confusion may also arise if the word dermatitis—a more generalized, often vague designation that refers to all cutaneous conditions with inflammation—is used synonymously with eczema or is coupled with it. In general, it is acceptable to use eczema and dermatitis interchangeably. Eczematous dermatitis, therefore, is somewhat redundant, although some might argue that the term is more inclusive than either word alone. The diversity of clinical images presented in this chapter is indicative of the protean clinical appearance of eczema.

The following clinical presentations of eczem a or associated conditions are discussed in this chapter: ATOPIC DERMATITIS (ATOPIC ECZEMA) CONTACT DERMATITIS AND DIAPER DERMATITIS CHRONIC HAND ECZEMA AND DYSHIDROTIC ECZEMA NUMMULAR ECZEMA LICHEN SIMPLEX CHRONICUS PRURIGO NODULARIS ASTEATOTIC ECZEMA NEUROTIC EXCORIATIONS NONSPECIFIC ECZEMATOUS DERMATITIS SEBORRHEIC DERMATITIS STASIS DERMATITIS

Hist o p at h o lo g y On a microscopic level, an eczematous epidermis contains intercellular and intracellular fluid that appears in a spongelike formation (spongiosis).Vasodilatation of the dermis also occurs. These abnormalities result in the clinical manifestations of acute eczema: edema, erythema, vesicles, and bullae (e.g., from poison ivy). Later, the epidermis thickens (acanthosis) and retains nuclei (parakeratosis), and an abundant cellular infiltrate develops in the dermis. These changes account for the scale and lichenification (see following) of chronic eczema (e.g., chronic lichenified atopic dermatitis). Acut e , Sub acut e , an d Ch ro n ic Ecze m a In reference to eczema, the designators acute, subacute, and chronic are somewhat arbitrary because they describe parts of a dynamic spectrum. A patient can present with lesions in any or all of the phases. 49

2.1 Acute allergic eczematous eruption of poison ivy. The red color and linear blistered appearance suggest an acute “boiling,” bubbling, second-degree burn.

Acute eczema is manifested by itchy erythematous patches, plaques, or papules that may become “juicy” and develop into vesicobullous lesions (FIG. 2.1). Alternatively, acute eczema may originate and continue as a less florid, nonvesicular, erythematous eruption. Subacute eczema is an intermediate stage between acute and chronic eczema. The term has little clinical value. It is best simply to be aware that acute oozing lesions dry into crusts (scabs; FIG. 2.2), and they can later develop scales that overlie an erythematous base. Subacute eczema may become chronic, resolve spontaneously, or resolve with treatment. Chronic eczema is also known as chronic eczematous dermatitis. Its hallmark is lichenification—plaque with an exaggeration or hypertrophy of the normal skin markings. Lichenification resembles the bark on a tree trunk; or, as implied, the skin appears lichenlike. (FIG. 2.3). In addition, scale and hemorrhagic crusts can result from scratched or drying vesicles. Older lesions may exhibit postinflammatory pigment alterations (PIPA), i.e., hyperpigmentation and/or hypopigmentation (FIG. 2.4).

2.3 Chronic eczematous dermatitis. This patient shows lichenification, an exaggeration of skin markings, which was caused by repeated scratching.

2.2 Subacute eczema. The crusts, scales, and erythema of subacute eczema are less intense than those seen in acute eczema.

2.4 Chronic eczematous dermatitis. This lesion shows no evidence of active inflammation. Lichenification and postinflammatory hyperpigmentation are apparent. 50

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

At o p ic Der m a t it is

(At o p ic Eczem a )

See also Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients.”

BASICS • Atopic dermatitis, also known as atopic eczema or endogenous eczema, is the most commonly seen type of eczema (FIGS. 2.5–2.9). It is a chronic, inflammatory, itchy skin condition with an unpredictable course of flares and remissions that affects an estimated 5% to 10% of the United States population. Atopic dermatitis is the most frequently seen skin condition among patients of Asian descent. • By definition, atopic dermatitis occurs in association with a personal or family history of hay fever, asthma, allergic rhinitis, sinusitis, or atopic dermatitis itself. A probing history taking is often necessary to uncover symptoms of atopy. For example, patients should be asked whether they or their family members are allergic to pollen, dust, house dust mites, ragweed, dogs, or cats. Inquiries should be made about chronic recurrent symptoms that suggest atopy, such as nasal pruritus and rhinitis, rhinorrhea, paroxysmal sneezing, or itchy or irritated eyes. A personal or family history of allergies to multiple medications is also important. Furthermore, secondary relatives (aunts, uncles, cousins, and grandparents) may have an atopic predisposition. • Most cases begin in childhood (often in infancy); however, atopic dermatitis may start at any age. The disease frequently remits spontaneously—reportedly in 40% to 50% of children—but it may return in adolescence or adulthood and possibly persist for a lifetime. Traditionally, patients and their families were advised that children “will grow out of eczema”; however, this optimistic prognosis is not always realized.

2.6 Atopic dermatitis. Lesions are widespread in this infant.

2.7 Atopic dermatitis. Antecubital involvement in a 2-year-old child.

2.5 Atopic dermatitis. The cheeks are a typical location in an infant.

2.8 Atopic dermatitis. Popliteal involvement is apparent in this toddler.

Chapter 2 • Eczem a

51

• Children with asthma—an increasing population in the inner cities of the United States—appear to have a higher prevalence of atopic dermatitis than do other children; atopic dermatitis often manifests in asthmatic children in a more extensive and chronic form. African-Americans and Asians, particularly those living in an urban setting, tend to develop atopic dermatitis at an earlier age. Severe eczema in childhood portends a worse prognosis in adulthood. • Atopic dermatitis can present with a wide spectrum of severity. Some patients may have only a mild, recurrent, localized, itchy rash on “dry” or “sensitive” skin; others may experience a more severe, extensive eruption that can be accompanied by unremitting pruritus, sleepless nights, secondary cutaneous bacterial or viral infections, embarrassing alligatorlike lichenification, and, rarely, an exfoliative erythroderma. Many patients with atopic dermatitis have multiple accompanying atopic ailments, as mentioned earlier. • In addition to the physical discomfort of atopic dermatitis, patients may suffer from embarrassment about the appearance of lesions. Psychosocial problems, such as poor selfimage, anger, and frustration, may lead to depression and social isolation.

2.9 Atopic dermatitis, generalized. Note the marked postinflammatory hyperpigmentation in this AfricanAmerican child.

COMMON MYTHS ABOUT ECZEMA Myt h : Soy form ulas im prove eczem a in infants. Fact : Food allergies that induce eczem a are rare. Urticaria (hives) is the usual skin m anifestation of a food allergy. Myt h : Infants and children who have atopic derm atitis should be bathed infrequently. Fact : The advantages of bathing far outweigh its disadvantages (see following). Myt h : Laundry detergents are a com m on cause of eczem a. Fact : Very rarely is this the case. Most detergents are rinsed out, with very little soap rem aining to cause a rash. Myt h : Potent topical steroids should not be used on infants or young children. Fact : Topical steroids, when used properly, are quite safe. Not using them can lead to undertreatm ent that can last for an indeterm inate period of tim e.

52

Pat h o g e n e sis • Atopic dermatitis is an inherited type I (immunoglobulin E–mediated) hypersensitivity disorder of the skin. In comparison with normal skin, atopic skin tends to be more prone to irritation, dryness, barrier abnormalities, and infection; it is also more likely to be negatively influenced by emotional stress. • The intense itching of atopic dermatitis is presumed to be produced by the release of vasoactive substances from sensitized mast cells and basophils in the dermis. The itching may be initiated by external agents such as woolen or synthetic fabrics; certain foods; alcohol; and overexposure to dry, cold weather or to very hot, humid conditions that predispose to sweating. Less commonly, pruritus has been reported to be triggered by house dust mites. There is considerable debate about whether atopic dermatitis is primarily an allergen-induced disease or, rather, an inflammatory skin disorder found in association with respiratory allergy or other atopic symptoms. Individuals find that an allergic condition is permanent, whereas they often outgrow atopic dermatitis; this supports the latter explanation. • Even though atopic dermatitis frequently remits spontaneously, patients, their families, and their health care providers—in particular, pediatricians and allergists— often relentlessly search for external sources that patients can avoid or eliminate from their environments. Avoidance of milk products and food preservatives and extreme dietary restrictions are not only very difficult to maintain on an ongoing basis, but they may also incite developmental problems in growing children; furthermore, they rarely, if ever, offer a cure.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

DESCRIPTION OF LESIONS • Although the character and distribution of the skin eruption tend to vary according to the patient’s age, the different phases of atopic dermatitis are not always clearly distinct. • Any or all manifestations of atopic dermatitis may exist in a single patient.

In fan t ile Ph ase • In patients aged 2 months to 2 years, the face (particularly the cheeks; see FIG. 2.5) scalp, chest, neck, and extensor extremities are most often involved. The eruption may become generalized (see FIG. 2.6). In many cases, atopic dermatitis first manifests with severe “cradle cap” or severe recalcitrant intertriginous (groin, neck, axillae) rashes. • As the patient approaches age 2, the flexor creases become involved. Lesions consist of scaly, red, and, occasionally, oozing plaques that tend to be symmetric (see FIGS. 2.7 and 2.8).

2.10 Atopic dermatitis. In this adult, the lichenified plaques tend to blend into the surrounding normal skin. Postinflammatory hyperpigmentation is seen here.

Ch ild h o o d Ph ase • Lesions seen in children aged 2 through 12 years tend to become lichenified because of repeated rubbing and scratching. • Lichenification occurs more commonly in Asian and African-American patients than in Caucasian patients (see FIG. 2.9). • The hallmark of atopic dermatitis is pruritus; children who have atopic dermatitis are typically very “busy” and cannot often sit quietly because of the pruritus. Dist rib u t io n o f Lesio n s

• Lesions tend to occur symmetrically, with a characteristic distribution in the flexural folds: the antecubital and popliteal fossae and the neck, wrists, and ankles. • Lesions may also occur on the eyelids, lips, scalp, and behind the ears. Ad o lescen t a n d Ad u lt Ph a se

2.11 Atopic dermatitis, follicular eczema. Atopic dermatitis of the hair follicles. Note the gridlike pattern of follicular papules. This is a common presentation in AfricanAmerican patients.

In adolescents and adults, lichenified plaques are generally prominent and tend to blend into surrounding normal skin. Postinflammatory hyperpigmentary and hypopigmentary changes may be seen (FIG. 2.10). Alternatively, lesions may consist of small, itchy, erythematous papules (e.g., follicular eczema; FIG. 2.11) or vesicles on the hands (e.g., dyshidrotic eczema; see below).

Chapter 2 • Eczem a

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Dist rib u t io n o f Lesio n s

The distribution of lesions may be similar to that seen in childhood (i.e., in the flexural folds). However, lesions may also appear in extensor locations: the dorsa of the hands, wrists, shins (FIG. 2.12), ankles, and feet, and the nape of the neck (FIG. 2.13). On the other hand, lesions may be limited to the lips (atopic cheilitis; FIG. 2.14); eyelids; vulvar or scrotal areas (FIGS. 2.15 and 2.16, respectively); or hands (as in chronic hand eczema or dyshidrotic eczema; see below), which may be the only features of atopic dermatitis in some adults. Nail dystrophy occurs when the proximal nail fold and the underlying nail matrix (root) are involved (FIG. 2.17). OTHER CLINICAL ASPECTS Additional associated features and findings that are clues to the diagnosis of atopic dermatitis include the following:

2.12 Atopic dermatitis. Lesions in this patient resemble both nummular and asteatotic eczema (see FIGS. 2.40 and 2.52).

2.13 Atopic dermatitis, lichen simplex chronicus. The nape of the neck is a common site of involvement.

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• Persistent xerosis, or dry, “sensitive” skin. • Dennie–Morgan lines. These comprise a characteristic double fold that extends from the inner to the outer canthus of the lower eyelid (FIG. 2.18). • “Allergic shiners.” This term refers to a darkened, violaceous, or tan coloring in the periorbital areas. Along with Dennie–Morgan lines, this dark coloring may be an instant clue to the diagnosis of atopic dermatitis (FIG. 2.19). • Hyperlinear palmar creases (FIG. 2.20).

2.14 Atopic cheilitis (atopic dermatitis of the lips). Note the lichenification and the ill-defined outline of the vermilion border of the upper lip.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

2.15 Atopic dermatitis limited to the vulvar and inguinal areas. This eruption was initially diagnosed and treated as a fungal infection by the patient’s health care provider.

2.16 Atopic dermatitis (lichen simplex chronicus) limited to the scrotum. This patient was also initially thought to have tinea cruris. Note the lichenification.

2.17 Atopic dermatitis. This patient’s middle fingernails show dystrophic changes, transverse ridging, and cuticle loss solely on those fingers where eczema is present in the proximal nail folds.

2.18 Atopic dermatitis, periorbital. Note lichenification and the characteristic double fold (Dennie-Morgan line) that extends from the inner to the outer canthus of the lower eyelid and the “allergic shiners,” the darkening color of the periorbital areas.

2.19 Atopic dermatitis, periorbital. The presence of “allergic shiners”—a darkened or violaceous hue, as in this child—is a clue to the diagnosis of atopic dermatitis.

2.20 Atopic dermatitis. Hyperlinearity of the palms is evident here. Chapter 2 • Eczem a

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Other associated dermatoses include the following: • Ichthyosis vulgaris. This condition is frequently associated with atopy. Lesions, which are most apparent on the shins, resemble fine fish scales. Characteristically, the flexor creases are spared in this condition (FIG. 2.21). • Keratosis pilaris. These tiny, horny, rough-textured, whitish or red, follicular papules or pustules occur most often during adolescence. Most commonly, keratosis pilaris is noted on the deltoid and posterolateral upper arms, the upper back and thighs, and the malar area of the face. It is frequently confused with acne (FIG. 2.22).

2.21 Ichthyosis vulgaris. Lesions resemble fish scales. Note the characteristic sparing of the popliteal creases.

CLINICAL MANIFESTATIONS AND POSSIBLE COMPLICATIONS • Pruritus may interfere with sleep. Itching is increased by repeated scratching and rubbing, which leads to lichenification, oozing, and secondary bacterial infection (impetiginization, or “honey-crusted skin”). • Secondary infection with Staphylococcus aureus may trigger relapses of atopic dermatitis. • Secondary infections with herpes simplex virus may result in eczema herpeticum (Kaposi’s varicelliform eruption), which is more commonly seen in childhood. DIAGNOSIS • Diagnosis of atopic dermatitis depends on excluding conditions such as fungal infections, seborrheic dermatitis, psoriasis, scabies, contact dermatitis, ichthyosis, and cutaneous T-cell lymphoma.

2.22 Keratosis pilaris. This teenager has tiny, roughtextured, red, follicular papules on his lateral upper arms.

DIFFERENTIAL DIAGNOSIS • The diagnosis of atopic dermatitis is generally not difficult, especially in patients with an atopic history in whom the following causes of eczema or eczemalike eruptions have been excluded.

Co n t act De rm at it is (See later in this chapter). • Determine whether the patient was exposed to a substance that could cause contact dermatitis. The location of the lesions may suggest an external cause.

Scab ie s (See Chapter 20, “Bites, Stings, and Infestations.”) • A history of exposure is important in diagnosing scabies. • Symptoms are present in other household members. • Characteristic distribution (e.g., in the webs between the fingers and on the flexor wrists) can mimic that of eczema. 56

• A positive scabies scraping is diagnostic of scabies.

Pso riasis See Chapter 3, “Psoriasis.” • Lesions generally appear on extensor locations—the elbows, knees, and other large joints—rather than on flexor creases. • Patients may have a positive family history of psoriasis. • Usually, psoriasis is less pruritic than eczema. • Psoriatic lesions tend to be clearly demarcated from normal surrounding skin, and the scale of psoriasis tends to be thicker and micaceous in appearance. However, psoriasis may at times be clinically indistinguishable from atopic dermatitis.

Tin e a Pe d is, Co rp o ris, Man uum , an d Cap it is (See Chapter 7, “Superficial Fungal Infections.”) • A positive potassium hydroxide (KOH) test or fungal culture result indicates these conditions.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

MANAGEMENT

To p ical St e ro id Th e rap y See also “Introduction: Topical Therapy.” Gen era l Prin cip les

• The application of an appropriately chosen topical steroid usually results in prompt improvement in most patients with atopic dermatitis. • Topical steroids should be used only as short-term therapy, if possible, and only to treat active disease (i.e., with itching and erythema). • Topical steroids should not be used for prevention of future lesions or for cosmetic concerns, such as postinflammatory hyperpigmentation. • “Stronger” is often preferable to “longer” in the use of topical steroids, because long-term application is more often associated with side effects. • Without question, the use of a superpotent topical steroid is preferable to the administration of a systemic steroid, with its potential side effects. • When the condition is under control, the frequency of application and the potency of the topical steroids are reduced (“downward titration”), or the agents are discontinued. Fa ce a n d Bo d y Fo ld s

• For the face and intertriginous regions (the axillae and inguinal creases are areas that are “naturally” occluded), treatment should be initiated with a low-potency (class 7) cream or ointment, such as over-the-counter (OTC) hydrocortisone 0.5% or 1%. • In more severe cases of atopic dermatitis, initial therapy may be with a more potent steroid, followed by a less potent preparation for maintenance. For example, a higher-potency (class 5) agent, such as hydrocortisone valerate 0.2% cream, could be used for 2 or 3 days, followed by a lower-potency (class 6) agent, such as desonide 0.05% or OTC hydrocortisone 0.5% to 1%, which is then used for maintenance as needed. Bo d y

• For nonintertriginous areas of the body, treatment can be initiated with a mid-strength (class 4) cream or ointment, such as triamcinolone acetonide 0.1%, or a midstrength (class 3) agent, such as fluocinonide 0.05%. Even a superpotent (class 1) agent, such as clobetasol 0.05%, may be used for limited periods (no more than 2 weeks) until control is achieved. Then therapy may be switched to a lower-potency (class 5) agent, such as hydrocortisone valerate 0.2%. Fluticasone 0.05% cream (Cutivate) is another lower-potency agent that has been shown to be effective as maintenance therapy when it is used twice weekly.

• Ointments are helpful for dry skin. Because of their occlusive properties, they are more lubricating than other formulations. They also tend to be less irritating and less sensitizing. Their popularity increases in colder, drier weather. For patients with widespread skin involvement, a 1-lb jar of triamcinolone acetonide cream or ointment 0.1% is quite economical. In fect io n

• If necessary, topical steroids can be given concurrently with systemic antibiotics. This combination is sometimes helpful if evidence of coexisting staphylococcal or streptococcal infection (“impetiginization”) of the skin is present. Oral antibiotics such as cephalexin or dicloxacillin are commonly used. Also, tetracycline derivatives, which may be prescribed in patients over 10 years of age, are effective. • During flare-ups, the acute, open, weeping, crusted lesions that develop from infection or scratching may be treated with a drying antibacterial agent, such as Burow’s solution, before topical steroids are applied. • Clorox bleach—1 to 2 teaspoonfuls per tubful of water, which can be increased up to 6 teaspoonfuls added to daily bath water—is a quite effective and inexpensive alternative to topical and oral antibiotics. • Another topical option is topical 2% mupirocin cream (Bactroban) or ointment (Centany).

To p ical Im m un o m o d ulat o r Th e rap y • Currently, these drugs are indicated for the short-term or intermittent treatment of atopic dermatitis and are considered as second-line therapy when conventional therapies are inadvisable, ineffective, or not tolerated. Photoprotection is advised when using these agents, although no evidence so far has implicated them in promoting skin cancer. • For information regarding the long-term safety of these agents, see “Introduction: Topical Therapy.” • Protopic ointment (tacrolimus) is a nonsteroidal immunomodulator that has been shown to reduce the symptoms of atopic dermatitis. It is used as an alternative to topical steroids, particularly when the eruption involves the face or intertriginous areas, such as the axillae and groin, where the long-term use of high-potency steroids is limited. Protopic has potential as a topical steroid–sparing agent. • When applied twice daily, Protopic may cause transient side effects, such as burning and itching. This burning and itching may result in patients’ refusal to continue applying the medication. • It is available as an ointment in 0.1% and 0.03% concentrations. continued on page 58

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MANAGEMENT Continued • The 0.1% concentration has been approved for the treatment of atopic dermatitis in adults. • The 0.03% concentration is designated for short-term and intermittent long-term treatment of atopic dermatitis in children (age 2 years and older) and in adults. • Elidel cream (pimecrolimus), in a 1% cream base, is less likely to be irritating, and it is not as greasy as Protopic ointment.

Ot h e r Th e rap e ut ic Me asure s • Oral H1 antihistamines such as diphenhydramine (Benadryl) and hydroxyzine (Atarax) probably do not reduce itching, but they are sometimes useful as inducers of sleep, an unacceptable side effect for many patients. • Oozing, exudative lesions may be soothed and dried with Burow’s solution or by bathing in a tub with antipruritic emollients, such as an Aveeno oatmeal bath preparation. • Sun exposure, ideally in the early morning and late afternoon—when humidity is lowest—may significantly improve atopic dermatitis in selected patients. • When a patient does not have access to natural sunlight, phototherapy with ultraviolet B rays and, less commonly, ultraviolet A rays, is often very effective for widespread skin involvement. • Less commonly used today, tar baths, as well as tar preparations formulated as ointments, pastes, and gels, may be used concurrently with topical steroids or alternated with them. (Before the advent of topical steroids, tar preparations were the mainstay of treatment.) • Emotional stress in patients or in their families may contribute to atopic dermatitis. Measures to reduce stress include support groups and family psychotherapy. • Before resorting to systemic steroids, a “soak and smear” regimen may be used. (See Introduction, “Topical Therapy.”) • Systemic steroids, immunosuppressive therapy with systemic agents such as cyclosporine, or short-term hospitalization is sometimes necessary in patients with severe unresponsive generalized atopic dermatitis. • For patients with secondary herpes simplex infection (Kaposi’s varicelliform eruption), oral antiviral therapy and possibly hospitalization may be required. Un succe ssful Tre at m e n t s • Treatments that do not seem to improve atopic dermatitis include vitamins, mineral or dietary supplements, and other nutritional supplements. • Topical ointments that include diphenhydramine and doxepin are potential contact allergens and thus are contraindicated.

Ge n e ral Man ag e m e n t Ba t h in g

How often the person who has atopic dermatitis should bathe has been the subject of controversy and misunderstanding. There are many reasons not to restrict frequent bathing: • Bathing removes crusts, irritants, potential allergens, and infectious agents. • Bathing provides pleasure and reduces stress. • Bathing hydrates the skin and allows better delivery of corticosteroids and moisturizers. • The addition of Clorox bleach to bath water (“bleach baths”) can be effective (see earlier discussion) for oozing or infected atopic dermatitis. Bathing Tips

• Mild, moisturizing soaps such as Dove or nonsoap cleansers such as Cetaphil Lotion should be used. • The patient should be cautioned not to use soap on lesional skin (many people are erroneously led to believe that scrubbing with “good soaps” may actually help inflamed skin). • Excessive bathing that is not followed immediately by application of a moisturizer tends to dry the skin. • Excessive toweling and scrubbing should be avoided. Preven t io n o f At o p ic Der m a t it is

The following measures may help the patient to avoid or reduce exposure to triggers such as dry skin, irritants, overheating and sweating, and allergens. • Dry skin: Moisturizers, particularly in the dry winter months, should be applied immediately after bathing to “trap” water in the skin. However, in warm climates or in the summer, moisturizers may actually be irritating or may interfere with healing. • Suggested ointments: Vaseline Petroleum Jelly, Aquaphor • Suggested creams and lotions: Eucerin, Cetaphil, Lubriderm, Curel, Moisturel • Barrier repair: Atopiclair, MimyX, and Epiceram are multiple-ingredient prescription, nonsteroidal barrier creams that are applied two or three times per day. Their efficacy as topical steroid–sparing agents has been suggested by several studies. The barrier cream and lotion CeraVe can be purchased OTC. • Irritants: Nonirritating fabrics, such as cotton, should be worn. Wool clothing may induce itching. • Overheating and sweating: Excess dryness or humidity should be avoided. An air conditioner or humidifier in a child’s bedroom may help to avoid the dramatic changes in climate that may trigger outbreaks. continued on page 59

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MANAGEMENT Continued (Unfortunately, humidifiers do not seem to help very much.) • Allergens: Some evidence indicates that the environmental elimination of certain airborne substances, such as house dust mites, may bring some lasting relief. A

SEE PATIENT HANDOUTS, “Burow’s Solution ” an d “Soak an d Sm ear In st ruct ion Sh eet ” ON THE SOLUTION SITE

POINTS TO REMEMBER • Topical steroids should be applied only to active disease (inflamed skin). • When topical steroids are applied immediately after bathing, their penetration and potency are increased. • Low-potency topical steroids are recommended for use on the face and in skin folds, such as the perineal area and underarms. • A very small number of children show some clinical improvement after measures to control house dust mites are instituted. • “Soak and smear” therapy can often be substituted for, or limit the use of, systemic steroids.

great deal of controversy surrounds the influence of dietary manipulation and the value of skin testing and hyposensitization on the course of atopic dermatitis. Although some foods may provoke attacks, elimination of them rarely brings a lasting improvement or cure. Skin tests and allergy shots may actually provoke attacks of atopic dermatitis.

HELPFUL HINTS • There are primarily two causes of eczema: one comes from the outside (contact dermatitis), and the other comes from the inside (atopic dermatitis). • Patients and their parents, caregivers, and teachers should be educated about the manifestations and management of atopic dermatitis. • The “gooiest” and cheapest moisturizer is petrolatum. • The National Eczema Association can be contacted at: • 415-499-3474 or 800-818-7546 • 4460 Redwood Highway, Suite 16-D, San Rafael, CA 94903-1953 • [email protected] or http://www. nationaleczema.org

SEE PATIENT HANDOUT “Atopic Derm atitis” ON THE SOLUTION SITE

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Co n t a ct Der m a t it is Contact dermatitis is an inflammatory reaction of the skin that is caused by an external agent. The appearance of the eruption and a careful history often give clues to the offending agent. The two types of contact dermatitis are irritant and allergic.

IRRITANT CONTACT DERMATITIS

2.23 Irritant contact dermatitis. The localized erythema on this boy’s face was caused by irritation from benzoyl peroxide in an acne preparation.

Also known as nonallergic contact dermatitis, irritant contact dermatitis (ICD) is an erythematous, scaly, sometimes eczematous eruption that is not caused by allergens (FIGS. 2.23 and 2.24). A direct toxic reaction to rubbing, friction, or maceration, or to exposure to a chemical or thermal agent, the severity of ICD depends on the concentration of the irritant, its thermal energy, its abrasiveness, and the duration of exposure, among other factors. ICD may occur in anyone. The eruption of ICD is confined to the areas of exposure, as exemplified by diaper rash, “dishpan hands,” and reactions that occur under an adhesive dressing (FIG. 2.25) or where a topical medication was applied. Examples of irritants include alkalis, acids, solvents, soaps, detergents, and numerous chemicals found in the home and workplace that damage the skin after repeated contact. Patients who have atopic dermatitis are more likely to develop ICD as a result of their inherent skin sensitivity and defective barrier function. Diagnosis, when not clearly evident, is based on a careful history and the ruling out of allergic contact dermatitis (ACD), which is discussed later. Management is fairly simple: Patients should be told to avoid the offending agent or to minimize contact with it.

Diap er Derm atitis (Diap er Rash ) BASICS 2.24 Irritant contact dermatitis. The erythema and scaling are obviously secondary to this child’s habit of licking her lips.

2.25 Irritant contact dermatitis. Chronic irritation from a stoma was the cause of this reaction. 60

• A common example of ICD is diaper dermatitis (diaper rash), referred to as “napkin dermatitis” in the United Kingdom. Diaper dermatitis applies to eruptions that occur in the area covered by a diaper. It can first present as early as the first few weeks of life or occur any time when diapers are worn. • Irritant diaper dermatitis is by far the most common rash in infancy, but it is not restricted to that age group because it can affect persons of any age group who wear diapers, such as incontinent patients.

Pat h o g e n e sis • Diaper dermatitis is essentially the result of overhydration of the skin that is irritated by chafing, by soaps and detergents, and by prolonged contact with urine and feces. The ammonia that is produced as a breakdown product of urea by bacteria in feces is considered an exacerbating factor. • Added to this wet, macerated, excrement-laden milieu are the occlusive effect of rubber or plastic diapers and the constant contact with moisture from cloth diapers when they are not changed as soon as possible.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

• Diaper dermatitis may also be caused by, or intensified by, the presence of atopic dermatitis, seborrheic dermatitis, or a secondary infection by Candida albicans. (C. albicans is often isolated from the perineal area in many of these infants; whether it is the cause or effect of the rash is controversial.) CLINICAL MANIFESTATIONS AND DESCRIPTION OF LESIONS • Erythema, scale, and possibly papules and plaques are present; occasionally, vesicles and bullae occur. • With neglect, lesions may erode and ulcerate. • “Beefy” redness and satellite papules and pustules suggest a primary or secondary infection of diaper dermatitis with C. albicans.

2.26 Irritant contact dermatitis. Diaper rash. The eruption conforms to the shape of the diaper.

DISTRIBUTION OF LESIONS • Lesions typically spare the creases (genitocrural folds) because such areas do not come into direct contact with the diaper (FIG. 2.26). Primary candidal diaper dermatitis should be considered in an immunocompromised patient, particularly if the creases are involved. • The eruption may conform to, and be limited to, the diaper area, and it may also affect the lower abdomen, genitalia, perineum, and buttocks.

DIFFERENTIAL DIAGNOSIS During infancy, the various causes of diaper dermatitis such as ICD, atopic dermatitis, seborrheic dermatitis, and psoriasis may be indistinguishable.

addition, other rare diseases such as Letterer-Siwe disease (a form of Langerhans cell histiocytosis) and acrodermatitis enteropathica (from zinc deficiency) should be considered in recalcitrant cases. Leiner’s disease is a very rare eruption resembling seborrheic dermatitis that is associated with diarrhea and a failure to thrive.

At o p ic De rm at it is • Atopic dermatitis. In general, patients with atopic dermatitis are more likely to experience ICD; nonetheless, the diaper area is often remarkably spared (FIG. 2.27). Other evidence of atopic dermatitis, such as involvement of the face and extensor areas, may be present, and the patient may have a family history of atopy. Se b o rrh e ic De rm at it is • Seborrheic dermatitis (intertriginous seborrheic dermatitis) (see “Seborrheic dermatitis” later in this chapter). The creases are involved, and the patient may have lesions elsewhere, such as the axillae or scalp (“cradle cap”). Other less common conditions to consider are tinea cruris, impetigo, child abuse (severe or repeated ulcerations), Kawasaki’s disease, and psoriasis, particularly if there is a positive family history or other evidence of psoriasis. In

2.27 Atopic dermatitis. Note involvement of the inguinal creases.

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MANAGEMENT General preventive measures to minimize friction, absorb moisture, and protect the skin from urine and feces include the following: • The use of disposable or superabsorbent diapers holds moisture in and keeps it away from the skin. • The diaper area should be dried gently after changing and aired out. • Frequent diaper changes should be made promptly after voiding or soiling. • It is sometimes recommended that the diaper area remain uncovered for long periods of time; however, this is quite impractical for most parents. Such an uncovered approach should be reserved when nonhealing erosions and ulcerations are present. • Rubber and plastic pants should be avoided. • Soap-free cleansers such as Cetaphil Lotion are recommended. • Absorbent baby powders such as Desitin cornstarch powder, Zeasorb powder, and Johnson’s Baby Powder are useful. • Aquaphor ointment and pure white petrolatum ointment (Vaseline Petroleum Jelly) act by trapping water beneath the epidermis.

•

•

•

•

•

•

Sp e cific Tre at m e n t Me asure s • The first-line therapy is zinc oxide ointment. There are many inexpensive OTC products that contain zinc oxide,

POINTS TO REMEMBER • Most cases are caused by irritation (ICD). • Avoid the use of high-potency topical steroids in the diaper area. • Educate parents and caregivers to change diapers frequently, to wash the patient’s genitalia with warm water and mild soap, and to use superabsorbent disposable diapers. • Consider referral to a dermatologist, particularly in persistent, unresponsive cases.

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such as Balmex, Desitin, and A D ointment. They should be applied thickly. Petrolatum, zinc oxide, aluminum acetate solution (1-2-3 Paste) is a “tried and true” combination product that both protects skin and has a drying effect. It should be applied after each diaper change. Low-potency OTC hydrocortisone 1% or 0.05% cream or ointment is often all that is necessary for uncomplicated diaper dermatitis. Stronger topical steroids (class 6) such as desonide 0.05% or hydrocortisone valerate 0.02% cream (class 5) or ointment (class 4) may be used for very short periods (1 to 4 days), if necessary. Potent topical steroids, particularly fluorinated preparations such as those contained in Lotrisone, are to be avoided in the diaper area. If the presence of C. albicans is suspected, particularly if there is no improvement after several days, a topical antifungal preparation such as the OTC miconazole (Micatin) may help; Vusion ointment (0.25% miconazole combined with 15% zinc oxide) is another option that is available only with a prescription. Consider adding nonabsorbable oral nystatin in recalcitrant cases.

ALLERGIC CONTACT DERMATITIS A true allergic reaction that precipitates eczematous dermatitis, ACD is caused by an allergen (antigen) that produces a delayed (type IV) hypersensitivity reaction. It occurs only in sensitized persons. ACD is not dose dependent, and it may spread extensively beyond the site of original contact. ACD is seen less commonly in young children, the elderly, and African-Americans. Examples of allergic contact sensitizers include jewelry, metal, cosmetics, topical medications, rubber compounds, plants, and the countless chemicals that are found in homes and work environments. The best-known example of ACD is rhus dermatitis, which is caused by poison ivy and poison oak.

Rh u s Derm atitis In the United States, poison ivy and poison oak are the principal causes of rhus dermatitis. Poison ivy is found throughout the country. Poison oak is found more commonly in the western United States. Poison sumac, another cause of rhus dermatitis, is found only in woody, swampy areas. The three plants belong to the same genus, Toxicodendron, which is the “poisonous” branch of the genus Rhus. Each of the three plants contains pentadecylcatechol and heptadecylcatechol, the sensitizing allergens, in their resinous oils (urushiol). The plants’ invisible oils may reach the skin not only through direct contact but also through garden tools, pet fur, golf clubs, or the smoke of a burning plant. Identical or related antigens are found in the resin of the Japanese lacquer tree, ginkgo trees, cashew nut shells, the dye of the India marking nut (used as a clothing dye in India), and the skin of mangoes. All cause similar skin rashes in sensitized people. In the eastern United States, rhus dermatitis occurs mainly in the spring and summer. In the western and southeastern United States, where outdoor activity is common all year, rhus dermatitis may occur in any season. Approximately 85% of the population develops a reaction on exposure to one of the plants.

2.28 Allergic contact dermatitis. Poison ivy caused this fiery red eruption. Note the “outside job” appearance of the linear streaks of papules and vesicles.

2.29 Allergic contact dermatitis. Poison ivy. The buttocks became involved after this patient used toilet paper that had been contaminated by the resin of poison ivy.

DESCRIPTION OF LESIONS

DIAGNOSIS

The characteristic eruptions, which consists of intensely pruritic linear streaks of erythematous papules, “juicy” vesicles, and blisters, appear to be caused by an outside agent (FIG. 2.28). The rash typically occurs 2 days after contact with the plant, but initial reactions have been noted within 12 hours of contact and as long as 1 week later. Generally, exposed areas of the body are affected first. The rash may later involve covered areas that have come into contact with the plant oil. For example, the external vulva or perianal areas may be affected after women use toilet paper that has been contaminated by plant oil from their hands (FIG. 2.29). In men, involvement of the penis is sometimes a diagnostic sign.

• The diagnosis of rhus dermatitis is based on history of exposure to an antigen and the characteristic distribution of the lesions. Contrary to common belief, the fluid in blisters does not contain the resinous oil, and it cannot transfer the rash to others or cause the rash to spread on the affected person. • Further dissemination, or autoeczematization, is believed to occur through hematogenous spread and subsequent immune-complex deposition in the skin. This spread may occur within 5 to 7 days after the initial exposure, and the resulting rash may last for 3 weeks or more.

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DIFFERENTIAL DIAGNOSIS Other dermatoses that may resemble rhus dermatitis include:

Plan t De rm at it is • Reactions to meadow grass and other plants may cause atopic dermatitis. In se ct Bit e Re act io n s • Bites, particularly those from bedbugs, often cause a linear eruption that may occasionally be confused with rhus dermatitis.

Scab ie s • In scabietic infestations, other household or family members may report itching. Scabies has its own characteristic distribution of lesions: in the finger webs, wrists, genitals, and axillae. He rp e s Zo st e r • Nonpainful herpes zoster, with its linear series of blisters, can cause diagnostic confusion.

MANAGEMENT A limited eruption and mild itching may be relieved by the following. • Cool showers and application of frozen vegetable packages (e.g., frozen peas) may help. • Cool baths with colloidal oatmeal agents such as Aveeno are recommended. • Cool compresses of Burow’s solution help dry vesicles and bullae. • Calamine lotion is useful. • Potent or superpotent topical corticosteroids (class 1), such as clobetasol cream 0.05% two or three times daily. • Oral antihistamines are helpful, particularly at bedtime. In severe cases with widespread eruption and marked

pruritus, topical therapy may need to be supplemented with the following: • Systemic corticosteroids. Prednisone is usually used, in a tapering dosage schedule that often starts at 1 mg/kg and decreases by 5 mg every 2 days for at least 2 weeks and for as long as 3 weeks. The dosage may be increased again if flares occur during the tapering regimen. Prednisone tablets should be taken with meals, and the entire daily dose may be taken all at once, rather than in divided doses throughout the day. (Possible side effects of short-term systemic corticosteroids include gastrointestinal upset, sleep disturbances, and mood changes. Hyperactivity, anxiety, depression, and even paranoia have been reported.) • Intramuscular corticosteroids. Triamcinolone diacetate or hexacetonide may be used if the patient has gastrointestinal intolerance to oral corticosteroids. SEE PATIENT HANDOUT “Burow’s Solut ion ” ON THE SOLUTION SITE

HELPFUL HINTS To prevent rhus dermatitis, patients can learn to recognize its plants: • “Leaves of three, let it be.” If work or hobbies involve frequent exposure to poisonous plants, a barrier cream may be applied before exposure. • When people come into contact with the plant or its oil, they should wash with soap and cold water as soon as possible. All exposed clothing should be laundered. • Vaccines against poison ivy and other immunizations given orally or as injections may result in serious negative side effects and often fail. • Medrol Dosepaks (methylprednisolone) usually do not provide enough days of treatment for most patients with severe rhus dermatitis. 64

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• During the tapering prednisone regimen for treatment of severe rhus dermatitis, patients may experience a rebound of the eruption and itching. When this rebound occurs, it may be suggested that patients increase the dosage back to the one that worked the day before and then titrate downward thereafter. • There are advantages to prescribing doses consistently in increments of 5 mg. It is easier for the patient and health care provider to keep track of the dosage schedule, and tablets usually do not have to be broken in half to decrease the dose.

POINT TO REMEMBER • In patients with severe rhus dermatitis, it is important to continue prednisone for 2 to 3 weeks because a shorter course may allow a rebound of the condition.

Oth er Form s of Allergic Con tact Derm atitis Other than the poisonous Toxicodendron species, the most common contact allergens are nickel, thimerosal (a mercurial preservative), neomycin (a topical antibiotic), formaldehyde (found in shampoo and cosmetics), paraphenylenediamine (found in certain hair dyes), and quaternium-15 (a preservative often found in cosmetics). Patterns of distribution and shapes of the rash may serve as clues to the specific allergen, as in, for example, dermatitis from rubber in underpants (FIG. 2.30), neomycin in eardrops (FIG. 2.31), or nickel in earrings (FIG. 2.32). 2.31 Allergic contact dermatitis. This contact dermatitis was caused by neomycin in this patient’s ear drops.

2.30 Allergic contact dermatitis. This patient reacted to the rubber in the elastic waistband of her underpants. Note sparing at the sites where the garment did not come into constant contact with the skin.

2.32 Allergic contact dermatitis. Nickel in earrings caused the dermatitis on the earlobe and neck of this girl, who wore long earrings.

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DIAGNOSIS THE TOP TEN ALLERGENS • Nicke l. Found in jewelry, clasps, and m etal buttons. ACD to nickel is m ore com m on in wom en than in m en. • Go ld . Found in jewelry. • Balsam o f Peru. Included in perfum es and skin lotions. • Th im ero sal. Used as a preservative in local antiseptics and vaccines. • Ne o m ycin sulfat e. Found in first aid cream s and in som e cosm etic products. • Frag ran ce m ix. Found in foods, cosm etics, perfum es, insecticides, dental products, etc. • Fo rm ald e h yd e. A preservative that is included in paper products, dry cleaning solvents, paints, and cosm etic products. • Co b alt ch lo rid e. In hair dyes and m etals. • Bacit racin . A topical antibiotic. • Quat ern ium -15. A preservative often found in cosm etics and industrial agents.

• Patients should be questioned regarding their daily habits and occupational exposures, so that any possible contactants can be revealed. • Patch testing is used to identify specific allergens in patients with histories suggestive of ACD (FIGS. 2.33A–B). The allergens most commonly responsible for ACD are standardized and are available commercially. The allergens, which are fixed in dehydrated gel layers, are taped against the skin of the patient’s back for 48 hours and are then removed. A final reading is performed after 96 hours. The area is examined for evidence of contact dermatitis. The presence of erythema, papules, or vesicles (i.e., an acute eczematous reaction) is strongly positive. A bullous reaction is extremely positive. • Interpretation of patch test results and correlation with clinical findings require experience and are generally performed by dermatologists. DIFFERENTIAL DIAGNOSIS Conditions to include in the differential diagnosis are the following: • ICD • Other types of acute and chronic eczematous dermatitis (especially atopic dermatitis) • Systemic drug reactions

MANAGEMENT Patients with ACD may be managed with the following:

A

• Identification and removal of the inciting agent • Advice on how to avoid the inciting agent • Treatment with topical or systemic corticosteroids, if necessary

POINT TO REMEMBER • Patch testing may be the only way to differentiate ACD from ICD.

HELPFUL HINT B 2.33 A an d B Allergic contact dermatitis. Test patches. A: These test patches were removed after 48 hours. B: The final reading at 96 hours shows positive reactions to various allergens.

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• When an immediate reaction to a contactant occurs (i.e., visible hives develop in less than 30 minutes after exposure), this may indicate a contact urticaria (not ACD), particularly if urticarial in appearance and if associated with other symptoms such as distant urticaria, wheezing, angioedema, or anaphylaxis. Rubber latex currently is the most important source of allergic contact urticaria.

At o p ic H a n d Eczem a (Ch ro n ic H a n d Der m a t it is) BASICS • When eczema involves the hands and is caused by exposure to an irritant or an allergic contactant, the diagnosis is contact dermatitis (see earlier). • The onset of atopic hand eczema is uncommon before adolescence. After middle age, the frequency of acute episodes tends to decrease. • When there is no suggestive history or documentation of an exogenous cause of hand eczema, the diagnosis is most likely atopic hand eczema (also known as chronic hand dermatitis). Most patients with atopic hand eczema report an atopic history, such as a personal or familial atopic diathesis (e.g., asthma, hay fever, sinusitis), or patients may have had a previous episode of atopic dermatitis or a concurrent manifestation elsewhere on the body. Even with these findings, a diligent history must be taken to rule out contactant etiology. • In addition, patch testing (see earlier in this chapter) with putative allergens may be performed if an exogenous cause is suspected. • It is also common for both exogenous (contact) and endogenous (atopic) factors to be at work in the same patient. Whatever the origin, hand eczema is often a cause of social embarrassment and can result in performance problems in the workplace. DESCRIPTION OF LESIONS, CLINICAL MANIFESTATIONS, AND DISTRIBUTION OF LESIONS For descriptive purposes, atopic hand eczema may be divided into two clinical types that may overlap in the same patient: a “wet” type and a “dry,” scaly type.

“We t ” Typ e Dyshidrotic eczema, the wet type (FIGS. 2.34 and 2.35), was formerly referred to as pompholyx (the Greek word for bubble), which describes the following: • Itchy, clear vesicles. • The vesicles are typically located on the sides of the fingers, but they can also occur on the palms and, less commonly, on the soles of the feet and the lateral aspects of the toes. The term “dyshidrotic” is a misnomer based on the erroneous assumption that the vesicles were caused by “trapped sweat.” We now understand that they result from inflammation and foci of intercellular edema (“spongiosis”), which becomes loculated in the thicker stratum corneum of the palms and soles. • Initially, the very small and clear vesicles resemble little bubbles. • Later, as they dry and resolve without rupturing, they generally turn a golden brown color. • Secondary impetiginization may occur.

2.34 Atopic hand eczema, dyshidrotic or “wet” type. The characteristic vesicles (pompholyx) are apparent in this patient’s palm.

2.35 Atopic hand eczema, dyshidrotic or “wet” type. The vesicles on the sides of the fingers (arrows) are shown here.

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“Dry,” Scaly Typ e In nondyshidrotic hand eczema—the dry, scaly type—the following are noted:

2.36 Atopic hand eczema (“dry,” scaly type). The fingers have become dry and fragile, with resultant painful fissures.

• Lesions are scaly and red. • Scaly, hyperkeratotic, lichenified plaques may arise. • The fingertips may become dry, wrinkled, red, and fragile, with resultant painful fissures and erosions (FIG. 2.36). • The central palm or palmar aspect of the hands and fingers is also commonly affected in patients with chronic hand eczema. It is characterized by highly itchy, scaly palms. • Fissures in the folds of the hands and fingers are painful and can limit the use of the hands. • As with the dyshidrotic type of hand eczema, oozing and secondary bacterial infection (“honey-crusted” skin) can occur. • With long-standing disease, patients’ fingernails may reveal dystrophic changes (e.g., irregular transverse ridging, pitting, thickening, discoloration) when the nail matrix (root) becomes involved (see FIG. 2.17). FACTORS THAT MAY TRIGGER RECURRENCES Many of the triggers that exacerbate eczema are ubiquitous in daily life and in certain work settings. They include the following: • Emotional stress. • Environmental conditions (including seasonal changes, hot or cold temperatures, humidity). • Contact allergens (including nickel, balsams, paraphenylenediamine, chromates) and irritants (including soaps). • Staphylococcus aureus. This microbe is thought to play a role in the exacerbation of eczema because it is virtually omnipresent on the skin of patients with atopic dermatitis. Colonization with S. aureus results in the secretion of toxins (superantigens) that promote skin inflammation. DIAGNOSIS • The diagnosis of atopic hand eczema is usually made on clinical grounds or when other causes are excluded.

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DIFFERENTIAL DIAGNOSIS

Co n t act De rm at it is (FIG. 2.37). • This is suspected, particularly if the eruption is on the dorsum of the hands or feet. • Contact dermatitis is considered when the patient has a history of exposure to a suspected contactant. • On occasion, contact allergy to nickel has been shown to cause dyshidrotic eczema.

• The patient may have evidence of psoriasis elsewhere on the body or a personal or family history of psoriasis.

Scab ie s (See Chapter 20, “Bites, Stings, and Infestations.”) • This diagnosis should be considered if there is an acute pruritic vesicular eruption in the web spaces of the fingers.

Tin e a Man uum FIGURE 2.38. • This is suggested by well-demarcated plaques on the palms (often on one palm only) and soles or a positive KOH examination or fungal culture.

Pso riasis o n t h e Palm s FIGURE 2.39. • This may be indistinguishable from hand eczema. • Pustular psoriasis of the palms may also, at times, be indistinguishable from pustular dyshidrotic hand eczema.

2.37 Contact dermatitis. This eczematous dermatitis on the dorsa of the hands was caused by exposure to latex gloves.

2.38 Tinea manuum. Only one palm shows a welldemarcated plaque. The scale of this palm was positive for fungus.

2.39 Psoriasis of the palms. These palmar lesions can easily be mistaken for eczema or tinea manuum.

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MANAGEMENT

Mild Case s Patients with mild cases of atopic hand eczema are managed as follows. • Mild cleansers or soap substitutes are recommended. • Protective cotton-lined gloves should be used for washing dishes or other similar tasks. • Fastidious hand protection is necessary, with emollient barrier creams, protective gloves, and the avoidance of irritants and allergens. • For oozing and infected lesions, compresses with Burow’s solution (aluminum acetate) are applied. This treatment promotes drying and has an antibacterial effect. The solution is applied in a 1:40 dilution two or three times daily until bullae resolve (usually within a few days). • Topical corticosteroids are the mainstay of treatment. Ointments penetrate skin better than creams do, but patients may prefer to use creams during the day. Most patients require medium-potency (class 3) corticosteroids (e.g., triamcinolone 0.1%), with or without occlusion. However, higher-potency (class 2) corticosteroids (e.g., fluocinonide 0.05%) can be used on an asneeded basis. Lower-strength (class 5) corticosteroids (e.g., hydrocortisone valerate 0.2%) may sometimes be applied for long-term maintenance. • Short-term application of Protopic ointment (tacrolimus) 0.1% or Elidel cream (pimecrolimus) 1% may also be effective.

Se ve re Case s Severe atopic hand eczema is often very difficult to manage. • Application of corticosteroids under occlusion is occasionally effective when it is done early in the course of an eruption. However, potent topical corticosteroids applied under plastic or vinyl occlusion and superpotent topical corticosteroids can be used only intermittently and for short periods, because they increase the risk of atrophy. • Systemic antibiotics should be administered for obvious or suspected secondary infection. • Short-term use of systemic corticosteroids may be required for very severe flares. However, they should be given very infrequently. • Treatment of hyperkeratotic palmar eczema is notoriously difficult. Acitretin (Soriatane), an aromatic retinoid, may help control hyperkeratosis. • Other measures, such as oral psoralen plus topical ultraviolet A (PUVA), oral cyclosporine, azathioprine, and low-dose methotrexate are used for severe, refractory cases. • Superficial X-irradiation (rarely used today) had been used to treat some patients with resistant chronic hand eczema.

SEE PATIENT HANDOUTS “Buro w’s So lut io n ” AND “Han d Ecze m a” ON THE SOLUTION SITE

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Eczem a Va ria n t s Numerous common clinical variants of eczema are recognized: nummular eczema, lichen simplex chronicus, prurigo nodularis, asteatotic eczema, neurotic excoriations, hand eczema, and nonspecific eczematous dermatitis. These disorders are usually found in patients with an atopic history. However, on occasion, they manifest in patients without an atopic predisposition; in such instances, a methodic search for an exogenous cause, such as a contact dermatitis, is often necessary. Included here are stasis dermatitis and seborrheic dermatitis, which are also eczematous eruptions that may or may not be related to an atopic history.

Nu m m u lar Eczem a DESCRIPTION OF LESIONS

2.40 Nummular eczema. Erythematous, coin-shaped lesions are seen in a typical location.

The round lesions of nummular eczema often have the shape of coins. The word “nummular” comes from the same root as “numismatic,” meaning “coin-shaped.” Lesions are usually itchy eczematous patches and plaques that often occur in clusters (FIGS. 2.40 and 2.41). Although this disorder is usually seen in patients who have a history of atopy, it is not uncommon in adult patients who do not have such a history. DISTRIBUTION OF LESIONS Lesions are seen mainly on the legs; less commonly, they arise on the arms and trunk. The patches or plaques sometimes clear centrally and resemble tinea corporis (“ringworm”). Healing or resolving lesions often display postinflammatory hyperpigmentation, particularly in dark-skinned patients. DIAGNOSIS • The diagnosis of nummular eczema is based on the clinical appearance and, if necessary, negative results of a KOH examination.

2.41 Nummular eczema. These coin-shaped scaly lesions show evidence of postinflammatory hyperpigmentation.

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Tin e a Co rp o ris FIGURE 2.42.

• In tinea corporis, the KOH examination or fungal culture is positive. • Nummular eczema is frequently misdiagnosed as tinea corporis (“ringworm”).

• Lesions of tinea corporis are often—but not always— clear in the center (annular).

Pso riasis FIGURE 2.43.

DIFFERENTIAL DIAGNOSIS

• Psoriasis is less likely to itch than nummular eczema. • Psoriatic lesions frequently occur on elbows and knees and may have a whitish or micaceous scale.

Lich e n Sim p le x Ch ro n icus (See later in this chapter.) • Focal lichenified plaques are noted. • Often, a positive atopic history is present.

2.42 Tinea corporis (ringworm). Initially treated as nummular eczema, this itchy eruption has a scaly border that demonstrated hyphae on potassium hydroxide examination. Note the resemblance to both nummular eczema and psoriasis. This is often referred to as “tinea incognito.”

MANAGEMENT • Nummular eczema can often be controlled by an intermediate-strength (class 3 or 4) topical corticosteroid, such as triamcinolone acetonide cream 0.1%, applied sparingly two to three times daily. • If necessary, a high-potency (class 1) topical corticosteroid, such as clobetasol cream 0.05% once or twice daily, may be used.

2.43 Psoriasis. This patient has erythematous papules with typical psoriatic scale. Again, note the similarity to nummular eczema.

• Recalcitrant cases may require occlusion—provided by a polyethylene wrap or Cordran tape (flurandrenolide)— or intralesional corticosteroid injections. • Long-term treatment can be accomplished with less potent topical corticosteroids.

POINT TO REMEMBER • Nummular eczema is frequently misdiagnosed as tinea corporis (“ringworm”) and is often inappropriately treated with topical antifungals as well as combination antifungal/topical steroid combinations. 72

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Lich en Sim p lex Ch ron icu s Also known as neurodermatitis, lichen simplex chronicus is a common, chronic, often solitary, pruritic eczematous eruption caused by repetitive rubbing and scratching. It is seen most commonly in adults, particularly in patients with other atopic manifestations, such as asthma and allergic rhinitis. CLINICAL MANIFESTATION AND DISTRIBUTION OF LESIONS Patients with lichen simplex chronicus have a focal lichenified plaque or multiple plaques, most often on the nape of the neck, scalp, external ear canals, wrists, extensor forearms, ankles (FIG. 2.44), pretibial areas, or inner thighs. Lichen simplex chronicus may also involve the vulvae, scrotum (FIG. 2.45), intragluteal area (FIG. 2.46), and perianal area (pruritus ani) (FIG. 2.47). Patients often have only one area of involvement. Chronic or paroxysmal pruritus is the primary symptom.

2.45 Lichen simplex chronicus. Scrotal lichenification in an atopic patient. This condition is often mistaken for tinea cruris.

DIAGNOSIS • The diagnosis is readily apparent and is made on clinical grounds.

2.46 Lichen simplex chronicus. A lichenified gluteal plaque is seen in this atopic patient.

2.44 Lichen simplex chronicus. This focal lichenified plaque involves the distal pretibial area and ankle. This patient not only scratched the lesion, but he also persistently rubbed it with his contralateral heel.

2.47 Lichen simplex chronicus. Perianal lichenification in an atopic patient. This is a frequent cause of pruritus ani.

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DIFFERENTIAL DIAGNOSIS IN GENITAL AREA

Tin e a Cruris an d Can d id iasis FIGURE 2.48. • A chronic itchy vulvar or scrotal rash may also suggest a fungal infection such as tinea cruris or candidiasis. • KOH examination or fungal culture is positive.

In ve rse Pso riasis an d In t e rt rig o FIGURES 2.49 and 2.50. • Inverse psoriasis and intertrigo should be considered when lesions involve the inguinal creases and perianal area.

2.49 Inverse psoriasis. KOH-negative erythema in a patient who has psoriasis.

2.48 Tinea cruris. This is a typical scaly, KOH-positive example of fungal infection. Note the scalloped shape of the lesions and the “active” scaly border. 2.50 Inverse psoriasis. This is the same patient as in the previous figure.

MANAGEMENT • The most important aspect of therapy is the elimination of scratching and rubbing. Unfortunately, many patients scratch themselves in their sleep. • As with nummular eczema, lichen simplex chronicus may be treated with an intermediate-strength (class 3 or 4) topical corticosteroid. If necessary, a high-potency (class 1) topical corticosteroid can be used. • Occlusion, when required, has the added advantage of preventing patients from scratching or rubbing—or, at least, reminding them not to do so. 74

• Oral antihistamines may be helpful at bedtime because of their sedative effect. • Protopic ointment (tacrolimus) 0.03% or 0.1% may prove beneficial in patients with vulvar or perianal lichen simplex chronicus. (Patients should be warned about the potential for stinging and burning when tacrolimus ointment is applied to these sensitive areas.) • Alternatively, Elidel cream 1% (pimecrolimus) may be effective. It is less irritating than Protopic ointment.

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Pru rigo Nod u laris Another chronic, but much less common, variant of atopic dermatitis is prurigo nodularis. It is seen in the same clinical context as lichen simplex chronicus and may be considered a papular or nodular form. DESCRIPTION OF LESIONS Lesions are reddish, brown, or hyperpigmented dome-shaped papules or nodules that resolve with postinflammatory hyperpigmentation (FIG. 2.51). CLINICAL MANIFESTATION AND DISTRIBUTION OF LESIONS • Lesions are most commonly noted on the pretibial shafts and sometimes on the extensor areas of the arms. • They are often crusted or excoriated—pruritus may be intense. • Healing generally results in significant postinflammatory hyperpigmentation. 2.51 Prurigo nodularis. These intensely pruritic excoriated papules on the pretibial shafts show marked postinflammatory hyperpigmentation.

MANAGEMENT • Prurigo nodularis tends to be very resistant to topical corticosteroids. • Occlusion topical steroid therapy with Cordran tape or a class 1 topical steroid are sometimes effective. • In recalcitrant cases, intralesional corticosteroid injections may be helpful.

• Thalidomide has been reported as effective in intractable cases. (Thalidomide should not be used in women who are pregnant. In the United States, only physicians who are part of a special registry are permitted to administer this drug.)

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Asteatotic Eczem a A common form of dermatitis, asteatotic eczema appears in dry, cold winter months. It is also referred to as winter eczema, and because its lesions consist of scaly patches with superficial fissures that resemble a cracked antique china vase, it is sometimes called erythema craquelé. It occurs only in adults. CLINICAL MANIFESTATION AND DISTRIBUTION OF LESIONS

2.52 Asteatotic eczema (erythema craquelé). The scaly patches on this patient’s shin demonstrate superficial fissures that resemble a cracked antique china vase or a dry riverbed.

• The condition may be pruritic. • Lesions consist of characteristic scaly patches with very shallow erythematous fissures resembling a cracked, dry riverbed (FIG. 2.52). • They are located most commonly on the shins, arms, hands, and trunk.

DIFFERENTIAL DIAGNOSIS MANAGEMENT • Asteatotic eczema is usually managed readily by having the patient bathe less frequently and apply moisturizers regularly. • A very effective treatment is Lac-Hydrin (12% ammonium lactate cream or lotion), which is available only by prescription, and the similar preparation, AmLactin, which can be obtained without a prescription. These agents are applied immediately after bathing. • If necessary, pruritic lesions respond readily to low- to moderate-strength (class 3 or 4) topical corticosteroids.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS • Nonspecific eczematous dermatitis is a diagnosis of exclusion when no underlying cause, such as a contact allergen, scabies, or occult fungal infection (tinea incognito), is found.

MANAGEMENT • Treatment consists of an intermediate-strength (class 3 or 4) topical corticosteroid.

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• The differential diagnosis of asteatotic eczema includes xerosis (dry skin) and nummular eczema.

“Neu rotic” Excoriation s an d Factitia Patients with neurotic excoriations, also referred to as neurodermatitis, compulsively pick at their skin. Lesions may accompany or exacerbate atopic dermatitis, or they may have been preceded by atopic dermatitis or an insect bite. Most often, no precipitating cause can be determined.

Non sp ecific Eczem atou s Derm atitis Many people, particularly the elderly, have chronic, recurrent, itchy, eczematous dermatitis without the typical distribution of atopic dermatitis. These patients may or may not have an apparent atopic history. Frequently, they complain of dry or sensitive skin that tends to become drier and itchier in winter months. The eruption tends to worsen with aging, as the skin loses some of its barrier function and lubrication (asteatosis). Itching with or without specific lesions tends to occur on the arms, legs, and upper back.

• If necessary, a higher-potency (class 1 or 2) topical corticosteroid may be used. Patients with nonspecific eczematous dermatitis should avoid the use of soap on affected areas. In dry winter months, moisturizers may be beneficial.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

CLINICAL MANIFESTATION AND DISTRIBUTION OF LESIONS • Lesions frequently suggest an external cause, often referred to as an “outside job” by dermatologists. Lesions are often noted to be erosions, linear crusts, or ulcerations that suggest manipulation by the patient. Postinflammatory hyperpigmentation and whitish hypopigmented lesions indicate chronicity (FIG. 2.53). • Deep ulcerations with geometric shapes suggest factitia (FIG. 2.54), a self-induced condition caused by habitual scratching or picking. In factitia, lesions tend to show a wide range of bizarre patterns (FIG. 2.55) uncharacteristic of any specific disease. The presence of factitia may imply that the patient has severe emotional problems. • The lesions of neurotic excoriation tend to be located on the upper back or ankles—areas that are easily reachable by the patient (see FIG. 2.53). • Factitial lesions may appear anywhere and often have bizarre shapes. • Many patients with neurotic excoriations or factitia may also show signs and symptoms of a neurosis (e.g., obsessive-compulsive disorder) or a delusional psychosis that underlies the repetitive self-destructive behavior.

2.53 Neurotic excoriations (neurodermatitis). Lesions tend to be located on the upper back or ankles, areas that are easily reachable.

DIAGNOSIS • The diagnosis is either given by the patient, who readily admits that the lesions are self-created, or the lesions themselves may be indicative. • Bizarre lesions and a la belle indifférence affect on the part of the patient suggest factitial dermatitis as the cause.

MANAGEMENT

2.54 Factitial ulcerations. These were created by the patient. Note their geometric appearance. The patient has a severe psychiatric disorder.

• High-potency topical corticosteroids, topical corticosteroids under occlusion, and intralesional corticosteroids are sometimes useful, but these treatments will be ineffective if the underlying psychologic cause is not addressed. • Bedtime antihistamines are sometimes helpful. • Psychotherapy and/or psychopharmacologic drugs should be used, if indicated.

HELPFUL HINT • When the diagnosis is in doubt, the lesions may be covered with a thick dressing, and the patient is then instructed not to remove it. Consequently, when the patient cannot access them, the lesions heal rapidly.

2.55 Factitial purpura. These purpuric lesions were obviously self-induced.

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Seb o r rh eic Der m a t it is (“Seb o r rh eic Eczem a ”) BASICS • Seborrheic dermatitis is a very common, chronic inflammatory dermatitis. Its characteristic distribution involves areas that have the greatest concentration of sebaceous glands: scalp, face, presternal region, interscapular area, umbilicus, and body folds (intertriginous areas). • Many people experience some degree of dandruff—a whitish scaling of the scalp that is sometimes itchy and is fairly easily controlled with dandruff shampoos. When dandruff is accompanied by erythema, a sign of inflammation, it is referred to as seborrheic dermatitis. When seborrheic dermatitis occurs in the body folds, it is called intertrigo, or intertriginous seborrheic dermatitis. • Seborrheic dermatitis is seen more commonly in male patients and often begins after puberty. There appears to be a hereditary predisposition to its development. When it presents in patients who are infected with the human immunodeficiency virus, seborrheic dermatitis may serve as an early marker of the acquired immunodeficiency syndrome. Seborrheic dermatitis is also seen commonly in patients with Parkinson’s disease and in patients taking phenothiazines. • Seborrheic dermatitis has many features in common with chronic eczema and psoriasis. Typical lesions of seborrheic dermatitis often appear in patients with psoriasis, and the histologic features of the lesions of seborrheic dermatitis resemble those of both eczema and psoriasis. In fact, some dermatologists do not consider seborrheic dermatitis a distinct nosologic entity but instead assign it to various forms of eczema or psoriasis. In the latter case, the term “seborrhiasis” has been used. In the United Kingdom, seborrheic dermatitis is referred to as “seborrhoeic eczema.”

Pat h o g e n e sis • Traditionally, seborrheic dermatitis has been described as idiopathic. However, some evidence indicates that Pityrosporon ovale, a small yeast, may play a part in its pathogenesis because seborrheic dermatitis occasionally responds to antifungal medications (see following). • Because seborrheic dermatitis occurs only where the sebaceous glands are found, sebum has also been thought to play a role, although no link has been shown. DESCRIPTION OF LESIONS The appearance of the lesions of seborrheic dermatitis varies depending on their location. • On the face, lesions are red, with or without an overlying whitish scale, or they may appear as orange-yellow greasy patches. • On the scalp, seborrheic dermatitis may range from a mild erythema and scaling to thick, armorlike plaques that are indistinguishable from psoriasis (“sebopsoriasis”) (FIG. 2.56).

2.56 Seborrheic dermatitis. Scale and erythema are evident along the frontal hairline.

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• When lesions occur in body folds, they often consist of sharply defined, bright red plaques that may develop fissures. DISTRIBUTION OF LESIONS The eruption of seborrheic dermatitis tends to be bilaterally symmetric in its distribution. • Scalp, face. Lesions appear on the forehead, eyebrows, eyelashes, cheeks, beard, and nasolabial folds (FIG. 2.57). • Ears. Lesions occur behind the ears and in the external ear canal (FIG. 2.58). • Body folds. Body folds and anogenital areas are affected— inframammary areas, axillae, inguinal creases, intragluteal crease, perianal area, and umbilicus. In these areas, seborrheic dermatitis is often clinically indistinguishable from tinea cruris and inverse psoriasis. • Presternal lesions are not unusual and are scaly or papular.

2.57 Seborrheic dermatitis. Here we see typical involvement of the cheeks, eyebrows, eyelashes, and nasolabial folds.

CLINICAL MANIFESTATIONS • On the scalp, there may be itching and scale with resultant dandruff that, embarrassingly, often falls on clothing. • Facial seborrheic dermatitis usually flares in the winter and improves in the summer. However, many patients report provocation of the condition after sun exposure. • When fissures develop in the body folds and umbilicus, symptoms may consist of burning, itching, oozing, and pain.

Clin ical Varian ts Nonspecific vulvitis and balanitis and the interscapular “itchy back syndrome” are considered variants of seborrheic dermatitis by some dermatologists. Seborrheic dermatitis in infants is generally self-limiting and usually disappears by 8 months of age. It presents either as “cradle cap,” a buildup of a scaly, greasy adherent plaque on the vertex of the scalp, or as erythematous lesions in body folds. Both these presentations are probably unrelated to adult seborrheic dermatitis.

2.58 Seborrheic dermatitis. This patient has involvement of the retroauricular area.

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DIFFERENTIAL DIAGNOSIS • The differential diagnosis of seborrheic dermatitis varies depending on the age, sex, and ethnic background of the patient and, particularly, on the location of lesions.

Scalp an d Ext e rn al Ears Pso ria sis

FIGURES 2.59 and 2.60. • Psoriatic lesions elsewhere on body • Family history of psoriasis Eczem a t o u s Der m a t it is

2.59 Psoriasis. This is quite similar to seborrheic dermatitis seen in FIG. 2.56.

• Eczematous lesions elsewhere on body • Atopic history • Onset often before adolescence Tin ea Ca p it is

• • • •

Preteen age group Prevalent in urban African-American toddlers Focal areas of alopecia Positive KOH examination or positive fungal culture

Face Er yt h ro t ela n giect a t ic Ro sa cea , Ro sa cea

FIGURE 2.61. • Telangiectasias • Acnelike papules and pustules “Bu t t er fl y” Ra sh o f Syst em ic Lu p u s Er yt h em a t o su s

2.60

Psoriasis. Note the similarity to FIG. 2.58.

• Positive antinuclear antibody test • Other features of lupus erythematosus Tin ea Fa cia le

• Lesions generally annular (ring-shaped) with an asymmetric distribution • Positive KOH examination or positive fungal culture

Bo d y Fo ld s an d Ge n it alia In verse Pso ria sis

FIGURES 2.49 and 2.50. • Often indistinguishable from seborrheic dermatitis (see Chapter 3, “Psoriasis”) • Negative KOH examination • No growth on fungal culture

2.61 Rosacea. This patient has typical acnelike papules and erythema in the central third of her face. (Note similarity to FIG. 2.57.) continued on page 81

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DIFFERENTIAL DIAGNOSIS Continued

• Fungal culture positive for Candida species • Most common in patients with diabetes mellitus

Tin ea Cr u ris

See FIGURE 2.48 and Chapter 7, “Superficial Fungal Infections.” • Arcuate shape with advancing “active border” with central clearing • Positive KOH examination or fungal culture

Eczem a t o u s Der m a t it is, Su ch a s At o p ic Der m a t it is

• Eczematous lesions elsewhere on the body • Atopic history • Marked pruritus

Ca n d id ia sis

See Chapter 7, “Superficial Fungal Infections.” • “Beefy” red plaques, “satellite pustules” • Positive KOH examination

MANAGEMENT Treatment options for seborrheic dermatitis vary according to the location of the lesions (TABLE 2.1).

Scalp Mild scalp seborrheic dermatitis generally responds to the numerous commercially available antidandruff, antiseborrheic shampoos that contain one or more of the following ingredients: zinc pyrithione, coal tar, salicylic acid, selenium sulfide, and/or sulfur, as well as the antifungals ciclopirox and ketoconazole. • The shampoos should be left on for at least 5 minutes after lathering. • For itching and inflammation, a medium-strength (class 3 or 4) topical steroid in a gel or solution, such as betamethasone dipropionate lotion 0.05% (Diprosone) or betamethasone valerate foam 0.12% (Luxiq foam), may be used, but only if necessary. Severe scalp seborrheic dermatitis (“sebopsoriasis”) is often managed in the same manner as psoriasis of the scalp. • Potent (class 2) agents such as fluocinonide gel 0.05% (Lidex) and superpotent (class 1) clobetasol propionate gel/lotion/foam 0.05% (Temovate, Olux foam, Clobex lotion) may be used. These topical steroids are frequently preceded by keratolytic agents to remove thick scale, allowing the medications to penetrate the scalp. • Scale may be removed with a keratolytic preparation (e.g., Salex, Keralyt) as often as necessary, usually two

to three times per week initially and then whenever it builds up again.

In t e rt rig in o us Bo d y Fo ld Are as • Other areas of the body. Body folds and genital areas are similarly treated with low-potency (class 4, 5, 6, or 7) topical steroids. Face • Seborrheic dermatitis of the face responds quickly to topical steroids, but this treatment requires long-term maintenance and vigilance to avoid atrophy, telangiectasias, and rosacealike side effects. • To minimize these unwanted reactions, low-potency topical steroids may be alternated with antifungals such as ketoconazole cream 2% (Nizoral), ketoconazole gel 2% (Xolegel), or ciclopirox 0.77% gel (Loprox). • Very low-potency (class 7) topical steroids are used, with caution, when treating seborrheic dermatitis of the eyelid. “Crad le Cap ” • Minor amounts of scale can be removed with mild antiseborrheic shampoos that contain sulfur and salicylic acid, such as Sebulex. Mineral oil or olive oil also help remove scale. • Stronger keratolytic agents such as Salex cream or lotion or Keralyt gel are used for thick, dense, adherent scale. • Very mild topical steroids may be applied to reduce inflammation and itching. continued on page 82

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MANAGEMENT Continued

Tab le 2.1 SEBORRHEIC DERMATITIS FORMULARY SCALP Shampoos/gels/lotions Antiseborrheics

Antifungals Keratolytics (agents that remove excessive scale) Topical corticosteroids Medium potency (class 4)

High potency (class 2) Superpotency (class 1)

Pyrithione zinc (Head & Shoulders*) shampoo Coal tar (Neutrogena T/Gel*) shampoo Coal tar (Zetar*) shampoo and emulsion 1% selenium sulfide (Selsun Blue*) shampoo 2.5% selenium sulfide shampoo 1% ketoconazole shampoo (Nizoral*) 2% ketoconazole shampoo (Nizoral), ciclopirox 0.77% (Loprox shampoo and gel) Sulfur 2%, salicylic acid 2% (Sebulex*) shampoo, or Salex cream or lotion, or Keralyt gel Tar plus salicylic acid (Neutrogena T/Sal*) shampoo Betamethasone valerate 0.1% (Valisone) Desoximetasone (Topicort) gel 0.05%, betamethasone valerate 0.12% (Luxiq Foam) Fluocinolone acetonide (Capex†) shampoo 0.01% Fluocinonide (Lidex) gel or solution 0.05% Clobetasol gel, foam, or scalp application 0.05%

FACE AND INTERTRIGINOUS AREAS Topical steroids Very low potency (class 7) Low potency (class 6) Medium potency (classes 4 and 5) Topical creams/ointments Antifungals

Immunomodulators

Hydrocortisone cream or ointment 0.5% to 1%* Desonide (DesOwen) cream, lotion 0.05%, desonide 0.05% foam (Verdeso) Hydrocortisone valerate (Westcort) cream, ointment 0.2% Ketoconazole (Nizoral*) 1% cream, ciclopirox 0.77% (Loprox gel), and (econazole cream 1% (Spectazole)* Ketoconazole (Nizoral) 2% cream, gel (Xolegel), foam (extina) Tacrolimus 0.03% and 0.1% (Protopic) ointment Pimecrolimus 1% (Elidel) cream

*Available over the counter. †This shampoo contains a mid-potent topical steroid. It is used two or three times weekly, as needed.

POINTS TO REMEMBER • Seborrheic dermatitis is often confused with psoriasis, rosacea, and fungal infections. • Topical steroids should be used only for brief periods for seborrheic dermatitis, as with all steroid-responsive dermatoses.

SEE PATIENT HANDOUT “Scalp Pso riasis: Scale Re m o val” ON SOLUTION SITE

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HELPFUL HINTS • Seborrheic dermatitis of the scalp is not seen in preadolescent children; therefore, excessive use of shampoos should not be encouraged in this age group. The child may actually have atopic dermatitis, which is only aggravated by frequent shampooing. • The application of topical antifungals may work as well or better than topical steroids in many cases. • The limited use of Protopic ointment (tacrolimus) 0.1% and Elidel cream (pimecrolimus) 1% may also be effective in the treatment of facial and intertriginous seborrheic dermatitis. • OTC ketoconazole (Nizoral) 1% cream or shampoo can be very effective for seborrheic dermatitis.

St a sis Der m a t it is BASICS • Stasis dermatitis (gravitational dermatitis) is an eczematous eruption that is most commonly located on the lower legs. It often appears on the medial ankles of middle-aged and elderly patients and rarely occurs before the fifth decade of life. • The dermatitis is a consequence of chronic venous insufficiency (“leaky valves”) and is seen more often in women, particularly those with a genetic predisposition to develop varicosities. It may also occur in patients with acquired venous insufficiency resulting from surgery (e.g., vein stripping or harvesting of saphenous veins for coronary bypass), deep venous thrombosis, or other types of traumatic injury to the lower venous system.

Pat h o g e n e sis • Traditionally, the following sequence of events has been proposed to explain the pathogenesis of stasis dermatitis:

2.62 Acute stasis dermatitis. This patient has the earliest signs of stasis dermatitis—pruritus, erythema, scale (eczematous dermatitis), and slight distal hyperpigmentation.

Varicose veins Reversed flow through incompetent valves Diminished venous return Increased hydrostatic capillary pressure Peripheral edema and relative tissue hypoxia • The preceding schema may account for the pruritic, eczematous eruption seen in the early stages of stasis dermatitis; however, several other theories offer explanations for the exact mechanism at the tissue level, and the issue is still a topic of debate. PROGRESSION OF LESIONS • Lesions begin with erythema and scale (eczematous dermatitis) (FIG. 2.62). Later, the rash may become subacute, with more intense erythema, edema, erosions, crusts, and secondary bacterial infection (FIG. 2.63). The rash may progressively lead to the chronic stages of stasis dermatitis, in which pigmentary changes occur. After an initial redness (from extravasated red blood cells), affected areas turn reddish brown (from iron left from the breakdown of red blood cells). • Postinflammatory hyperpigmentation (from melanin) also occurs. These colors may overlie a cyanotic background. • Ultimately, the skin thickens and becomes less supple and nonpitting, and it feels permanently bound down and fibrotic (“woody”) on palpation.

2.63 Subacute stasis dermatitis. This patient shows symptoms of more advanced stasis dermatitis—increased scale, peripheral edema, erosions, crusts, and secondary bacterial infection (“impetiginization”).

DISTRIBUTION OF LESIONS • Most cases of stasis dermatitis and associated ulcers are located on the medial malleolus. When symptoms progress, lesions may spread to the foot or calf.

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CLINICAL MANIFESTATIONS • Large venous varicosities may be evident proximal to the eruption, and superficial varicosities may surround the affected area (FIG. 2.64). • Pruritus may occur. • Ankle edema that is initially pitting later becomes fibrotic and nonpitting. • Even during inactive periods of the eruption, the skin remains thickened and permanently pigmented. Possible complications of stasis dermatitis include the following:

2.64 Chronic stasis dermatitis. Large venous varicosities are evident proximal to the eruption, and superficial varicosities surround the affected area.

• Venous stasis ulcers that are presumably caused by microcirculatory abnormalities and the generation of an inflammatory response. The ulcers may be exacerbated by trauma (e.g., scratching), bacterial infection, or improper care of the eczematous rash (FIG. 2.65). Such ulcers sometimes produce a dull pain. • Induration may progress to lipodermatosclerosis, which has a classic “inverted water bottle” appearance (FIGS. 2.66 and 2.67). • Autoeczematization (id reaction) is a widespread, often explosive, acute eczematous eruption that is presumably triggered by secondary bacterial infection (impetiginization) of eczema, with resultant circulating immune complexes released from the site of the stasis dermatitis lesions (FIGS. 2.68A–B). It is hypothesized that patients become sensitized to their own tissue breakdown products.

2.65 Cellulitis. This patient has a painful, tender, pretibial plaque. Image courtesy of Joseph Eastern, M.D.

2.66 Stasis dermatitis with venous stasis ulcer. Note the eczematous eruption, the nonpitting edema (“woody” fibrosis) surrounding the ulcer (lipodermosclerosis). 84

2.67 Lipodermosclerosis. Chronic stasis dermatitis has produced a circumferential fibrosis that gives the leg an “inverted water bottle” appearance.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

DIFFERENTIAL DIAGNOSIS

Ce llulit is • Typical stasis dermatitis is generally an obvious diagnosis, but it is often confused with cellulitis. Cellulitis (see FIG. 2.65) is an acute infection of skin and soft tissues characterized by localized pain, swelling, tenderness, erythema, and warmth. It is usually caused by gram-positive aerobic cocci (e.g., S. aureus, S. pyogenes). Ot h e r Diag n o se s • The presence of ulceration should point to other possible conditions, such as arterial disease, cryoglobulinemia, the antiphospholipid syndrome, protein C deficiency, skin cancer, or pyoderma gangrenosum.

A

B 2.68 A an d B Stasis dermatitis with secondary impetiginization. Autoeczematization. The same patient as in the previous figure. This patient’s ankle eruption has become widespread as a result of impetiginization of the eczema on her legs.

MANAGEMENT

St asis De rm at it is Dim in ish ed Ven o u s Ret u r n

• Venous return can be increased by engaging in regular exercise, such as brisk walking and bicycling. • Furthermore, the affected leg(s) should be elevated above the level of the heart. (Sitting with the leg elevated by a stool is inadequate.) • At night, leg elevation can be accomplished by propping up the foot end of the bed with 1 to 2 inches of plywood or a bedding fabric such as sheets. Ed em a

Significant edema may be managed with compressive therapy, which augments the “calf pump,” the mainstay of therapy for venous insufficiency. However, in the pres-

ence of arterial insufficiency, compression is contraindicated. • Support hose help decrease the stretching of blood vessels. Elastic bandages and specialized compression (Jobst-type) stockings that deliver a controlled gradient of pressure are strongly recommended. • The patient’s peripheral arterial circulation should be assessed (clinically or with a Doppler study) before compression is recommended. Ra sh

• The eczematous rash (stasis dermatitis) should be carefully managed with topical therapy. Burow’s solution soaks to help dry oozing or infected areas. • Twice-daily application of a low- to moderate-strength (class 4, 5, or 6) topical corticosteroid ointment (such as continued on page 86

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MANAGEMENT Continued desonide 0.05%, hydrocortisone valerate 0.2%, or, if necessary, triamcinolone 0.1%) is usually sufficient to treat the eczematous rash and alleviate any itching. • Patients should be advised not to apply topical corticosteroid preparations directly to stasis ulcers because the preparations may interfere with healing. Long-term use of potent topical corticosteroids may promote atrophy and should be avoided. • OTC preparations that contain benzocaine, lanolin, or neomycin should also be avoided, since patients with stasis dermatitis tend to develop contact dermatitis quite easily. In fect io n

• Obvious superficial infections (impetiginization) should be treated with systemic antibiotics that have activity against S. aureus and Streptococcus species (e.g., dicloxacillin, cephalexin, or a fluoroquinolone). • A widespread autoeczematized eruption may require treatment with both systemic corticosteroids and oral antibiotics.

St asis Ulce rs Stasis ulcers are managed by treating the underlying eczematous dermatitis, controlling weight, preventing infection, and using compression dressings. Venous ulcers at times produce a dull pain that is relieved by elevation. • Unna’s boot is a commercially available bandage (DomePaste bandage, Gelocast bandage) that is impregnated with zinc oxide paste. It is best applied in the morning, before edema progresses. After application, the bandage hardens into a cast. The boot decreases edema, promotes healing, and serves as a barrier from trauma (e.g., scratching). It should be changed weekly until the ulcer heals. • If feasible, corrective surgery, such as skin grafts or vascular procedures, may be another option. • The areas surrounding the ulcer may be treated with topical steroids, whereas the ulcer itself can be treated with moist wound healing methods, high-compression therapy, fibrinolytic agents, and newer modalities, such as growth factors, matrix materials, and biologically engineered tissue. (These methods are beyond the scope of this chapter.)

SEE PATIENT HANDOUT “Buro w’S So lut io n ” ON THE SOLUTION SITE

POINTS TO REMEMBER • Stasis dermatitis is often misdiagnosed as cellulitis. • Infected stasis dermatitis should be considered in patients who develop a sudden onset of extensive generalized eczematous dermatitis (autoeczematization). • Contact dermatitis or autoeczematization should be considered in patients who become clinically worse despite appropriate topical treatment. • Compression is the mainstay of therapy for venous insufficiency and venous leg ulceration.

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HELPFUL HINTS • Sitting in a reclining chair while reading or watching television can help promote venous return. • Walking regularly at a brisk pace should be encouraged. • Physical therapy should be considered. • Smoking and long periods of standing or sitting should be discouraged.

C H AP T ER

Psoriasis

3 OVERVIEW Psoriasis (psoriasis vulgaris) is a red and scaly chronic skin condition of unknown cause. The primary concern to most patients is the unsightly appearance of lesions whose visibility and persistence often lead them to feel self-conscious and unclean. The emotional toll and the personal struggle to come to terms with psoriasis are expressed in an autobiographic short story, “At War with my Skin,” by John Updike, an author with severe psoriasis. After undergoing an operation for a broken leg, Updike reflected, “I chiefly remember amid my pain and helplessness being pleased that my shins, at that time, were clear and I would not offend the surgeon.” Psoriasis affects 1% to 2% of the world’s population. The condition is much less common in West Africans, AfricanAmericans, Native Americans, and Asiatic people than it is in whites. It is found equally in men and women. Psoriasis most frequently begins in the second or third decade of life, but it can first present in infants or in the elderly. About 30% of patients with psoriasis have a family history of the disease. Patients may also develop psoriatic arthritis, which may precede or follow the onset of skin lesions. Psoriasis can be a major blow to one’s ego. It may stifle social activities and sexual spontaneity, interfere with job opportunities, and inhibit participation in sports and the use of beaches and public swimming pools. Because psoriasis is a visible disease, it may arouse a fear of contagion, as well as repugnance and avoidance, from persons who are not used to seeing it. The young child with psoriasis has the additional burden of embarrassment caused by the undisguised scrutiny and thoughtless remarks of other children. A parent may have to cope with guilt for having genetically passed psoriasis on to his or her child. A person who has psoriasis often spends an excessive amount of time treating skin lesions and trying to hide them, as well as searching for external causes and possible cures. The National Psoriasis Foundation provides information about psoriasis to educate patients, the public, and health care providers. The contact information is as follows: 6600 S.W. 92nd, Suite 300, Portland, OR 97223; 800-723-9166; www.psoriasis.org.

The clinical presentations of psoriasis listed here create a som ewhat artificial classification, which is based on the characteristics or m orphology of the predom inant type of lesion and its distrib ution. There m ay be com p osites of these different types in a given patient. Because each type is m anaged som ewhat differently and has its own differential diagnosis, each is discussed separately. LOCALIZED PLAQUE PSORIASIS GENERALIZED PLAQUE PSORIASIS ACUTE GUTTATE PSORIASIS (SEE ALSO CHAPTER 27, “SPECIAL CONSIDERATIONS IN THE SKIN OF PEDIATRIC AND ELDERLY PATIENTS”) ERYTHRODERMIC PSORIASIS (EXFOLIATIVE DERMATITIS SECONDARY TO PSORIASIS) (SEE ALSO CHAPTER 25, “CUTANEOUS MANIFESTATIONS OF SYSTEMIC DISEASE”) PSORIASIS IN CHILDREN (SEE ALSO CHAPTER 27, “SPECIAL CONSIDERATIONS IN THE SKIN OF PEDIATRIC AND ELDERLY PATIENTS”) HIV-INDUCED PSORIASIS (SEE ALSO CHAPTER 24, “CUTANEOUS MANIFESTATIONS OF HIV INFECTION”) INVERSE PSORIASIS (ON THE GROIN, PENIS, AXILLAE, AND PERIANAL AND INFRAMAMMARY REGIONS) PSORIASIS OF THE PALMS AND SOLES SCALP PSORIASIS PSORIATIC NAILS (SEE ALSO CHAPTER 13, “DISEASES AND ABNORMALITIES OF NAILS”) PSORIATIC ARTHRITIS OTHER RARE CLINICAL VARIANTS: LOCALIZED PUSTULAR PSORIASIS (HALLOPEAU) AND THE RARE GENERALIZED PUSTULAR PSORIASIS OF VON ZUMBUSCH

87

Pat h o p h ysio lo g y • Psoriasis is essentially an inflammatory skin condition with abnormal epidermal differentiation and hyperproliferation. It is suggested that the inflammatory process is immunologically based and most likely set off—and maintained by—T cells in the dermis. • The lesions of psoriasis result from an increase in epidermal cell turnover. The cell’s transit time from the basal layer of the epidermis to the stratum corneum is decreased from the normal 28 days to 3 or 4 days. • This “turned-on” epidermis, with its rapid accumulation of cells, accounts for the characteristic lesion of psoriasis: a red papule or plaque (FIG. 3.1). It also explains the accumulation of white or silvery (micaceous) scale; the great increase in cellular kinetics does not allow time for shedding (FIGS. 3.2 and 3.3). • Because psoriasis is now considered to be an immunologic disease, most current therapies, including topical corticosteroids, phototherapy, photochemotherapy, methotrexate, and cyclosporine, are directed at the suppression of responsible T cells.

3.1 Psoriasis. This is a typical location for the characteristic lesions of psoriasis. Note the well-circumscribed erythematous plaques surmounted by a fine scale.

3.2 Psoriasis. Here the scale is thicker (hyperkeratotic) and white in color.

3.3 Psoriasis. The silvery, shiny luster of the micaceous scale is obvious.

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Hist o p at h o lo g y The histopathologic findings demonstrate the altered cell kinetics of psoriasis (ILL. 3.1):

Scales

Excessive cell division

Inflammation

• Increased mitosis of keratinocytes, fibroblasts, and endothelial cells. Skin biopsies typically show: • Marked thickening (acanthosis) and also thinning of the epidermis with resultant elongation of the rete ridges • Parakeratosis (nuclei retained in the stratum corneum) • Inflammatory process: • Dermal inflammation (lymphocytes and monocytes) • Epidermal inflammation (polymorphonuclear cells) in the stratum corneum that may form the so-called microabscesses of Munro Psoriasis

DISTRIBUTION OF LESIONS The distribution of thickened, reddened, silvery or whitish, scaly papules or plaques can range from only a few small asymptomatic lesions on the elbows and knees to larger plaques that cover extensive areas of the body.

I3.1 Psoriasis. Scales, excessive cell division, and inflammation.

• Psoriasis tends to be remarkably symmetric. It usually spares the face. Lesions are most commonly located as follows: • On large extensor joints (elbows, knees, and knuckles) • On the scalp • On the anogenital region (perineal and perianal areas, glans penis) • On the palms and soles • Trunk lesions may be small, guttate (teardrop-shaped) plaques or large plaques. • When psoriasis involves only the scalp and retroauricular areas, it is sometimes referred to as “sebopsoriasis” or “seborrhiasis” (see FIGS. 2.56 and 2.58). • When the entire body is involved, generalized, disseminated plaques or exfoliative erythroderma may be evident. • When lesions occur primarily in the intertriginous areas (inguinal creases, axillae, and inframammary, perineal, and perianal areas), this manifestation is referred to as inverse psoriasis. • Psoriasis is commonly a cause of nail deformity, which is often mistaken for, and treated incorrectly as, a nail fungus infection (onychomycosis). • Psoriatic arthritis occurs in 5% to 10% of patients who are diagnosed with psoriasis. CLINICAL MANIFESTATIONS

Prurit us • Psoriasis generally is asymptomatic, but it can become quite pruritic and uncomfortable, particularly during acute flareups or when it involves the scalp or intertriginous regions.

Chap ter 3 • Psoriasis

89

Th e Kö b n e r Re act io n (Iso m o rp h ic Re sp o n se ) • Patients commonly recognize the phenomenon that new lesions may appear at sites of injury or trauma to the skin. • Noxious stimuli, such as scratching and rubbing, or a sunburn can elicit a Köbner reaction (FIGS. 3.4 and 3.5; see also FIG. 4.16). Fissurin g o f Plaq ue s • Painful fissures may occur when lesions are present over joints, intragluteally, or on the palms and soles.

3.4 Psoriasis. The Köbner phenomenon is localized to the area of sunburn. The region that had been covered by the patient’s bathing suit is almost free of lesions.

3.5 Psoriasis. The Köbner phenomenon is evident in this diabetic patient, who developed psoriatic plaques at the sites of insulin injections.

90

Psych o so cial Pro b le m s The health care provider should be attuned to the psychologic ramifications of psoriasis—anxiety, social isolation, alcoholism, depression, suicidal ideation—as possible associations and outcomes of this essentially benign skin disease. Stress has been implicated in the acute exacerbations and progression of psoriasis. In a vicious cycle, the poor self-image that may be incited by lesions can create more stress. Factors that may adversely influence psoriasis include: • Alcohol. Alcohol overindulgence has been reputed to exacerbate psoriasis, which, once again, can create a vicious cycle of worsening the alcohol overindulgence. • Drugs. Antimalarials, beta-blockers, angiotensin-converting enzyme inhibitors, certain nonsteroidal anti-inflammatory drugs (e.g., indomethacin), systemic interferon, and lithium carbonate have been reported to worsen psoriasis; however, preexisting psoriasis is not necessarily a contraindication to their use. Both systemic and potent topical steroids have been known, albeit rarely, to trigger a severe, acute, potentially fatal pustular psoriasis (pustular psoriasis of von Zumbusch) that tends to occur after withdrawal of the medication. • Physical trauma. Surgery, thermal and chemical burns, and infections potentially exacerbate psoriasis. For example, an increase in psoriasis activity has been observed in patients who are, or become, infected with the human immunodeficiency virus (HIV). • Sunlight. A small minority of patients find that their psoriasis is worsened by strong sunlight, probably via the Köbner reaction (FIG. 3.4), whereas the vast majority of patients generally consider sunlight to be beneficial. • Other factors. There is evidence that psoriasis is associated with smoking, obesity, and dyslipidemia. It has also been noted that severe psoriasis appears to increase the risk of a myocardial infarction.

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

Co urse • Psoriasis is an erratic condition with an unpredictable, waxing-and-waning course. It has no known cure; however, there are many methods of keeping it under control. • Many patients tend to improve during the summer and worsen during the colder periods of the year. This fluctuation is presumably the result of the positive influence of sunlight on psoriasis. • There have been anecdotal reports of patients with psoriasis who were “cured,” and some patients claim that they “grew out of it.” This situation may be explained by either a misdiagnosis of the original skin problem or by cases of acute guttate psoriasis (see later discussion) that resolved without recurrence.

DIFFERENTIAL DIAGNOSIS The differential diagnosis of psoriasis varies, depending on the type and location of lesions. In general, psoriasis most often must be differentiated from the following: • • • • • •

Eczematous dermatitis Superficial fungal infection Seborrheic dermatitis Pityriasis rosea Drug eruption Parapsoriasis and mycosis fungoides (cutaneous T-cell lymphoma) • Secondary syphilis, the “great imitator”

DIAGNOSIS • The diagnosis of psoriasis is made on clinical grounds. • A skin biopsy or fungal studies may be performed to rule in or rule out other possible diagnoses.

SEE PATIENT HANDOUT, “Psoriasis” ON THE SOLUTION SITE

Chap ter 3 • Psoriasis

91

Lo ca lized Pla q u e Pso ria sis BASICS In its mildest manifestation, psoriasis is an incidental finding and consists of mildly erythematous, scaly patches on the elbows or knees. Localized plaque psoriasis, the most common presentation of psoriasis, may remain limited and localized (FIGS. 3.6–3.8), or it may become unstable and become widespread. DIAGNOSIS

3.6

Psoriasis. Note the symmetry of the plaques.

3.7

Psoriasis. Typical lesions on knuckles.

• If the typical well-demarcated whitish or silvery plaque is present in the usual locations, the diagnosis of psoriasis is quite evident. • Other helpful diagnostic features include a family history of psoriasis and nail findings (see later in this chapter and also Chapter 13, “Diseases and Abnormalities of Nails”). • If necessary, other tests, such as a skin biopsy and fungal examinations, can be performed to rule out other conditions. For example, Bowen’s disease, parapsoriasis, and mycosis fungoides are diagnosed by skin biopsy (see FIG. 3.12).

3.8 Psoriasis. Widespread plaques on buttocks (compare to FIGS. 3.12 and 3.13).

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DIFFERENTIAL DIAGNOSIS

Ecze m at o us De rm at it is (Lich e n Sim p le x Ch ro n icus an d At o p ic De rm at it is) FIGURE 3.9 and see Chapter 2, “Eczema.” • The patient or a close relative may have a history of atopy. • Lichenification (an exaggeration of normal skin markings) may be present. Lesions are poorly demarcated; they blend gradually into normal surrounding skin. • Usually, lesions itch, and crusts and excoriations may be seen.

Num m ular Ecze m a FIGURE 3.10. • An atopic history may or may not be present. • An extensor or flexural distribution is noted, most often on the legs. • “Coin-shaped” patches and plaques are present. • Usually, lesions itch (often a major differentiating factor from psoriasis), with possible crusts, excoriations, and lichenification.

Tin e a Co rp o ris FIGURE 3.11. • Patients may have a history of exposure to fungus. • Lesions usually are annular (“ringlike”)—round and clear in the center but may present a plaques. • The potassium hydroxide (KOH) examination or fungal culture is positive. • Lesions usually itch.

3.10 Nummular eczema. Pruritic, round, nummular (coin-shaped), itchy patches with erythema, crusts, and lichenification.

Bo we n ’s Dise ase (Sq uam o us Ce ll Carcin o m a in Sit u) • The solitary lesion may resemble a typical psoriatic plaque. • The condition is unresponsive to topical steroids.

3.11 Tinea corporis. Asymmetric erythema and KOHpositive scale (“active border”). This patient has a “psoriasiform” plaque.

3.9 Eczema (lichen simplex chronicus). Note the lichenification and poor demarcation of these lesions (they blend gradually into normal surrounding skin).

continued on page 94

Chap ter 3 • Psoriasis

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DIFFERENTIAL DIAGNOSIS Continued

Parap so riasis • The term “parapsoriasis” derives from the fact that the condition clinically resembles psoriasis but in fact is a completely different entity. • Idiopathic multiple, barely elevated patches are usually found on the trunk and arms. • There are small and large plaque variants. Myco sis Fun g o id e s (Cut an e o us T-Ce ll Lym p h o m a) FIGURE 3.12. • “Smudgy” patches and plaques or tumors are noted, usually on the buttocks and trunk. • Lesions are often pruritic. • A biopsy may demonstrate a cutaneous T-cell lymphoma.

MANAGEMENT

Ge n e ral Prin cip le s • Because psoriasis is a chronic skin condition, any approach to its treatment must be considered for the long term. Treatment regimens must be individualized according to age, sex, occupation, personal motivation, other health conditions, and available resources. Disease severity is defined by the number and extent of plaques present, as well as by the patient’s perception and acceptance of the disease. Treatment, therefore, must be designed with the patient’s specific expectations in mind. • Therapy for psoriasis is aimed at decreasing size and thickness of plaques, reducing pruritus, alleviating arthritic symptoms if present, and improving emotional well-being. Ultimately, the determination of successful treatment includes both objective and subjective measures. • The types of treatment selected are determined by some of the following factors: • Age of the patient: Many oral agents that are used to treat severe psoriasis, such as methotrexate and oral retinoids, are less likely to be used in children. Very young children, particularly infants, are not able to cooperate with phototherapy treatment (described later). • Type of psoriasis. • Site and extent of involvement. • Health care provider’s experience in managing psoriasis. (Management of mild to relatively moderate psoriasis can be performed by primary care clinicians. 94

3.12 Mycosis fungoides (cutaneous T-cell lymphoma). Lesions have characteristic “smudgy,” poorly defined patches and plaques as seen here in a typical location.

Moderate to severe psoriasis is best treated by dermatologists.) • Availability of facilities, such as a phototherapy unit. • Presence of psychosocial problems, such as anxiety, depression, alcoholism, and substance abuse. • Three basic treatment modalities are available for the overall management of psoriasis: (a) topical agents, (b) phototherapy, and (c) systemic agents, including biologic therapies. These treatments may be used alone or in combination. • Topical therapy is the first-line approach in the treatment of plaque psoriasis (TABLES 3.1 and 3.2). A number of topical treatments are available (e.g., corticosteroids, coal tar, anthralin, calcipotriene, tazarotene). No single topical agent is ideal, and many are often used concurrently in a combined approach. Auxiliary agents such as scale-removing keratolytics can often be added to these preparations. • Phototherapy and systemic therapy are initiated only after topical treatments have been unsuccessful (see also the later section titled “Generalized Plaque Psoriasis”). These treatments are considered for patients with very active psoriasis or patients who have disease that is physically, psychologically, or socially disabling.

Sp e cific Tre at m e n t o f Lo calize d Plaq ue Pso riasis To p ica l Co r t ico st ero id s

The use of a potent topical steroid for a limited period, followed by a less potent topical steroid for maintenance, is

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continued on page 95

MANAGEMENT Continued the most common method for treating psoriasis and many inflammatory dermatoses (see “Introduction”). Advantage

• Rapid onset in decreasing erythema, inflammation, and itching Disadvantages

• Drug tolerance (tachyphylaxis) is not uncommon • Expensive and time consuming, especially when large areas are treated

Occlu sio n o f To p ica l St ero id s

Generally a medium- or high-potency agent is applied and then covered with polyethylene wrap (e.g., Saran Wrap) for several hours or overnight, if tolerated. Cordran tape (see “Introduction: Topical Therapy”) is similarly effective (see also Chapter 2, “Eczema”). Advantage

• Increases the absorption, and thus potency, of topical steroids

continued on next page

Tab le 3.1 SHORT LIST OF TOPICAL STEROIDS POTENCY

GENERIC NAME

BRAND NAMES

Class I

Clobetasol propionate cream/gel/ointment/foam, lotion 0.05% Flurandrenolide (small and large rolls) Desoximetasone/0.05% gel Fluocinonide cream/ointment/solution/gel 0.05% Fluticasone ointment 0.005% Triamcinolone acetonide ointment 0.1% Betamethasone valerate 0.12% Hydrocortisone valerate cream 0.2% Triamcinolone acetonide cream 0.1% Desonide ointment 0.05% Desonide cream 0.05%, foam Hydrocortisone cream/ointment/lotion 0.5%, 1.0%*

Temovate, Olux foam, Clobex lotion, Cormax scalp solution Cordran tape small roll, large roll Topicort Lidex Cutivate Kenalog Luxiq foam Westcort Kenalog DesOwen DesOwen, Verdeso foam Hytone, Cortizone-10, and many other brands

Class II Class III Class IV

Class V Class VI Class VII

Most preparations are available in tubes of 15, 30, or 60 g. Lotions and solutions are available in bottles of 20 to 60 mL. *Available over the counter.

Tab le 3.2 OTHER TOPICAL AGENTS GENERIC NAME Keratolytic agents Salicylic acid 6% Salicylic acid 6% Topical vitamin D3 Calcipotriene 0.005% Topical vitamin D3 –topical steroid combination Calcipotriene–betamethasone dipropionate 0.064% Topical retinoids Tazarotene 0.05%, 0.1%, cream/gel

BRAND NAME Keralyt gel (1 oz) Salex cream (400 g) and lotion (441 mL) Dovonex cream, scalp solution

Taclonex

GENERIC NAME Topical immunomodulators Tacrolimus ointment 0.03%, 0.1% Pimecrolimus 1% cream Anthralin preparations Anthralin 0.1%, 0.25%, 0.5% Anthralin 0.25%, 0.5% Anthralin 1% cream Tar preparations

BRAND NAME Protopic ointment Elidel Drithocreme Dritho-Scalp Psoriatec Estar* PsoriGel* Balnetar* Doak tar oil*

Tazorac cream/gel

Note: All tar preparations (except liquor carbonis detergents) must be used in grease- or oil-based vehicles. Tar is commonly available in shampoos and is often combined with salicylic acid. Liquor carbonis detergens is an alcohol-extracted tar. *Available over the counter. continued on page 96 Chap ter 3 • Psoriasis

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MANAGEMENT Continued Disadvantage

• Side effects of topical steroids (described previously) are more common. Additional Suggestion

• A plastic shower cap can be used during treatment of the scalp with topical steroids; the resultant occlusion increases efficacy. In t ra lesio n a l St ero id s

Intralesional triamcinolone acetonide (Kenalog, 2.5 to 5 mg/mL) is delivered intradermally with a 30-gauge needle. The plaque is infiltrated until it blanches. This procedure may be repeated at 4- to 6-week intervals. Advantages

• Useful with limited number of lesions • Acts rapidly • Provides longer period of remission Disadvantages

• Painful • Possible local atrophy and telangiectasias • Requires office visits to administer injections To p ica l Vit a m in D 3 (Do vo n ex )

• Calcipotriene is a form of synthetic vitamin D3. It slows down the rate of skin cell growth, flattens psoriasis lesions, and removes scale. • Dovonex is available as a cream, ointment, and scalp solution in a 0.005% strength. Advantages

• Dovonex is used in combination with many other treatments. • Unlike topical steroids, Dovonex has few side effects. • Dovonex scalp solution is a water- and alcohol-based formulation specifically designed for treating scalp psoriasis. • Combining Dovonex with topical steroids may help. For example, a combined maintenance treatment of daily Dovonex plus weekend use of a superpotent topical steroid (called pulse therapy) may prolong remissions. • Dovonex increases the effectiveness of ultraviolet treatments. Disadvantages

• Dovonex is not very effective at decreasing inflammation and does not work as quickly as superpotent topical steroids. • The most common minor side effect is skin irritation, usually in the form of stinging or burning.

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• The face, genitals, and skin folds can be sensitive to Dovonex irritation. • The active ingredient in Dovonex is easily inactivated, particularly by acidic compounds such as salicylic acid. To p ica l Vit a m in D 3 –Po t en t St ero id Co m b in a t io n

• Calcipotriene and betamethasone dipropionate; Taclonex ointment Advantages

• The calcipotriene slows down the rate of skin cell growth, flattens psoriasis lesions, and removes scale. • The steroid helps reduce inflammation and itching. • The preparation is applied once a day. Disadvantages

• Because Taclonex contains a potent topical steroid, it should not be applied to the face, armpits, groin, or other skin folds. • The preparation is expensive. To p ica l Ta r Prep a ra t io n s

• Before the advent of topical steroids, tar preparations such as crude coal tar were the mainstay of therapy for psoriasis as well as most inflammatory dermatoses. Currently, they are used much less often. • Agents such as liquor carbonis detergens, Balnetar, Doak Tar oil, Estar gel, PsoriGel, and T/Derm tar oil are the traditional tar preparations. To p ica l An t h ra lin

• Anthralin is a coal tar derivative that evolved as an answer to many of the side effects of crude coal tar. It may be used for shorter periods than coal tar, such as for half an hour. • This short-term anthralin treatment is referred to as short-contact anthralin therapy (SCAT). Its major drawbacks are the possible occurrence of skin irritation and a reversible brownish purple staining of the skin.

In n o vat ive Man ag e m e n t St rat e g ie s Ro t a t io n a l Th era p y

• An innovative approach to the management of psoriasis consists of cycling or rotating different treatment modalities. This strategy presumably decreases cumulative side effects and drug tolerance (tachyphylaxis), and it often allows for lower dosages and shorter durations of therapy for each agent. • For example, a superpotent (class 1) topical steroid, such as clobetasol, may be applied for 2 weeks, discontinued for 1 or 2 weeks, and then restarted. Alternatively, clobetasol may be used on weekends only, and Dovonex ointment can be used during the week.

Part One • Com m on Skin Cond itions: Diagnosis and Managem ent

Gen era lized Pla q u e Pso ria sis BASICS • Psoriasis can flare very quickly and unexpectedly to cover 20% to 80% of the body. Therapy for widespread psoriasis differs from that used for more localized disease. • In case of extensive psoriasis, topical therapy alone becomes less effective, more expensive, time consuming, and labor intensive when it is administered to larger regions (FIG. 3.13).

3.13 Psoriasis. Extensive, large plaques are evident on this patient.

MANAGEMENT

Ph o t o t h e rap y • It is well known that most cases of psoriasis improve with sunlight exposure. This observation has led to the development of various methods to deliver ultraviolet (UV) light artificially. UV treatment is used only in the presence of extensive and widespread moderate-to-severe plaque psoriasis that is not responding to topical treatment. • The two forms of UV light that are used clinically are UVB and UVA. Bro a d b a n d UVB

• Broadband UVB therapy uses light with wavelengths of 290 to 320 nm (visible light range, 400 to 700 nm). Advantages

• UVB is one of the safest and most effective treatments for psoriasis. • UVB has fewer side effects than does UVA; thus, it is tried first. • There is no evidence of increased risk of skin cancer from UVB treatment for psoriasis. • UVB exposure has been shown to induce disease remission in more than 80% of patients.

• UVB can be combined with an oral retinoid derivative (ReUVB) to decrease the cumulative dose of UVB radiation to the skin as well as the dosage of retinoid. • UVB is often combined with one or more topical treatments. Disadvantages

• The major drawback of this therapy is the time commitment required for treatments and the lack of accessibility of UVB equipment. If administered at home, UVB therapy can overcome some of the logistical problems associated with phototherapy. However, home units are expensive; therefore, they are most suitable for patients who require long-term maintenance therapy or for those who live a great distance from UVB equipment. • Burning may be a problem. • An average of 30 treatments is often required to reach maximum improvement of psoriasis lesions. Na r ro w b a n d UVB

• Narrowband UVB phototherapy uses a fluorescent bulb with a narrow emission spectrum that peaks at 311 nm (UVB spectrum, 290 to 320 nm). continued on page 98

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With RePUVA, it is possible to lower the dosage of both treatment modalities and to achieve better clinical responses in many patients.

MANAGEMENT Continued Advantages

• Narrowband UVB is becoming more widely used. The major difference between broadband and narrowband UVB is that narrowband UVB units emit a more specific range of UV wavelengths. • This selective and relatively longer wavelength is more effective and has less risk of burning than broadband UVB. • Narrowband UVB clears psoriasis faster with fewer treatments per week and produces longer remissions than broadband UVB. • Narrowband UVB is also emerging as an alternative to treatment with oral psoralen plus topical ultraviolet A (PUVA; see section on UVA treatment below) and may be safer over the long term. Ex cim er La ser UVB

• This can deliver high-dose light to limited plaques. Advantages

• With an excimer laser, it is possible to clear psoriasis with as little as a single treatment with moderately long remission. • This handheld device is selectively directed toward lesional skin, thus sparing the surrounding normal skin from unnecessary radiation exposure. Disadvantages

• Expensive • Not widely available UVA

• UVA irradiation uses light with wavelengths of 320 to 400 nm. • UVA is administered with an oral photosensitizing drug, methoxsalen (8-methoxypsoralens). This is known as PUVA. The psoralen is activated by the skin’s exposure to UV light. • PUVA is administered in a dermatologist’s office or a psoriasis daytime treatment center. • PUVA interferes with DNA synthesis, decreases cellular proliferation, and induces apoptosis of cutaneous lymphocytes, leading to localized immunosuppression. Advantages

• More than 85% of patients report relief of disease symptoms with 20 to 30 treatments. Therapy is usually administered two to three times per week in an outpatient setting, with maintenance treatments every 2 to 4 weeks until remission. • As with ReUVB (see previous discussion), PUVA has been combined with oral retinoid derivatives (RePUVA).

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Disadvantages

• Adverse effects of PUVA therapy include nausea (from oral psoralens), pruritus, and a burning sensation. • Studies have indicated a link between PUVA therapy and the development of squamous cell and basal cell carcinomas and possibly malignant melanoma. • An increased sensitivity to sunlight or sunburn may result, and there is a theoretical risk of cataracts if the eyes are left unprotected.

Syst e m ic Th e rap y Methotrexate, cyclosporine, oral retinoids, and biologic therapies all have helped induce and maintain remission in severe cases of plaque psoriasis. Methotrexate, as well as several of the biologics (see below), are effective in treating both skin disease and joint disease. Biologics should be introduced and added in combination while these systemic agents are gradually tapered. Met h o t rex a t e

• This antimetabolite inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in tissues with high rates of turnover, such as those found in psoriatic plaques. • Dosage: • Methotrexate is often prescribed in a low-dose weekly regimen. • In light of its hepatotoxicity, this drug should be used only with extreme care because it has been associated with hepatic fibrosis and bone marrow suppression. • The adult dose is 2.5 mg/week PO initially; it is administered in three doses over a 24-hour period, then titrated to a dose between 12.5 and 25 mg/week, depending on response. • Folic acid 1 mg daily should be taken on nontreatment days. Advantages

• Methotrexate should be considered as an option for the treatment of extensive chronic plaque psoriasis, erythrodermic psoriasis, or generalized pustular psoriasis. • It may be administered intramuscularly or subcutaneously. • It is effective for psoriatic arthritis. • It is quite inexpensive. Disadvantages

• The main limitation of methotrexate is hepatotoxicity. Therefore, complete blood counts and monthly liver and renal function blood tests should be monitored.

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continued on page 99

MANAGEMENT Continued • Liver enzymes cannot be relied on to monitor liver health, because bridging necrosis can occur in the presence of normal liver enzymes. • Liver biopsy is recommended after a total of 1.5 g of methotrexate have been taken. • Many drug interactions are possible. • Long-term, continuous use may lead to myelosuppression and carcinogenicity. Acit ret in (So ria t a n e)

• Acitretin is in the retinoid family of drugs related to vitamin A. • The mechanism of action in treating psoriasis is unknown, but probably the drug induces cellular differentiation; it has antiproliferative, anti-inflammatory, and antikeratinizing effects. In addition, it inhibits neutrophil chemotaxis. • Dosage: • Initial: 25 mg/day PO; then increase • Maintenance: 20 to 50 mg/day PO Advantages

• Acitretin should be considered as an option for the treatment of palmoplantar, erythrodermic, or generalized pustular psoriasis. • Useful in combination with UVA (RePUVA) and UVB (ReUVB). Disadvantages

• Acitretin is a teratogen and is absolutely contraindicated in pregnancy as well as in women who are likely to become pregnant, intend to become pregnant within 3 years following cessation of treatment, or in those women who cannot use reliable contraception while undergoing treatment (and for at least 3 years after discontinuation). • Side effects are numerous. • Cheilitis is seen in virtually all patients taking retinoids. • The drug also may cause lipid elevation, muscle weakness, myalgias, hair loss, nail changes, skin fragility, premature epiphyseal closure or calcification, and ossification of ligaments and tendons. Cyclo sp o rin e (Neo ra l, Sa n d im m u n e)

• Cyclosporine suppresses humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity. The drug acts by inhibiting production of interleukin 2, the cytokine responsible for inducing T-cell proliferation. • Dosage: • Initially, 2 to 5 mg/kg/day PO in divided doses is used. • After control is achieved, maintenance therapy is continued at lower doses.

Advantages

• Remission is rapid for severe, uncontrollable psoriasis. • Cyclosporine is mostly useful for short-term treatment of significant exacerbations. Disadvantages

• Lesions tend to recur within days to weeks after treatment is stopped, and “rebounds” (with worse symptoms than before treatment) are not uncommon. • Many drug interactions are possible. • Evaluation of renal and liver functions should be performed often by measuring blood urea nitrogen, serum creatinine, serum bilirubin, and liver enzyme levels. Frequent monitoring of blood pressure is also necessary. • Risk of myelosuppression, infection, and lymphoma may be increased. • Side effects include nephrotoxicity and hypertension. Hirsutism and gingival hypertrophy have also been reported. Ro t a t io n a l Th era p y

• The use of a rotational approach with the various systemic agents can minimize the toxic effects of long-term treatment with any one of them. • For example, the use of agents such as UVB, PUVA, methotrexate, acitretin, or cyclosporine, which are reserved for more severe, extensive psoriasis, can also be rotated; for example, one treatment may be used from 12 to 24 months and then another modality may be used. On clearing of the condition, treatment is stopped until the psoriasis recurs, at which point another agent is used.

Ne we r Syst e m ic Ap p ro ach e s (t h e “Bio lo g ics”) Relatively new systemic therapies provide selective, immunologically directed intervention at key steps in the pathogenesis of the disease. They interact with specific targets in T-cell–mediated inflammatory processes and have an anti-inflammatory effect. These steps include: • • • •

Inhibition of cytokine release Prevention of T-cell activation Depletion of pathologic T cells Blocking the interactions that lead to T-cell activation or migration into tissue • Alteration of the balance of T-cell types • Inhibition of key inflammatory cytokines, such as tumor necrosis factor (TNF) Et a n ercep t (En b rel)

• Etanercept is a fusion protein containing the human TNF receptor bound to the Fc portion of human immunoglobulin G (IgG) antibody. continued on page 100

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MANAGEMENT Continued • It acts by binding and inhibiting TNF, the cytokine that contributes to inflammatory and immune responses. • It is administered subcutaneously. Advantages

• Can be given at home • Prevents bony erosions in patients with psoriatic arthritis • Leads to tuberculosis activation less commonly than infliximab and adalimumab • Effective in recalcitrant palmoplantar psoriasis and generalized pustular psoriasis Disadvantages

• Results in injection site reactions • Rare effects: congestive heart failure, drug-induced lupus, lymphoma, and unmasking of multiple sclerosis and tuberculosis

In flixim ab (Re m icad e ) • Infliximab is a monoclonal antibody that targets TNF alpha and inhibits its activity. • Patients must be tested for tuberculosis exposure with purified protein derivative (PPD) placement prior to treatment. • It is necessary to monitor platelet counts and perform liver function studies.

• It is administered subcutaneously. • Patients must be tested for tuberculosis exposure with PPD placement prior to treatment. Advantages

• Rapid acting • Indicated for reducing signs and symptoms of active arthritis in psoriatic arthritis Disadvantage

• Rare reports of lupus-like symptoms. Efa lizu m a b (Ra p t iva )

• Efalizumab is a recombinant humanized IgG1-kappa isotype monoclonal antibody that inhibits stimulation of T cells and T-cell migration into the skin. • It is administered subcutaneously. • No CD4 testing is necessary. Advantages

• Fairly rapid acting • Effective in psoriatic arthritis Disadvantages

• Rebound flares occur with abrupt withdrawal. • Thrombocytopenia and hemolytic anemia are possible. • Worsening of psoriasis occurs in a small percentage of patients.

Advantages

Alefa cep t (Am evive)

• Is rapid acting • Is used in patients with psoriatic arthritis

• Alefacept is a monoclonal antibody that binds to lymphocyte antigen (CD2) and inhibits LFA-3/CD2 interaction and lymphocyte activation. • It is administered intramuscularly.

Disadvantages

• Is administered intravenously • Common infusion reactions: pruritus, hives, nausea, and headache • Contraindications: congestive heart failure class III or IV

Advantages

• Long-lasting benefit when effective • Probably the safest of the biologics

Ad a lim u m a b (H u m ira )

Disadvantages

• Adalimumab is a recombinant humanized IgG1 monoclonal antibody that binds to TNF alpha. • It is effective in reducing signs and symptoms of active arthritis and psoriatic arthritis.

• Slow onset of action • Ineffective in a comparatively high percentage of patients • Lowering of CD4 counts

HELPFUL HINTS • Systemic drugs such as methotrexate and cyclosporine should not be abruptly discontinued because of the risk of marked rebound of disease activity. 100

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Ex fo lia t ive Derm a t it is

(Ex fo lia t ive Er yt h ro d er m a )

BASICS Rarely, a patient may develop a sudden or subacute appearance of generalized scaling and erythema (FIG. 3.14), often with accompanying fever and chills. This condition, exfoliative dermatitis, can be the presenting symptom of psoriasis or a subsequent complication of limited psoriatic disease (see Chapter 25, “Cutaneous Manifestations of Systemic Disease,” for a discussion of exfoliative dermatitis). Some of the trigger factors that may lead to exfoliative dermatitis in patients with psoriasis are as follows: • Administration of systemic or superpotent topical corticosteroids in patients with preexisting psoriasis • Topical therapy that is irritating or produces severe contact dermatitis • High levels of emotional stress • Medical procedures (e.g., surgery) or certain conditions (e.g., infections)

3.14 Psoriasis. Erythrodermic variant of exfoliative dermatitis.

Alternatively, psoriasis may initially present as exfoliative dermatitis.

MANAGEMENT Treatment of exfoliative dermatitis secondary to psoriasis may involve some of the measures used for generalized plaque psoriasis (e.g., UV light therapy, oral agents) in addition to the following: • • • • • •

Bed rest Cool compresses Lubrication with emollients Antipruritic therapy with oral antihistamines Low- to moderate-strength topical corticosteroids Hospitalization in extreme cases

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Acu t e Gu t t a t e Pso ria sis See also Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients.”

BASICS This type of psoriasis refers to the sudden onset of multiple guttate (teardrop-shaped) lesions (FIG. 3.15). It is often the initial presentation of psoriasis in children or young adults. Acute guttate psoriasis is occasionally preceded by a group A beta-hemolytic streptococcal pharyngitis (positive throat culture or serologic evidence of antistreptolysin O). These patients should be treated promptly with appropriate antibiotic therapy, because it has been reported that some of these patients have self-limited cases of psoriasis. Long-term follow-up has indicated that many of these patients with “onetime” cases of psoriasis eventually proved to have recurrences, suggesting typical psoriasis.

3.15 Psoriasis (acute guttate). This patient had a recent group A beta-hemolytic streptococcal pharyngitis.

DIFFERENTIAL DIAGNOSIS • • • •

Pityriasis rosea (FIG. 3.16) Drug eruption Parapsoriasis Secondary syphilis

MANAGEMENT • UVB phototherapy or natural sunlight exposure • Appropriate antibiotic therapy, such as penicillin or erythromycin for group A beta-hemolytic streptococcus • High-potency (class 1, 2, or 3) topical steroids or SCAT (described earlier)

3.16 Pityriasis rosea. Typical distribution of elliptic, scaly lesions (see also Chapter 4, “Inflammatory Eruptions of Unknown Cause”).

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Pso ria sis in Ch ild ren See also Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients.”

BASICS In approximately 10% of patients, psoriasis begins before the age of 10 years. An early onset portends more severe disease, and there is often an associated family history of the disease.

In some infants, psoriasis begins as a diaper rash, which may be difficult to distinguish from irritant dermatitis, atopic dermatitis, or cutaneous candidiasis. The rash may clear; however, the child may later develop psoriasis. Conversely, psoriasis may present with typical plaques, such as those seen in adults. Infantile or childhood psoriasis deserves particular attention. It requires intensive educational guidance and counseling of the patient and family.

MANAGEMENT Many of the treatments that are used in adults, such as superpotent topical steroids, phototherapy, methotrexate, and retinoids, are generally avoided in children. Low- to medium-potency topical steroids, SCAT (described earlier), and natural sunlight, if available, are also used in children. All of these treatments should be administered with caution.

3.17 Psoriasis in an infant. This eruption was initially considered to be a simple diaper rash.

3.18 Acute guttate psoriasis. This child also had a streptococcal throat infection.

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Sca lp Pso ria sis BASICS Psoriasis may involve the scalp alone, or the scalp may be affected along with other areas of the body. The plaques are often thick and well demarcated with a whitish scale (FIG. 3.19). They are frequently hidden in the scalp or behind the ears, but often they extend beyond the hairline and become more obvious when the hair is held back and when the retroauricular area is examined. Often, the external ears and ear canals are involved (FIG. 3.20). Features of scalp psoriasis include:

3.19 Psoriasis of the scalp. This discrete, scaly plaque is one of many this patient has on her scalp.

• Pruritus and scratching, which may exacerbate the condition (Köbner reaction). • Lesions that range from flaky dandruff to thick, extensive, armorlike plaques. • Possibly problematic management. When severe, it is particularly difficult to treat because hair blocks UV light as well as the topical application of psoriatic medications.

3.20 Psoriasis of the scalp and ears. Note the crusted excoriations behind this patient’s ear and along his hairline.

DIFFERENTIAL DIAGNOSIS

Ad ult s Seb o r rh eic Der m a t it is a n d Eczem a t o u s Der m a t it is o f Sca lp

FIGURES. 3.21 and 3.22. • Both conditions are very common and may be clinically indistinguishable from scalp psoriasis. • Both conditions may be present elsewhere on the body. Eczem a t o u s Der m a t it is o f Sca lp

• Eczematous lesions may be present elsewhere on the body. • An atopic history is usually present.

3.21 Seborrheic dermatitis. Finer, thinner scale than is shown in FIGURES. 3.19 and 3.20. continued on page 105

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

DIFFERENTIAL DIAGNOSIS Continued

Ch ild re n Tin ea Ca p it is

• A KOH test and/or fungal culture may be positive.

3.22 Seborrheic dermatitis. Retroauricular erythema and scale. Compare to FIGURE. 3.20. (See also Chapter 2, “Eczema.”)

MANAGEMENT

Mild Case s • In patients with minimal scaling and thin plaques (similar to what is seen in seborrheic dermatitis (see Chapter 2, “Eczema”), the psoriasis can often be managed with antidandruff shampoos and a mid-potency (class 3 or 4) topical steroid, used as needed for itching. • Over-the-counter options include shampoos that contain tar (Zetar, T/Gel), selenium sulfide (Selsun Blue, Head & Shoulders), or salicylic acid (T/Sal). To p ica l St ero id s

• Low-potency (class 6) topical steroids include preparations such as Capex shampoo or Verdeso foam. Gel, foam, or solution preparations reach the scalp more readily than do ointments or creams. An t ifu n ga ls

• Shampoos containing the antifungals ketoconazole 2% (Nizoral) and ciclopirox (Loprox) are available by prescription.

Se ve re Case s • In patients with thick scales and plaques, the scale must be removed before the plaques can be treated effectively. Scale removal is accomplished by applying either Keralyt gel or Salex cream or lotion one to three times per week. This regimen may be sufficient to keep scale under control, thus allowing penetration of a topical steroid. • After the scale is removed, a medium- to high-potency (class 2, 3, or 4) topical steroid is used. For example, fluocinonide solution or gel or desoximetasone (Topicort) gel can be applied once or twice daily as needed, under shower cap occlusion overnight, or for 3 to 4 hours during the day. If necessary, a superpotent (class 1) topical steroid such as clobetasol propionate lotion, foam, or gel can be used without occlusion. In recalcitrant situations, the superpotent topical steroid can be applied under occlusion once or twice per week. • Dovonex lotion can be used as maintenance or rotational therapy (see earlier section). • Injections of intralesional triamcinolone (3 to 5 mg/mL) in a limited amount (1 to 2 mL or less per treatment) every 4 to 8 weeks are used to target particularly itchy areas and may bring longer remissions.

SEE PATIENT HANDOUT, “Scalp Pso riasis: Scale Re m o val” ON THE SOLUTION SITE

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In verse Pso ria sis BASICS • Psoriasis seen in intertriginous areas such as the axillae, inframammary folds, perineal and perianal areas, scrotum, glans penis, and inguinal creases is referred to as inverse psoriasis (FIGS. 3.22–3.27). • Typically, lesions are red, glistening, well-demarcated plaques that generally lack scale. This manifestation is seen when two apposing surfaces of skin rub together, such as under the breasts. Such constant rubbing does not allow scale to build up. • Fissures may occur in the groin and gluteal creases.

3.23 Inverse psoriasis. Axillary involvement is shown here. Both axillary psoriasis and inframammary psoriasis are often misdiagnosed as cutaneous candidiasis. (Compare to FIG. 3.28)

3.24 Inverse psoriasis. Well-demarcated inframammary lesions. (Compare to FIG. 3.29)

3.26 Inverse psoriasis. Typical psoriatic lesions on the penis are not unusual.

3.25 Inverse psoriasis. Note involvement of the scrotum, foreskin, and glans. This is often misdiagnosed as cutaneous candidiasis or tinea cruris. (Compare to FIG. 3.30)

3.27 Inverse psoriasis. Intragluteal involvement is also not unusual. Note the painful fissure.

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

DIFFERENTIAL DIAGNOSIS • Inverse psoriasis is commonly misdiagnosed by nondermatologists as tinea or candidiasis. Accordingly, it is often incorrectly treated with topical antifungal agents.

In t e rt rig o o r Co n t act De rm at it is A common inflammatory condition of skin folds (FIG. 3.28), intertrigo occurs when opposing skin surfaces rub against each other, such as seen in diaper dermatitis (see also Chapter 27, “Special Considerations in the Skin of Pediatric and Elderly Patients”). Common features include: • Induction or aggravation by heat, hyperhidrosis, moisture, maceration, and friction • May be caused by contactants such as antiperspirants or dry cleaning solvents • Location in the axillae and inguinal and intragluteal creases; often occurs under pendulous breasts and abdominal folds • Possible colonization by secondary infection such as Candida albicans, particularly in patients with diabetes (FIG. 3.29) • Often complicates obesity

3.28 Irritant intertrigo. This patient’s eruption is caused by irritation from antiperspirants used to treat hyperhidrosis. This problem is common when opposing skin surfaces rub against each other.

Tin e a Cruris • Lesion with a scalloped, active border (FIG. 3.30) • Generally spares the scrotum and penis • Positive KOH examination and fungal cultures for dermatophytes Cut an e o us Can d id iasis • “Beefy red” color to the lesions • Satellite pustules seen beyond the border of the plaques • Positive KOH examination for budding yeast • Positive culture for Candida species

3.29 Cutaneous candidiasis. Note the “beefy red” plaque and “satellite pustules” in this diabetic patient.

At o p ic De rm at it is • Eczematous lesions that occur elsewhere on the body • Patients have an atopic history Se b o rrh e ic De rm at it is • May be indistinguishable from inverse psoriasis (intertriginous seborrheic dermatitis) Ot h e r Co n sid e rat io n s • When lesions are present on the glans penis, nonspecific balanitis (more commonly seen in elderly men) and balanitis from candidal species should be considered in the differential diagnosis. • Pruritus ani also may be confused with inverse psoriasis. • Secondary overgrowth with Candida species and tinea must also be considered.

3.30 Tinea cruris. Note the scalloped border. The KOH examination is positive. The scrotum is spared in most cases.

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POINT TO REMEMBER MANAGEMENT • The lowest-potency nonfluorinated topical steroids are used to avoid atrophy and striae. • To achieve rapid improvement, treatment may be initiated with a higher-potency (class 5) steroid that is used for several days before it is changed to a lowerpotency (class 6 or 7) agent. • Dovonex cream or ointment may be used primarily (if it is not irritating) or in rotation with a mild topical steroid. • Tacrolimus (Protopic) ointment 0.03% or 0.1% can be applied once or twice daily. • Pimecrolimus (Elidel) cream 1% may be used once or twice daily.

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• Intertriginous areas are moist and occluded; therefore, the penetration and efficacy of topical agents are increased in these regions; consequently, topical steroids are more likely to produce striae (linear atrophy).

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Pso ria sis o f t h e Pa lm s a n d So les BASICS Psoriasis that manifests on the palms and soles presents a difficult therapeutic challenge. The palms or soles alone may be affected, or these areas may be a part of more extensive psoriasis on the body. As with inverse psoriasis (see earlier), palmoplantar psoriasis, by virtue of its location, cannot benefit from UV light therapy. There are two variants: • Hyperkeratotic. Like its counterparts elsewhere, this form of psoriasis is characterized by well-demarcated, scaly plaques (FIGS. 3.31 and 3.32). The location of these lesions presents additional problems such as pain, impairment of function, fissuring, bleeding, and embarrassment. • Pustular. This rare form of psoriasis has historically had many clinical descriptions and eponyms. It is most commonly seen in adults, and lesions tend to be symmetric and well defined. It favors the insteps of the feet, the heels, and the thenar and hypothenar eminences. Less commonly, it appears on the palms (FIG. 3.33).

3.32 Psoriasis. Note the clear demarcation between involved and uninvolved skin. Similar lesions were present on this patient’s palms.

3.31 Psoriasis. This patient’s lesions are symmetric and well-demarcated.

3.33

Psoriasis. This is the pustular variant of psoriasis.

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DIFFERENTIAL DIAGNOSIS

Co n t act De rm at it is • This is suspected, particularly if the eruption is on the dorsum of the hands or feet. • The patient has a history of exposure to a suspected contactant. Han d Ecze m a o r Dysh id ro t ic Ecze m a See Chapter 2, “Eczema.”

MANAGEMENT Topical treatment is the first line of therapy. Because of their thick stratum corneum, the palms and soles present the greatest barrier to cutaneous penetration; potent topical steroids are used, often under occlusion. Treatment options include the following: • Superpotent (class 1) topical steroids, such as clobetasol propionate, are first tried without occlusion, but occlusion (under vinyl or rubber gloves) may be used if necessary. • Salicylic acid preparations such as Keralyt gel or Salex cream or lotion may be used to remove scale, if necessary. • Calcipotriene (Dovonex) ointment or cream can be used.

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• “Sago-grain” vesicles are visible. • Pruritus is present. • The patient has evidence of eczema elsewhere on the body or a personal or family history of atopy. • May be indistinguishable from palmoplantar psoriasis.

Tin e a Man uum an d Pe d is • A “two-feet, one-hand” presentation is noted (see Chapter 7, “Superficial Fungal Infections”). • The KOH examination or fungal culture is positive.

• Anthralin, overnight or as SCAT, may be useful. • Emollients may be useful. When a patient is not responding to topical therapies, treatment options can include: • PUVA (see earlier discussion): topical UVA therapy using a “hand-foot box” • Oral retinoids, such as etretinate • RePUVA (low-dose etretinate combined with PUVA) • Oral methotrexate • Oral cyclosporine • Biologics (see earlier discussion). Raptiva is increasingly considered the biologic of choice for hand–foot disease. Raptiva plus low-dose acitretin has been shown to be an excellent regimen for severe, disabling hand–foot disease.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Pso ria t ic Na ils BASICS Involvement of nails is very common in patients with psoriasis (see also Chapter 13, “Diseases and Abnormalities of Nails”). Psoriatic nail dystrophy is a chronic, primarily cosmetic condition. However, in some instances, thickened psoriatic toenails can become painful, and psoriatic fingernail deformities may result in interference with function. Psoriatic nail dystrophy is more commonly noted in patients who have psoriatic arthritis. Typical nail changes may involve: • Pitting, which is the most characteristic nail finding in psoriasis. It is produced by tiny punctate lesions that arise from the nail matrix (nail root) and appear on the nail plate as it grows (FIG. 3.34). • Onycholysis, which represents a separation of the nail plate from the underlying pink nail bed. The separated portion is white or yellow-white and opaque, in contrast to the pink translucence of the attached portion (FIG. 3.35).

3.34 Psoriasis (pitting). The result of tiny punctate lesions that arise from the nail matrix, pitting appears on the nail plate as it grows.

3.35 Psoriasis (onycholysis). Several nail plates have separated from the underlying pink nail bed. The separated portion is white or yellow-white and opaque, in contrast to the pink translucence of the attached portion. Note the typical psoriatic plaque on this patient’s knuckle.

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• “Oil spots” or “drops,” which are orange-brown colorations appearing under the nail plate. They are presumably the result of psoriasis of the nail bed (FIG. 3.36). • Thickening, or subungual hyperkeratosis, which is a buildup of scale beneath the nail plate. It resembles onychomycosis, with which it is often confused and may coexist, particularly in toenails (FIG. 3.37).

DIFFERENTIAL DIAGNOSIS

3.36 Psoriasis (“oil spots” or “drops”). Orange-brown coloration appears under the nail plate, presumably the result of psoriasis of the nail bed. Onycholysis is also evident.

3.37 Psoriasis (subungual hyperkeratosis). A buildup of scale beneath the nail plate resembles onychomycosis. Also note in this figure “oil spots” and onycholysis.

MANAGEMENT Treatment is generally unrewarding, but some measures can be helpful: • Careful trimming and paring of the nails are recommended. • The application of a super-potent (class 1) topical steroid to the proximal nail folds is followed by covering with plastic wrap, Cordran tape, or a plastic glove. • Tazarotene (Tazorac) gel 0.01%, applied to the proximal nail fold nightly, has been shown to reduce onycholysis and pitting of psoriatic nails. (It has no effect on thickening and severe dystrophy.) 112

On ych om yco sis • In onychomycosis, the KOH examination or fungal culture is positive (FIG. 3.38). Ecze m at o us De rm at it is • Eczematous dermatitis with secondary nail dystrophy lacks subungual hyperkeratosis. Eczema is noted in the area of the proximal nail fold (see FIG. 2.17).

3.38 Onychomycosis. The subungual hyperkeratosis is similar to psoriasis; however, a fungal culture grew a dermatophyte.

• Intralesional corticosteroids can be injected into the nail matrix. The proximal and/or lateral nail fold is sprayed first with a refrigerant spray for anesthesia, and 2.5 mg/mL is injected with a 30-gauge needle every 4 to 6 weeks. • At present, three systemic medications are most commonly used to treat psoriasis and nail psoriasis: methotrexate, retinoids, and cyclosporine. All have potential serious side effects and toxicities, and, in most cases, the psoriatic nail disease recurs after the systemic therapy is stopped. • Systemic agents such as biologics are reserved for intractable cases, particularly when psoriatic arthritis is also present.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Pso ria t ic Ar t h rit is BASICS Although psoriatic arthritis can be seen at any age, it most often begins between the ages of 35 and 45 years. It develops before or, more often, after the outbreak of skin manifestations of psoriasis. Overexpression of TNF alpha is thought to play a key role. Multiple human leukocyte antigen associations are known. An earlier onset of psoriatic arthritis in adulthood can portend a worse prognosis that may include destructive arthropathy. Psoriatic arthritis has the following clinical features: • A test for the rheumatoid factor is usually negative. • It is seen in 5% to 10% of patients with psoriasis. • It is more likely seen in patients with severe cutaneous disease. • Nail involvement is more frequently noted. • Peripheral psoriatic arthritis may be indistinguishable from Reiter’s syndrome.

3.39 Psoriatic arthritis. “Sausage finger deformity” of the distal interphalangeal joint.

There are five clinical patterns of psoriatic arthritis: • Asymmetric involvement of one or several small or medium-sized joints is the most common initial presentation of psoriatic arthritis. If a finger joint is affected initially, the result is sometimes referred to as a “sausage finger deformity” (FIG. 3.39). • Mild involvement of the distal interphalangeal joints is considered the classic form of psoriatic arthritis. It is often accompanied by nail disease. • Symmetric joint involvement is difficult to distinguish from rheumatoid arthritis. (However, a test for rheumatoid factor is negative.) • Involvement of the joints in the axial skeleton that resembles, and may overlap with, ankylosing spondylitis can occur. • Mutilating, grossly deforming, arthritis mutilans may occur (FIG. 3.40).

3.40 Psoriatic arthritis (“arthritis mutilans”). This patient has severe psoriatic arthritis with marked deformities and subluxations of the small bones of the hands. Note also the characteristic onycholysis on the nails.

MANAGEMENT • Treatment consists of analgesics, primarily nonsteroidal anti-inflammatory drugs, and methotrexate. • Biologics may also be helpful (see earlier discussion).

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C H AP T ER

4

Inflam matory Eruptions of Unknown Cause OVERVIEW

PITYRIASIS ROSEA • Classic • Atypical or inverse • Pityriasis rosea-like eruption in association with various drugs GRANULOMA ANNULARE • • • •

Childhood Adult Subcutaneous Dissem inated LICHEN PLANUS

• Hypertrophic • Atrophic • Erosive (m ucosal) • Follicular (lichen planopilaris) Other eruptions resem bling lichen planus are seen in the following conditions: • Drug-induced • Lichenoid reactions associated with graft-versus-host disease • LP associated with hepatitis C

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Pityriasis rosea, granuloma annulare, and lichen planus are unique inflammatory conditions of unknown etiology. Each has various clinical presentations, and distinctive patterns of anatomic distribution. Most often the diagnosis can be readily made based upon the typical signs and symptoms of these curious dermatioses. There are conflicting reports about the association of these entities with certain infectious and metabolic conditions. For example, pityriasis roses is thought to represent a viral exanthem possibly caused by a herpesvirus. An association has been noted between lichen planus and hepatitis C, chronic active hepatitis, and primary biliary cirrhosis and widespread granuloma annulare is considered by some investigators to be associated diabetes mellitus.

Pit yria sis Ro sea BASICS Pityriasis rosea (PR), which means “fine pink scale,” is an acute, benign, self-limiting eruption with a characteristic clinical course. PR tends to occur in the spring and fall, and although it may occur at any age, it is seen mostly in young adults and older children. The cause is unknown; however, the occasional clustering of cases and seasonal appearances suggest an infectious, transmissible origin. A single outbreak tends to elicit lifelong immunity, although repeat cases have reportedly been observed.

Pat h o g e n e sis A viral etiology has been suggested, but this has not been confirmed. Despite the prevailing opinion that PR is caused by an infectious agent, it does not appear to be contagious; household contacts and schoolmates usually do not develop the eruption.

4.1 Pityriasis rosea. This patient has a herald patch on her chest. Other, smaller, elliptical lesions can be seen.

DESCRIPTION OF LESIONS • The typical course of PR often begins with the larger herald patch (FIG. 4.1), a 2- to 5-cm, scaly lesion that may exhibit central clearing and therefore may mimic, and often be confused with, tinea corporis. • The herald patch is followed in several days to 2 weeks by multiple characteristic oval or elliptic erythematous patches with fine, thin scale on their surfaces (FIG. 4.2). • Individual lesions often develop a thin, circular, collarette of scale (see “Introduction: Reaction Patterns, Shapes, and Configurations”). Lesions in very dark-skinned patients may lack the typical pink color of PR and may appear darker than the surrounding skin. DISTRIBUTION OF LESIONS

4.2 Pityriasis rosea. Note the characteristic elliptic (“football”) shape of lesions.

• The initial lesion, the herald patch, is most commonly observed on the trunk, neck, or extremities (FIG. 4.3). The absence of the herald patch does not necessarily rule out the diagnosis; it may be absent or hidden in an obscure location such as the scalp or groin. • Subsequent lesions appear on the trunk, neck, arms, and legs in an “old-fashioned bathing suit” distribution.

4.3 Pityriasis rosea. The herald patch is on this child’s flexor forearm.

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• The long axis of the lesions runs parallel to skin tension lines. This gives a so-called “Christmas tree” pattern on the trunk (FIG. 4.4). CLINICAL MANIFESTATIONS • Itching is usually absent or mild but may be severe in a minority of patients. • PR is a self-limiting, benign disorder; it usually lasts for 6 to 8 weeks. • On resolution, postinflammatory pigment changes (hyperpigmentation) can occur, particularly in dark-skinned people (FIG. 4.5). • Recurrences are rare. CLINICAL VARIANTS

4.4 Pityriasis rosea. Here the lesions are more exuberant and the “Christmas tree” pattern is evident.

• PR can occur with less typical presentations such as those in which the herald patch is not noted by the patient or clinician. Moreover, in dark-skinned patients, the lesions may be vesicular and uncharacteristically pruritic. • The eruption may be limited in its distribution, or it may present in an inverse fashion involving the groin (FIG. 4.6), axillae, or distal extremities (inverse PR). • Infrequently, eruptions resembling those of PR also can occur in association with many drugs. These include barbiturates, bismuth, captopril, clonidine, diphtheria toxoid, gold, isotretinoin, ketotifen, levamisole, metronidazole, and D-penicillamine. DIAGNOSIS The diagnosis is made clinically in most cases. In general, laboratory tests are not necessary or helpful, with the following exceptions:

4.5 Pityriasis rosea. Note the hyperpigmented lesions in this African-American patient.

• A potassium hydroxide (KOH) examination may be helpful when only the herald patch is present, to help rule in or rule out tinea corporis; similarly, a KOH examination may be used to distinguish tinea versicolor (see Chapter 7, “Superficial Fungal Infections”) from PR. • A rapid plasma reagin (RPR) or venereal disease research laboratory (VDRL) test should be performed in all patients with PR. • A skin biopsy may be performed when the eruption is atypical, the diagnosis is uncertain, or the disease has not resolved after 3 to 4 months.

4.6 Pityriasis rosea. Atypical (inverse). The larger herald patch is present in the left inguinal area. 116

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

DIFFERENTIAL DIAGNOSIS

Gut t at e Pso riasis FIGURE 4.7. • Guttate psoriasis often follows streptococcal pharyngitis, and its abrupt onset and appearance can easily be confused with PR. • Scale is generally thicker than that of PR.

Se co n d ary Syp h ilis FIGure 4.8. • Lesions are often seen on the palms, soles, and face, as well as the trunk, and may be indistinguishable from PR. • The RPR or VDRL test is positive.

4.7 Guttate psoriasis. Here the plaques are thicker and more round or oval in shape than those seen in PR.

4.8 Secondary syphilis. Papulosquamous lesions appear on the trunk, similar to PR. (Image courtesy of Ed Zabawski, D.O.).

Tin e a Ve rsico lo r FIGure 4.9.

• Parapsoriasis should be considered in PR that persists for longer than 8 weeks.

• Round or oval macules or patches are present. • Pigmentation may be varied (“versicolor”). • The KOH examination is positive.

Drug Erup t io n o r Viral Exan t h e m • Lesions are redder, less scaly, and tend to be itchier than in PR. • There may be other symptoms (e.g., fever). Num m ular Ecze m a • “Coin-shaped” patches and plaques are present. • Lesions tend to be on the legs; they are less common on the arms. • This condition generally itches. Parap so riasis • Lesions may be similar to those of PR. • Despite its similar name, parapsoriasis is unrelated to psoriasis.

4.9 Tinea versicolor. The oval, tan patches are positive on KOH examination.

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MANAGEMENT • Treatment is often unnecessary, because PR is usually a self-limiting, asymptomatic condition with no sequelae. • All that is usually necessary is to advise the patient about the usual course of the rash and its noncontagious nature. • Exposure to sunlight or administration of ultraviolet B by a dermatologist may speed resolution of the eruption.

• Follow-up or referral to a dermatologist should be made if the rash persists more than 8 weeks. • In cases of severe pruritus, oral antihistamines or topical steroids may help alleviate the itching. The sedative effect of the antihistamines may help the patient sleep better at night. On occasion, systemic steroids (prednisone, 0.5 to 1 mg/kg/day for 7 days) can be used in patients with severe pruritus.

POINTS TO REMEMBER • Lesions characteristically appear “from the neck to the knees.” • PR is observed in otherwise healthy people, most frequently in children and young adults. • Patients should be told that PR is a benign condition that will resolve over 6 to 8 weeks without treatment. • Secondary syphilis should be considered in the differential diagnosis, especially when lesions are present on the palms and soles.

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Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Gra n u lo m a An n u la re BASICS Granuloma annulare (GA) is an idiopathic, generally asymptomatic, ring-shaped grouping of dermal papules. The papules are composed of focal granulomas that coalesce to form curious circles or semicircular plaques, which are often misdiagnosed as “ringworm.” Familial cases of GA in identical twins and siblings suggest the possibility of a hereditary component. • In very young children, GA is often self-limiting. • In adults, GA tends to be a chronic condition that occurs in women (2.5:1 female-to-male ratio). GA has been associated with diabetes mellitus based on an increased number of GA patients in a small case series.

Pat h o p h ysio lo g y Proposed pathogenic mechanisms include cell-mediated immunity (type IV), immune complex vasculitis, and an abnormality of tissue monocytes. None of these theories has convincing supporting evidence.

4.10 Granuloma annulare. These dermal plaques are typical ringlike lesions.

DESCRIPTION OF LESIONS • Lesions are skin-colored or red firm dermal papules, with no epidermal change (scale). • The lesions may be individual, isolated papules, or they may be joined in annular or semiannular (arciform) plaques with central clearing (FIGS. 4.10 and 4.11). The centers of the lesions may be slightly hyperpigmented and depressed relative to their borders. • Occasionally, GA may present as subcutaneous nodules that are similar to rheumatoid nodules. 4.11 Granuloma annulare. An annular plaque of the dorsal foot.

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DISTRIBUTION OF LESIONS • Although any part of the cutaneous surface may be involved, lesions are most often distributed symmetrically on dorsal surfaces of hands, fingers, and feet (acral areas). • In adults, lesions may also be found around the elbows (FIG. 4.12) and on the trunk (FIG. 4.13). • Subcutaneous nodules may be seen on the arms and legs. CLINICAL MANIFESTATIONS • GA is generally asymptomatic and is primarily a cosmetic problem, although many patients tend to find it alarming.

4.12 Granuloma annulare. Papules of granuloma annulare are located below the elbows in this middle-aged woman.

DIAGNOSIS • The diagnosis is most often made on clinical grounds. • GA has a characteristic histopathologic appearance. It consists of foci of altered collagen and mucin surrounded by granulomatous inflammation of histiocytic and lymphocytic cells. The degenerative collagen is referred to as necrobiosis.

4.13 Granuloma annulare. Note the similarity of these annular lesions to FIGURES 4.14 and 4.15.

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DIFFERENTIAL DIAGNOSIS

Tin e a Co rp o ris (“Rin g wo rm ”) • Scale is present at the “active border” (FIG. 4.14). • Lesions tend to be “ringlike” (clear in the center), and they are not firm and infiltrated as seen in GA. • An asymmetric distribution of lesions is apparent. • The KOH examination or fungal culture is positive. • Lesions are often pruritic. Eryt h e m a Mig ran s Rash o f Lym e Dise ase (See also Chapter 20, “Bites, Stings, and Infestations.”) • Lesions of erythema migrans are larger than those associated with GA (FIG. 4.15). • They are often associated with a history of tick bite. • The rash is self-limited. • Lesions are not as firm to palpation as in GA.

4.14 Tinea corporis. KOH-positive scale is present at the “active border.”

Cut an e o us Sarco id o sis • This condition is most commonly seen in black and Scandinavian adults. • Lesions often appear around orifices (e.g., the mouth, nose, ocular orbits) or develop in scars (see FIGS. 25.35 and 25.36). • Other diagnostic features of sarcoidosis are usually present. • Annular sarcoidosis may be indistinguishable from GA. Rh e um at o id No d ule s • These may be indistinguishable from subcutaneous nodules of GA. Ne cro b io sis Lip o id ica Diab e t ico rum • Necrobiosis lipoidica diabeticorum (NLD) is characterized by yellow-red to brown, translucent plaques, with epidermal atrophy and telangiectasia (see FIGS. 25.1 and 25.2). • NLD is seen more frequently in people with type 1 diabetes and may occur before the onset of clinical diabetes. • A minority of patients have no clinical evidence or family history of diabetes; in these patients, the term necrobiosis lipoidica is used.

MANAGEMENT • The patient should be reassured of the benign nature of this condition but advised that it may be a harbinger of diabetes mellitus particularly in case of disseminated granuloma annulare. • Localized lesions on nonvisible skin in children are best left untreated. • Topical steroids such as class 2 high-potency fluocinonide 0.5% cream (Lidex) or super-potent class 1

4.15 Erythema migrans rash of Lyme disease. Lesions tend to be larger than those associated with GA.

clobetasol 0.05% cream may be applied. Cordran tape is another option (see “Introduction: Topical Therapy”). • Intralesional triamcinolone acetonide (Kenalog), in a dose of 2.5 to 5 mg/mL, is injected directly into the elevated border of the lesions with a 30-gauge needle. The plaque is infiltrated until it blanches. • This may be repeated at 4- to 6-week intervals.

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Lich en Pla n u s BASICS

4.16 Lichen planus. The Köbner phenomenon (isomorphic response) results from scratching.

Lichen planus (LP) is a relatively uncommon cutaneous inflammatory disorder. “Classic” (idiopathic) LP is a pruritic, idiopathic eruption with characteristic shiny, flat-topped (Latin planus, “flat”) papules on the skin, often accompanied by mucous membrane lesions. The papules are characterized by their violaceous color, polygonal shape, and, sometimes, fine scale. LP is most commonly found on the extremities, genitalia, and mucous membranes. Less commonly lesions can also involve the hair and nails. LP is seen predominantly in adults and occurs in women more often than men. More than two-thirds of patients are between 30 and 60 years of age; however, the condition can occur at any age. LP is rare in children and the geriatric population.

Pat h o p h ysio lo g y LP is a cell-mediated immune response of unknown origin. An association is noted between LP and hepatitis C infection, chronic active hepatitis, and primary biliary cirrhosis. DESCRIPTION OF LESIONS

4.17 Lichen planus. Flat-topped, violaceous, polygonal papules on the flexor wrists are present. There are active and resolving lesions. Note the postinflammatory hyperpigmentation.

Th e “Se ve n Ps” 1. Lesions are often pruritic, but they may be asymptomatic. 2. Lesions are often purple (actually red to violet). 3. Lesions tend to be planar (flat-topped) (FIG. 4.16). 4. Lesions form papules or plaques. 5. Lesions may be polygonal (FIG. 4.17). 6. Lesions may be polymorphic in shape and configuration— that is, oval, annular, linear, confluent (plaquelike), large, and small, even on the same person. 7. Lesions tend to heal with residual postinflammatory hyperpigmentation, leaving darkly pigmented macules in their wake (FIG. 4.18).

4.18 Lichen planus. Postinflammatory hyperpigmentation in a characteristic distribution. 122

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ot h e r Clin ical Fin d in g s Asso ciat e d wit h Lich e n Plan us • New lesions may be noted at sites of minor trauma such as scratches or burns (the Köbner reaction [isomorphic response]; see FIG. 4.16). See also Chapter 3, “Psoriasis,” for another example of this phenomenon. • Wickham’s striae are characteristic white, lacelike streaks that are best visualized on the surfaces of lesions after mineral oil is applied. If present, they are virtually pathognomonic of LP. • Mucous membrane lesions may be characterized by white lacy streaks in a netlike pattern (FIG. 4.19) or by atrophic erosions or ulcers (see Chapter 12, “Disorders of the Mouth, Lips, and Tongue”). DISTRIBUTION OF LESIONS

4.19 Lichen planus. Oral lesions, with a white, lacy, reticulated, pattern on the buccal mucosa.

• The flexor areas such as the wrists, forearms, dorsa hands, dorsa feet, pretibial shafts, scalp, trunk, sacrum, glans penis, and labia minora are most often affected. Hypertrophic (verrucous) lesions tend to occur on the lower legs. Lesions may also become generalized. • Mucous membrane involvement is common and may be found without skin involvement. Lesions are most commonly found on the tongue and buccal mucosa but may also be noted on the gingiva, palate, or lips. • Genital involvement is common in men with cutaneous disease. Typically, an annular configuration of papules is seen on the glans penis (FIG. 4.20). Less commonly, linear white streaks (Wickham’s striae) can be seen on male genitalia. Vulvar involvement can range from reticulate papules to severe erosions. CLINICAL MANIFESTATIONS • Pruritus, which may be severe, and the cosmetic appearance of lesions are the major concerns to patients. • The course of LP is unpredictable. The onset may be abrupt or gradual. The lesions may resolve spontaneously, recur intermittently, or be chronic for many years. Chronicity is especially likely when hypertrophic lesions appear. • Mucous membrane involvement may become erosive and painful, particularly if ulcers are present. Rarely, malignant transformation to squamous cell carcinoma has been documented. • Vulvar lesions can result in dyspareunia, burning, and pruritus. • Nail lesions may exhibit symptoms ranging from a mild dystrophy to a total loss of the nails. • Scalp lesions result in a permanent, patchy, scarring follicular alopecia (lichen planopilaris, see Chapter 10, “Hair and scalp Disorders.”).

4.20 Lichen planus. Typical flat-topped papules are noted on the glans and the distal shaft of this patient’s penis (compare to psoriasis of penis in FIGURE 4.24).

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Clin ica l Va ria n t s Variations in LP include the following: • Hypertrophic: These extremely pruritic lesions are most often found on the extensor surfaces of the lower extremities (FIG. 4.21), especially around the ankles. Hypertrophic lesions are often chronic; residual pigmentation and scarring can occur when the lesions eventually clear. • Atrophic: Atrophic LP is characterized by a few lesions, which often develop into hypertrophic lesions. • Erosive: These lesions are found on the mucosal surfaces. • Follicular: Lichen planopilaris is characterized by keratotic papules that may coalesce into plaques. Scarring alopecia may result. Other eruptions resembling LP are seen in the following conditions: • Drug-induced LP, associated with gold, thiazides, captopril, and antimalarials • Lichenoid reactions associated with graft-versus-host disease • LP associated with hepatitis C DIAGNOSIS 4.21 Lichen planus, hypertrophic. Darkly pigmented hypertrophic lesions are present on the pretibial shaft.

• LP is often very easy to diagnose by its appearance, despite its range of clinical presentations. • The presence of Wickham’s striae is diagnostic. • Characteristic oral lesions are helpful in making the diagnosis. • Skin biopsy is performed, if necessary. • Serology for hepatitis B and C should be obtained if history is suggestive.

DIFFERENTIAL DIAGNOSIS

Lich e n Sim p le x Ch ro n icus an d Ot h e r Varian t s o f Ecze m at o us De rm at it is See Chapter 2, “Eczema,” and FIGure 4.22. • Lichenification may be present. • Condition may be clinically indistinguishable from LP. • Patient often has a positive atopic history.

Drug -In d uce d o r Ch e m ically In d uce d Lich e n o id (“Lich e n Plan us–Like ”) Erup t io n s • Causal drugs include thiazides, furosemide, beta-blockers, sulfonylureas, antimalarials, penicillamine, gold salts, and angiotensin-converting enzyme inhibitors. • Rarely, photodeveloping chemicals, dental materials, and tattoo pigments are involved. • There is generally a latent period of several months between drug introduction and the appearance of lesions.

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4.22 Lichen simplex chronicus. This patient has itchy pretibial hypertrophic plaques.

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DIFFERENTIAL DIAGNOSIS Continued • Lesions resolve when the inciting agent is discontinued, often after a prolonged period. • Skin lesions are indistinguishable from those of classic LP. • Oral lesions are lacking.

Ot h e r Diag n o se s t o Co n sid e r • Pityriasis rosea • Drug eruption • Guttate psoriasis • Tinea corporis • Discoid lupus erythematosus • Lichen nitidus • Oral mucous membranes (see Chapter 12, “Disorders of the Mouth, Lips, and Tongue”) • Normal bite line (FIG. 4.23) • Leukoplakia • Oral hairy leukoplakia • Candidiasis • Squamous cell carcinoma (particularly in ulcerative lesions) • Aphthous ulcers • Herpetic stomatitis • Secondary syphilis • Genital mucous membranes • Psoriasis (penis and labia) (FIG. 4.24) • Lichen sclerosis • Fixed drug eruption (penis) • Candidiasis (penis and labia) • Hair and scalp • Scarring alopecia (pseudopelade) • Folliculitis decalvans

MANAGEMENT • Mild cases can be treated symptomatically with potent topical steroids. Patients with more severe cases, especially those with scalp, nail, and mucous membrane involvement, may require systemic therapy. • High-potency (class 2) or super-potent (class 1) topical steroids may be used alone or with polyethylene occlusion, or with Cordran tape (see “Introduction: Topical Therapy”).

4.23 Normal bite line. This is a common finding on the buccal mucosa that is often confused with oral lichen planus.

4.24 Psoriasis. This is a common location for psoriasis. There are typical psoriasiform papules and plaques on this patient’s penis.

• The first-line treatments of cutaneous LP are potent topical steroids. • Systemic steroids (e.g., prednisone beginning at 0.5 to 1 mg/kg daily) in short, tapering courses may be necessary for symptom control and possibly more rapid resolution. • Oral acitretin (Soriatane) has been occasionally helpful. • For symptomatic LP of the oral mucosa, topical steroids are usually tried first. Alternatively, topical tacrolimus (Protopic) ointment 0.1% has been tried with some success.

POINT TO REMEMBER • Serial oral or genital examinations are indicated for erosive/ulcerative lesions to rule out squamous cell carcinoma. Chap ter 4 • Inflam m atory Erup tions of Unknown Cause

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5

Superficial Bacterial Infections, Folliculitis, and Hidradenitis Suppurativa OVERVIEW

IMPETIGO FOLLICULITIS • Staphylococcal folliculitis • Pseudom onas (hot tub) folliculitis FOLLICULITIS: OTHER TYPES • Irritant, frictional, or chem ical folliculitis • Steroid-induced acne and rosacea (see also Chapter 1, “Acne and Related Disorders”) • Eosinophilic pustular folliculitis (see also Chapter 24, “Cutaneous Manifestations of HIV Infection”). • Pityrosporum folliculitis • Majocchi’s granulom a • Viral folliculitis: herpes virus folliculitis (see Chapter 6, “Superficial Viral Infections”) FURUNCULOSIS (“BOILS”) HIDRADENITIS SUPPURATIVA (ACNE INVERSA)

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Bacteria such as Corynebacterium, Brevibacterium, Acinetobacter, and some Staphylococcus species, are commonly found on normal skin and are not pathogenic. Propionibacterium bacteria reside in hair follicles and contribute to acne. The two gram-positive cocci, Staphylococcus aureus and the group A -hemolytic streptococci, account for the vast majority of cutaneous infections. They may colonize normal skin or be secondary invaders of cutaneous ulcers, surgical or traumatic wounds, as well as in eczematous dermatitis, a skin disorder in which the barrier function of the skin is defective. Methicillin resistant Staphylococcus aureus (MRSA) is the term used for bacteria of the S. aureus group that are resistant to the traditional antibiotics used against them. Problems arise because antibiotic choice becomes very limited.

Im p et igo BASICS Impetigo is a primary superficial bacterial infection of the superficial layers of the epidermis. Traditionally, impetigo has been divided into two forms—bullous and nonbullous (crusted). These conditions are clinically more or less indistinguishable; therefore, it is probably less confusing to use the term impetigo to describe both of them. Impetigo is a common, highly contagious finding in preschoolers. The incidence of impetigo in children younger than 6 years of age is higher than it is in adults; however, the condition may occur in persons of all ages. Impetigo rarely progresses to systemic infection, although poststreptococcal glomerulonephritis is a rare complication. Impetigo is caused most often by Staphylococcus aureus; less often, group A beta-hemolytic streptococci (GABHS) may be the primary pathogen. In fact, both organisms can be present at the same time in the affected sites. In recent years, methicillin-resistant S. aureus (MRSA) has been noted as a cause of impetigo; this infection is observed more commonly with the nonbullous form of impetigo than the bullous form.

5.1 Impetigo. This child has a mixture of intact bullae and drying crusts.

Se co n d ary Im p e t ig o (Im p e t ig in izat io n ) Impetigo can, and often does, emerge as a secondary infection of preexisting skin disease or traumatized skin; it is then referred to as secondary impetiginization. Examples include impetiginized eczema. Patients who have atopic dermatitis or other inflammatory skin conditions often have skin colonized by S. aureus. Other conditions that may lead to impetiginization include the following: • • • •

Stasis dermatitis Herpes simplex and varicella infections Scabies and insect bites Lacerations and burns

5.2 Impetigo. In this 2-year-old child, intact blisters are not present; only the flaccid remains (scaly collarettes) of bullae are seen.

DESCRIPTION OF LESIONS • Impetigo begins as a crust or thin-roofed, fragile vesicle or bulla that ruptures and often leaves a peripheral collarette of scale or a darker, hemorrhagic, crusted border. Intact bullae are not usually present because they are very fragile; rather, they often demonstrate a collarette of scale or the flaccid remains of bullae (FIGS. 5.1 and 5.2). • Oozing serum dries and gives rise to the classic goldenyellow, “honey-crusted” lesion. Lesions appear to be stuck on (FIG. 5.3).

5.3 Impetigo. Oozing “honey-crusted” lesions in a typical location.

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• In time, a varnishlike crust (FIG. 5.4) develops centrally that, if removed, reveals a moist red base. DISTRIBUTION OF LESIONS • In children, the face is commonly involved, particularly in and around the nose and mouth, along with other exposed parts of the body (e.g., arms, legs), sparing the palms and soles. • In adults, lesions may occur anywhere on the body. CLINICAL MANIFESTATIONS Spread of lesions is by autoinoculation. 5.4 Impetigo (gladiatorum). This is a college wrestler (see also discussion of herpes gladiatorum in Chapter 6).

• Lesions are usually asymptomatic; occasionally they may itch. • The infection is self-limiting—even without treatment— and generally spontaneously resolves after a few weeks. It also typically clears with topical or oral antibiotics; only rarely do serious complications occur (see below). • Healing takes place without scarring, but it may cause temporary postinflammatory hyperpigmentation in dark-skinned persons. • Recurrent or persistent impetigo may indicate a carrier state in the patient or the patient’s family. DIAGNOSIS • Diagnosis is usually made on clinical grounds. • Bacterial culture and sensitivity testing are recommended if standard topical or oral treatment does not result in improvement. • A bacterial culture of the nares may be obtained to determine whether a patient is a carrier of S. aureus. • Urinalysis is necessary to evaluate for acute poststreptococcal glomerulonephritis if the patient develops edema or hypertension. Hematuria, proteinuria, and cylindruria are indicators of renal involvement.

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DIFFERENTIAL DIAGNOSIS

Tin e a Co rp o ris FIGURE 5.5. • The potassium hydroxide examination or fungal culture is positive. • Central clearing of lesions is noted. • Honey-colored crusts are absent. Ot h e r Diag n o se s • Rare considerations include primary bullous diseases such as bullous dermatosis of childhood and bullous pemphigoid. RARE COMPLICATIONS • Cellulitis, lymphangitis, scarlet fever, erysipelas, bacteremia with subsequent pneumonitis, septic arthritis, and septicemia may develop; rarely, bacterial endocarditis may also occur. • Staphylococcal scalded skin syndrome occurs more commonly in younger children. (See Chapter 9, “Bacterial Exanthems”) • Acute glomerulonephritis develops in 2% to 5% of individuals with impetigo caused by GABHS, most often in

MANAGEMENT • Antibacterial soaps such as povidone-iodine (Betadine) or chlorhexidine (Hibiclens) are used twice daily. • Gentle débridement of lesional crusts is done with a washcloth and the antibacterial soap. • Mupirocin 2% (Bactroban, Centany) ointment or cream applied three times daily may be used alone to treat very limited cases of impetigo. It is used until all lesions are cleared. Topical application of these preparations has been shown to be as effective as oral antibiotics. • For widespread involvement, an oral staphylocidal penicillinase-resistant antibiotic, such as cephalosporin,

5.5 Tinea corporis (faciale). This young boy was initially treated with topical antibiotics for presumptive impetigo. children aged 2 to 4 years. The onset is usually 10 days after the lesions of impetigo first appear, but it can occur from 1 to 5 weeks later. Transient proteinuria and hematuria may occur during impetigo and resolve before renal involvement develops. • Ecthyma, a deep dermal infection, can result, after which subsequent scarring can occur.

dicloxacillin, or erythromycin, may be used alone or in conjunction with topical antibiotics. • If bacterial cultures reveal MRSA, tetracyclines, trimethoprim/sulfamethoxazole (Bactrim), clindamycin, or linezolid are effective oral antibiotics. • In patients who have been determined to be chronic nasal carriers and have recurrent impetigo, and for those with MRSA, mupirocin 2% cream or ointment can be applied inside the nostrils three times daily for 5 days each month to reduce bacterial colonization in the nose. • Patients who are chronic nasal carriers also can be treated with rifampin (see later in this Chapter).

HELPFUL HINTS

POINTS TO REMEMBER • Rarely, poststreptococcal glomerulonephritis (but not rheumatic fever) has been reported to follow impetigo caused by certain strains of streptococci. • Family members should be evaluated as potential nasal carriers of S. aureus and treated, if necessary.

• Chronic or recurrent impetigo should alert the clinician to the possibility of an impaired immune status. • Strains of S. aureus are usually resistant to penicillin and may be resistant to erythromycin. • An emerging problem is MRSA, which may appear in both immunocompromised and immunocompetent patients. If infectious skin lesions do not improve during treatment intended for methicillin-sensitive S. aureus, the diagnosis of MRSA should be considered, and definitive antibacterial therapy should be determined on the basis of in vitro antibiotic sensitivity.

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Fo llicu lit is BASICS

5.6 Folliculitis. This woman had a leg waxing. Note the crusted papules.

Folliculitis, in its broadest sense, may be defined as a superficial or deep infection or inflammation of the hair follicles. It has multiple causes: various infections, physical or chemical irritation, occlusive dressings or clothing, and the use of topical or systemic steroids. Hereditary forms of folliculitis such as follicular eczema are generally classified as atopic dermatitis (see Chapter 2, “Eczema”). The deeper forms of inflammatory folliculitis that involve the entire follicular structure, such as folliculitis decalvans, occur most commonly in black men and women (see Chapter 10, “Hair and Scalp Disorders Resulting in Hair Loss”). Folliculitis may also be seen as a secondary infection in conditions such as eczema, scabies, and excoriated insect bites. It is more commonly found in patients who are diabetic, obese, or immunocompromised. Viral folliculitis may be seen in patients with herpes simplex infections, particularly in patients with human immunodeficiency virus (HIV) infection.

Stap h ylococcal Follicu litis Coagulase-positive S. aureus is the responsible pathogenic bacterium in most cases of infectious folliculitis. CAUSES AND PRECIPITATING FACTORS As in cases of inflammatory folliculitis (see Chapter 2, “Eczema”), bacterial folliculitis may be seen after the following:

5.7 Folliculitis. Intact follicular pustules and crusted papules.

• Repeated trauma (such as waxing, plucking, and shaving of the face, legs, and pubic areas) • Wearing of restrictive clothing, such as tight jeans • Excessive sweating DESCRIPTION OF LESIONS • A pustule or papule with a central hair is the primary lesion in folliculitis. The central hair shaft may not always be visible. • Follicular lesions tend to manifest a gridlike pattern on hairbearing areas of the body (FIGS. 5.6 and 5.7). • Lesions are often polymorphic, displaying a mixture of papules and pustules, or they may be monomorphic and consist solely of papules. • In darkly pigmented patients, primary lesions may consist of obvious papules or pustules; alternatively, only secondary, hyperpigmented lesions arranged in a follicular pattern may be all that is clinically visible.

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DISTRIBUTION OF LESIONS • Lesions occur on hair-bearing areas—the face, scalp, thighs, and body folds. • The axillae, groin, and legs are particularly prone to folliculitis when they are regularly shaved. CLINICAL MANIFESTATIONS • Lesions of folliculitis elicit mild discomfort and cosmetic concern. CLINICAL VARIANTS • Tender, painful, folliculitis involving an eyelash is called a hordeolum, or “sty.” • Similarly, folliculitis may affect a single nasal hair follicle and may produce a tender erythematous papule or pustule in or on the distal nose or near the tip of the nose (FIG. 5.8).

5.8 Folliculitis. This patient has a tender papule that originated in a nasal hair follicle.

DIAGNOSIS This is generally diagnosed by clinical findings. In cases that are resistant to treatment, the following procedures may be performed: • Gram stain and bacterial culture. In typical cases, a Gram stain shows gram-positive cocci, and culture grows S. aureus. • Nasal culture. The patient and, if necessary, the patient’s family members may require a nasal culture to look for S. aureus.

DIFFERENTIAL DIAGNOSIS

Acn e Vulg aris an d Ot h e r Acn e like Co n d it io n s • Keratosis pilaris is frequently confused with acne and folliculitis (see Chapter 2, “Eczema”). • Because keratosis pilaris involves the hair follicles, it manifests in a gridlike pattern, similar to that of folliculitis. • Lesions have a rough texture and are persistent. In se ct Bit e Re act io n s • Lesions are grouped in a nonfollicular pattern (see Chapter 20, “Bites, Stings, and Infestations”).

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MANAGEMENT

Mild Case s • Mild cases of bacterial folliculitis can sometimes be prevented or controlled with antibacterial soaps. • In addition, topical antibiotics, such as erythromycin 2% topical solution or clindamycin (Cleocin) 1% solution, may be applied once or twice a day to the affected areas. Ch ro n ic an d Re curre n t Case s Chronic and recurrent cases of bacterial folliculitis present a difficult therapeutic problem. • If staphylococcal colonization is present, mupirocin 2% (Bactroban) ointment should be applied to the nasal

vestibule twice a day for 5 days to eliminate the S. aureus carrier state. • Family members may be treated similarly, if necessary. Rifampin (600 mg/day for 10 to 14 days) may also eliminate the carrier state. • Even in cases of negative bacterial cultures, a systemic antibiotic is often needed for coverage of S. aureus because it is the most common pathogen. This organism is often resistant to penicillin, and thus dicloxacillin (250 to 500 mg four times a day) or a cephalosporin, such as cephalexin (1 to 4 g/day in two doses) is generally the first choice. Minocycline (50 to 100 mg twice a day) is sometimes used for MRSA.

Pseudom onas (Hot Tu b) Follicu litis

POINTS TO REMEMBER • Bacterial cultures should be considered for cases that are resistant to therapy. • Culturing and treating of family members should be considered in cases of chronic bacterial folliculitis.

Pseudomonas folliculitis, which may be acquired from communal hot tubs, is caused by Pseudomonas aeruginosa infection. Although hot tubs have increased the incidence of folliculitis, they are often overlooked as a cause. Jacuzzis, therapeutic whirlpools (“whirlpool folliculitis”), public swimming pools, and the use of loofah sponges can be sources of Pseudomonas infection. Pseudomonas folliculitis has been found to occur under diving areas and after wax depilation. DESCRIPTION OF LESIONS • Lesions of hot tub folliculitis consist of intensely pruritic or tender follicular papules or pustules that are most often found on the trunk, particularly on areas covered by a bathing suit (FIG. 5.9). CLINICAL MANIFESTATIONS • Pruritic lesions occur 1 to 3 days after bathing in a hot tub, whirlpool, or public swimming pool. DIAGNOSIS • The diagnosis is based on a history of exposure. • Pseudomonas organisms can be isolated in patients with this condition.

MANAGEMENT

5.9 Hot tub folliculitis (“hot tub buns”). Multiple pruritic follicular papules and pustules occurred on the buttocks of this young man 3 days after he had bathed in a hot tub. Bacterial culture grew Pseudomonas aeruginosa. 132

• Hot tub folliculitis usually resolves spontaneously, but it may not if it is very extensive or symptomatic. • If necessary, it may be treated with oral ciprofloxacin (500 mg twice a day for 5 days).

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Follicu litis: Oth er Typ es Irrit an t , Frict io n al, o r Ch e m ical Fo lliculit is Nonbacterial, or sterile, folliculitis can arise from physical or chemical irritation. Such irritants include leg waxing, leg shaving, axillary shaving, and hair plucking. Chemical depilatories, electrolysis, occlusive dressings, and excessive sweating can also contribute to this problem, as well as wearing tight clothing. Nonbacterial folliculitis may also be related to working conditions, such as the use of greases or oils, and to the application of various cosmetics. Bacteria such as S. aureus are not infrequent secondary invaders. St e ro id -In d uce d Acn e an d Ro sace a Topical or systemic steroid treatment may lead to steroidinduced acne, which is actually a form of folliculitis. Diagnosis of these conditions is aided by a history of potent topical or systemic steroid use (FIG. 5.10 and also see Chapter 1, “Acne and Related Disorders”). Eo sin o p h ilic Pust ular Fo lliculit is Eosinophilic pustular folliculitis, another form of sterile folliculitis, has intensely pruritic lesions that resemble urticaria papules. It is seen in patients with acquired immunodeficiency syndrome (see Chapter 24, “Cutaneous Manifestations of HIV Infection”). Fun g al Fo lliculit is Pit yrospor u m Fo llicu lit is

This acnelike eruption, seen on the trunk, is caused by Malassezia furfur, which is a lipophilic yeast. Lesions are chronic, erythematous, pruritic papules and pustules that usually appear on the back and chest of young adults. The eruption appears in a follicular pattern. This condition is seen more frequently in the summer. Pityrosporum folliculitis should be considered as a diagnosis when folliculitis resists antibiotic treatment. It looks like acne, but it does not respond to acne therapy (See Chapter 7, “Superficial Fungal Infections”).

5.10 Systemic steroid-induced folliculitis. This patient is taking long-term oral prednisone for sarcoidosis.

POINTS TO REMEMBER • Bacterial, fungal, or viral cultures should be considered in cases that are resistant to therapy. • In HIV-positive patients, a skin biopsy should be performed for suspected cases of eosinophilic pustular folliculitis.

Ma jo cch i’s Gra n u lo m a

Tinea corporis of the lower legs may produce tinea folliculitis in women who shave their legs. The organism is introduced into the hair follicle by shaving.

Viral Fo lliculit is: He rp e s Virus Fo lliculit is This form of folliculitis is caused most often by an infection by herpes simplex virus type 1. It is found in areas adjacent to a primary cold sore and is spread by shaving. See also Chapter 6, “Superficial Viral Infections.”

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Fu ru n cu lo sis

(“Bo ils”) BASICS Folliculitis may evolve into a furuncle (“boil”), which is a deeper infection; the term carbuncle refers to an aggregation of furuncles. S. aureus is the customary responsible pathogenic bacterium. Furuncles are painful nodules or abscesses (walled-off collections of pus) in an infected hair follicle; they are more common in boys and young adults. Chronic or recurrent furunculosis is a difficult therapeutic problem that is often the result of nasal carriage of S. aureus. Like folliculitis, furunculosis is more common in diabetic patients and in obese persons. DESCRIPTION OF LESIONS

5.11 F uruncle. This patient has a tender “boil” located in his axilla.

• A furuncle is a tender, painful nodule with overlying erythema (FIG. 5.11). • As the lesion evolves, a fluctuant abscess may form (FIG. 5.12). • If untreated, it may rupture and drain spontaneously. DISTRIBUTION OF LESIONS • Hair-bearing areas are commonly involved, with body folds the preferred sites. • The scalp, face, buttocks, thighs, axillae, and inguinal areas are affected. • Furuncles are often seen in the axillae, groin, posterior neck, thighs, and buttocks. When they occur in a contiguous cluster on the occipital scalp, they are referred to as carbuncles. CLINICAL MANIFESTATIONS

5.12 Abscess. This patient has the follicular occlusion triad (“tetrad” in this case), which consists of hidradenitis suppurativa, acne conglobata, and dissecting cellulitis of the scalp. This walled-off lesion began as a pilonidal sinus that later developed into an abscess. Note the older violaceous scars from previous furuncles and cystic acne lesions.

• Furuncles can cause throbbing pain and can be quite tender. DIAGNOSIS • This is based on the clinical presentation. • Gram stain generally reveals gram-positive cocci; culture often grows S. aureus.

DIFFERENTIAL DIAGNOSIS

Hid rad e n it is Sup p urat iva See the following section. • • • •

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Abscesses resembling furuncles are noted. Bacteria are secondary invaders. The condition is more common in women. It may be indistinguishable from furunculosis in its early stages.

MANAGEMENT • Furuncles come to a “head” with warm compresses, or they may be incised and drained. • Systemic staphylocidal antibiotics such as dicloxacillin, erythromycin, or cephalosporin may be added. Minocycline is sometimes used for MRSA. • The daily coating of the distal nasal mucosa with mupirocin should be considered in carriers or recurrent cases.

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H id ra d en it is Su p p u ra t iva BASICS Hidradenitis suppurativa (HS) should not be classified as an infection; rather, it is a chronic, recurrent, scarring, inflammatory disease that affects the regions of the skin-bearing apocrine sweat glands: the axillae, inguinal folds, suprapubic area, anogenital area, buttocks, areola, and under the female breasts. Bacterial involvement is not a primary pathogenic event. Autosomal-dominant inheritance has been described. HS appears after puberty, and most cases develop during the second and third decades of life. It is seen mostly in women and only rarely before puberty. When HS occurs in African-American women, it tends to be more severe.

Pat h o p h ysio lo g y The exact cause of HS is unknown. Traditionally, it had been considered a primary inflammatory disorder of the apocrine glands (and was sometimes referred to as apocrinitis or apocrine acne). The current hypothesis suggests that poral occlusion of the hair follicle leads to retention of the secretory products and subsequent inflammation. This hypothesis is supported by the finding that in most biopsy specimens, the apocrine glands are intact and unaffected, and follicular occlusion is constant. Inflammation of the apocrine glands is thus considered to be secondary or incidental. Bacterial involvement is also considered a secondary pathogenic event. The plugged structure dilates, ruptures, becomes infected, and progresses to abscess formation, draining, and fistulous tracts.

(Acn e In versa )

In the chronic state, secondary bacterial infection probably is a major cause of exacerbations. Like acne vulgaris, HS is related to androgen excess and often flares with menstruation. Symptoms often improve during the estrogen-elevation phases of the menstrual cycle. Moreover, HS frequently improves during pregnancy, only to flare during the postpartum period. DESCRIPTION OF LESIONS AND CLINICAL MANIFESTATIONS • Initially, HS presents with nodules and abscesses that may be indistinguishable from furunculosis or common “boils.” • Lesions are painful and tender, and they often become infected secondarily and exude a serosanguineous or foulsmelling purulent material that may stain clothing. • HS is often a cause of embarrassment and, possibly, social isolation. • Lesions recur, new lesions crop up, and old lesions scar in a frustrating, unrelenting process. • Frequently there is a menstrual flare. • Chronic HS is indicated by the appearance of sinus tract and fistula formation, ulcerations, and, eventually, hypertrophic, ropelike linear bands of scars and dermal contractures (FIG. 5.13). • Characteristic multiple open comedones (“blackheads”) develop in long-standing cases.

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DISTRIBUTION OF LESIONS • The most common area of involvement is the axillary area (FIG. 5.13); the groin is also frequently involved (FIG. 5.14). • However, lesions may also be seen on the perineum, inframammary areas, the buttocks, and, rarely, the neck and scalp. DIAGNOSIS • The multiple lesions of HS that scar and form sinus tracts should be easily distinguishable from other conditions.

5.13 Chronic hidradenitis suppurativa. This patient has involvement of the axilla with bandlike hypertrophic scars and draining abscesses.

5.14 Hidradenitis suppurativa. This patient has involvement of the inguinal areas, labia majora, and mesial thighs.

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DIFFERENTIAL DIAGNOSIS In its early stages, HS is most often confused with the following: • Recurrent folliculitis and furunculosis (FIGS. 5.15 and 5.16). Solitary lesions resemble a furuncle, lymphadenitis, or an infected epidermoid cyst.

5.15 Folliculitis. This patient has multiple superficial papules and pustules in her axillary vault.

MANAGEMENT • HS is a difficult, frustrating condition to control. • Large cysts should be incised and drained. Smaller cysts respond to intralesional injections of triamcinolone acetonide (Kenalog, 2.5 to 10 mg/mL). • Weight loss helps reduce the activity and severity of HS. • Actively discharging lesions should be cultured. Repeated bacteriologic assessment is advisable in all cases. • Antibiotics are the mainstay of treatment, especially for the early stages of the disease. Long-term oral antibiotics such as tetracycline (500 mg twice daily), erythromycin (500 mg twice daily), doxycycline (100 mg twice daily), or minocycline (100 mg twice daily) may prevent disease activation. Lower doses may be effective for maintenance once control is established. Topical clindamycin may also be effective.

Pre ve n t ive Me asure s Durin g Re m issio n s • Wearing of ventilated cotton clothing is advised. • Other therapeutic measures involve the use of absorbent powders and bacteriostatic soaps.

• In the vaginal area, an infected Bartholin’s cyst may resemble a solitary lesion of HP. Other conditions appear to be related to HS and may coexist in the same patient. The so-called follicular occlusion triad, which consists of HS, acne conglobata, and dissecting cellulitis of the scalp, has been well documented. Pilonidal sinus was later added to the triad, making it a tetrad (see FIG. 5.12).

5.16 F urunculosis. This patient has multiple painful, “pointing” furuncular papules and nodules in her axilla.

To p ical Th e rap y • Limited and very early disease may be helped somewhat by the daily use of topical antibiotics, such as clindamycin or erythromycin. • Intralesional corticosteroid injections inserted directly into painful lesions are used to treat limited acute exacerbations. Syst e m ic Th e rap y • Prednisone can be used in short courses, particularly if inflammation is severe. A short course of prednisone, 40 to 60 mg daily, to be tapered over 2 to 3 weeks is often quite effective. • Prednisone may be given alone or, most often, in combination with oral antibiotics, such as minocycline, erythromycin, ciprofloxacin, cephalosporins, or semisynthetic penicillin, given in the usual doses used for soft tissue infections. For example, minocycline, in doses ranging from 50 to 100 mg twice a day, may be used on an episodic basis for weeks or, if necessary, months at a time and then tapered to the lowest dosage that relieves continued on page 138

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MANAGEMENT Continued

•

•

•

•

symptoms. Long-term administration of an antibiotic, such as minocycline, can also be used to prevent episodic flares. The efficacy of minocycline seems to be attributable to its anti-inflammatory action rather than its antibiotic effect. Alternative antibiotics that can be helpful include erythromycin (250 to 500 mg three or four times a day), ciprofloxacin (500 mg twice a day), cephalexin (250 to 500 mg four times a day), and dicloxacillin (250 to 500 mg twice a day). Systemic retinoids, such as oral isotretinoin (Accutane), have been used with limited benefit in early disease that has not yet produced significant scarring. The systemic retinoids are not as effective in treating HS as they are in treating severe nodular acne; moreover, relapses are very common after seemingly effective treatment is stopped. Certain oral contraceptives, such as cyproterone acetate (which is not available in the United States), have been reported to be helpful in some cases. Cyclosporine has also been reported to be of some value. Infliximab (Remicade) is a monoclonal antibody that targets tumor necrosis factor alpha and inhibits its activity that is used in the treatment of psoriasis (see Chapter 3, “Psoriasis”). It has been anecdotally reported to be

effective in some severe cases of HS; however, toxic events and lack of efficacy have been demonstrated in one recent series.

Surg ical Me asure s • Incision and drainage are performed only on fluctuant lesions. This approach affords short-term relief of troublesome, painful abscesses. Repeated incision and drainage may lead to more scarring and sinus tract formation. • Severe refractory HS is best treated with wide, complete surgical excision of the involved area, which may produce a definitive cure. • A narrow excision of inflamed areas may help temporarily, but this method has a high recurrence rate. • Ablation techniques using a carbon dioxide laser that spares normal tissue have been tried successfully. These techniques may become the standard of surgical treatment. Pro g n o sis The course of HS varies. • Some patients have very mild disease that may be indistinguishable from chronic furunculosis. • Remissions may occur more frequently as the patient ages or as more scar tissue develops; however, total spontaneous resolution is rare. More commonly reported is a decline in severity at or after menopause.

POINTS TO REMEMBER • Recurrent tender furuncles or sterile abscesses in the axillae or groin, on the buttocks, or below the breasts suggest the diagnosis of HS. • Many cases, especially of the thighs and vulva, are mild and misdiagnosed as recurrent furunculosis. • Chronic disease is indicated by the presence of old scars, sinus tracts, and open comedones.

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C H AP T ER

Superficial Viral Infections

6 OVERVIEW Viruses are capable of causing a wide variety of disorders of the skin and mucous membranes. Specific skin lesions vary greatly and include vesicles, pustules, papules, ulcers, and tumors. Cutaneous viral infections present in various reaction patterns, most commonly, vesicobullous, vascular (viral exanthems), or papulosquamous (pityriasis rosea). Certain viral infections—warts in particular—vary greatly in their gross clinical manifestations despite all being caused by the same, albeit different subtypes, of human papilloma virus (HPV). For example, the clinical appearances of warts often differ markedly and manifest as papillomatatous (common warts), threadlike (filiform warts), flat (planar warts), to exuberant moist papules (condyloma acuminata), or tumors (giant condyloma acuminatum of BuschkeLöwenstein). See Chapter 19, “Sexually Transmitted Diseases.” In contrast, lesions of molluscum contagiosum tend to be quite monomorphic and uniform in appearance and vary primarily by size. The virus of varicella-zoster (VZV) may produce the clinical syndrome of either chickenpox or herpes zoster. Herpes simplex virus (HSV) lesions may manifest in ways that produce systemic problems, whereas the virus of warts and molluscum contagiosum are entirely localized to the skin (dermatotrophic) and do not cause systemic symptoms. Systemic viral disorders such as varicella are discussed in Chapter 8, “Viral Exanthems.”

WARTS (NONGENITAL) • • • •

Com m on warts Plantar warts Flat warts Filiform warts MOLLUSCUM CONTAGIOSUM HERPES SIMPLEX (NONGENITAL)

• Prim ary orolabial herpes sim plex • Recurrent orolabial herpes sim plex • Clinical variants of herpes sim plex infections HERPES ZOSTER • Dissem inated herpes zoster • Post herpetic neuralgia

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Wa rt s

(No n gen it a l)

BASICS The emergence of common warts (verrucae vulgaris) and other forms of cutaneous warts is extremely common, particularly in children and young adults. An estimated 20% of school-age children will at some time have at least one wart. In children, warts tend to regress spontaneously. In many adults and in immunocompromised patients, however, warts often prove difficult to eradicate. All warts are caused by the human papillomavirus (HPV); to date, more than 150 different subtypes have been identified. The virus infects epidermal keratinocytes, which stimulates cell proliferation. Viral transmission occurs primarily through skin-to-skin contact such as handshaking or kissing. The recently shed virus can also be found on almost anything in a moist, warm environment, including doorknobs, hand railings, and floors of locker rooms, as well as around swimming pools. Contact with any of these surfaces is another means of viral transmission; the virus is virtually impossible to avoid. Often, several family members develop warts. Whether this reflects a genetic susceptibility or is simply a result of the ubiquitous nature of the contagion has not been determined.

Fact o rs t h at Pre d isp o se t o Hum an Pap illo m avirus In fe ct io n • Infection with the human immunodeficiency virus (HIV) or the presence of other immunosuppressive diseases, such as lymphomas, can predispose one to become infected.

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• Taking drugs that decrease cell-mediated immunity (e.g., prednisone, cyclosporine, chemotherapeutic agents) is another predisposing factor. Transplant recipients who, by necessity, use such medications on a long-term basis have warts that can be very resistant to treatment. • Handling raw meat, fish, or other types of animal matter in one’s occupation (for example, butchers) increases susceptibility. DESCRIPTION OF LESIONS • Warts are most often diagnosed based on their clinical appearance, but a biopsy can be performed if the diagnosis is in doubt. A typical wart is a papillomatous, corrugated, hyperkeratotic growth that is confined to the epidermis. Despite a common misconception, warts have no “roots,” and there is no “mother wart.” • Warts may be skin colored to tan and measure 5 to 10 mm in diameter. However, they may coalesce into clusters (mosaic warts) that can be up to 3 cm in diameter. • Warts often vary widely in shape, size, and appearance. The different names for warts generally reflect their clinical appearance, location, or both. For example, filiform warts are threadlike, planar warts are flat, and plantar warts are located on the plantar surface of the feet. • Genital warts (condyloma acuminata) may be large and cauliflowerlike, or they may consist of small papules.

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DISTRIBUTION OF LESIONS • Warts may develop anywhere on the body, but they are most often found at sites subject to frequent trauma, such as the hands and feet. • The distribution is generally asymmetric, and lesions are often clustered. • Viral protein and infectious particles have been detected in the absence of visible skin surface lesions using electron microscopy, polymerase chain reaction, and DNA hybridization techniques. Thus, it is well documented that HPV can exist in a subclinical or latent state. • This latency explains the not infrequent recurrence of warts at the same site or at an adjacent site, even when they had been apparently “cured” many years before.

CLINICAL VARIANTS

6.1 Common warts (verruca vulgaris). This young boy has multiple common warts.

Com m on Warts • Verrucae vulgaris, or common warts (FIG. 6.1), occur most often on the hands and fingers and in the nail area—both around (periungual) and under (subungual) nail areas (FIGS. 6.2 and 6.3). They are frequently seen on the knees and elbows, especially in children. • Their distribution is generally asymmetric, and lesions are often grouped.

6.2

Common warts (verruca vulgaris). Periungual warts.

6.3 Common wart (verruca vulgaris). This subungual lesion could easily be mistaken for onychomycosis, and, in rare instances, prove to be a squamous cell carcinoma (when only one nail is involved).

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DESCRIPTION OF COMMON WARTS • Common warts generally have a verrucose, or vegetative, appearance. • Lesions show loss of normal skin markings (e.g., fingerprints and handprints). • “Black dots,” or thrombosed capillaries, are pathognomonic (FIG. 6.4). • Usually warts are asymptomatic, but they can be tender and often cause embarrassment.

6.4 Common warts (verruca vulgaris). These lesions demonstrate loss of normal skin markings, and “black dots,” or thrombosed capillaries, are pathognomonic.

DIFFERENTIAL DIAGNOSIS OF COMMON WARTS

Pe d iat ric • Molluscum contagiosum (see FIG. 6.15) Ad ult / Eld e rly • Seborrheic keratosis • Acrochordon (skin tag) • Solar keratosis and cutaneous horn • Squamous cell carcinoma • Keratoacanthoma Se b o rrh e ic Ke rat o sis See Chapter 21, “Benign Skin Neoplasms.” • These benign lesions occur in middle-aged and older people. • They are most often seen along the frontal hairline, face, and trunk. • They have a “stuck-on” appearance. • They may be clinically indistinguishable from warts.

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So lar Ke rat o sis (Act in ic Ke rat o sis) See Chapter 22, “Premalignant and Malignant Skin Neoplasms.” • These lesions occur in elderly, fair-complexioned persons, and they are sometimes associated with a cutaneous horn. • They are rough-textured papules that appear in sunexposed areas. • Biopsy may be necessary to distinguish these lesions from squamous cell carcinoma.

Sq uam o us Ce ll Carcin o m a Un d e r t h e Nail • Biopsy is necessary. • This lesion can easily be misdiagnosed as a subungual wart. On ych o m yco sis See Chapter 7, “Superficial Fungal Infections.” • The potassium hydroxide examination or fungal culture is positive.

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Plan tar Warts • Plantar warts are seen on the plantar surface of the feet and occur mostly in children and young adults. • They usually appear on the metatarsal area, heels, insteps (FIG. 6.5), and toes in an asymmetric distribution. DESCRIPTION AND DISTRIBUTION OF PLANTAR WARTS • Plantar warts may be painful and can impair ambulation, particularly when present on a weight-bearing surface, such as the sole of the foot during walking. • Lesions may be solitary or multiple, or they may appear in clusters (mosaic warts) (FIG. 6.6). • There is loss of normal skin markings (dermatoglyphics). Often, there are pathognomonic “black dots” (thrombosed dermal capillaries) and punctate bleeding that become evident after paring with a no. 15 blade (FIG. 6.7).

6.5 Mosaic plantar warts. Characteristic “black dots” are seen in this cluster of plantar warts.

6.6 Mosaic plantar warts. Note the clustering, “kissing lesions” on this patient’s toes.

6.7 Plantar wart. Characteristic punctate bleeding is present after paring. Note the loss of skin markings.

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DIFFERENTIAL DIAGNOSIS OF PLANTAR WARTS • Corns (clavi) are sometimes difficult to distinguish from warts. Similar to calluses, corns are thickened areas of the skin that form in response to excessive pressure and friction. • They are usually hard and circle-shaped, with a polished or central translucent core, like the kernel of corn from which they take their name (FIG. 6.8). • Corns do not have “black dots,” and skin markings are retained, except for the area of the central core. • Corns most commonly develop on the tops and the tips of toes and along the sides of the feet. Lesions are also typically seen between the fourth and fifth toes (“kissing corns”). • Wearing high-heeled shoes—particularly shoes that shift the body weight into a narrow, tapering toe box—can produce corns.

6.8 Corn (clavus). After paring, the circular central translucent core resembles a kernel of corn.

Flat Warts Verrucae planae, or flat warts, are commonly found on the face (FIGS. 6.9 and 6.10), arms (FIG. 6.11), dorsa of hands, and the shins (women), where lesions are often spread by leg shaving.

6.10 F lat warts (verruca planae). Very subtle, fleshcolored papules are present on this woman’s chin.

6.9 F lat warts (verruca planae). Lesions are slightly elevated papules the color of the patient’s skin. Note the linear configuration resulting from autoinoculation of lesions on the bridge of this child’s nose. 144

6.11 F lat warts (verruca planae). Lesions are slightly elevated, flat-topped papules. Linear autoinoculation is apparent.

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DESCRIPTION OF FLAT WARTS • These small, flat-topped, papular warts are slightly elevated and well-defined. • Papules are skin-colored or tan to brown in color, and they range in size from 1 to 5 mm. Side lighting may be necessary to see them. • Sometimes, flat warts show a linear configuration caused by autoinoculation. • In men, flat warts are spread by shaving. Flat warts tend to resolve spontaneously, sometimes after a sudden increase in number, size, and inflammation.

DIFFERENTIAL DIAGNOSIS OF FLAT WARTS • Flat warts may resemble molluscum contagiosum (see later text), which manifests as shiny, waxy, domeshaped papules with a central white core.

Filiform Warts These tan, slender, delicate, fingerlike growths that emanate from the skin, filiform warts, are most commonly seen on the face (FIG. 6.12)—usually around the ala nasi, mouth, eyelids— and on the neck.

DIFFERENTIAL DIAGNOSIS OF FILIFORM WARTS • These finger-like papules that are seen in the elderly, usually on sun-exposed areas, may overlie a wart or a squamous cell carcinoma.

MANAGEMENT

Ge n e ral Prin cip le s The management of warts is often challenging, and there is no ideal treatment. The abundance of therapeutic modalities described in this chapter is a reflection of the fact that none of them is uniformly effective (see also TABLE 6.1). The method of treatment depends on the following: • • • •

The age of the patient The patient’s pain threshold The type of wart The location of the lesion

6.12 Filiform and common warts. This child has filiform warts on her nose and a common wart on her finger.

Providing no treatment at all may be safe and cost effective, because many warts resolve on their own. Painful, aggressive therapy should be avoided, unless there is a pressing need to eliminate the wart.

Ch ild re n • In children, most warts tend to regress spontaneously, which is probably related to a host immune response. • Social factors are also important. For example, a 2-yearold child with a filiform wart located near the ala nasi, or with multiple hand warts, should warrant less aggressive continued on page 146 Chapter 6 • Superficial Viral Infections

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MANAGEMENT Continued

Tab le 6.1 TOPICAL WART MEDICATIONS FORMULARY AGENT

APPLICATION

FORMS

Topical Agents: Over-the-Counter DuoFilm solution DuoFilm patch Dr. Scholl’s Callus Removers Occlusal-HP solution Compound W gel

Apply daily under occlusion Apply daily Apply daily Apply daily Apply daily

17% salicylic acid 40% salicylic acid in rubber-based vehicle 40% salicylic acid in rubber-based vehicle 17% salicylic acid in polyacrylic solution 17% salicylic acid in flexible collodion

Topical Agents: Prescription Aldara

Nightly as tolerated

5% imiquimod cream; 12 packets in a box

treatment than a 6-year-old child with similar lesions who may suffer from the teasing of other children.

• Treat one digit at a time. • Expect that after several weeks, the wart will become smaller, soft, and macerated and hopefully disappear.

Du ct Ta p e (“Du ct o -Th era p y”)

For stubborn common warts around and under the fingernails, the patient (or parent) is instructed in the following safe, easy, painless, inexpensive method that has been reported to help promote wart resolution: • Cut a roll of shiny, electrical (duct) tape into 1-inch strips. • Completely wrap the affected area with two “layers” of the tape (ILL. 6.1), making it airtight. Do not wrap the tape too tightly. • Leave the tape on for 6 days, and then remove it for half a day. Leave the tape on during bathing, working, school, and all activities. • Repeat this procedure (6 days on, 6 days off).

Ad ult s an d Im m un o co m p ro m ise d Pat ie n t s • In many adults and immunocompromised patients, warts often prove difficult to eradicate. • It is necessary to explain to patients that there is no known practical way actually to kill HPV, and in many patients, when warts regress it is not because they have been “cured” but because the infection has become latent. • Patients may also be reminded that so far there are no cures for acquired immunodeficiency syndrome (AIDS) or the common cold—both of which are caused by viruses— so it is not surprising that the virus that causes warts is difficult to eradicate. Treatment often takes numerous sessions, and, on occasion, warts fail to resolve. • In short, the immune system apparently plays the most significant role in the expression of HPV. Treatment merely prompts or stimulates the immune system into dealing more effectively with the virus. • The following treatment suggestions are given in a stepwise fashion, beginning with the least painful methods. (Note: The use of many of the following topical chemical approaches may be contraindicated during pregnancy or in women who are likely to become pregnant during the treatment period.) H o m e Trea t m en t : To p ica l Sa licylic Acid

• Salicylic acid is a keratolytic (peeling) agent that can be self-administered. It has a role in exfoliating the hyperkeratotic “dead skin” of warts and inducing inflammation. • Salicylic acid is available in numerous over-the-counter (OTC) trade name preparations such as Compound W gel and solution and Duofilm gel, patch, and solution. I6.1 Treating warts using “ducto-therapy.” (Modified courtesy of Jerome Z. Litt, M.D.). 146

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MANAGEMENT Continued • For best results with any keratolytic agent, the affected area should be hydrated first by soaking it in warm water for 5 minutes before application of the agent. Advantages

These preparations provide the best treatment for small children in whom warts are usually self-limiting. • • • • •

Usable on periungual warts Nonscarring Painless to apply Relatively inexpensive Do not require office visits

• This treatment can cause painful blisters. • On darkly pigmented skin, cryotherapy can result in hypopigmentation or hyperpigmentation, or even depigmentation, because LN2 destroys melanocytes. • Overaggressive treatment may cause scarring. • Treatment often requires multiple office visits. Elect ro ca u t er y a n d Blu n t Dissect io n

• In electrosurgical procedures, the wart is burned by an electrical current that uses heat conduction from a hot probe heated by a direct current. • These methods are best for warts on the knees, elbows, and dorsa of hands. They are also effective for filiform warts.

Disadvantages

Advantages

• Slow response • Often no response • Time-consuming

• Treatment is tolerable in most adults. • Warts are removed on the day of treatment. Disadvantages

Cr yo t h era p y w it h Liq u id Nit ro gen

• Liquid nitrogen (LN2) may be applied with a cotton swab or with a cryotherapy gun (Cryogun) (see Chapter 26, “Diagnostic and Therapeutic Procedures”). The goals are a rapid freeze and a slow thaw. Repeated freeze–thaw cycles increase cell damage. Cryotherapy is best for warts on hands. • Regardless of whether LN2 is applied with a saturated cotton swab or with a cryotherapy gun, one should aim to create a 2- to 3-mm zone of freeze around the lesion for a total of 4 to 5 seconds. The time of application varies, depending on the thickness of the lesion. • If possible, an attempt should be made to freeze lesions at a right angle; this approach may lessen the patient’s pain and may minimize collateral damage to normal surrounding skin. • The procedure is repeated at 2- to 3-week intervals, based on patient tolerance or on previous treatment results, degree of pain, and posttreatment morbidity. Advantages

• Treatment is rapid. • Many lesions can be treated during a single office visit. • It works well for hand warts. Disadvantages

• This approach necessitates the availability of an LN2 unit and holding tank. • Treatment is painful and must be used cautiously on fingertips and on periungual lesions.

• Local anesthesia is required. Treatment sometimes necessitates a digital block, which can be painful, especially on the fingers and the soles of the feet. • Treatment may cause scarring. • It can cause nail deformity after injury to the nail matrix. La ser Ab la t io n

• Laser destruction of warts is reserved only for large or refractory lesions. • This method is expensive and requires local anesthesia. • One study concluded that laser ablation is no more effective in eradicating recalcitrant warts than are the less costly conventional methods described herein. Im m u n o t h era p y Interferon Induction

• Aldara cream 5% (imiquimod), a local inducer of interferon that stimulates immune up-regulation, may be applied at home by the patient. It is available as a 5% cream that is approved for the treatment of genital warts (condyloma acuminatum) (See Chapter 19, “Sexually Transmitted Diseases”). • There have been numerous anecdotal reports of the successful off-label use of imiquimod on common warts and plantar warts. It is applied under duct tape occlusion after hydrating the area to be treated. This is best done at bedtime and washed off after 6 to 10 hours. It is applied to facial flat warts without occlusion (see later discussion).

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MANAGEMENT Continued Sensitizing Agents

• The deliberate induction of allergic reactions by injecting or applying sensitizing agents is sometimes used to treat warts. • Intralesional injection of the Candida skin test antigen has been associated with some reports of total clearance of warts in sites that were remote from the location of injection. • There are other contact (applied) immunotherapy agents, such as diphencyprone, dinitrochlorobenzene (DNCB), and squaric acid dibutylester (SADBE), that produce a delayed-type hypersensitivity reaction; however, there are possible mutagenic and side effects with these agents. Oral Therapy

• The results in treating recalcitrant warts with high-dose oral cimetidine (Tagamet) have been disappointing in most placebo-controlled studies. However, this agent may at times to be effective in children. Vesica n t s

• Cantharidin (Cantharone), or “bug juice,” a vesicant (blister-producing agent), is a chemical that was originally derived from the green blister beetle. It is applied in an office setting. • The preparation is applied to individual warts in a thin coat, using a cotton-tipped applicator or a toothpick. A waterproof bandage is used to cover the lesion(s). The procedure is painless. The occlusive dressing is left in place for 4 to 6 hours, and the skin is washed with soap and water. • The cantharidin causes the skin under the wart to blister, and the wart is thus lifted off the skin. When the blister dries, the wart—if treatment is successful—detaches with the blistered skin. • There usually is no scarring. Although cantharidin does not hurt when it is applied, the resulting blister can be painful. • The combination of cantharidin, salicylic acid, and podophyllin in flexible collodion (Cantharone Plus) is a very potent alternative to the use of Cantharone alone; this approach may cause severe blisters and pain and should be used with caution. Ca u st ic Agen t s

• Dichloroacetic acid, trichloroacetic acid, podophyllin, formic acid, 5-fluorouracil, formaldehyde, and glutaraldehyde have all been used, with varying results. • Intradermal injections of bleomycin, a chemotherapy agent that inhibits cell division, is another treatment for highly resistant warts. This agent is expensive and causes severe pain and possible tissue necrosis.

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• Topical benzoyl peroxide and retinoids are sometimes used for facial flat warts (see below).

Tre at m e n t o f Sp e cific Typ e s o f Wart s Co m m o n Wa rt s

• LN2 or electrosurgery is effective. • Topical cantharidin (Cantharone) when LN2 fails or is not tolerated; this is an excellent treatment for periungual lesions. Pla n t a r Wa r t s

• Paring with a no. 15 blade parallel to the skin surface often immediately relieves pain on walking. • Instruct the patient to apply salicylic acid preparations between visits, as well as to perform “sanding” with an emery board, a foot file such as Dr. Scholl’s Callous Removers, or a pumice stone, which keeps the wart flat and thus painless. Application of OTC Salactic film (17% salicylic acid solution) or Mediplast, a 40% salicylic acid plaster cut to the size of the wart, follows. The patient should leave the solution on overnight; he or she may leave the plaster on for 5 to 6 days or use a pumice stone. • LN2, blunt dissection, electrodesiccation, and curettage are reserved for more recalcitrant warts or when patients insist on aggressive therapy. • Aldara cream under occlusion may be used (see earlier discussion). Fla t Wa rt s

• Cautious application of LN2 therapy (e.g., with a cottontipped applicator) or light (low-intensity) electrocautery are appropriate treatment options. • These destructive measures may be used in combination with the daily application of imiquimod cream (Aldara cream), which may hasten resolution of lesions. When applied to the face, imiquimod cream is used without occlusion. • Benzoyl peroxide and retinoids are applied topically. • Topical retinoids such as tretinoin (retinoic acid, Retin-A) are used; there is less scarring than with cryotherapy or surgery, and these may be best for warts on the face. Instruct patients to apply them twice daily for 4 to 6 weeks. • Lactic-salicylic acid (Duofilm) or Occlusal-HP, a salicylic acid, requires daily treatment for about 3 months. • Salicylic acid (Trans-Ver-Sal) in a transdermal delivery system requires daily treatment for about 6 weeks. • Flat warts are notoriously recalcitrant to therapy.

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MANAGEMENT Continued Filifo rm Wa r t s

• A virtually painless method is to dip a mosquito hemostat into LN2 for 10 seconds and then gently grasp the wart for about 4 to 5 seconds (FIG. 6.13 A and B). • The frozen wart is generally shed in 7 to 10 days (see also Chapter 21 and FIG. 21.24). This method often requires multiple office visits. • A “snip excision” or electrocautery may be used following local anesthesia.

Alt e rn at ive Tre at m e n t s • Hypnosis has been used to treat refractory warts. Several published studies have documented the success of hypnotherapy. • Hyperthermia involves immersing the involved surface in hot water (113ºF) for 30 to 45 minutes, two to three times per week. • An OTC freezing device is now sold in many drug counters. It consists of a canister filled with a liquid mixture of the compressed gases dimethyl ether, propane, and isobutane. No success with this device has been documented. • Raw garlic cloves have been demonstrated to have antiviral activity. This can be rubbed onto the wart nightly, followed by occlusion. • Vaccines are currently in development.

A

B

6.13 A and B Filiform wart treatment. A relatively painless method is to dip a mosquito hemostat into LN2 for 10 seconds and then gently grasp the wart for about 4 to 5 seconds. This treatment is repeated four to five times during each visit as tolerated.

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POINTS TO REMEMBER • Freezing and other destructive treatment modalities do not kill the virus but merely destroy the cells that harbor HPV. In other words, when you treat a wart, only the “host” is destroyed, not the virus itself. • Because HPV persists after therapy, some degree of infectivity and the potential for recurrence may remain, even in the absence of clinical lesions. • Patients always ask, “How do you know when the warts are gone?” Answer: “When they don’t recur.” • How to avoid getting warts? Never shake hands. Never kiss anyone. Never walk barefoot. Never share towels. Live in a bubble . . . and there’s still a good chance you’ll get one.

• No single therapy for warts is uniformly effective or superior; thus, treatment involves a certain amount of trial and error. • Conservative, nonscarring treatments are preferred. Each treatment is associated with a 60% to 70% cure rate. A clinical “cure” is achieved when the skin lines are restored to a normal pattern and there is no recurrence.

Im p o rt an t In fo rm at io n Ab o ut Plan t ar Wart s On ly • Melanoma can mimic a plantar wart. • Verrucous carcinoma, a slow-growing, locally invasive, well-differentiated squamous cell carcinoma, may also be easily mistaken for a plantar wart.

WART HEROES The hero of successful wart treatm ent is usually the last person to treat the wart, or the last person to recom m end a treatm ent, before the wart regresses. The “wart hero” m ay have been a wart charm er, a derm atologist, a hypnotist, or a person who recom m ends a folk m edicine rem edy, such as the application of garlic or aloe vera. More often than not, warts tend to “cure” them selves over tim e, especially in im m unocom petent patients. This outcom e should be borne in m ind and explained to patients early in the course of therapy.

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SEE PATIENT HANDOUT “Wart s” ON THE SOLUTION SITE

Mo llu scu m Co n t a gio su m BASICS Molluscum contagiosum (MC) is a common superficial viral infection of the epidermis. It is spread by skin-to-skin contact and is caused by a large DNA-containing poxvirus. It is seen most often in three clinical contexts: • It occurs in young, healthy children (infants and preschoolers), in whom the incidence decreases after the age of 6 or 7 years. Most often it arises in young children who have atopic dermatitis. • It occurs in HIV-positive patients. • It occurs in young adults who are sexually active and not HIV seropositive. DESCRIPTION OF LESIONS • MC lesions are dome-shaped, waxy or pearly papules with a central white core (FIG. 6.14). Less frequently, the papules are the color of the patient’s skin. • Lesions are generally 1 to 3 mm in diameter, but they may coalesce and become giant mollusca. • Frequently, the lesions are grouped. • The number of lesions varies from 1 to 20 up to hundreds.

6.14 Molluscum contagiosum. Characteristic domeshaped, shiny, waxy papules have a central white core.

DISTRIBUTION OF LESIONS • Lesions of MC most often appear on the face and eyelids (FIG. 6.15), the trunk, the axillae, genitalia, and the extremities. • Usually, lesions are asymmetric in distribution, depending on the sites of initial inoculation. • They are spread by autoinoculation from picking and rubbing. • MC can appear in areas of the skin that are traumatized or inflamed, as seen in the flexural creases and axillae in children who have underlying atopic dermatitis at these sites (FIG. 6.16).

6.15 Molluscum contagiosum. This is a typical distribution of lesions on a child’s face. Note the eyelid lesions.

6.16 Molluscum contagiosum. Lesions are present on a background of atopic dermatitis of the flexural creases.

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• Lesions may be seen on the external genitalia (FIG. 6.17), on the lower abdominal wall, on the inner thighs, and on the pubic area. • Such lesions are often spread sexually in adults, and their presence in these locations may—in rare occasions—be considered a sign of sexual abuse in children. CLINICAL MANIFESTATIONS

6.17 Molluscum contagiosum. Characteristic domeshaped, shiny, waxy papules are present on the penis.

• Generally asymptomatic, MC may itch slightly, may be scratched, and may become secondarily infected. • In children, the course is self-limiting; 70% of the time lesions of MC resolve within 6 to 8 months. Recurrences are rare in immunocompetent persons. • MC in HIV-positive patients is common (see Chapter 24, “Cutaneous Manifestations of HIV Infection”). • More than 100 lesions may be seen. • They appear most commonly on the face and are spread by shaving (FIG. 6.18). • The giant molluscum or coalescent double or triple lesions are frequently seen in these patients. • The lesions are often chronic and are difficult to eradicate. DIAGNOSIS • Typical papules are easily recognized. • Inspection with a handheld magnifier often reveals the central core. • A short application of cryotherapy with LN2 accentuates the central core (FIGS. 6.19 A and B).

6.18 Molluscum contagiosum. Note the double and “giant lesions” on the face of a patient with acquired immunodeficiency syndrome.

A

B

6.19 A an d B Molluscum contagiosum. A: Short application of liquid nitrogen (LN2). B: LN2 accentuates the central core. 152

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• A direct microscopic smear of a lesion (crush preparation) demonstrates characteristic “molluscum bodies” (FIG. 6.20). • A shave biopsy is performed, if necessary. Identification of characteristic intracytoplasmic inclusion bodies in histologic or cytologic preparations is made by hematoxylin and eosin staining of biopsy sections.

6.20 Molluscum contagiosum. “Molluscum bodies” (hematoxylin and eosin stain).

DIFFERENTIAL DIAGNOSIS

Wart s (No n g e n it al), Esp e cially Sm all Flat Wart s Distinguishing features are as follows: • Warts are not waxy. • They are tan or brown. • They have no central white core.

Wart s (Ge n it al) • Condyloma acuminatum appears on the inner thighs, pubic area, vulvae, and penis.

MANAGEMENT

Ho m e Tre at m e n t Lesions may be ignored until they resolve spontaneously, or MC may be treated by the patient or caregiver with: • A topical OTC antiwart preparation, such as liquid salicylic acid in a rubber-based vehicle (DuoFilm), which is applied daily to the core of each lesion with a toothpick. • Imiquimod 5% cream (Aldara cream) available only by prescription, is applied three times per week at bedtime. It is very expensive.

Office Tre at m e n t If MC lesions cause social embarrassment and exclusion from activities (e.g., school, day care, swimming), the following treatments are available:

• A biopsy may be necessary to differentiate these lesions from molluscum contagiosum.

Ot h e r Diag n o se s • Disseminated cryptococcosis, toxoplasmosis, and histoplasmosis in HIV-infected patients should also be considered. • A biopsy may be necessary to differentiate these infections from MC.

Cr yo t h era p y

• In adults and older children, the lesions may be frozen lightly for 3 to 5 seconds with LN2 applied with a cotton swab or a Cryogun (see FIG. 6.19). Ca n t h a rid in Th era p y

• In young children, a topical vesicant (blistering agent), such as cantharidin (Cantharone), is daubed on carefully with a toothpick or the wooden end of a cotton swab to each lesion and allowed to dry. This is done every 3 to 4 weeks, or until lesions are resolving. • This method is less painful and better tolerated than LN2. Care should be taken to avoid applying the agent to the uninvolved surrounding skin. Treated areas should not be occluded. continued on page 154

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MANAGEMENT Continued • Parents should be instructed to wash off the agent with soap and water 2 to 4 hours later. In axillary and other skin-to-skin areas, the Cantharone should be washed off in 2 hours. • The face should not be treated with Cantharone.

Ot h e r Tre at m e n t s • Electrodesiccation and curettage may be necessary for patients with refractory lesions.

• Trichloroacetic acid peels have been performed with some success in HIV-infected patients with extensive lesions. • For refractory lesions in HIV-infected patients, highly active antiretroviral therapy has been very effective in reducing the incidence of MC in recent years. • Systemic treatment with agents such as griseofulvin and cimetidine has been anecdotally reported to be effective in the treatment of MC; however, no controlled studies have been performed to confirm this.

HELPFUL HINTS

POINTS TO REMEMBER • Lesions on an infant or a young preschool child should not be treated aggressively. The pain and emotional trauma associated with curettage and cryotherapy make them undesirable treatments in this age group. • MC—particularly if it is located on the face of an adult—should alert the clinician to the possibility of HIV infection. • MC in healthy, immunocompetent persons generally is self-limiting and heals after several months or longer.

• For anxious children, a topical anesthetic such as EMLA (eutectic mixture of local anesthetics) cream can be applied under occlusion 1 hour before treatment to decrease the discomfort associated with procedures such as curettage, local anesthetic injections, or cryosurgery. • Because many children with MC also have atopic dermatitis, further spread of the MC lesions is perpetuated by itching and scratching. Consequently, it is best to treat and control all eczematous lesions before the lesions of MC are addressed.

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Part One • Com m on Skin Conditions: Diag nosis and Managem ent

H erp es Sim p lex BASICS Herpes simplex virus (HSV) infections are caused by two virus types: HSV-1 and HSV-2. HSV-1 causes most nongenital infections. These highly contagious viruses are spread by direct contact with the skin or mucous membranes. After the primary infection resolves, the virus retreats to a dorsal root ganglion, where it becomes incorporated into the genetic material of the cell. The virus remains latent until it is reactivated by precipitating factors or triggers, such as sunlight exposure, menses, fever, common colds, and, possibly, stress. Primary infections are acquired in infancy and early childhood; most are subclinical. Patients who have AIDS or who are under treatment with immunosuppressants for organ transplantation or cancer chemotherapy are at greatest risk for contracting severe recalcitrant HSV infections. Nongenital HSV infection is extremely common. In fact, herpes-specific antibody (for type 1 and, less commonly, type 2) can be found in the serum of many lesion-free adults. Asymptomatic shedding probably accounts for the widespread transmission of this ubiquitous virus. Since the 1980s, the public attention that genital herpes has attracted has led to misconceptions about HSV infection and to its overdiagnosis, especially in regard to lesions that occur within the oral cavity. For example, many people who suffer from recurrent nonherpetic painful intraoral mouth sores (aphthous stomatitis, or canker sores) are given a diag-

(No n gen it a l)

nosis of “herpes,” and thus they may feel the stigma associated with sexually transmitted diseases. Because recurrent aphthous stomatitis—which has no known viral association—has a clinical appearance and course similar to those of recurrent herpes labialis, the two conditions are often confused by patient and clinician alike. HSV lesions, particularly recurrent ones, occur inside the mouth very infrequently, unless the virus is a primary infection or occurs in immunocompromised patients.

Pat h o p h ysio lo g y Intimate contact between a susceptible person (without antibodies against the virus) and an individual who is actively shedding the virus or with body fluids containing the virus is required for transmission of HSV infection to occur. Contact must involve mucous membranes or open or abraded skin. HSV invades and replicates in neurons as well as in epidermal and dermal cells. Virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion, where latency is established. Viral replication in the sensory ganglia leads to recurrent clinical outbreaks. These outbreaks can be induced by various stimuli, such as trauma, ultraviolet radiation, extremes in temperature, stress, immunosuppression, or hormonal fluctuations. Viral shedding, leading to possible transmission, is most likely to occur during the period of primary infection, during subsequent recurrences, and during periods of asymptomatic viral shedding.

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DESCRIPTION OF LESIONS The following sequence of events describes the easily recognizable evolution of HSV “cold sores” or “fever blisters”: • A single vesicle or a group of vesicles overlies an erythematous base (FIG. 6.21). Vesicles may sag in the center (umbilicate). • The vesicles may become pustules (FIG. 6.22), or they may dry and become crusts or erosions (FIG. 6.23). • The lesions generally heal without scarring (because they are intraepidermal).

Prim ary Orolabial Herp es Sim p lex 6.21 Herpes simplex virus. In this typical grouping, umbilicated vesicles overlie an erythematous base.

Herpes labialis is most commonly associated with HSV-1 infection. It often occurs in childhood and is usually asymptomatic. DISTRIBUTION OF LESIONS When symptoms are present during a primary HSV infection, the oral cavity (the lips, gums, buccal mucosa, fauces, tongue, and hard palate) is the area generally affected (FIG. 6.24).

6.22 Herpes simplex virus. Here, most vesicles have evolved into pustules.

6.23 Herpes simplex virus. The presacral and gluteal areas are common locations of herpes simplex type 2 in women. This patient shows drying crusts (scabs) and erosions.

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6.24 Primary herpes simplex virus infection. This infant has multiple vesicles and pustules as well as gingivostomatitis.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

CLINICAL MANIFESTATIONS Most cases of primary HSV are subclinical. • Symptomatic primary HSV infections tend to be more severe than those of recurrent disease; they include gingivostomatitis, fever, sore throat, and submandibular or cervical lymphadenopathy. • Distinguishing primary HSV infection from severe cases of recurrent HSV can be difficult. • Painful vesicles develop on the lips, the gingiva, the palate, or the tongue and are often associated with erythema and edema. Lesions tend to ulcerate and heal within 2 to 3 weeks. • Encephalitis and aseptic meningitis are rare complications.

Recu rren t Orolabial Herp es Sim p lex

6.25 Recurrent herpes simplex virus infection (herpes labialis). Lesions are evident on the vermilion border of the lip and beyond.

DISTRIBUTION OF LESIONS • Lesions tend to recur at or near the same location within the distribution of a sensory nerve. • Recurrences are most often seen on or near the vermilion border of the lip (herpes labialis) (FIG. 6.25). CLINICAL MANIFESTATIONS • Symptoms are generally milder and the number of lesions fewer than those associated with primary HSV. • Patients commonly experience a prodrome of itching, pain, or numbness. • The recurrent vesicular lesions eventually ulcerate or form a crust. • Infrequently, regional lymphadenopathy occurs. • Over time, recurrences decrease in frequency and often stop altogether. • Persistent ulcerative or verrucous vegetative lesions may be seen in immunocompromised patients. • Most cases of recurrent erythema multiforme minor accompany, and appear to be caused by, recurrent (both clinical and subclinical) HSV episodes (see Chapter 18, “Diseases of Vasculature”). DIAGNOSIS OF HERPES SIMPLEX The diagnosis of HSV is usually based on clinical appearance and history. At the time of an office visit, patients often present with only nonspecific crusted lesions or merely with a history consistent with recurrent HSV. When necessary, the following tests may be administered on fresh lesions: • A Tzanck preparation, if positive, suggests HSV or varicella-zoster virus (VZV) infection. This test is used to rapidly determine the presence of HSV or VZV; it does not distinguish between these two viruses (FIG. 6.26) (see the description of the Tzanck procedure in the sidebar).

6.26 Positive Tzanck preparation. Note the typical multinucleated giant cells with large nuclei. This test does not distinguish between herpes simplex and herpes zoster. Note the presence of nuclei of normal-sized keratinocytes, which are the size of neutrophils. Chapter 6 • Superficial Viral Infections

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TZANCK PREPARATION A Tzanck preparation is used to aid in the diagnosis of HSV, herpes zoster, and VZV. This technique furnishes an inexpensive, efficient provisional diagnosis, but it does not enable one to distinguish HSV from VZV. 1. For best results, a fresh, intact vesicle or bulla usually present for less than 24 hours is preferred. 2. After the lesion is swabbed with an alcohol preparation, the blister is unroofed by piercing it with a no. 11 blade or a needle, followed by blotting with a sponge. 3. The underlying m oist base of the lesion is then scraped with a no. 15 scalpel blade, and a thin layer of m aterial is spread onto a glass slide. 4. The specim en is then air dried and is stained with a supravital stain such as Giem sa, Wright’s, or m ethylene blue, which is left on for 1 m inute. 5. The specim en is then gently flooded with tap water for 15 seconds to rem ove any rem aining stain. 6. Exam ination, initially under 40-power m agnification and then 100-power oil im m ersion, helps identify the characteristic m ultinucleated giant cells (see FIG. 6.26).

• Detection and typing of HSV are performed by obtaining a culture from intact vesicles, ideally early in the course of the infection, but the false-negative rate increases after 48 hours of lesion onset. • HSV tissue culture using monoclonal antibodies requires only 24 hours. The test is 90% sensitive, but it is expensive. • Polymerase chain reaction for HSV DNA detection can be conducted; however, like the monoclonal antibody method, it is expensive. • Serologic tests for HSV are generally not very useful because so much of the general adult population has antibodies to herpes simplex; however, primary HSV infection can be documented by demonstration of seroconversion, high titers, or rising titers.

DIFFERENTIAL DIAGNOSIS: OROLABIAL HERPES SIMPLEX

Ap h t h o us St o m at it is • Lesions of aphthous stomatitis are small, punched-out erosions that occur on the tongue and on the buccal, labial, and gingival mucosa (see Chapter 12, “Disorders of the Mouth, Lips, and Tongue”) (FIG. 6.27). • Lesions typically consist of painful, shallow, gray or yellow 2- to 3-mm erosions.

• Mouth ulcers, a high fever, sore throat, and headache are characteristic. • Symptoms may precede the appearance of lesions.

Han d -Fo o t -an d -Mo ut h Dise ase • Oval erythematous erosions are most often seen on the soft palate and uvula (see Chapter 8, “Viral Exanthems”). • Lesions are asymptomatic. • Lesions may also appear on the hands and feet. • Lesions are shallower than those of primary HSV. He rp an g in a • Small, painful vesicular or ulcerative lesions occur on the roof of the mouth and in the throat. • Lesions have a white to whitish-gray base and a red border. • The condition is usually caused by coxsackie virus, typically coxsackie group A viruses. • Typically, it occurs during the summer and frequently affects children, but it also may occur in young adults.

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6.27 Aphthous stomatitis. This shallow erosion is surrounded by a ring of erythema.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

DIFFERENTIAL DIAGNOSIS: EXTRAOROLABIAL HERPES SIMPLEX • Although HSV infections may occur anywhere on the body, 70% to 90% of HSV-1 infections occur above the umbilicus. • In contrast, 70% to 90% of HSV-2 infections occur below the umbilicus. Lesions also tend to occur on the presacral area in women, but they may be found anywhere on the cutaneous surface (see Chapter 19, “Sexually Transmitted Diseases”).

He rp e s Zo st e r • Lesions of herpes zoster are unilateral, dermatomal, and often painful (see the discussion of herpes zoster later in this chapter). • Lesions are also grouped but tend to vary in size. • The condition may be clinically indistinguishable from HSV when lesions are located in a single focus.

6.28 Herpes whitlow. This infection in a health care worker was caused by a needle puncture.

Clin ical Varian ts of Herp es Sim p lex In fection s He rp e t ic Wh it lo w • Painful herpetic whitlow results from the direct inoculation of the virus to the fingertip (FIG. 6.28). • Before the current stringent infection control measures and the widespread use of gloves by health care providers, herpetic whitlow was an occupational hazard among dental and medical health care personnel whose fingertips came in contact with infected oral or respiratory excretions. Ecze m a He rp e t icum FIGURE 6.29. • Also known as Kaposi’s varicelliform eruption, eczema herpeticum is an uncommon disseminated form of HSV infection caused by HSV-1. It occurs mainly in children who have severe atopic dermatitis, burns, or other inflammatory skin conditions. He rp e s Glad iat o rum • This is caused by HSV-1 and is seen as papular or vesicular eruptions on the torsos of athletes in sports involving close physical contact (classically, wrestling).

6.29 Eczema herpeticum (Kaposi’s varicelliform eruption). This patient has an uncommon disseminated form of HSV infection. She has underlying atopic dermatitis. (Image courtesy of Joseph Eastern, M.D.).

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Disse m in at e d He rp e s Sim p le x • Infection can occur in individuals who are immunocompromised. • These patients may present with atypical signs and symptoms of HSV, and the condition may be difficult to diagnose. Larger lesions or necrotizing ulcers may occur, and widespread areas may be involved. Ne o n at al He rp e s Sim p le x • Newborns are exposed to HSV-2 via the birth canal of an actively infected mother. • Infection occurs most often peripartum, although in utero transmission also occurs.

MANAGEMENT

To p ical Th e rap y Skin symptoms may be eased by soaking in Burow’s solution (aluminum acetate or aluminum sulfate) two to three times daily. Alternatively, soaks with water or saline may help dry the eruption and may prevent secondary infection. • Topical acyclovir 5% (Zovirax) ointment, penciclovir 1% (Denavir) cream, and docosanol 10% (Abreva) cream are not very effective treatments, but they may help reduce healing time. • Patients in whom sun exposure incites recurrent HSV of the lips can apply an opaque sun-blocking agent before sun exposure. • Patients can lessen the discomfort of oral HSV lesions by applying viscous lidocaine applications or OTC “caine” products, taking oral analgesics, or sucking on ice cubes.

He rp e t ic Syco sis • This follicular infection with HSV may present as a vesiculopustular eruption in the beard area in men. • It often results from autoinoculation after shaving through a recurrent herpetic outbreak. Ocular He rp e s Sim p le x • Herpes conjunctivitis, keratitis, uveitis, optic neuritis, and retinitis are possible sequelae of HSV.

• The use of valacyclovir is contraindicated in some patients (e.g., in some renal and bone marrow transplant recipients and in those infected with HIV) because of reports of thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome. Trea t m en t w it h An t ivira l Agen t s Prim ary Herpes Sim plex

• Valacyclovir (Valtrex) (1 g twice daily for 7 to 10 days) • Famciclovir (Famvir) (250 mg three times daily for 7 to 10 days) • Acyclovir (200 mg five times daily or 400 mg three times daily for 10 days) Recurrent Herpes Sim plex

This treatment should be initiated at the first sign of prodrome, because it can often abort the lesions. Following are treatment options:

Syst e m ic Th e rap y Pharmacologic agents used for the treatment of HSV include acyclovir, valacyclovir, and famciclovir. Valacyclovir is rapidly converted to acyclovir, and its bioavailability is three to five times greater than that of acyclovir. Similarly, famciclovir is converted to the more bioavailable penciclovir. For these reasons, acyclovir has been supplanted by valacyclovir and famciclovir in the treatment of HSV in adults.

• Valacyclovir (Valtrex) (2 g twice daily for 1 day taken about 12 hours apart). This is a shorter, more economical course. • Famciclovir (Famvir) (single-day therapy; 1,000 mg in the morning and 1,000 mg in the evening, or 125 mg twice daily for 5 days). In HIV-positive patients, 500 mg twice a day is given for 7 days. • Acyclovir (200 mg twice daily or 400 mg three times daily for 5 days).

• Dose reduction is recommended for patients who have renal impairment.

continued on page 161

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MANAGEMENT Continued For frequent recurrences (more than six recurrences per year), persistent HSV, severe disease, or recurrent erythema multiforme minor, long-term suppressive oral therapy may be used. After 1 year of treatment with these agents, the medication should be discontinued to determine the recurrence rate, and the dosage can be adjusted as needed.

SEE PATIENT HANDOUT “He rp e s Sim p le x” ON THE SOLUTION SITE

• Valacyclovir (1 g daily for 6 to 12 months; afterward, the clinician should attempt to taper the dose to 500 mg or to discontinue the agent) • Famciclovir (250 mg twice daily for 12 months) • Acyclovir (400 mg twice daily for 12 months) Immunocompromised hosts, those with Kaposi’s varicelliform eruption, or those with HSV encephalitis often require intravenous acyclovir therapy.

POINTS TO REMEMBER • Intraoral ulcers in immunocompetent patients are most likely canker sores (aphthous stomatitis). • Recurrent HSV attacks can be aborted by treatment on a short-term basis with oral antivirals administered during the prodromal stage. • Frequent recurrences can be aborted by treatment with suppressive oral antivirals. • A truly effective topical treatment for HSV has yet to be found. • Pregnant women with active genital HSV may need a cesarean section to prevent neonatal HSV, a potentially fatal disease.

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H erp es Zo st er BASICS • Herpes zoster (“shingles”) is caused by the same herpesvirus that causes varicella, or chickenpox. The virus first manifests as varicella (see Chapter 8, “Viral Exanthems”), a primary infection usually seen in childhood. Subsequently, when the same latent virus is reactivated, its second episode manifests as herpes zoster. • The risk of herpes zoster increases with age and is 8 to 10 times more likely to develop in people 60 years of age or older as in younger people. • The disease also develops frequently in immunocompromised patients, such as transplant recipients and those with HIV infection or malignant disease, particularly lymphoproliferative malignancies (e.g., Hodgkin’s disease). • Elderly persons and immunocompromised patients also tend to have more severe disease, with complications such as postherpetic neuralgia (PHN), disseminated zoster, and chronic zoster.

• The infectious course of herpes zoster infection, or VZV infection, is similar to that of HSV infection. • After the primary infection resolves, the virus retreats to the dorsal root ganglion, where it remains in a dormant state. Reactivation—into dermatomal “shingles”—may be caused by severe illness or infection with HIV, but most often it occurs spontaneously, without an obvious precipitating cause. It is most likely a sign that immunity to VZV, which most people acquire in childhood, has decreased. • The reemergence as a local vesicobullous eruption derives from the anterograde migration of virions through the axon to the skin of a single dermatome or several adjacent ones. In immunocompetent patients, recurrent or bilateral herpes zoster episodes are extremely uncommon; immunity to the virus is presumably boosted by the initial episode of herpes zoster. • The pain of herpes zoster is thought to result from nerve damage caused by the spread of the virus to the skin through the peripheral nerves. An inflammatory reaction leads to scarring of the peripheral nerves and dorsal root ganglia. PHN presumably results from the consequent hyperexcitability of neurons, which tend to discharge spontaneously. • VZV infection occurs occasionally in pregnant women. A primary VZV infection (varicella) may result in severe fetal abnormalities; however, the development of herpes zoster during pregnancy does not appear to harm the developing fetus. DESCRIPTION OF LESIONS The following sequence of events describes the evolution of herpes zoster:

6.30 Herpes zoster. These umbilicated vesicles of various sizes are grouped on an erythematous base.

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• Lesions begin as “juicy” erythematous papules that rapidly mature into clustered vesicles or bullae on top of an erythematous base. They tend to vary more in size than do the lesions of HSV (FIG. 6.30).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

• Successive crops continue to appear for 6 to 8 days. The blisters sometimes umbilicate (sag in the middle); occasionally, they become pustular and hemorrhagic. • In time, lesions dry into crusts or erosions that may heal and disappear completely or resolve with postinflammatory hyperpigmentation or hypopigmentation and, possibly, scarring. • Lesions of herpes zoster in HIV-infected patients tend to be more verrucous and ulcerative, and they often heal with scars. • Infrequently, dermatomal neuralgia may be accompanied or followed by nonbullous or urticarialike lesions (FIG. 6.31). Rarely, skin lesions are absent (“zoster sine herpete”). DISTRIBUTION OF LESIONS • Lesions of herpes zoster occur in a characteristic unilateral dermatomal (“zosteriform”) distribution. • Occasionally, lesions involve contiguous dermatomes or extend beyond the midline. • Although it can affect any dermatome, herpes zoster is most commonly found on the thoracic (FIG. 6.32), trigeminal, lumbosacral (FIG. 6.33), and cervical areas. • Immunocompromised patients have a greater risk of multidermatomal zoster, recurrent zoster, and dissemination beyond the skin (e.g., into the eyes or the lungs) (see FIG. 24.6).

6.31 Herpes zoster. “Juicy,” erythematous, urticarialike papules are seen here in a “zosteriform” distribution.

6.32 Herpes zoster. Drying hemorrhagic crusts appear in a “zosteriform” distribution. In this immunocompromised patient, the lesions will probably heal with scars.

6.33 Herpes zoster. This patient has painful lesions of the vulva and perineum in a dermatomal distribution. Chapter 6 • Superficial Viral Infections

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CLINICAL MANIFESTATIONS Several days before the cutaneous eruption, patients may experience the following focal (dermatomal) symptoms: pain, numbness, pruritus, paresthesia, and skin tenderness or sensitivity (tactile allodynia).

6.34 Herpes zoster ophthalmicus. This condition affects the first branch of the fifth cranial nerve.

Disse m in at e d He rp e s Zo st e r See FIGURE 24.6. • In immunocompromised patients, the eruption usually begins with typical dermatomal herpes zoster. The lesions may then become widespread, with 25 or more lesions found outside the primary dermatome. • The condition can become chronic and indistinguishable from varicella. DIAGNOSIS • Herpes zoster can most often be diagnosed on the basis of clinical appearance and the presence of pain in a dermatomal distribution. • If necessary, a Tzanck smear should be obtained from the base of a fresh lesion (see the discussion of Tzanck preparation earlier in this chapter). A positive result suggests either HSV or VZV infection. • A skin biopsy is generally unnecessary, but it can help to confirm the diagnosis.

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• In children, herpes zoster is often asymptomatic. • In contrast to the disease in children, both the likelihood and severity of pain (acute and chronic) associated with herpes zoster are significantly increased in patients older than 50 years. • Second episodes of herpes zoster in immunocompetent people are rare, probably because of the immunologic “boosting” effect of the first episode. • Pain and paresthesia in the affected dermatome may accompany the eruption or may precede it by 1 to 2 weeks. The neuropathic pain of some patients has been described as “boring,” “burning,” “crushing,” or “stabbing.” Some patients presenting with such pain have been thought to have a myocardial infarction or pleurisy, until the characteristic eruption of herpes zoster establishes the diagnosis.

Co m p licat io n s • PHN is defined as pain persisting for more than 1 month after the eruption of the initial herpes zoster lesions. The pain may also develop after a pain-free interval. The frequency of PHN increases with age. It occurs more commonly in people with compromised immune systems, such as HIV-infected patients. • In many elderly patients, PHN can cause chronic depression, anxiety, and social isolation. • When herpes zoster occurs in the ophthalmic division of the fifth, or trigeminal, nerve, it is called herpes zoster ophthalmicus (FIG. 6.34). Eye involvement, such as conjunctivitis, acute retinal necrosis, uveitis, and retinal arteritis, can lead to blindness. Ophthalmic zoster warrants an immediate ophthalmologic consultation. • VZV involvement of the geniculate ganglion is called the Ramsay Hunt syndrome. This condition results in motor and sensory neuropathy of the seventh cranial nerve.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

DIFFERENTIAL DIAGNOSIS

He rp e s Sim p le x Virus In fe ct io n • When HSV presents in a site usually occupied by herpes zoster, or when it occurs in a semidermatomal distribution, it may be clinically indistinguishable from herpes zoster. • The vesicles of herpes simplex, however, tend to be more uniform in size and are much less painful than those seen in herpes zoster. • Recurrence strongly suggests HSV infection.

MANAGEMENT

To p ical Th e rap y For the acute episode of herpes zoster, the following treatments are available without a prescription: • Burow’s solution. Wet dressings with Burow’s solution (aluminum acetate or aluminum sulfate) are soothing and drying; so are moist soaks with water or saline. • Topical anesthetic “caines” such as benzocaine may be helpful.

Syst e m ic Th e rap y Pain control is generally the paramount concern in herpes zoster. • Oral analgesics, such as acetaminophen, aspirin, and other nonsteroidal anti-inflammatory drugs, as well as mild narcotics, are helpful in mild, self-limited cases. • Both valacyclovir and famciclovir are most effective when they are given within 72 hours of the appearance of the zoster rash. They are equally effective in accelerating cutaneous healing, in shortening the duration of acute episodes, and in decreasing the chronic pain of PHN. • Valacyclovir is much less expensive than famciclovir; however, its use is contraindicated in HIV-infected patients. Both valacyclovir and famciclovir are superior to acyclovir, which is reserved for use in children and for intravenous administration.

Po iso n Ivy • Also known as rhus dermatitis, poison ivy often occurs in a linear distribution of blisters that corresponds to, or suggests, a dermatome. • Rhus dermatitis, however, is pruritic and painless. Most patients with rhus dermatitis offer a history of contact with poison ivy or poison oak.

Regim en s

Following are the treatment options for immunocompetent adult patients with herpes zoster: • Valacyclovir (Valtrex) 1 g (two 500-mg caplets) three times daily for 7 days • Famciclovir (Famvir) 500 mg three times daily for 7 days • Acyclovir 800 mg five times daily for 7 days Immunocompromised patients may require intravenous acyclovir. Intravenous foscarnet is used for acyclovir-resistant VZV infection. Co rt ico st ero id s

• The use of systemic corticosteroids in combination with oral acyclovir, valacyclovir, or famciclovir has been controversial. Anecdotal reports claim a faster resolution of acute pain and a decreased incidence of PHN. The rationale for adding corticosteroids is that they may decrease nerve inflammation. However, no double-blind studies demonstrate the efficacy of systemic corticosteroids, and the theoretical risk of dissemination of the virus is an issue. • Elderly patients, in whom PHN more often occurs, are more likely to experience significant adverse side effects from systemic corticosteroids than are younger patients. Potential relative contraindications to the use of corticosteroids include hypertension, diabetes, glaucoma, and peptic ulcer disease. continued on page 166

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MANAGEMENT Continued

Ch ro n ic Pain Treatment of PHN is problematic. The following measures have met with varying degrees of success. Their great number reflects the finding that none of them appears to be totally satisfactory. Optimally, the acute episode of herpes zoster should be treated as quickly as possible after onset to decrease the risk of PHN. • Lidocaine patches. These bandages, impregnated with lidocaine, are the only treatment for PHN approved by the United States Food and Drug Association. • Capsaicin (Zostrix). The active molecule in hot chili peppers, capsaicin depletes substance P, a pain impulse transmitter. It is available OTC and is applied three to five times daily. Unfortunately, many patients cannot tolerate the burning sensation that occurs after application. • Low-dose tricyclic antidepressants. These agents (e.g., amitriptyline) may be helpful. Higher doses of tricyclic antidepressants—used alone or in combination with phenothiazines—may also be tried. • Neurontin (gabapentin), an antiseizure drug, has been helpful in some patients. • Neurosurgical procedures include nerve blocks with local anesthetics. • Intralesional corticosteroids may be given as subcutaneous injections.

• Transcutaneous electrical nerve stimulation may be useful. • Acupuncture may be tried. • Biofeedback may be helpful.

Pre ve n t io n Va ccin a t io n

The recent introduction of the vaccine Zostavax promises to reduce the risk of developing herpes zoster and result in less frequent, less painful, and shorter courses of PHN episodes. The preventive effect of the vaccine is thought to be a result of its boosting effect on an older person’s cellmediated immunity to VZV. • Zoster vaccination (a single dose of the vaccine) is approved for everyone older than 60 years of age who has had chickenpox. Zostavax contains the same attenuated virus as the varicella vaccine but is far more potent. • Zoster vaccination is contraindicated in people with active, untreated tuberculosis and in pregnant women. Whether to vaccinate immunocompromised persons is a controversial issue that is important to resolve because of increased risk of herpes zoster in this population, because the vaccine is a live attenuated virus, it is contraindicated. Ta i Ch i

A recent study suggests that tai chi may help prevent shingles. Further studies are necessary to confirm these findings.

POINTS TO REMEMBER • Herpes zoster, particularly if it is recurrent or disseminated, may be an early indicator of an immunosuppressive disorder or a lymphoproliferative disease. • An evolving herpes zoster eruption should be treated with antiviral drugs as early as possible. • PHN is unusual in people younger than 50 years. • Patients with herpes zoster can transmit the virus as chickenpox to persons who have not already been infected with this virus.

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C H AP T ER

Superficial Fungal Infections

7 OVERVIEW Superficial fungi are capable of germinating on the dead outer horny layer of skin. They produce enzymes (keratinases) that allow them to digest keratin, with resulting epidermal scale (e.g., tinea pedis, tinea versicolor); thickened, crumbly nails (onychomycosis); and hair loss (tinea capitis). In the dermis, an inflammatory reaction may result in erythema, vesicles, and, infrequently, a more widespread autoeczematous eruption known as an “id” reaction. Infection may be acquired by the following means: • Person-to-person contact • Animal contact, especially with kittens and puppies • Contact with inanimate objects (fomites) Environmental and hereditary factors leading to fungal infections are as follows: • Warm, moist, occluded environments such as the groin, axillae, and feet • Family history of tinea infections • Lowered immune status of the host, such as seen in patients with acquired immunodeficiency syndrome (AIDS), diabetes, collagen vascular diseases, or long-term systemic steroid therapy • Diagnosis can often, but not always, be made on clinical grounds. • A direct potassium hydroxide (KOH) examination or a fungal culture is necessary to make a definitive diagnosis. • Periodic acid–Schiff stain on biopsy specimens can be helpful. • Wood’s lamp examination may be useful in some cases of tinea capitis and tinea versicolor.

DERMATOPHYTE INFECTIONS The term tinea refers to an infection by derm atophytes. Tinea is nam ed according to the location on the body: • • • • •

Tin e a Tin e a Tin e a Tin e a Tin e a

p e d is an d t in e a m an uum (feet and hands) cruris (inguinal folds) cap it is (scalp) co rp o ris an d t in e a faciale (body and face) un g uium ( o n ych o m yco sis) (nails)

YEAST INFECTIONS • Tinea versicolor Tinea versicolor is an exception; in fact, it is not caused by a derm atophyte but rather by a yeastlike organism . Tinea versicolor is referred to as pityriasis versicolor by m any authors. • Ca ndidia sis Cutaneous candidiasis is also caused by yeast.

167

Tin ea Ped is

(“At h let e’s Fo o t ”) BASICS Tinea pedis is an extremely common problem seen mainly in young men. Ubiquitous media advertisements for athlete’s foot sprays and creams are testimony to the commonplace occurrence of this annoying dermatosis. Most cases are caused by Trichophyton rubrum, which evokes a minimal inflammatory response, and less often by T. mentagrophytes, which may produce vesicles and bullae; less frequently, Epidermophyton floccosum may be responsible. There are three clinical types of tinea pedis: type 1: interdigital; type 2: chronic plantar; and type 3: acute vesicular.

Typ e 1: In terd igital Tin ea Ped is BASICS This is the most common type of tinea pedis. It is seen predominantly in men between the ages of 18 and 40 years. 7.1 Interdigital tinea pedis (toe web infection). Note fissuring and maceration.

DESCRIPTION OF LESIONS • Scale, maceration, and fissures are characteristic (FIG. 7.1). DISTRIBUTION OF LESIONS • Toe web involvement is seen, especially between the third and fourth and the fourth and fifth toes; however, any web space may be involved (FIG. 7.2). CLINICAL MANIFESTATIONS • It is often asymptomatic; however, it may itch intensely. • Marked inflammation and fissures suggest secondary bacterial superinfection. • There may be coexistent yeast or saprophytic fungi present.

7.2 Interdigital tinea pedis. Here the lesions are more inflammatory.

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DIAGNOSIS • A positive KOH examination or fungal culture is diagnostic.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

DIFFERENTIAL DIAGNOSIS

At o p ic De rm at it is FIGURE 7.3. • Atopic dermatitis and dyshidrotic eczema may be clinically indistinguishable from tinea pedis (see Chapter 2, “Eczema”).

• There is a positive atopic history. • It is seen especially in children on the dorsal or plantar surface of the feet (tinea pedis is unusual in preteens).

Co n t act De rm at it is (FIG . 7.4) • This occurs most often on the dorsum of the feet.

7.3 Atopic dermatitis. Note the lichenification on the dorsal toes. The distinction from tinea pedis was based on a negative KOH and a positive atopic history.

7.4 Contact dermatitis. In this case it was determined that the patient was allergic to a component of his shoe leather.

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169

Prevention consists of maintaining dryness in the area by:

MANAGEMENT • For acute oozing and maceration, Burow’s solution compresses are used two to three times daily. (See handout Burow’s Solution) • Broad-spectrum topical antifungal agents such as ketoconazole (Nizoral), ciclopirox (Loprox), or clotrimazole (Lotrimin) are applied once or twice daily. (See TABLE 7.1.)

• Using a hairdryer after bathing. • Applying powders, such as Zeasorb-AF, that contain miconazole as an active ingredient.

Tab le 7.1 ANTIFUNGAL DRUG FORMULARY AGENT

APPLICATION

FORMS

COMMENTS

Cream, solution, spray Cream, lotion, solution Cream, lotion, spray Cream Shampoo

Tinea (not indicated for Candida) Tinea, Candida, tinea versicolor Tinea, Candida, tinea versicolor Tinea Tinea versicolor

Powder

Tinea, Candida, tinea versicolor; antifungal, antifriction/drying agent

Once daily 4 weeks, once daily

Cream Cream

4 weeks, as needed Once daily 4 weeks, twice daily 4 weeks, twice daily 4 weeks, once to twice daily

Cream, lotion, shampoo Cream, gel Cream, solution Cream Cream, lotion

Tinea, Candida, tinea versicolor Tinea, Candida, tinea versicolor, Gram-positive bacteria Lotion preferred for nail penetration Tinea; has anti-inflammatory activity Tinea, Candida, tinea versicolor Tinea, Candida, tinea versicolor Tinea, Candida, tinea versicolor

Topical agents: over-the-counter Terbinafine 1% (Lamisil) 1 to 4 weeks, twice daily Clotrimazole 1% (Lotrimin) Twice daily Miconazole 2% (Micatin) Twice daily Tolnaftate 1% (Tinactin) Twice daily Selenium sulfide 1% Apply daily to wide area (Selsun Blue) for 10 minutes, followed by a shower Miconazole 2% As needed (Zeasorb-AF powder) Topical agents: prescription Ketoconazole 2% (Nizoral) Econazole 1% (Spectazole) Ciclopirox 0.77% (Loprox) Naftifine 1% (Naftin) Sulconazole (Exelderm) Miconazole (Monistat-Derm) Oxiconazole 1% (Oxistat) Systemic antifungal agents Griseofulvin (Fulvicin, Grisactin, Gris-PEG)

Terbinafine (Lamisil)

Microsized: 250-, 500-mg tablets; ultramicrosized: 125-, 250-, 333-mg tablets. Pediatric: Microsized: 125 mg/tsp pediatric suspension

Effective only against dermatophytes Contraindicated in pregnancy Fungistatic Take with fatty meals Alcohol should be avoided Occasional headache Gastrointestinal upset Photosensitivity Elevation of liver function tests Significant drug interactions (phenobarbital, warfarin, other drugs metabolized in liver)

250-mg tablets 125-mg oral granules 187.5-mg oral granules

Side effects minimal; include rare hepatotoxicity, reversible taste loss Many fewer drug interactions than with itraconazole; blood levels decreased by cimetidine and terfenadine and increased by rifampin; lowers cyclosporine levels continued on page 171

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MANAGEMENT Continued

Tab le 7.1 ANTIFUNGAL DRUG FORMULARY (Continued) AGENT

APPLICATION

Itraconazole (Sporanox)

FORMS

100-mg capsules Oral solution (10 mg/mL)

Fluconazole (Diflucan)

50-, 100-, 150-, 200-mg tablets; oral solution 10 mg/mL, 40 mg/mL

COMMENTS Severe hepatotoxicity including liver failure has been reported in patients with no pre-existing liver disease. A baseline hepatic profile (alanine and aspartate aminotransferase) levels is recommended for all patients before initiating therapy with this agent. These tests should be monitored in patients receiving continuous treatment for more than 1 month or patients who develop signs or symptoms suggestive of liver disease. Side effects minimal; rare hepatotoxicity Significant drug interactions and contraindications: drugs not to be taken with itraconazole include astemizole, cisapride, terfenadine, triazolam, midazolam, lovastatin, and simvastatin Studies report a risk for developing congestive heart failure (CHF) from negative inotropic effects of this drug. Because of this risk, itraconazole should not be used in the treatment of onychomycosis in patients with ventricular dysfunction such as CHF or a history of CHF. Side effects minimal; rare hepatotoxicity Liver toxicity must be monitored if used long term Not to be taken with cisapride

SEE PATIENT HANDOUT “At h le t e ’s Fo o t (Tin e a Pe d is)” ON THE SOLUTION SITE

Chap ter 7 • Superficial Fungal Infections

171

Typ e 2: Ch ron ic Plan tar Tin ea Ped is BASICS • Tinea pedis (“moccasin” type) is relatively common. DESCRIPTION OF LESIONS • Lesions consist of diffuse scaling of the soles (FIG. 7.5). DISTRIBUTION OF LESIONS 7.5 Tinea pedis. Chronic scaly infection of the plantar surface of the foot in a “moccasin” distribution. Note involvement of the nails.

• The entire plantar surface of the foot is usually involved. • Borders are distinct along the sides of the feet. • There is often nail involvement. CLINICAL MANIFESTATIONS • Symptoms are minimal, unless painful fissures occur. DIAGNOSIS • The KOH examination or fungal culture is positive.

“Two Fe e t , On e Han d ” (Palm ar/ Plan t ar) Tin e a • Tinea can present on one or both palms (tinea manuum). Not infrequently, it appears in a “two feet, one hand” distribution. This is pathognomic for tinea (FIG. 7.6). • Management is similar to that for chronic tinea pedis.

7.6 “Two feet, one hand” variant of tinea pedis. The scale is present on one hand only. Note the nail involvement. These findings are pathognomonic.

DIFFERENTIAL DIAGNOSIS

Pso riasis • Psoriasis has sharply demarcated plaques (FIG. 7.7). At o p ic De rm at it is • Atopic dermatitis usually is pruritic, whereas chronic plantar tinea pedis is generally asymptomatic. • There is a positive atopic history.

7.7 Psoriasis. A well-demarcated plaque that spares the instep is seen here.

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MANAGEMENT This is the most difficult type of tinea pedis to cure, because topical agents do not effectively penetrate the thickened epidermis. Treatment generally requires oral antifungal agents such as the following (TABLE 7.1): • Terbinafine (Lamisil) 250 mg once daily for 30 days or longer, if necessary

• Itraconazole (Sporanox) 200 mg once daily for 30 days or longer, if necessary • Fluconazole (Diflucan) 150 to 200 mg once daily for 4 to 6 weeks, if necessary Nail involvement requires longer treatment because nails may serve as a reservoir for reinfection and take much longer to grow out normally (see later in this chapter).

Typ e 3: Acu te Vesicu lar Tin ea Ped is BASICS This is the least common clinical variant. DESCRIPTION OF LESIONS • Vesicles and bullae generally occur on the sole, great toe, and instep of the foot. CLINICAL MANIFESTATIONS • Acute vesicular tinea pedis is pruritic (FIG. 7.8). 7.8 Acute vesicular tinea pedis. A KOH culture specimen is obtained from under the roof of a vesicle.

DIAGNOSIS • For diagnosis, the specimen should be obtained from the inner part of the roof of the blister for KOH examination or culture.

DIFFERENTIAL DIAGNOSIS Dyshidrotic eczema is easily confused with acute tinea pedis (FIG. 7.9). • Patients often have a positive atopic history. • It is KOH negative.

7.9 Dyshidrotic eczema. Note the small vesicles and the similarity to acute tinea pedis.

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173

Clin ical Varian t MANAGEMENT See TABLE 7.1. • For symptomatic relief of severe inflammation and itching, a potent topical steroid, such as triamcinolone acetonide cream, may be used for 4 to 5 days. The resultant anti-inflammatory effect also helps to increase the yield of obtaining organisms on KOH examination or culture. • Treatment is similar to that of type 1, although systemic as well as topical antifungals are often necessary. • Prevention involves decreasing wetness, friction, and maceration. Absorbent powders, such as miconazole (Zeasorb-AF) powder, should be applied after the eruption clears to prevent recurrence.

HELPFUL HINTS • When the diagnosis is in doubt, a potent topical steroid may be applied—for a week or so only—to relieve the acute itch and burning. • To increase positive yields, KOH examination or fungal cultures should be obtained only after the patient has not used topical therapy for at least 24 to 48 hours. • Positive results of KOH examination and fungal cultures are not necessarily proof of pathogenesis, because some organisms, especially yeasts and molds, may be saprophytes, or “contaminants.” • When there is a rash on the palms, the feet should always be examined.

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Uncommonly, an id reaction (dermatophytid) may occur. This is considered to be a hypersensitivity to fungal elements. Clinically, lesions consist of itchy, sterile (KOH and culture negative) vesicles on the hands similar to dyshidrotic eczema; this resolves when the primary acute process on the feet resolves.

POINT TO REMEMBER • Not all rashes of the feet are fungal. In fact, if a child younger than 12 years has what appears to be tinea pedis, it is probably another skin condition, such as eczema.

• A common error is automatically to assume that a rash of the feet, or “athlete’s foot,” is fungal in origin. Often, these conditions are mistakenly treated with topical antifungal preparations alone or in combination with topical steroids with a “shotgun” approach. Careful observation and a positive KOH examination reveal the true nature of the problem. This caveat also applies to tinea cruris (see following section). Type 2 (Chronic Plantar and/or Palmar) Only: • In patients in whom oral antifungal agents are contraindicated, a keratolytic agent such as Salex cream or lotion can be used to remove scale, followed by a topical antifungal agent such as ketoconazole cream.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Tin ea Cru ris BASICS Tinea cruris (“jock itch”) is a common infection of the upper inner thighs that most often occurs in postpubertal male patients. It is generally caused by the dermatophytes T. rubrum and E. floccosum. In contrast to candidiasis and lichen simplex chronicus, it generally spares the scrotum. DESCRIPTION OF LESIONS • Lesions are bilateral, fan-shaped, or annular plaques (plaques with central clearing), with a slightly elevated scaly “active border” (FIG. 7.10). DISTRIBUTION OF LESIONS • Lesions may involve the upper thighs, the crural folds, and possibly the pubic area and buttocks (see FIG. 3.12). • It generally spares the scrotum and penis.

7.10 Tinea cruris. Note the scalloped shape with an “active border.”

CLINICAL MANIFESTATIONS • Generally, the lesions are pruritic, “burning,” or irritating. • Frequently, the patient also has tinea pedis. • The condition may be chronic or recurrent, depending on environmental factors and exercise. • The likelihood of the spread of tinea cruris between sexual partners appears to be very small. DIAGNOSIS • A positive KOH examination or fungal culture is found most easily by sampling from the borders of the lesions.

DIFFERENTIAL DIAGNOSIS

Lich e n Sim p le x Ch ro n icus (Ecze m at o us De rm at it is) FIGURE 7.11 (see also FIG. 2.45). • It often involves the scrotum. • KOH examination and fungal cultures are negative for fungus. • Often, there is an atopic history. • Lesions are confluent (no central clearing). • Lichenification occurs as the condition becomes chronic.

7.11 Lichen simplex chronicus (chronic eczematous dermatitis). Lichenification of scrotal and inguinal skin results from relentless scratching and rubbing. continued on page 176

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175

DIFFERENTIAL DIAGNOSIS Continued

In ve rse Pso riasis FIGURE 7.12 (see also FIG. 3.24.) • It often involves the scrotum. • Evidence of psoriasis may be noted elsewhere. • KOH examination and fungal cultures are negative for fungus. • Lesions are confluent (no central clearing). OTHER DIAGNOSES

Se b o rrh e ic De rm at it is, Can d id iasis, In t e rt rig o , an d Irrit an t De rm at it is • All of these conditions may be clinically indistinguishable from one another.

MANAGEMENT See TABLE 7.1. • Topical antifungal creams, applied once or twice daily, are often effective in controlling, and sometimes curing, uncomplicated, localized infections. Over-the-counter (OTC) preparations of miconazole (Micatin), terbinafine (Lamisil), and clotrimazole (Lotrimin) are available. • For severe inflammation and itching, a mild OTC hydrocortisone 1% preparation or moderate-strength hydrocortisone valerate 0.2% (Westcort) may be used for 4 to 5 days for symptomatic relief.

7.12 Inverse psoriasis. Note the well-demarcated plaques with no “active border.

• Systemic antifungal therapy may be necessary in cases that do not respond to topical therapy and cases of chronic recurrent tinea cruris, particularly in immunocompromised patients. Prevention aims toward decreasing wetness, friction, and maceration by: • Using an absorbent powder such as miconazole (Zeasorb-AF). • Drying the area with a hairdryer after bathing. • Wearing loose clothing; briefs are less frictional than boxer shorts.

SEE PATIENT HANDOUT “Tin e a Cruris (Jo ck It ch )” ON THE SOLUTION SITE

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Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Tin ea Ca p it is BASICS Tinea capitis, or “ringworm,” most commonly occurs in prepubertal children. In the United States, African-American children are disproportionately affected by this superficial fungal infection of the hair shaft. The incidence of tinea capitis has been increasing and presents a growing public health concern, especially in overcrowded, impoverished inner-city communities. T. tonsurans is, by far, the most common etiologic agent; more than 90% of cases are caused by it. Other species, such as Microsporum audouinii, which is spread from human to human, and M. canis, which is spread from animals (cats and dogs), are more often seen in white children. Patients frequently have a family member, pet, or playmate with tinea. Tinea capitis is quite contagious and is generally spread by person-to-person contact. Studies have demonstrated a 30% carrier state of adults exposed to a child with T. tonsurans. The organism has also been isolated from such inanimate objects as hairbrushes and pillows.

7.13 Tinea capitis. Scaly, alopecic patches mimic seborrheic dermatitis.

DESCRIPTION OF LESIONS

Clin ical Typ e s There are essentially five clinical expressions of tinea capitis, with some overlapping physical presentations: • Inflamed, scaly, often alopecic patches, mimicking seborrheic dermatitis, are especially common in infancy until the age of 6 to 8 months (FIG. 7.13). • A diffuse scaling is seen with multiple round areas, characterized by alopecia that occurs secondary to broken hair shafts, leaving residual black stumps ( “black dot” ringworm) (FIG. 7.14). It is seen uncommonly and is often mistaken for alopecia areata. • The “gray patch” type (FIG. 7.15) consists of round, scaly plaques of alopecia in which hairs are broken off close to the surface of the scalp. • Tender pustular nodules or plaques called kerions may occur. • A kerion is a boggy, pustular, indurated, tumorlike mass, which represents an inflammatory hypersensitivity reaction to the fungus. A kerion can result in localized scarring.

7.14

Tinea capitis. “Black dot” ringworm.

7.15 Tinea capitis. “Gray patch type.” Note alopecia with broken off hairs close to scalp surface. Microsporum canis was found on culture, and the area fluoresced green with a Wood’s lamp.

Chap ter 7 • Superficial Fungal Infections

177

• Secondary bacterial invaders such as Staphylococcus aureus and some gram-negative organisms may sometimes be recovered from a kerion. Often, there is accompanying nontender regional adenopathy (FIG. 7.16). • Occasionally, a pustular variety, with or without alopecia, can mimic a bacterial infection. DIAGNOSIS

7.16 Tinea capitis with kerion. There is also a palpable, asymptomatic, nontender right occipital lymph node (arrow).

• A KOH preparation or fungal culture confirms the diagnosis. • When in doubt, or when a KOH preparation is negative, a fungal culture placed on Sabouraud’s agar should be done. This can be performed by obtaining broken hairs and scale by stroking the affected area with a sterile toothbrush, a familiar object to a child and one that is less frightening than a surgical blade or forceps (see Chapter 26, “Diagnostic and Therapeutic Procedures”). The collected material is then tapped onto the surface of Sabouraud’s agar. • An alternative method of harvesting broken hairs is by rubbing a moistened gauze pad on the involved area of scalp and then using forceps to place the hairs on the culture medium or slide. Pustules generally are sterile or grow bacterial contaminants. • A biopsy is rarely necessary. • In the past, Wood’s light examination was a valuable screening tool to diagnose tinea capitis easily (because Microsporum species are usually fluorescent), but it has largely lost its usefulness because most cases are caused by the nonfluorescing T. tonsurans.

DIFFERENTIAL DIAGNOSIS

Alo p e cia Are at a FIGURE 7.17. • This has a well-demarcated, symmetric patch of alopecia. • It is smooth and free of scales. • The KOH test is negative

At o p ic De rm at it is • This is a common cause for an itchy, scaly scalp in children • No hair loss is noted Se b o rrh e ic De rm at it is • Infants show “cradle cap” with thick scale. • Alopecia is absent in adults who have scalp involvement.

7.17 Alopecia areata. This child has smooth, welldemarcated, noninflammatory, asymptomatic patches of alopecia. continued on page 179

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DIFFERENTIAL DIAGNOSIS Continued

Ot h e r Diag n o se s • Psoriasis • Trichotillomania (a self-induced cause of hair loss) (see Chapter 10, “Hair and Scalp Disorders Resulting in Hair Loss”) • Tinea amiantacea (FIG. 7.18), which is a KOH-negative local patch or plaque of adherent scale (“tinea” is a misnomer for this condition, See Chapter 27, “Special Considerations in Pediatric and Elderly Skin”) • Bacterial scalp infection • Secondary syphilis • Acute and chronic cutaneous discoid lupus erythematosus

7.18 Tinea amiantacea. An inflammatory condition of the scalp in which heavy white or yellow (from sebum) scales extend onto the hairs and bind the proximal portions together; it is not caused by a fungus despite its name. “Pityriasis amiantacea” is probably a better name for this condition.

MANAGEMENT See TABLE 7.1. • Topical therapy is of little or no value in treating tinea capitis, although an adjunctive antifungal shampoo such as ketoconazole 1% to 2% (Nizoral) or selenium sulfide 1% to 2.5% (Selsun) may be used by the infected person and contacts to prevent reinfection and spread.

Syst e m ic Th e rap ie s Griseofulvin • In children, systemic therapy with a liquid suspension of griseofulvin has been the mainstay of therapy. • The dosage of microsized griseofulvin is 20 to 25 mg/kg/day and is sometimes as high as 25 mg/kg/day in divided doses. Ultramicrosized griseofulvin is given as a dosage of 15 to 20 mg/kg/day. It should be given with milk or food, which increases its absorption. It should be continued until the patient is clinically cured, generally 6 to 8 weeks. Some patients may require longer therapy. • Occasionally, an “idlike” reaction occurs shortly after the initiation of griseofulvin therapy. This consists of multiple small sterile papules on the face or

body, and it probably represents a hypersensitivity response. • Treatment failure, which is uncommon with griseofulvin, may indicate inadequate doses or duration of therapy, drug resistance, reinfection from another family member, poor compliance, or immune incompetence. • It is also believed that resistance to griseofulvin is currently rising. • Itraconazole, terbinafine, and fluconazole are newer and more efficacious agents. They have been used in some cases of griseofulvin treatment failure. • Pediatric dosages are as follows: • Itraconazole (Sporanox) (5 mg/kg/day). This drug is available as 100-mg capsules or as an oral solution (10 mg/mL). • Terbinafine (Lamisil). Dosage should be reduced according to weight: Children weighing less than 20 kg should receive one fourth of a tablet (62.5 mg) per day; children 20 to 40 kg are given 125 mg/day; children weighing more than 40 kg receive 250 mg/day (the medication is available as 250-mg tablets only). Formerly, children reluctant to swallow tablets were given terbinafine by crushing a tablet and mixing it in their food. Currently, there is a new Food and Drug continued on page 180

Chap ter 7 • Superficial Fungal Infections

179

MANAGEMENT Continued Administration–approved formulation of “childfriendly” Lamisil granules. The formulation has been approved for use by children 4 years of age and older. The amount of granules corresponds to 125 mg and 187.5 mg of terbinafine. Parents are instructed to

sprinkle it on the food of a child who may not like to take medicine. • Fluconazole (Diflucan) (6 mg/kg/day for 2 weeks; repeat at 4 weeks if indicated). This drug is available in 100-mg, 150-mg, and 200-mg tablets and as an oral solution (10 and 40 mg/mL).

HELPFUL HINTS • The pustular variety of tinea capitis can mimic a bacterial infection, and antibiotics are sometimes given before the correct diagnosis is made. • When a child has scaling alopecia and enlarged lymph nodes in the posterior auricular or occipital area, obtain a fungal culture and consider starting empiric antifungal treatment. • In many instances, therapy may have to be initiated in a patient with negative KOH examination and fungal cultures, based solely on clinical appearance. • Siblings of tinea capitis patients should be evaluated, or else the infection might be “ping-ponged “ back and forth within the family. • Occasionally, concomitant systemic steroid therapy is warranted in addition to griseofulvin when the patient is experiencing a severe, tender, or painful kerion. A very short course (usually 3 or 4 days) of oral prednisone, 1 mg/kg/day, is sufficient.

180

POINTS TO REMEMBER • The current standard of diagnosis is a positive KOH examination or culture. • Topical therapy does not work. • Systemic therapy must be in an adequate dosage and duration.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Tin ea Co rp o ris

(“Rin gw o r m ”)

BASICS Tinea corporis is commonly referred to as “ringworm,” a term used by laypersons, and, frequently, many in the health care community, to describe practically any annular or ringlike eruption on the body. In fact, there are many nonfungal conditions that assume an annular “ringwormlike” configuration: granuloma annulare, erythema multiforme, erythema migrans (seen in acute Lyme disease), and figurate erythemas such as urticaria. Tinea corporis (described as tinea faciale if it is located on the face) is most often acquired by contact with an infected animal, usually kittens and occasionally dogs. It may also spread from other infected humans, or it may be autoinoculated from other areas of the body that are infected by tinea such as tinea pedis or tinea capitis. Another common method of transmission of tinea corporis is noted in wrestlers (tinea gladiatorum, see FIG. 5.4). M. canis, T. rubrum, and T. mentagrophytes are the usual pathogens.

7.19 Tinea corporis. Multiple lesions are present, with a border of scale.

DESCRIPTION OF LESIONS • Lesions are generally annular, with peripheral enlargement and central clearing. Odd gyrate or concentric rings may appear (FIGS. 7.19 and 7.20). • The scaly, “active border” can sometimes be pustular or vesicular. • Lesions are single or multiple. DISTRIBUTION OF LESIONS • If multiple lesions are present, their distribution is typically asymmetric. • Lesions are found most often on the extremities, face, and trunk.

7.20 Tinea faciale. Two erythematous, scaly, annular lesions are noted on this child’s face.

Chap ter 7 • Superficial Fungal Infections

181

CLINICAL MANIFESTATIONS • Lesions may be pruritic or asymptomatic. • Majocchi’s granuloma is a follicular deep form of tinea corporis. It may result when inappropriate therapy, such as topical steroids, or shaving drives the fungi into hair follicles. • Tinea corporis is very often misdiagnosed and treated with topical steroids (“tinea incognito”) (FIG. 7.21). DIAGNOSIS

7.21 Tinea corporis (“tinea incognito”). This patient was treated with topical steroids for months until the correct diagnosis was made. The topical steroids modified the typical clinical appearance of tinea corporis; in fact, her lesions look more like psoriasis.

• Diagnosis is confirmed by a positive KOH examination or fungal culture (it is especially easy to find hyphae in those patients who have been previously treated with topical steroids). • A skin biopsy may be necessary for diagnosis. • A history of a newly adopted kitten, or of another infected contact, is helpful.

DIFFERENTIAL DIAGNOSIS

Urt icaria FIGURE 7.22. • Erythema with no scale (i.e., epidermal involvement)

Acut e Lym e Dise ase (Eryt h e m a Mig ran s) FIGURE 7.23. • Erythema with no scale • Characteristic targetlike appearance

7.22 Urticaria. Dermal vasodilatation occurs, with no epidermal change (scale).

7.23 Acute Lyme disease (erythema migrans). Note the targetlike concentric rings with no scale. continued on page 183

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DIFFERENTIAL DIAGNOSIS Continued

Gran ulo m a An n ulare FIGURE 4.10. • • • •

Skin-colored or red firm papules Absence of scale Symmetric distribution of lesions Lesions slightly firm to palpation

Ot h e r Diag n o se s • Atopic dermatitis • Psoriasis (FIG. 7.24) • Subacute lupus erythematosus • Mycosis fungoides (cutaneous T-cell lymphoma)

7.24 Psoriasis. Extensive annular, serpiginous lesions are present in this patient.

POINT TO REMEMBER MANAGEMENT • Inquire about sports activities, such as wrestling. See TABLE 7.1. • Topical antifungal agents are useful. • Systemic antifungal agents (see the earlier discussion of tinea cruris) are sometimes necessary when multiple lesions are present or in areas that are repeatedly shaved, such as men’s beards (tinea barbae) or, especially, women’s legs, in which granulomatous lesions (Majocchi’s granuloma) may appear. • If pets appear to be the source of infection, they may also need antifungal treatment after evaluation by a veterinarian.

Chap ter 7 • Superficial Fungal Infections

183

On ych o m yco sis

(Tin ea Un gu iu m ) BASICS The term onychomycosis refers to an infection of the fingernails or toenails caused by various fungi, yeasts, and molds. In contrast, the term tinea unguium refers specifically to nail infections caused by dermatophytes. Onychomycosis is uncommon in children, but its prevalence increases dramatically with advancing age, with prevalence rates as high as 30% in those 70 years and older. The major causes of onychomycosis are as follows:

7.25 Distal subungual onychomycosis. The nail is dystrophic and discolored, and there is a buildup of keratin underneath it (subungual hyperkeratosis).

• The dermatophytes E. floccosum, T. rubrum, and T. mentagrophytes • Yeasts, mainly Candida albicans • Molds, such as Aspergillus, Fusarium, and Scopulariopsis species DESCRIPTION OF LESIONS Distal subungual onychomycosis (FIG. 7.25) accounts for more than 90% of all cases of onychomycosis. It is usually characterized by the following: • Nail thickening and subungual hyperkeratosis (scale buildup under the nail) • Nail discoloration (yellow, yellow-green, white, or brown) • Nail dystrophy • Onycholysis (nail plate elevation from the nail bed) CLINICAL MANIFESTATIONS

7.26 Superficial white onychomycosis. A KOH specimen was easily obtained from the surface of this lesion.

• Aside from footwear causing occasional physical discomfort and the psychosocial liability of unsightly nails, onychomycosis is usually asymptomatic. • Left untreated, onychomycotic nails, can, however, infrequently act as a portal of entry for more serious bacterial infections of the lower leg, particularly in patients with diabetes. • Distal subungual onychomycosis is sometimes associated with chronic palmoplantar tinea (i.e., “two feet, one hand” variant of tinea).

Clin ical Varian ts • In superficial white onychomycosis (FIG. 7.26), the fungus is superficial, and material for scraping may be obtained from the dorsal surface of the nail. • Proximal white subungual onychomycosis (FIG. 7.27) may be seen in persons with human immunodeficiency virus (HIV) infection. DIAGNOSIS 7.27 Proximal white subungual onychomycosis. HIV infection should be suspected in this patient.

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• A positive KOH examination or growth of dermatophyte, yeast, or mold on culture is diagnostic.

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DIFFERENTIAL DIAGNOSIS See also Chapter 13, “Diseases and Abnormalities of Nails.”

Pso riasis o f t h e Nails FIGURE 7.28. • This may be indistinguishable from, or coexist with, onychomycosis. • Usually, evidence of psoriasis is found elsewhere on the body. • The KOH examination is generally, but not always, negative. • Characteristic nail pitting and nail discoloration (“oil spots,” yellowish brown pigmentation) may be present.

7.28 Psoriasis of nails. Subungual hyperkeratosis and “oil spots” are noted.

Ch ro n ic Paro n ych ia FIGURE 7.29. • This is seen in patients with an altered immune status (e.g., diabetic patients) and in people whose hands are constantly in water. • Erythema and edema of the proximal nail fold are noted. • The cuticle is absent. • There is nail dystrophy. • Culture may be positive for Candida and/or bacteria.

Pseudomona s In fe ct io n o f t h e Nail (Gre e n Nail Syn d ro m e ) FIGURE 7.30. • Onycholysis occurs, with secondary bacterial (pseudomonas) colonization. • A distinctive green coloration is apparent. • This is usually found in women with long finger nails.

7.29 Chronic paronychia. Note the swelling of the proximal nail fold, the loss of the cuticle, and the dystrophy of the nail plate.

Ot h e r Diag n o se s Onycholysis unrelated to a fungus or psoriasis can be idiopathic or associated with nail trauma, thyroid disease, use of nail polish or nail hardeners, and oral tetracyclines, especially demeclocycline (Declomycin), coupled with sun exposure.

7.30 Green nail, onycholysis. The green color is the result of a secondary infection with Pseudomonas.

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MANAGEMENT Media attention has brought scores of patients to their health care providers to have their unsightly nails treated with the oral antifungal agent terbinafine (Lamisil). Lamisil and itraconazole (Sporanox) have replaced griseofulvin, which is less effective and is associated with a high recurrence rate (TABLE 7.1).

Oral Th e rap y Important factors to consider before starting oral therapy: • Diagnostic confirmation by KOH examination or fungal culture • Patient motivation and compliance • Family history of onychomycosis • Patient’s age and health • Drug cost • Possible drug interactions and side effects (see TABLE 7.1) Terb in a fi n e (La m isil) Ta b let s

• It is fungicidal, especially against dermatophytes. • Long-term cure rate is probably no greater than 40% to 50%. • Side effects are infrequent. However, baseline liver function tests are performed, and the tests are repeated in 4 to 6 weeks. • This drug has a reservoir effect. Because it persists in the nail for up to 4 to 5 months, there is no need to wait until the nail appears clinically normal; there is continued clearing even after cessation of therapy. Baseline liver function tests should be done, and the tests should be repeated in 6 to 8 weeks if therapy is long term. Dosage

• Adults: 250 mg/day for 6 weeks for fingernails; 250 mg/day for 12 weeks for toenails • Alternatively, pulse dosing with 250 mg/day for 1 week monthly for 4 months • Children: weight 20 to 40 kg: 125 mg/day; weight more than 40 kg: 250 mg/day for 6 to 12 weeks It ra co n a zo le (Sp o ra n o x ) Ca p su les

• This is a broad-spectrum fungistatic agent. • The primary drawback to the use of this drug is the risk for significant drug interactions. • Long-term cure rate is probably no greater than 40% to 50%.

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• Side effects are infrequent. However, liver function tests should be performed at baseline and repeated in 4 to 6 weeks. • This drug also has a reservoir effect. Dosage

• 200 mg/day for 6 weeks for fingernails; 12 weeks for toenails • Alternatively, pulse dosing with 200 mg twice daily, taken with full meals, for 7 days of each month (3 months for fingernails, 4 months for toenails) Flu co n a zo le (Difl u ca n ) Ta b let s

• This is a broad-spectrum fungistatic agent. • It is more extensively used in patients with HIV infection. • It has many fewer drug interactions than itraconazole. • Side effects are minimal. Liver toxicity must be monitored if the drug is used long term. Dosage

• 150 to 400 mg daily for 1 to 4 weeks or 150 mg once per week for 9 to 10 months

Ot h e r Tre at m e n t Me t h o d s Other treatments include the following: • Surgical ablation of nails is rarely indicated and is generally ineffective. • Topical agents are generally ineffective because of poor nail penetration. In early distal subungual and superficial white onychomycosis, these drugs may be used as adjuvant therapy or to prevent recurrences after clearing with oral agents. • One such preparation is Carmol 40 Gel, which contains 40% urea, a keratolytic agent; this is applied once daily to thickened nails. It may be used in conjunction with other topical antifungal agents. • Penlac Nail Lacquer Topical Solution 8% is a topical nail lacquer containing the antifungal agent ciclopirox; it is used in conjunction with oral antifungal agents or alone for the prevention of recurrent infection. The overall efficacy of this agent remains to be determined. • Amorolfine nail lacquer (available in Europe) is reported to be effective when it is applied for at least 12 months.

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POINTS TO REMEMBER • Onychomycosis should be confirmed with a positive KOH test or culture before initiating oral therapy. • Nails that appear abnormal do not always have a fungal infection. • Onychomycosis is generally asymptomatic, and treatment with the newer systemic antifungal agents is expensive and not always curative. • Pre-existing liver disease is a relative contraindication to the use of antifungal agents for onychomycosis. • A patient with a family history of onychomycosis is less likely to have a successful treatment outcome than a person without such a history.

HELPFUL HINTS The following important questions must be answered before oral therapy is prescribed: • What are the patient’s age and health status? • Can the patient afford the cost of the drug? • Is the patient taking any other medications that could interact adversely with the antifungal agent?

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Cu t a n eo u s Ca n d id ia sis BASICS Cutaneous candidiasis is a superficial fungal infection of the skin and mucous membranes caused by Candida albicans. It is seen much less commonly than tinea infections. C. albicans thrives on moist, occluded sites, particularly as a secondary invader. It occurs in the following: • People who continually expose their hands to water (e.g., dishwashers, health care workers, florists) • Obese persons • Infants (in the diaper area or mouth) It is also found in persons with an altered immune status, such as: 7.31 Cutaneous candidiasis of the axillae. This patient has diabetes. Note the satellite pustules.

• • • •

Patients with diabetes Patients taking long-term systemic steroid therapy Patients with AIDS Patients with polyendocrinopathies

DESCRIPTION OF LESIONS • The appearance of lesions varies according to the location.

Can d id al In t e rt rig o • Initially, pustules appear, followed by well-demarcated erythematous plaques with small papular and pustular lesions at the periphery (“satellite pustules”). • Erythematous areas later become eroded and “beefy red” (FIGS. 7.31 and 7.32). • Lesions are not annular (they have no central clearing), as seen in tinea infections. DISTRIBUTION OF LESIONS 7.32 Cutaneous candidiasis of skin folds. This patient with pendulous breasts has rheumatoid arthritis and is on immunosuppressive therapy. Note the “beefy red” plaque and satellite pustules.

• Lesions are seen in intertriginous areas, such as under pendulous breasts (see FIG. 7.32), the axillae, the groin, the intergluteal fold, the perineal region including the scrotum (FIG. 7.33), and at the corners of the mouth (perlèche).

Ot h e r Lo cat io n s an d De scrip t io n s o f Clin ical Varian t s • “Erosio interdigitalis blastomycetes.” Superficial interdigital scaly, erythematous erosions or fissures occur in the web spaces of the fingers. • Candidal diaper dermatitis occurs in the area occluded under diapers. • Candidal folliculitis is characterized by follicular pustules. • Candidal balanitis is seen in men with diabetes. Erythema, edema, and moist curdlike accumulations occur on the glans penis, with possible fissuring and ulceration of the foreskin. • Candidal vulvitis/vulvovaginitis consists of erosions, pustules, and erythematous plaques.

7.33 Cutaneous candidiasis of the groin. The characteristic “beefy red” plaque and satellite pustules are seen here. 188

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• Candidal paronychia is characterized by edema, erythema, and purulence of the proximal nail fold with secondary nail dystrophy (see Chapter 13, “Diseases and Abnormalities of Nails”). • Oral candidiasis (“thrush”) is characterized by white, creamy exudate or plaques, which, when removed, appear eroded and beefy red. Oral candidiasis appears in infants (“thrush”) and in the clinical settings of immunosuppression and diabetes (see Chapter 24, “Cutaneous Manifestations of HIV Infection”).

DIFFERENTIAL DIAGNOSIS • • • • •

Inverse psoriasis Tinea infections Irritant intertrigo (FIGS. 7.34 and 7.35) Atopic dermatitis Seborrheic dermatitis

CLINICAL MANIFESTATIONS • Cutaneous candidiasis is characterized by itching and burning. DIAGNOSIS • The organism is KOH positive for pseudohyphae, budding yeast, or mycelia (see Chapter 26, “Diagnostic and Therapeutic Procedures”). • Fungal culture on Sabouraud’s media reveals creamy, dullwhite colonies.

7.34 Irritant intertrigo. This itchy eruption was caused by the patient’s deodorant. MANAGEMENT See TABLE 7.1. • Burow’s solution in cool wet soaks two to three times daily is helpful. This solution can be applied to decrease moisture and maceration. • The intertriginous area should be kept dry with powders, such as miconazole (Zeasorb-AF) powder, and by drying with a hairdryer after bathing. • Topical broad-spectrum antifungal creams, such as prescription ketoconazole (Nizoral) cream or the over-the-counter preparations of clotrimazole (Lotrimin) and miconazole (Micatin), can be applied. • Systemic antifungal agents, such as itraconazole or fluconazole, are used for widespread involvement or recalcitrant infections.

7.35 Irritant intertrigo. This is often mistaken and treated for candidiasis. The maceration and pendulous breasts are the cause of this woman’s problem.

POINT TO REMEMBER • Cutaneous candidiasis is frequently confused with inverse psoriasis and irritant intertrigo; thus, documentation of candidal organisms should be made.

Chap ter 7 • Superficial Fungal Infections

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Tin ea Versico lo r BASICS Tinea versicolor, also known as pityriasis versicolor, is a very common superficial yeast infection caused by the hyphal form of Pityrosporum ovale. The organism is also known as P. orbiculare and Malassezia furfur. Seen mostly in young adults, it is unusual in very young and elderly persons. Tinea versicolor is primarily of cosmetic concern and is generally asymptomatic. The term “versicolor” refers to the varied coloration that tinea versicolor can display. The color of the lesions may vary from whitish to pink to tan or brown (Figs. 7.36–7.38). It is a chronic relapsing condition because the causative fungus is part of the skin’s normal flora. It is ubiquitous in tropical and subtropical countries. 7.36 Tinea versicolor. This patient has hypopigmented lesions. Note the similarity to vitiligo.

DESCRIPTION OF LESIONS • The primary lesions are well-defined round or oval macules with an overlay of fine scales; the lesions often coalesce to form larger patches. • The condition is more common in consistently hot climates and recurs during the summer in more temperate zones. DISTRIBUTION OF LESIONS • Lesions are most often distributed on the trunk, upper arms, and neck; however, they may also be seen on the face.

7.37 Tinea versicolor. This patient has light tan (fauncolored) tinea versicolor.

7.38 Tinea versicolor. Here the lesions are dark brown and confluent.

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DIAGNOSIS • If scale is present, KOH examination is positive, and the typical “spaghetti and meatball” hyphae are abundant and easily found (FIG. 7.39; see FIG. 26.7), diagnosis is positive. • Wood’s light examination is used to demonstrate the extent of the infection and may help to confirm the diagnosis, because lesions often fluoresce an orange-mustard color when the Wood’s light is held close to lesions in a dark room.

7.39 Tinea versicolor. In this photomicrograph of a KOH examination, note the short, wavy hyphae (“spaghetti”) and several clusters of spores (“meatballs”).

DIFFERENTIAL DIAGNOSIS

Vit ilig o • The whitish (hypopigmented) variety of tinea versicolor is frequently mistaken for vitiligo (FIG. 7.40) Pit yriasis ro se a • A Pityriasis rosea may also be a cause of diagnostic confusion (see Chapter 4, “Inflammatory Eruptions of Unknown Cause”).

7.40 Vitiligo. Note the complete depigmentation and the lack of scale.

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• Alternatively, topical ciclopirox (Loprox) gel or shampoo, which is available only by prescription, may be applied. • This treatment regimen may be repeated for 3 or 4 weeks. It is also a good idea to repeat this regimen before the next warm season or before a tropical vacation.

MANAGEMENT See TABLE 7.2.

To p ical Ag e n t s • For mild, limited tinea versicolor, topical therapy is applied in the shower. Daily applications of selenium sulfide (Selsun Blue) shampoo, pyrithione zinc (Head & Shoulders) shampoo, and ketoconazole 1% (Nizoral) cream or shampoo are inexpensive OTC methods that often clear the eruption. • In addition, application of topical antifungals such as miconazole (Micatin), clotrimazole (Lotrimin), or terbinafine (Lamisil) sprays (Micatin and Lamisil sprays allow for easy application on the back) is useful. The topical agents are used once or twice daily.

Syst e m ic Th e rap y • For stubborn or widespread disease, systemic therapy with ketoconazole, itraconazole (Sporanox) or fluconazole (Diflucan) may be prescribed (see formulary in TABLE 7.2). • Although administered for a very short term (3 to 5 days), systemic therapy should not be given routinely for this essentially cosmetic problem.

Tab le 7.2 FORMULARY FOR TINEA VERSICOLOR AGENT

DOSAGE

Topical agents: over-the-counter Selenium sulfide 1% (Selsun Blue) shampoo Selenium sulfide 1%, zinc pyrithione (Head & Shoulders) shampoo Miconazole 2% (Micatin) spray Clotrimazole (Lotrimin) 1% cream Terbinafine (Lamisil) 1% cream

Spray on once daily for 2 weeks Apply once daily for 2 weeks Apply 1 to 4 weeks, twice daily

Topical agents: prescription required Ketoconazole 2% gel (Xolegel, foam [extina]) Ketoconazole 2% (Nizoral) shampoo Selenium sulfide 2.5% (Selsun 2.5%) shampoo Ciclopirox shampoo Ciclopirox (Loprox) gel

Apply daily to wide area for 10 minutes, followed by a shower Apply daily to wide area for 10 minutes, followed by a shower Apply daily to wide area for 10 minutes, followed by a shower Apply 1 to 4 weeks, twice daily

Systemic agents Ketoconazole (Nizoral) Itraconazole (Sporanox) Fluconazole (Diflucan)

200 mg for 5 days 100 mg for 5 days 150 mg for 5 days

Apply daily to wide area for 10 minutes, followed by a shower Apply daily to wide area for 10 minutes, followed by a shower

HELPFUL HINTS

POINTS TO REMEMBER • Patients should be advised that the uneven coloration of the skin may take several months to disappear after the fungus has been successfully eliminated. • Recurrences are very common, especially in warm weather.

• Prophylactic application of ketoconazole cream or shampoo once or twice weekly may prevent recurrences. • Topical therapy can be repeated 1 week before the next exposure to warm weather.

SEE PATIENT HANDOUT “Tin e a Ve rsico lo r” ON THE SOLUTION SITE 192

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

C H AP T ER

8

Viral Exanthems Kenneth Howe

OVERVIEW Viral exanthems are the cutaneous manifestation of an acute viral infection. In most exanthems, viral particles are present within the visible lesions, having reached the skin through the bloodstream. It is unclear whether the observed exanthem results from active viral infection of the skin, the immune response to the virus, or a combination of these two. Most common in children, viral exanthems may present as distinct, clinically recognizable illnesses such as measles or chickenpox. More frequently, however, a nonspecific eruption is seen that makes an exact diagnosis elusive. More than 50 viral agents are known to cause exanthems, and many of these rashes are indistinguishable from one another. Because most viral illnesses are benign and self-limited, a specific diagnosis is often not made. In some situations, however, determining the precise etiology may be of vital importance. Examples include the appearance of a viral exanthem during pregnancy or in an immunocompromised patient. It is also important to distinguish viral exanthems from rashes caused by treatable bacterial or rickettsial infections and from hypersensitivity reactions to medications.

VARICELLA (CHICKENPOX) HAND-FOOT-AND-MOUTH DISEASE ERYTHEMA INFECTIOSUM (FIFTH DISEASE) ROSEOLA INFANTUM RUBELLA (GERMAN MEASLES) RUBEOLA (MEASLES)

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Va ricella

(Ch ick en p o x ) BASICS • Varicella, or chickenpox, is an infection caused by the varicella-zoster virus (VZV). Transmission occurs by aerosolized droplet spread, with initial infection occurring in the mucosa of the upper respiratory tract. Traveling through the blood and lymphatics (primary viremia), a small amount of virus reaches cells of the reticuloendothelial system, where the virus replicates during the remainder of the incubation period. Nonspecific host defenses contain the incubating infection at this point, but in most cases these defenses are eventually overwhelmed, and a large secondary viremia results. It is through this secondary viremia that VZV reaches the skin. The viremia occurs cyclically over a period of approximately 3 days and results in successive crops of lesions. • Most cases occur during childhood, and half of the patients are younger than 5 years of age. • Epidemics have a peak incidence during late winter and spring. DESCRIPTION OF LESIONS

8.1

Varicella. “Dewdrops on rose petals.”

• The characteristic lesions begin as red macules and progress rapidly from papules to vesicles to pustules to crusts. The entire cycle may occur within 8 to 12 hours. The typical vesicles are superficial and thin walled, and they are surrounded by an irregular area of erythema, giving them the appearance of “a dewdrop on a rose petal” (FIG. 8.1). • The lesions are usually pruritic. • Involvement of the oral mucous membranes (enanthem) occurs as well, most commonly on the palate. Because vesicles in these sites quickly rupture, it is common to observe shallow erosions. • Because the lesions appear in successive crops, a characteristic feature of varicella is the simultaneous presence of lesions in varying stages of development. In any given area, macules, vesicles, pustules, or crusts may be seen. • Crusts usually fall off within 1 to 3 weeks, depending on the depth of involvement. • Large blisters can also be seen in varicella, often resulting from superinfection with Staphylococcus aureus. Hemorrhagic lesions may occur in patients with thrombocytopenia. • Scarring is not unusual in uncomplicated varicella. Facial “punched-out” scars are common. DISTRIBUTION OF LESIONS

8.2

194

Varicella. Vesicles and crusts.

• The eruption typically begins on the face, scalp, and trunk and then spreads to involve the extremities. • Successive crops appear over 3 to 5 days, resulting in a diffuse, widespread eruption of discrete lesions (FIG. 8.2).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

CLINICAL MANIFESTATIONS

DIAGNOSIS

In cub at io n Pe rio d • The duration typically is 2 weeks (range, 10 to 21 days). • During this period, children are usually asymptomatic, with the onset of the rash being the first sign of illness. • In older children and adults, symptoms are typically more severe. The rash is frequently preceded by 2 to 3 days of fever and flulike symptoms, which often persist during the acute illness.

• The diagnosis of varicella is usually straightforward, based on the characteristic presentation and clinical findings. • A Tzanck smear can be helpful in confirming the diagnosis (see Chapter 6, “Superficial Viral Infections”). When the test is positive, it reveals characteristic multinucleated giant cells. Identical findings are seen in herpes zoster virus or herpes simplex virus (HSV) infections.

Co m p licat io n s • Complications in healthy children are rare; complications are more common in infected adults. • Varicella pneumonia is a relatively uncommon complication that usually occurs in adults and immunocompromised children. It begins 1 to 6 days after onset of the rash, with pulmonary symptoms such as cough, dyspnea, and pleuritic chest pain. The severity of the symptoms is out of proportion to the findings on physical examination. Chest radiographs typically reveal diffuse nodular densities.

DIFFERENTIAL DIAGNOSIS

Ot h e r Viral Exan t h e m s • Vesicular exanthems of coxsackievirus and echovirus infections may be mistaken for varicella. • These exanthems may show a characteristic distribution, as in hand-foot-and-mouth disease. Disse m in at e d He rp e s Zo st e r See FIGURE 24.6. • Patients have a previous history of primary varicella. • There is often a typical vesicular eruption accentuated in one unilateral dermatome in a typical “zosteriform” pattern. This is seen in addition to a widespread rash that is indistinguishable from varicella. • The patient is generally immunocompromised, secondary to medications, malignant disease, or human immunodeficiency virus infection.

Lab o rat o ry Te st in g • Smears obtained from active lesions can be tested by the direct immunofluorescence technique, which uses fluorescent-labeled antibodies to detect the presence of VZV. This technique has a sensitivity and specificity nearly equal to those of culture, with the advantage of providing rapid results. • Active lesions can also be cultured for VZV. Culturing of the VZV virus is technically difficult and positive less than 40% of the time.

• Direct immunofluorescence or culture results indicative of HSV infection.

At yp ical Me asle s • This occurs in adults who received killed measles virus vaccine between 1963 and 1967. • The eruption begins on the palms and soles and then spreads proximally. • Pneumonia is a common feature. • The diagnosis can be confirmed by a rise in measles antibody titers. Im p e t ig o • The patient generally feels well. • Typical moist, honey-colored crusts are present, often in a periorificial distribution (See Chapter 5, “Superficial Bacterial Infections”).

Ecze m a He rp e t icum (Kap o si’s Varice llifo rm Erup t io n ) See FIGURE 6.29. • Preexisting skin disease such as atopic dermatitis becomes secondarily infected with HSV.

Chap ter 8 • Viral Exanthem s

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MANAGEMENT

Acut e Varice lla • Uncomplicated varicella in otherwise healthy children is generally treated with supportive care such as antipruritics and antipyretics. Aspirin should be avoided because of the risk of Reye’s syndrome. • Oral acyclovir is warranted in patients who are at an increased risk of complications, and, in general, it should be started within 24 hours of the onset of the rash. These patients include: • Otherwise healthy, nonpregnant patients 13 years of age or older. • Children older than 12 months of age with chronic skin or pulmonary conditions or who are receiving longterm salicylate therapy. • Children receiving short, intermittent, or aerosolized courses of corticosteroids. • Intravenous acyclovir is indicated in immunocompromised patients or in patients with virally mediated complications of varicella. Varice lla Vaccin e The VZV vaccine (Varivax) is recommended for universal immunization in all children. • It is optimally given between 12 and 18 months of age; it may be administered in a single dose at any time before 13 years of age.

• In older adolescents or adults, two doses of vaccine should be administered 4 to 8 weeks apart. • The appearance of breakthrough varicella, seen in previously immunized persons, has indicated that the effectiveness of the vaccine wanes over time. Consequently, a revaccination booster immunization is now recommended for children between 4 and 6 years of age.

Varice lla an d Pre g n an cy • Peripartal maternal varicella poses a particular risk to the newborn. Neonates born 2 days before or 5 days after the onset of maternal varicella should be given varicella immunoglobulin (VZIG). Those newborns who develop varicella should be treated with intravenous acyclovir. • Oral acyclovir is not recommended in pregnant women with uncomplicated varicella because the risks and benefits to the fetus are unknown. • Pregnant patients who develop varicella in the first trimester have a 2.3% to 4.9% risk of delivering a child with the fetal varicella syndrome. • This syndrome is a congenital malformation complex with features such as intrauterine growth retardation, prematurity, cicatricial lesions in a dermatomal distribution, limb paresis and hypoplasia, chorioretinitis, and cataracts. • It is not known whether the administration of acyclovir prevents these complications.

POINT TO REMEMBER • Patients remain contagious until all cutaneous lesions are crusted.

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H a n d -Fo o t -a n d -Mo u t h Disea se BASICS • Hand-foot-and-mouth disease is an acute viral infection that manifests as a vesicular eruption with a characteristic distribution. The infection is caused by enteroviruses, most commonly coxsackievirus A16. The virus is spread from person to person by the fecal-oral route. • Outbreaks are typically in the summer or early fall, and epidemics may occur. Transmission is more likely in crowded environments. • Young children (1 to 5 years of age) are most commonly infected. • The incubation period ranges from 4 to 6 days. DESCRIPTION OF LESIONS • Oral lesions (enanthem) are the first manifestation of hand-foot-and-mouth disease. Although initially vesicular, it is more common to see multiple shallow erosions, because the vesicles are very fragile. • Individual lesions may range in size from 1 to 5 mm in diameter, and they may exhibit a rim of erythema. These oral lesions may be painful, and they frequently interfere with eating (FIG. 8.3). • The exanthem consists of round or angulated, grayish white vesicles that are typically 3 to 7 mm in diameter. • These vesicles, which are located on the palms and soles, have a characteristic oval or linear shape and tend not to rupture (FIG. 8.4). DISTRIBUTION OF LESIONS

8.3 Hand-foot-and-mouth disease. Oral lesion. Note the oval shape and rim of erythema.

• The enanthem appears most commonly on the tongue and buccal mucosa and occasionally on the lips, palate, and gums. • The exanthem is characteristically present on the hands and feet. Lesions occur on the dorsal or lateral aspects of the fingers and toes and on the palms and soles. All three sites may not be involved at the time of presentation. • The diaper area in infants may show a greater concentration of lesions. • Occasionally, an eruption of erythematous papules on the proximal extremities may occur, in addition to the acral lesions. CLINICAL MANIFESTATIONS • The illness most frequently begins as a sore throat or mouth. In young children, refusal to eat is often a presenting sign. • Occasionally, a 1- to 2-day prodrome of fever and abdominal pain may be seen. • The acral eruption follows the development of oral lesions. It is usually not pruritic, although it may be painful.

8.4 Hand-foot-and-mouth disease. Oval intact vesicles are noted on the palm.

Chap ter 8 • Viral Exanthem s

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DIFFERENTIAL DIAGNOSIS

Prim ary Oral He rp e s Sim p le x (See also Chapter 12, “Disorders of the Mouth, Lips, and Tongue) • Usually, the lips and gingiva are affected, and the back of the throat is spared. • There are recurrent outbreaks. • The Tzanck smear and culture are positive for HSV. Ap h t h o us Ulce rs • Lesions are painful. • As with herpes simplex, the lips and gingiva are usually affected, and the back of the throat is spared.

• In contrast to most viral illnesses, lymphadenopathy is absent to minimal. • Although in general complications are rare, the one seen most frequently is aseptic meningitis. DIAGNOSIS • Diagnosis is made on the basis of the characteristic clinical presentation. • Although not routinely indicated, laboratory testing can confirm the diagnosis. Virus can be cultured from throat washings or stool, with the latter giving a higher yield. Acute and convalescent sera show an elevation in antibody titer to the causative virus.

POINT TO REMEMBER • The course of the illness is self-limited, lasting less than a week in most cases.

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MANAGEMENT • Treatment is with supportive care. Antipyretics and a clear liquid diet while the throat is sore are typically all that is necessary.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Er yt h em a In fect io su m

(Fift h Disea se)

BASICS • Erythema infectiosum is a common viral illness caused by infection with parvovirus B19. Transmission is from person to person, probably through respiratory secretions. • It occurs most commonly in the late winter and spring. Epidemics are frequently seen, particularly among schoolage children. • The incubation period lasts 4 to 14 days, but it may be as long as 3 weeks. • By the time the characteristic exanthem appears, the patient is unlikely to be infectious. DESCRIPTION OF LESIONS • Erythema infectiosum is most commonly identified in children by its characteristic facial erythema. Bright red and tending to involve the malar surfaces, this eruption is described as having a “slapped cheek” appearance (FIG. 8.5A). • A photosensitive exanthem also appears on the extremities and trunk. This develops 1 to 4 days after the facial erythema, and it begins as a macular or macular and papular erythema that later clears centrally to produce a characteristic reticular (“lacy”) pattern (FIGS. 8.5B and C). • Although the exanthem usually resolves in 1 to 2 weeks, the reticular erythema may show a recrudescent course in some patients. In these cases, the erythema tends to flare in response to physical stimuli, such as exercise, excitement, sunlight, or warm baths.

A 8.5A Erythema infectiosum. “Slapped cheeks”: The erythema favors the malar surfaces. The slapped cheek appearance is further accentuated by a tendency to spare the nasal bridge and the periorbital and perioral areas.

DISTRIBUTION OF LESIONS • The facial erythema favors the malar surfaces. The “slapped cheek” appearance is further accentuated by a tendency to spare the nasal bridge and the periorbital and perioral areas. • The reticular erythema most commonly affects the extensor surfaces of the extremities and the buttocks. The palms and soles are usually spared.

B 8.5B Erythema infectiosum. This child has the characteristic reticular (“lacy”) pattern of lesions on her arms.

CLINICAL MANIFESTATIONS • Although facial erythema is the most common initial presentation, some patients experience a mild prodrome of low-grade fever, malaise, upper respiratory or gastrointestinal symptoms, and myalgias. • It can be associated with joint symptoms in adults, particularly in women. A symmetric polyarthropathy develops, involving the hands, feet, elbows, and knees. • The illness is benign and self-limited, with the exanthem resolving within 1 to 2 weeks. • Although joint symptoms generally resolve within 2 to 3 weeks, it is not uncommon for them to persist for several months.

C 8.5C

Erythema infectiosum. Similar lesions on legs.

Chap ter 8 • Viral Exanthem s

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DIFFERENTIAL DIAGNOSIS

Syst e m ic Lup us Eryt h e m at o sus • This may be difficult to differentiate from erythema infectiosum with associated joint symptoms. • The patient often has history of photosensitivity. • Positive antinuclear antibodies are present. • Other signs of systemic involvement such as serositis, renal disease, and central nervous system symptoms are noted (See Chapter 25, “Systemic Cutaneous Manifestals).

• Erythema infectiosum during pregnancy may result in fetal death because of the development of hydrops fetalis. The risk of fetal death with maternal infection is estimated at 4.2% to 9%, with greater risk when the infection occurs during the first 20 weeks of pregnancy. • Infection with parvovirus B19 can lead to aplastic crisis in patients with chronic anemias such as sickle cell disease, hereditary spherocytosis, and thalassemia intermedia. • Immunocompromised patients who develop chronic parvovirus B19 infection are at risk of chronic red cell aplasia or more generalized bone marrow failure. DIAGNOSIS

POINTS TO REMEMBER • Facial erythema is often absent in infected adults. • Because they are at risk for aplastic crisis, all patients with erythema infectiosum who have chronic anemia should have a complete blood cell count.

• The diagnosis is based on the characteristic clinical presentation. • Although usually unnecessary, serologic testing is the most accurate method of confirming infection. The presence of immunoglobulin M (IgM) antibodies to parvovirus B19 is indicative of recent infection. These antibodies appear approximately 3 days after the onset of the exanthem and begin to decline 1 to 2 months later.

MANAGEMENT • Supportive care is all that is required for uncomplicated cases. • No effective antiviral therapy exists for parvovirus B19.

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Ro seo la In fa n t u m BASICS • Roseola infantum, or exanthem subitum, is an acute viral illness marked by a high fever that characteristically resolves with the onset of the rash (FIG. 8.6). • It is caused by infection with herpesvirus type 6 (HHV-6). • Although the exact route of transmission is not known, it is probably spread through oral or respiratory secretions. • After HHV-6 exposure, there is an incubation period of 7 to 15 days before the onset of symptoms. • As with other herpesvirus infections, it is likely that HHV-6 establishes a latent infection after the acute illness. The isolation of HHV-6 from the saliva of healthy adults supports this view. DESCRIPTION OF LESIONS

8.6 Roseola. (Courtesy of Bernard A. Cohen, M.D.; http://dermatlas.org.)

• The exanthem appears 1 day before to 1 day after defervescence. • It consists of discrete macules or papules, 1 to 5 mm in diameter, often with a surrounding rim of pallor. The color of these lesions has been described as “rose pink.” Frequently, the individual lesions coalesce to form areas of confluent erythema. • The exanthem typically clears within 1 to 2 days, although it may persist for up to 10 days. DISTRIBUTION OF LESIONS • A widespread distribution is seen, with lesions appearing on the trunk, buttocks, neck, and, occasionally, the face and limbs. CLINICAL MANIFESTATIONS • A febrile illness typically precedes the exanthem by 3 to 5 days. Characteristically, this prodrome is marked by a high fever in an otherwise well child. • On occasion, the fever is accompanied by coryza, cough, headache, or abdominal pain. • Occipital, cervical, and postauricular lymphadenopathy is commonly present. • Complications are uncommon and include seizures, encephalitis, and thrombocytopenia.

Chap ter 8 • Viral Exanthem s

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DIAGNOSIS MANAGEMENT • During the prodromal phase of illness, antipyretics are often useful, particularly because they may reduce the risk of febrile seizures.

• The characteristic clinical presentation is usually sufficient for diagnosis. • Although rarely necessary, the diagnosis can be confirmed by laboratory studies demonstrating either the presence of IgM to HHV-6 or a fourfold rise in IgG titers to the virus.

DIFFERENTIAL DIAGNOSIS

POINT TO REMEMBER • Infection with HHV-6 is one of the most common causes of febrile illness in young children.

Ot h e r Fe b rile Viral Exan t h e m s Other conditions such as enterovirus, rubella, and measles must be excluded. Scarle t Fe ve r • This has severe constitutional symptoms and characteristic oral changes. It resolves with acral desquamation (See Chapter 9, “Bacterial Exanthems”). Drug Re act io n • This is typically not preceded by high fever. • The rash is usually of longer duration. (See Chapter 17, “Drug Eruptions”)

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Ru b ella

(Ger m a n Mea sles)

BASICS • Rubella is a mild viral illness that, because of its devastating effects on the developing human fetus, is recognized as a major public health issue. • Maternal infection may lead to fetal death or permanent damage. The consequences are more severe when the infection occurs during the first 8 weeks of gestation. Fetal damage is rare after 5 months of gestation. • Sensory neural hearing loss, cataracts, and cardiac anomalies are the most common defects of congenital rubella. • The rubella virus is an RNA virus of the Togaviridae family. Humans are the only known natural hosts. The initial infection occurs in the nasopharyngeal mucosa. • The incidence of rubella has declined markedly since mass immunization for rubella began in 1969. DESCRIPTION OF LESIONS • The eruption consists of pink to red macules with faint pinpoint papules. • Initially discrete, the lesions may coalesce to form an erythematous rash reminiscent of scarlet fever. • The eruption may be pruritic, particularly in adults. DISTRIBUTION OF LESIONS • The eruption begins on the face and spreads within 24 hours to the trunk and extremities (FIG. 8.7). • The exanthem of rubella is characteristically short-lived, with resolution beginning on the first or second day of the rash. Resolution proceeds in a cephalocaudad direction, and it may be accompanied by fine, branny desquamation. CLINICAL COURSE • A mild prodromal illness is the earliest clinical feature of infection. • A mild fever develops, accompanied by lymphadenopathy. The lymphadenopathy, which most commonly affects the postauricular, suboccipital, and posterior cervical lymph nodes, may be impressive. • In older patients, the prodrome may be longer and more severe. • Constitutional symptoms usually resolve within 24 hours of the onset of the rash. In some cases, however, the lymphadenopathy persists for weeks. • Complications are rare.

8.7

Rubella.

DIAGNOSIS • The clinical features of rubella are not distinctive enough to allow one to make the diagnosis with certainty based on the clinical presentation alone. • Acute and convalescent antibody titers can confirm the diagnosis. Although unnecessary in most cases, these tests are important in pregnant women who may have been exposed to rubella. Chap ter 8 • Viral Exanthem s

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DIFFERENTIAL DIAGNOSIS

Me asle s • Prodromal symptoms are of greater severity. • Koplik’s spots are present. • The rash lasts longer. Ro se o la • A high prodromal fever occurs in the absence of other symptoms. • The morphologic appearance and duration of the exanthem are similar to those of rubella. Mo n o n ucle o sis • Prominent lymphadenopathy, hepatosplenomegaly, and exudative pharyngitis are noted. • Atypical lymphocytes and heterophile antibodies are found in the blood.

Eryt h e m a In fe ct io sum • Patients have a distinctive “slapped cheek” erythema. • A lacy, reticular eruption occurs on the extremities. • The exanthem lasts longer than in rubella. En t e ro virus In fe ct io n • This is distinguished by a prominent enanthem. Scarle t Fe ve r • Severe constitutional symptoms and pharyngitis are noted. • Patients have a “strawberry tongue.” • A “sandpapery” exanthem occurs. • Marked desquamation is associated with resolution (See FIGS. 9.1 A and B). Drug Re act io n • It may be associated with marked pruritus. • The exanthem lasts longer than in rubella.

POINT TO REMEMBER MANAGEMENT • Rubella immunization should be well documented in young women; if antirubella antibiotic titers are negative, rubella immunization should be given.

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• No specific therapy is available. When necessary, supportive care should be provided. Such care includes antipyretics or anti-inflammatory medications for arthralgias. • Infected patients should be isolated from susceptible persons.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ru b eo la BASICS • Measles is a viral illness characterized by a distinctive exanthem and enanthem. The primary site of infection is the respiratory epithelium of the oropharynx. • The measles virus is a single-stranded RNA virus of the Paramyxoviridae family. Humans are the natural host for the virus, although other primates may be infected as well. • Transmission occurs by the respiratory aerosol route. The incubation period lasts from 9 to 11 days. • The incidence of measles in the United States has decreased dramatically since the introduction of the measles vaccine. • Measles has been all but eradicated in the Western Hemisphere. Almost all the cases most recently reported in the United States can be traced to immigrants from nations where measles is more common. • The disease still rages outside the West. It kills more than 800,000 children worldwide each year, more than half of them in central Africa.

(Mea sles)

• A characteristic enanthem known as Koplik’s spots appears 2 days before the onset of the exanthem. The lesions are 1-mm, bluish white macules that develop on a background of erythematous oral mucosa. These lesions are pathognomonic for measles and, because they develop before the rash, they provide an opportunity for early diagnosis. DISTRIBUTION OF LESIONS • The rash most characteristically begins on the forehead or behind the ears. It then spreads to involve the remainder of the face, the trunk, and the arms and legs over 2 to 3 days. It follows a cephalocaudad order in its development, and it later resolves in the same direction. • Koplik’s spots are most prominent on the buccal mucosa opposite the molars, although they may appear on the labial and gingival mucosa as well. CLINICAL MANIFESTATIONS

DESCRIPTION OF LESIONS • The exanthem appears 3 to 5 days after the onset of the prodromal illness. Lesions begin as discrete erythematous macules and papules, which soon coalesce into areas of confluent erythema. Pruritus is usually absent. The rash lasts 4 to 7 days before resolving, often with fine desquamation.

• The illness begins with a 2- to 4-day prodrome of fever; hacking, barklike cough; coryza; conjunctivitis; and photophobia. These patients appear acutely ill, and they often have cervical and preauricular lymphadenopathy on examination. • In most cases, measles is a benign and self-limited infection. Recovery is usually complete within 14 days of the onset of the prodrome.

Chap ter 8 • Viral Exanthem s

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DIFFERENTIAL DIAGNOSIS • • • • • •

Atypical measles Rubella Erythema infectiosum Scarlet fever Roseola Drug hypersensitivity reaction

Co m p licat io n s • Pneumonia is the most common complication. In children, this most frequently takes the form of primary measles pneumonitis, whereas in adults, secondary bacterial pneumonias are more common. Measles pneumonia is particularly severe in immunosuppressed patients. • Encephalitis occurs in 1 to 2 patients per 1,000 cases of measles. • Patients vaccinated with the killed virus vaccine, which was in use from 1963 to 1967, are at risk of developing atypical measles. After a 2- to 3-day prodrome of fever, dry cough, headache, and abdominal pain, a macular and papular exanthem appears. In contrast to classic measles, this eruption begins on the palms and soles and then spreads proximally. Pneumonia is often present in these patients as well. DIAGNOSIS • The diagnosis of measles is usually made on clinical grounds. • Although usually unnecessary, serologic testing is available. A fourfold or greater rise in antibody titers between acute and convalescent sera confirms the diagnosis.

MANAGEMENT • No specific therapy for measles virus infection exists. Supportive care should be provided, and patients should be isolated from susceptible persons. • Passive immunization should be given to pregnant women, infants younger than 1 year, and immunocom-

promised patients who lack antibodies to the measles virus. Immunoglobulin preparations containing a high antimeasles titer should be administered within 6 days of exposure. • Routine immunization is recommended for all children 15 months of age or older.

POINTS TO REMEMBER • A patient with measles becomes contagious 3 days before onset of the rash and remains so until desquamation of the rash. • All cases should be reported to local public health officials.

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C H AP T ER

9

Bacterial Exanthem s Kenneth Howe and Herbert P. Goodheart

OVERVIEW The term exanthem refers to a widespread, symmetric, erythematous rash that begins with macules and papules that remain discrete or become confluent. The eruption may or may not be pruritic and is usually accompanied by systemic symptoms such as fever, malaise, and headache. In pediatric populations exanthems are usually caused by infectious agents such as viruses and bacteria; infrequently, they may be due to a drug reaction. Bacterial exanthems represent either a reaction to a bacterial toxin, direct injury to the skin by the organism itself, or an immune response. Many common childhood bacterial exanthems have characteristic features, distributions, durations, and systemic symptoms. As with viral exanthems (see Chapter 8, “Viral Exanthems”), when there are no typical lesions or distinctive prodromal signs or symptoms, a specific diagnosis is often difficult, if not impossible, to make. However, a definitive diagnosis may be critical, particularly if a pregnant woman or an immunocompromised patient has been exposed to an infected individual. Furthermore, some of these conditions can become life threatening if not treated promptly with appropriate medications, e.g., Kawasaki’s disease.

SCARLET FEVER TOXIN-MEDIATED STREPTOCOCCAL AND STAPHYLOCOCCAL DISEASE KAWASAKI’S SYNDROME

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Sca rlet Fever BASICS • Scarlet fever (SF) is a streptococcal infection of the pharynx associated with widespread mucocutaneous changes that are caused by an erythrogenic exotoxin-producing strain of group A beta-hemolytic streptococci. Less commonly, SF may follow streptococcal wound infections or burns, as well as upper respiratory tract infections. • In the past, SF was a major public health threat. However, its morbidity, mortality, and incidence have declined markedly, both because of the development of antibiotics and because of a reduction in the virulence of the streptococci causing the condition. • The cutaneous manifestations of SF represent a delayed hypersensitivity response to streptococcal products. Thus, prior exposure to streptococci is a necessary precondition for SF.

Et io lo g y • Usually, group A beta-hemolytic Streptococcus pyogenes is the pathogenic organism. Uncommonly, exotoxin-producing Staphylococcus aureus may be responsible. DESCRIPTION OF LESIONS • A finely papular erythematous rash appears on the trunk and extremities. This rash may be referred to as “sandpapery” or “scarlatiniform.” • The skin around the mouth may show a characteristic pallor (circumoral pallor). Linear streaks of petechiae called Pastia’s lines may develop in flexural areas such as the antecubital fossae, the axillae, and the inguinal region. • Mucosal findings include erythema and edema of the pharyngotonsillar area, punctate erythematous macules and petechiae on the palate, and “strawberry tongue.” The last is a characteristic finding and is caused by prominence of the papillae on the surface of the tongue. • During the convalescent phase of the illness, the skin of the palms and soles frequently desquamates. This desquamation may be sheetlike, and the original infection may have passed unnoticed. In such instances, the patient may seek medical attention solely for the desquamation (FIGS. 9.1 A and B).

A

DISTRIBUTION OF LESIONS • The scarlatiniform eruption is widespread and symmetric, primarily affecting the trunk and extremities. CLINICAL MANIFESTATIONS B

9.1 A an d B Scarlet fever. Skin peeling from this patient’s palms and soles during the convalescent phase of his illness. This exuberant desquamation occurred two weeks after he had fever and a truncal exanthem that began as a streptoccocal throat infection. 208

• SF typically begins with the abrupt onset of fever, sore throat, headache, and chills. • Complications are uncommon but may include pneumonia, pericarditis, meningitis, hepatitis, glomerulonephritis, and rheumatic fever. Erythema nodosum and acute guttate psoriasis may also follow or accompany an infection with group

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

A beta-hemolytic streptococci (see Chapter 25, “Cutaneous Manifestations of Systemic Disease,” and Chapter 3, “Psoriasis”). • SF can recur, with reported recurrence rates as high as 18%. DIAGNOSIS • The diagnosis of SF is often made on clinical grounds. • The isolation of group A streptococci from the pharynx, or the presence of serologic tests such as an elevation of antistreptolysin-O titers, can help confirm the diagnosis.

MANAGEMENT • First-line treatment is with penicillin. Alternatives include erythromycin, cephalosporins, ofloxacin, rifampin, and newer macrolide antibiotics. • Emollients can be used to soothe the scarlatiniform eruption.

DIFFERENTIAL DIAGNOSIS • Streptococcal or staphylococcal toxic shock syndromes are distinguished by hypotension and multiorgan system involvement. • Kawasaki’s syndrome (see discussion later in this chapter) is characterized by prominent lymphadenopathy. • Febrile drug reactions cause a blotchy, erythematous rash. Pastia’s lines and strawberry tongue are not present. • Viral exanthem is a possible diagnosis. • Flaccid bullae are the predominant feature of staphylococcal scalded-skin syndrome, which occurs in newborns and in infants younger than 2 years (see Chapter 27, “Special Considerations in Pediatric and Elderly Skin.”)

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To x in -Med ia t ed St rep t o co cca l a n d St a p h ylo co cca l Disea se BASICS Some streptococcal and staphylococcal species are capable of producing circulating toxins. Patients infected with these toxinproducing bacteria exhibit clinical manifestations distant from the site of local infection. Several distinct syndromes related to these toxins have been recognized, including toxic shock syndrome (TSS) and, rarely, streptococcal toxic shock syndrome (STSS). The principal features of STSS are the same as those of classic TSS: a local infection leads to various clinical manifestations in distant organ systems, resulting from the action of a toxin produced by the infecting bacteria. In most cases of STSS, group A streptococci are isolated from the local infection. The responsible toxins act as superantigens, bypassing the normal sequence of immune system activation, to stimulate an immune response in a general, nonspecific manner. This nonspecific immunologic activation leads to damage in various organ systems. Certain physical signs—such as strawberry tongue, acral erythema with subsequent desquamation, and an erythematous eruption with perineal accentuation—are shared in common by several of the toxin mediated syndromes.

Toxic Sh ock Syn d rom e BASICS • TSS is a systemic illness caused by infection with toxinproducing strains of S. aureus. Originally described in association with tampon use, TSS now occurs more commonly with a local wound infection, particularly in the postoperative setting.

function test results, leukocytosis and thrombocytopenia, and increased serum creatine kinase levels. • In nonmenstrual TSS, the classic signs of erythema, tenderness, and purulence may be absent in the local infection, thereby making its identification difficult. DIAGNOSIS • Diagnosis is made when the characteristic clinical findings of fever, rash, and hypotension are present in patients who have an infection with S. aureus or in menstruating women who use tampons. • Diagnosis also is made when laboratory tests such as Gram’s stain and cultures of vaginal exudate or wounds are positive for S. aureus or, rarely, group A streptococci.

DIFFERENTIAL DIAGNOSIS • Hypotension does not occur in scarlet fever. • A febrile drug reaction is not associated with hypotension. • Kawasaki’s syndrome (see following section) usually occurs in children and causes prominent lymphadenopathy. • Staphylococcal scalded-skin syndrome occurs in newborns and in infants younger than 2 years.

MANAGEMENT DESCRIPTION OF LESIONS • A diffuse macular erythema is often present, which may be scarlatiniform (i.e., “sandpapery” to the touch) and may show accentuation in the flexures. • Erythema and edema of the palms and soles are often seen. • Desquamation of the palms and soles, as seen in many bacterial toxin-mediated disorders, occurs 1 to 2 weeks after the onset of illness (see FIGS. 9.1 A and B). • Hyperemia of the conjunctiva and mucous membranes and “strawberry tongue” are often present (see FIG. 9.3).

• Treatment of TSS includes the administration of penicillinase-resistant antibiotics and drainage of any abscesses. • Supportive care may include hydration and vasopressors for hypotension. • Management of STSS is similar to that of classic TSS. • Intravenous gamma globulin has been reported to be effective in treating STSS, but it is not yet in widespread use.

DISTRIBUTION OF LESIONS • The erythematous eruption is diffuse, with accentuation in flexures such as the antecubital folds. • The mucous membranes, palms, and soles are also sites of characteristic changes. CLINICAL MANIFESTATIONS • Patients with TSS have a high fever. • Multiorgan involvement is a hallmark of this condition. Systemic manifestations may include hypotension, elevated blood urea nitrogen and creatinine levels, abnormal liver 210

HELPFUL HINTS • Look for a cutaneous site of infection or for a forgotten or retained vaginal tampon. • STSS may be clinically identical to TSS, but it is usually distinguished by a more marked soft tissue infection at the site of origin, with localized pain in an extremity the most frequent initial complaint. • Blood cultures are positive in more than 50% of patients with STSS. • Antibiotic coverage for both staphylococci and penicillin-resistant streptococci should be given.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ka w a sa k i’s Syn d ro m e BASICS • Kawasaki’s syndrome (KS), also known as mucocutaneous lymph node syndrome, is an acute, febrile, multisystem illness that primarily affects young children. Its most serious complications are the result of systemic vasculopathy. • In fact, KS is best regarded as a generalized vasculitis that involves small to medium-sized arteries. The extent of the coronary vascular involvement is so significant that KS has now surpassed rheumatic fever as the leading cause of acquired heart disease in children from developed nations. • The peak incidence of KS is between 1 and 2 years of age. It is more common in boys. • In the United States, children of Asian ancestry are affected six times more often than are white children. • KS occurs sporadically and in epidemics. A seasonal predilection has been observed, with cases occurring more often in the winter and spring. • Although the exact cause of KS is unknown, it is most likely the result of a superantigen produced by an infectious agent such as S. aureus, resulting in massive cytokine release.

• The presence of scarlatiniform erythema in the perianal or inguinal area (FIG. 9.2) may be a useful diagnostic sign. The rash in this area progresses to desquamation before the palms and soles begin to peel. • Characteristic findings are present in the mouth, on the lips, and on the tongue. The earliest manifestations are seen on the lips, with bright red erythema accompanied by fissuring and swelling. Prominent papillae create the appearance of a “strawberry tongue” (FIG. 9.3). Examination of the oropharynx reveals a diffuse erythema without vesicles, erosions, or ulcers.

DESCRIPTION OF LESIONS • The truncal rash of KS is polymorphous and can be macular, papular, urticarial, erythrodermatous, targetoid, or composed of fine micropustules, but it is never vesicular or bullous. The eruption is usually pruritic. • Changes of the hands and feet are distinctive. An intense erythema appears on the palms and soles on days 3 to 5 of the illness, followed by an indurated edema. A sharp demarcation may be seen at the wrists and the sides of the hands and feet. As noted in SF, during the convalescent phase of the illness, the skin of the fingertips and toes peels off in sheets (FIG. 9.4). 9.3

9.2 Kawasaki’s syndrome. Desquamation in the genital area. This sheetlike desquamation occurred 2 weeks after the original infection.

Kawasaki’s syndrome. “Strawberry tongue.”

9.4 Scarlet fever. Skin peeling from fingertips. This desquamation occurred during the convalescent phase of the illness. It can be a useful diagnostic sign. Chapter 9 • Bacterial Exanthem s

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• Eye involvement (FIG. 9.5) consists of bilateral, nonpurulent conjunctival injection. Patients may exhibit signs of photophobia. DISTRIBUTION OF LESIONS • The polymorphic eruption favors the trunk and proximal extremities, but it may be generalized. CLINICAL MANIFESTATIONS

9.5

Kawasaki’s syndrome. Ocular involvement.

• Fever usually marks the onset of KS. Elevated temperature shows a remittent pattern, with spikes to 103°F and even up to 105°F. The average duration of the fever is 11 days. • Seen in 75% of patients, cervical lymphadenopathy is the least common diagnostic feature of KS. It usually manifests as a single, enlarged, nonsuppurative lymph node on the side of the neck. • Cardiac involvement is the most worrisome complication of KS. During the acute phase of the illness, tachycardia may develop, with gallop rhythm, subtle electrocardiographic changes, pericardial effusion, tricuspid insufficiency, or mitral regurgitation. Coronary artery aneurisms have been reported to occur in approximately 25% of untreated patients and may result in thrombosis with subsequent infarction. DIAGNOSIS The diagnosis of KS is based on recognition of its clinical features and is supported by compatible laboratory findings; however, laboratory findings are nonspecific. None of the following diagnostic guidelines are in themselves diagnostic, but their presence may be helpful: • • • • • •

Fever persisting 5 days or more Polymorphous rash Bilateral conjunctival injection Oral mucous membrane changes Cervical lymphadenopathy Changes of peripheral extremities: erythema of palms and soles, indurative edema of the hands and feet, desquamation of the fingertips

Lab o rat o ry Fin d in g s • During the acute phase of the illness, leukocytosis with a predominance of immature and mature granulocytes is common, with 50% of patients having a white blood cell count 15,000/mL. • Nonspecific abnormalities of acute phase reactants, such as the erythrocyte sedimentation rate and C-reactive protein levels are usually present.

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DIFFERENTIAL DIAGNOSIS • • • • • •

Staphylococcal TSS or STSS (see earlier section) SF (see earlier section) Rubella and rubeola Febrile viral exanthems Mononucleosis Hypersensitivity reactions (including Stevens-Johnson syndrome) • Drug eruptions with accompanying fever • Infantile polyarteritis nodosum

MANAGEMENT • Most children with KS must be hospitalized for a complete workup and supportive care. Because high temperatures and irritability make feeding difficult, intravenous fluids are often needed for hydration. • The initial goals of therapy are to reduce the fever and the inflammation of the myocardium and to prevent subsequent cardiac sequelae. • Children with evidence of cardiac disease may require intensive support. • Once the diagnosis of KS has been established, therapy with intravenous immune globulin (IVIG), or gamma globulin, and aspirin should be started. • The current recommended therapy for KS in the acute phase includes a single infusion of intravenously administered IVIG and aspirin.

POINTS TO REMEMBER • All patients with KS should have an echocardiogram during the acute illness and 3 to 6 weeks after the onset of fever. • Prompt treatment with aspirin and IVIG significantly decreases the risk of cardiac complications. • Although most patients recover with little to no limitations on physical activity, a delay in diagnosis results in a greater likelihood of coronary lesions and related complications.

• High-dose aspirin at a dose of 80 to 100 mg/kg/day PO in four equally divided doses is continued during the acute phase for its anti-inflammatory effects. It is continued at this dose until day 14 of the illness or until the patient has been afebrile for 48 to 72 hours. • IVIG has a synergistic effect with aspirin and reduces acute inflammation, with the maximal benefits seen when it is given within the first 10 days of the illness. IVIG has been shown to reduce the rate of coronary aneurysms from greater than 25% in untreated patients to 1% to 5% in treated patients. IVIG may decrease autoantibody production and increase solubilization and removal of immune complexes.

HELPFUL HINTS • KS should be considered in children with an unexplained fever lasting more than 5 days who have a polymorphous rash that may look like SF or measles and conjunctivitis without pus. • Some children may present with an incomplete clinical picture and may not exhibit sufficient clinical signs to fulfill the diagnostic criteria; therefore, a high level of suspicion is required to recognize these patients.

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C H AP T ER

10

Hair and Scalp Disorders Resulting in Hair Loss Herbert P. Goodheart and Hendrik Uyttendaele

OVERVIEW ANDROGENIC ALOPECIA ALOPECIA AREATA DIFFUSE ALOPECIA • Telogen effluvium • Anagen effluvium • Senescent alopecia SCARRING ALOPECIA • • • • • •

Chronic cutaneous lupus erythem atosus Lichen planopilaris Central centrifugal cicatricial alopecia Traction alopecia Sarcoidosis Folliculitis decalvans

Hair has great social and cultural significance in all human societies. It is found on most areas of the human body, except on the palms of the hands, the soles of the feet, and mucous membranes. TYPES OF HAIR • Lanugo, the fine hair that covers nearly the entire body of fetuses. • Vellus, the short, fine, “peach fuzz” body hair that grows in most places on the body. Vellus hairs are soft and short. It is seen in areas of male pattern baldness. • Terminal, the fully developed hair, which is generally longer, coarser, thicker, and darker than vellus hair and does not appear until puberty.

PSEUDOFOLLICULITIS BARBAE AND ACNE KELOIDALIS

HAIR TEXTURE AND SHAPE Hair texture and shape is genetically determined to be straight, curly or wavy, and it can change over time. It can also be affected by hair styling practices such as chemical straighteners, braiding, or curlers. Whether hair is curly or straight is determined by the shape of the follicle itself and the direction in which each strand grows out of its follicle. For example, curly hair is shaped like an elongated oval and grows at a sharp angle to the scalp (see ILL. 10.1). CYCLES OF HAIR GROWTH Hair grows in long cycles over many months: a growth (anagen) phase (see ILL. 11.1) is followed by degenerative (catagen) phase, then a resting (telogen) phase, with different hairs alternating phases.

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An d ro gen ic Alo p ecia HAIR LOSS Some degree of scalp hair loss or thinning generally accompanies aging in both sexes, and it’s estimated that half of all men are affected by male pattern baldness by the time they are 50 years of age. Drugs used in cancer chemotherapy frequently cause a temporary loss of hair, because they affect all rapidly dividing cells, not just the malignant ones. Certain diseases and traumas can cause temporary or permanent loss of hair (e.g., systemic lupus erythematosus, thyroid disease). BASICS Androgenic alopecia (AGA), also known as common baldness (male- or female-pattern baldness), is an extremely common, noninflammatory type of alopecia whose incidence increases greatly with advancing age. AGA is not a disease but a normal consequence of aging. In most, if not all, cultures, hair plays a powerful role in a person’s psychosexual identity and selfimage. It is not surprising that in our youth- and image-driven society, hair replacement and retention methods have taken on almost the status of a subspecialty in health care. • AGA is seen more frequently in men than it is in women because women’s hair loss tends to be less apparent, is less extensive, and generally begins at a later age than it does in men. • The condition is genetically determined (autosomal dominant with variable penetrance). The incidence and severity of AGA tend to be highest in white men, followed by white women; it is second highest in Asians and AfricanAmericans and lowest in Native Americans and Eskimos.

Pat h o g e n e sis • AGA is caused by an androgenic action on hair follicles that shortens the anagen (growth) phase of the hair cycle, thus producing thinner, shorter hairs in a process known as miniaturization. • It occurs through the gradual conversion of terminal hairs into indeterminate hairs and finally to short, wispy, nonpigmented vellus hairs. • In men, this type of alopecia usually begins in late adolescence, with hair loss often starting at the parietal hairline. • In women, the onset is more gradual and the loss of hair is more subtle, and it tends to become obvious later (most often after menopause, but occasionally in the third or fourth decade). This produces a thinning of the hair rather than areas of marked baldness. It is thought that estrogen protects against androgen-mediated miniaturization, which explains both the reduction in severity and the increase in incidence after menopause.

10.1 Male-pattern alopecia. This is characterized by an M-shaped pattern of hair loss on the front and vertex of the head.

10.2 Female-pattern alopecia. A midparietal pattern of decreasing hair loss is noted here. The integrity of the frontal hairline is maintained.

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CLINICAL MANIFESTATIONS • AGA usually produces a patterned type of hair loss. In men and women, hair loss is mostly restricted to the vertex and frontal scalp; hair density on the occipital scalp remains unaffected. • In men, this type of alopecia usually begins in late adolescence, with hair loss often starting at the parietal hairline (FIG. 10.1). • In women, the loss of hair is more subtle, and it tends to begin later in life (FIG. 10.2). DESCRIPTION AND DISTRIBUTION OF LESIONS

10.3 Female-pattern alopecia. The characteristic “widened part” in a “Christmas-tree” pattern toward the vertex is seen in this patient.

DIFFERENTIAL DIAGNOSIS • It should be kept in mind that the following conditions are not only independent causes of hair loss but may coexist and exacerbate AGA; they are discussed later in this chapter. • Telogen effluvium (shedding of resting hairs) • Anagen effluvium (shedding of growing hairs) • Hair loss from thyroid disease • Hair loss caused by iron-deficiency anemia and insufficient calories, protein, or vitamins • Hair loss caused by androgen excess in women • Blood tests and other laboratory studies are necessary only when the diagnosis is in doubt, or other coexisting reasons to explain alopecia are warranted by the history or physical examination (see later section, “Diffuse Alopecia”).

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• Androgenic alopecia produces two typical patterns of hair loss. • In men, the process usually begins in an M-shaped pattern on the front and vertex of the head (this is often referred to as male-pattern baldness). • In women, a thinning of the crown in a “Christmas-tree,” midparietal pattern (female-pattern baldness) is usually noted initially (FIG. 10.3). • Hair loss may progress in both sexes but is often more extensive in men. Thus, in the end stages of androgenic alopecia, many men have only a fringe of remaining hair, whereas women tend to maintain the frontal hairline and do not become frankly bald (see earlier section on “Pathogenesis”). DIAGNOSIS • The diagnosis of AGA is generally based on the clinical pattern of baldness coupled with an absence of clues pointing to a specific disease that may cause hair loss.

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MANAGEMENT

Wo m e n • Minoxidil (2% solution, applied twice daily) may reduce shedding and may possibly contribute to some regrowth. (The 5% solution of minoxidil may be more effective, but it has not yet been approved for use in women.) The mechanism of action is unknown; however, minoxidil appears to lengthen the duration of the anagen phase, and it may increase the blood supply to the hair follicle. Regrowth is more pronounced at the vertex than in the frontal areas and may not be noted for at least 4 months. Continuing topical treatment with the drug is necessary indefinitely because discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern. The incidence of facial hair growth appears to be increased with the use of the higher-concentration formulation. Patients who respond best to this drug are those who have a recent onset of AGA and small areas of hair loss. In general, women respond better to topical minoxidil than men. • Women with excess androgen may benefit from systemic antiandrogen therapy with agents such as spironolactone, flutamide, or oral contraceptives that decrease

ovarian and adrenal androgen production, especially agents that contain a nonandrogenic progestin.

Me n • Minoxidil 5% solution and foam (Rogaine), applied twice daily, may reduce shedding and may possibly contribute to some regrowth. • Finasteride (Propecia), 1 mg/day, is an antiandrogen that acts by inhibiting type II 5-alpha reductase, the enzyme that converts testosterone to dihydrotestosterone. • In much higher doses, finasteride is used as a treatment for benign prostatic hyperplasia and prostate cancer. • Recognized side effects include erectile dysfunction and, less often, gynecomastia. It is teratogenic and has not been approved by the U.S. Food and Drug Administration for the treatment of AGA in women. Me n an d Wo m e n • Hair transplantation is performed by harvesting hairs from donor sites such as the occipital scalp. Hair transplantation, which uses a micrografting technique in which a small incision is used to insert one or more donor hairs, is particularly effective in women, because unlike men, women rarely become completely bald.

POINTS TO REMEMBER • A patient’s anxiety regarding hair loss should be taken seriously by his or her health care provider. Hair loss should not simply be “brushed off” as an insignificant cosmetic complaint. The time spent listening to the patient may be helpful in uncovering other emotional or physical problems. • Evaluation of a female patient with AGA may include a complete blood count and testing of thyroid-stimulating hormone and serum iron levels.

• Women with symptoms or signs of virilization should undergo a careful history and evaluation for an androgenexcess syndrome. These patients require hormonal studies and may need referral to an endocrinologist. • AGA is very common; therefore, it may coexist with other forms of hair loss. Consequently, a search for treatable causes of telogen effluvium (e.g., anemia, hypothyroidism), especially in patients with an abrupt onset or a rapid progression of their disease, is indicated.

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Alo p ecia Area t a BASICS • A common, noninflammatory, idiopathic disorder, alopecia areata (AA) is characterized by well-circumscribed round or oval areas of nonscarring hair loss. Alopecia totalis is a loss of all or almost all scalp hair and eyebrows. Alopecia universalis refers to a total loss of body hair. • AA most commonly affects young adults and children. Occasionally, a family history of AA exists; often, onset is attributed to recent stress or a major life crisis.

10.4 Alopecia areata. The hair is lost in a round patch. Note the absence of scales or inflammation.

Pat h o g e n e sis The origin of AA is generally considered autoimmune, because biopsy findings demonstrate T-cell infiltrates surrounding the hair follicles and because AA is sometimes associated with other putative autoimmune disorders, such as the following: • Vitiligo • Thyroid disease (Hashimoto’s disease) • Pernicious anemia DESCRIPTION OF LESIONS • AA most commonly presents as oval, round, or geometric patches of alopecia (FIG. 10.4). • On occasion, a hand lens may reveal tiny “exclamation mark” hairs at the periphery of lesions. • Increased friction (not the expected smoothness) is felt on palpation of lesional skin because of the loss of vellus hairs (FIG. 10.5).

10.5 Alopecia areata. Increased friction is noted on palpation of lesional skin as a result of the loss of vellus hairs.

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DISTRIBUTION OF LESIONS • Lesions are most often found on the scalp, eyebrows, eyelashes, and areas of the face that bear hair, such as the beard (FIG. 10.6) or mustache on men. • The entire scalp (alopecia totalis) may rarely be involved, or even the entire body (alopecia universalis), including pubic, axillary, and nasal hair (FIG. 10.7). • Infrequently, nails may demonstrate a characteristic pitting (“railroad tracks”). CLINICAL MANIFESTATIONS • There is usually asymptomatic shedding of hair, which is often discovered by the patient’s hairdresser or a family member. • Frequently, hair spontaneously regrows; however, a recurrence of hair loss may be seen in 30% of patients who had experienced regrowth. Regrowing hair is initially thin and sometimes white (vitiliginous) (FIG. 10.8). • A poorer prognosis is associated with extensive alopecia, an atopic history, and chronicity. Also, when bands of alopecia occur along the hairline margins (ophiasis), (FIG. 10.9) that partially or completely encircle the head, a poorer prognosis is also probable. • Both alopecia universalis and alopecia totalis are generally refractory to therapy and usually last a lifetime; spontaneous regrowth is rare.

10.6 Alopecia areata. This man’s AA is limited to his beard.

DIAGNOSIS • The diagnosis of AA is generally based on its clinical appearance; however, a scalp biopsy may be performed if the diagnosis is in doubt. • A potassium hydroxide (KOH) test and fungal culture to rule out tinea capitis is negative.

10.9 Alopecia areata, ophiasis pattern. A band of alopecia occurs along the hairline margins encircling the head.

10.7 Alopecia areata, alopecia universalis. This patient has lost all of his hair. He has no eyelashes, intranasal hair, pubic hair, or axillary hair; he also has no hair on his extremities.

10.8 Alopecia areata, regrowing hair. In this patient with AA, clusters of hair regrew after intralesional triamcinolone acetonide injections. Some of the regrown hairs are white (vitiliginous). Chap ter 10 • Hair and Scalp Disorders Resulting in Hair Loss

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DIFFERENTIAL DIAGNOSIS

Tin e a Cap it is See Chapter 7, “Superficial Fungal Infections.” • This is seen most frequently in African-American children and uncommonly in African-American adults. • The scalp is often scaly, itchy, and inflamed. • The diagnosis is confirmed when the KOH examination is positive for hyphae or when a fungus grows on Sabouraud medium.

Seco n d a r y Syp h ilis

Secondary syphilis should always be considered in cases of unexplained patchy hair loss (see FIG. 19.19). • The hair loss is referred to as “moth-eaten” in appearance. • Serologic tests for syphilis are generally reactive.

Te lo g e n Effluvium See also later section. • The hair loss is diffuse. • There is often a history of antecedent illness or childbirth, for example.

Tract io n Alo p e cia an d Ho t -Co m b Alo p e cia See later discussion. Ot h e r Diag n o se s Trich o t illo m a n ia

Trichotillomania is also known as compulsive hair pulling (FIG. 10.10).

10.10 Trichotillomania. This condition is seen most often in young girls. Hairs tend to be broken at different lengths. The areas of alopecia are not completely devoid of hair.

• This is seen most often in young girls. • Hairs tend to be broken at different lengths. • There is an asymmetric loss of scalp hair.

MANAGEMENT • Because mild cases of AA often show spontaneous regrowth, therapy is often unnecessary. • The daily application of superpotent topical steroids, such as clobetasol cream 0.05%, may speed hair regrowth. To increase drug penetration, potent topical steroids, such as fluocinonide cream 0.05%, may be applied, occluded with a plastic shower cap, and left on overnight. • If necessary, intralesional steroid injections into the alopecic patches with triamcinolone acetonide may be administered every 6 to 8 weeks.

few are very effective. The success rates associated with the following measures have ranged from no response to varying degrees of partial success: • Irritant therapy involves using a topical anthralin (a coal tar derivative) preparation. • Topical minoxidil in a 2% or 5% concentration, scalp massage, heat, aloe vera, vitamins, hypnotherapy, oral psoralens combined with exposure to ultraviolet light in the A range (PUVA), topical cyclosporine, and immunotherapy by induction of contact dermatitis with chemical compounds have all been tried. • The most important part of widespread AA management is providing emotional support to the patient.

Furt h e r Tre at m e n t Mo d alit ie s The numerous treatment modalities for severe extensive AA that have been tried over the years reflect the fact that

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POINTS TO REMEMBER • Alopecia totalis and universalis, the most severe forms of AA, generally spark great emotional problems in patients and their families. • Consider workup for other diseases (e.g., thyroid disease) that may be suggested by the history or examination.

HELPFUL HINT • The National Alopecia Areata Foundation is an excellent resource for information and can direct patients to AA support groups and information about wigs, for example. It can be reached at: National Alopecia Areata Foundation, 14 Mitchell Boulevard, San Rafael, CA 94903; phone number: 415.472.3780; Web site: http://www.naaf.org/default2.asp.

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Diffu se Alo p ecia BASICS POINTS TO REMEMBER • The evaluation of diffuse hair loss in women—and in men—should be a careful, thoughtful, and sympathetic process. • Excessive hair loss should not be dismissed as simply a cosmetic issue. • History taking should include questions about the patient’s physical and mental health status, antecedent illnesses, medications, traumatic events (e.g., loss of a loved one), hairstyling techniques, and family history. • In addition, masculinizing signs or symptoms should be noted.

• Diffuse alopecia is defined as a uniform, generally nonscarring reduction in hair density over all portions of the scalp. In contrast, a patterned alopecia such as AGA or alopecia caused by androgen excess has a characteristic presentation of hair loss in specific locations that typically spares the temples and occipital regions. • A large majority of patients who complain about diffuse hair loss are women. • Unfortunately, the explanation for such hair loss frequently presents a confusing and frustrating challenge for primary care providers as well as for dermatologists. The diagnosis of the manifestations of telogen and anagen effluvium (described later) is made on the basis of history. In many cases, the hair loss may not be apparent to the examiner and at times the cause may be difficult, if not impossible, to determine.

Telogen Efflu viu m • This disorder refers to the shedding of hairs from telogen follicles. • Hair follicles show intermittent activity that cycles between a growing anagen phase (lasting approximately 3 years) and a resting telogen phase (lasting about 3 months). • Each hair grows to a maximum length and is retained for a period without further growth (telogen). It then goes through a catagen phase, is shed, and is replaced by a growing anagen hair (see ILL. 11.1). • At the end of the telogen phase, the hair is lost, and a new hair starts growing within the follicle in a new anagen phase. • The normal scalp contains approximately a 100,000 hairs, and about 10% to 15% of follicles are in the telogen phase. Hence, it is normal to shed about 100 hairs per day. • A telogen effluvium occurs when a large number of hairs (greater than 15%) enter the telogen phase at one time, which results in a sudden and increased number of shedding hairs. • The precipitating event usually precedes hair loss by 6 to 16 weeks, which is the time required for a catagen hair to become a telogen hair. The marked loss of hair can manifest as a blockage of a bathtub drain, or it may be more subtle and chronic.

10.11 Telogen effluvium, acute. This patient presented with a plastic bag full of hair that had been shed over the course of 1 month.

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Acut e Te lo g e n Effluvium • The acute type lasts for 3 to 6 months. • The hair shedding is typically sudden, rather than a gradual thinning. The patient may state that the shedding hair may be seen on pillows, on combs and brushes, and in the bathtub, and she or he may bring in a plastic bag full of hair as proof of the dramatic alopecia (FIG. 10.11).

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• The possible causes of acute telogen effluvium include medications, major illness, fever, physical trauma, surgery, general anesthesia, significant weight loss such as that caused by “crash” dieting, or severe emotional stress. The patient may describe a recent history of such an event that typically occurred 3 to 4 months before the onset of alopecia. • The medications that are most often implicated in acute telogen effluvium are anticoagulants, beta-blockers, cholesterol-lowering medications, antidepressants, angiotensinconverting enzyme inhibitors, propylthiouracil (which induces hypothyroidism), carbamazepine, oral retinoids, and immunizations. • When an acute telogen effluvium occurs in women in their childbearing years, it may be associated with giving birth (postpartum effluvium and post-breastfeeding effluvium), aborted pregnancy, or the discontinuation of oral contraceptives.

Ch ro n ic Te lo g e n Effluvium • The chronic type lasts for more than 6 months. • This type may be caused by the persistent presence of a trigger (such as medications) or by a rapid succession of several acute telogen effluviums. Chronic telogen effluvium may also have metabolic causes, such as iron or zinc deficiency, or result from low-protein diets, thyroid disease, or chronic systemic illnesses such as systemic lupus erythematosus or syphilis. • The patient may complain of both increased shedding, albeit less severe than in acute telogen effluvium, and hair thinning is manifested by a more visible scalp. DESCRIPTION OF LESIONS AND CLINICAL MANIFESTATIONS

DIAGNOSIS • The diagnosis is more often based on history, because the diffuse loss of telogen effluvium is more often barely perceptible to the clinician. • There is a loss of 400 or more hairs per day (normal shedding is 40 to 100 hairs a day). A gentle hair pull (of approximately 20 hairs) often yields more than four hairs per pull. The lost hairs are telogen hairs that can be identified by having a small white “bulb” at their proximal ends. • A scalp biopsy reveals an increased telogen-to-anagen ratio (above 15%).

Lab o rat o ry Te st s When the cause of telogen effluvium is not apparent, the following laboratory tests should be assessed when warranted by the history or physical examination: • Baseline chemistries and liver function tests may detect a systemic cause of hair shedding. • A complete blood count, sexually transmitted disease testing, and antinuclear antibody tests should be performed. • Thyroid-stimulating hormone level should be determined. • Serum ferritin and erythrocyte sedimentation rate (ESR) levels should be tested, because both ESR and ferritin determinations can be elevated as acute-phase reactants. A ferritin value greater than 50 g/L is optimal. • Serum dehydroepiandrosterone-sulfate (DHEA-S), free testosterone, prolactin, and morning cortisol levels should be obtained if virilization is evident. • When diffuse AA is suspected, or an inflammatory or scarring alopecia is present, a scalp biopsy may be necessary to make the diagnosis.

• This diffuse (nonpatterned) hair shedding involves the entire scalp and is usually not obvious to the clinician. Scarring and inflammation of the scalp are not seen. • Occasionally, patients state that the scalp hair simply feels less dense, that more of the scalp seems to be visible, and that the hair has changed in texture. This is often seen in chronic telogen effluvium. Complete alopecia is not seen. • If the precipitating event is removed, it usually takes about 1 year to completely return to the pre-effluvium hair volume, but hair may not grow back completely.

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DIFFERENTIAL DIAGNOSIS

MANAGEMENT • The patient should be reassured that, most often, hair tends to grow back normally. • The management of telogen effluvium often involves treating or eliminating the underlying cause. Once the trigger is removed, it may be sufficient simply to wait for the hair to grow back. • Consultation with a dietitian may sometimes be necessary to ensure adequate caloric, vitamin, iron, zinc, and protein intake. • Iron supplementation and correction may reverse the chronic telogen effluvium caused by this deficiency. • However, correction of thyroid function unfortunately does not always result in a reversal of the effluvium.

An d ro g e n ic Alo p e cia See earlier discussion of AGA. • This has a patterned distribution.

An ag e n Effluvium Se co n d ary t o Drug s See discussion later in this chapter. • It is more diffuse and more rapid than telogen effluvium. • Cancer chemotherapy and immunotherapy drugs are causes.

POINTS TO REMEMBER • A careful history should be taken to look for antecedent illness, recent childbirth, ingestion of drugs, or trauma 3 to 4 months before the onset of rapid alopecia. • In women with AGA, there is usually a positive family history of patterned alopecia. However, because AGA is quite prevalent, it should also be kept in mind that a diffuse alopecia may coexist with AGA.

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An agen Efflu viu m BASICS • In comparison with telogen effluvium, anagen effluvium produces a more extensive and a more rapid and dramatic hair loss. • At any given time, 80% to 90% of hair follicles on the scalp are in the anagen stage; hence a tremendous amount of shedding may occur.

Pat h o g e n e sis • Anagen effluvium is usually precipitated by a toxic event, such as a reaction to certain drugs. However, an acute and severe systemic illness such as systemic lupus erythematosus (SLE) may also result in an anagen effluvium. The dramatic hair loss usually starts 1 to 2 weeks after the precipitating event. • Among the agents that have been commonly associated with anagen hair loss are: • Drugs used for cancer chemotherapy (e.g., doxorubicin, nitrosoureas, cyclophosphamide) • Immunotherapeutic medications (cyclosporine, methotrexate, colchicine) • Intoxication of thallium or mercury • Radiation therapy CLINICAL MANIFESTATIONS • Anagen effluvium presents as a diffuse, nonscarring, noninflammatory type of hair loss (FIG. 10.12). Hence, the presence of scale, pustules, or scars indicating inflammation may suggest a different cause for the hair loss. • The hair pull is grossly positive, pulling more than four hairs per pull. In contrast to telogen effluvium, pulled hairs have a tapered end that is caused by the sudden cessation of hair shaft production.

10.12 Anagen effluvium. This patient’s alopecia resulted from chemotherapy for lung cancer. Her hair loss was diffuse, and her hair is now regrowing.

MANAGEMENT • Management of anagen effluvium simply involves the identification and removal, if feasible, of the precipitating cause. • Laboratory tests are not necessary unless causes of telogen effluvium or intoxication are suspected. • Local cooling of the scalp has been proposed to prevent hair loss during chemotherapy.

Pro g n o sis • Anagen effluvium is entirely reversible, and patients should be reassured that the hair loss is temporary. New hair growth starts a few weeks after the termination of treatment. However, the color and texture of the new hair may be different.

DIAGNOSIS • The diagnosis tends to be straightforward because of an obvious triggering event, such as chemotherapy.

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Sen escen t Alop ecia MANAGEMENT BASICS • No treatment has been shown to be effective for this condition. • Patient education and reassurance that this type of hair loss is part of the normal process of aging may be helpful.

• Aging results in a gradual decrease of scalp hair density. Whereas a newborn has about 1,100 hairs per square centimeter, by age 30 this has decreased to about 600 hairs per square centimeter, and by age 50 this has further decreased to about 500 hairs per square centimeter. • This type of alopecia affects men and woman equally and is seen in patients 50 years and older. CLINICAL MANIFESTATIONS • Patients generally complain of thinning of the scalp and do not report increased shedding. • Senescent alopecia is a diffuse, nonscarring, noninflammatory type of hair loss. It represents a diagnosis of exclusion.

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Sca r rin g Alo p ecia BASICS • Scarring alopecia, also known as cicatricial alopecia, comprises a large group of heterogenous disorders. Based on the pathogenic mechanism, they can be divided into inflammatory and noninflammatory categories. The inflammatory alopecias can be further subdivided into either infectious (see Chapter 7, “Superficial Fungal Infections: Tinea Capitis”) or noninfectious groupings. • This section will focus on the scarring alopecias that are caused by an inflammatory noninfectious process. Such scarring alopecias affect all ethnic groups and races; however, certain types of scarring alopecias are more prevalent in African-American and Afro-Caribbean women. • Because many African-American and Afro-Caribbean women use grooming techniques to straighten the natural kinkiness of their hair, a traumatic alopecia can be a consequence of these practices. Alopecia may result from the use of hair reshaping products (e.g., relaxers, straighteners, hot combs, foam rollers, and permanent wave products) or hair braiding methods (e.g., cornrows) that are popular in the black community. • It is a common misconception that these techniques are used solely to make hair more becoming and stylish; in fact, they are used as much to make hair more manageable. Traction alopecia, chemical alopecia, and hot-comb alopecia (also known as follicular degeneration syndrome) may be caused by the use of any of these methods, either alone or in combination, and may ultimately result in permanent alopecia.

Ch ron ic Cu tan eou s Lu p u s Eryth em atosu s See also Chapter 25, “Cutaneous Manifestations of Systemic Disease.” BASICS

Pat h o g e n e sis • There are many hypotheses regarding the pathogenesis of some of the scarring alopecias, including autoimmune phenomena, superantigen response of cytokines, infection, and altered host response. • Also, certain hairstyling practices can result in damage and permanent destruction of the hair follicles (see discussion of the variant central centrifugal cicatricial alopecia).

• Chronic cutaneous lupus erythematosus (CCLE) accounts for about one third of cases of cicatricial alopecia. It occurs more frequently in African-American women. Evidence of SLE or other cutaneous signs of lupus may or may not be present. • Discoid lupus erythematosus—so-named for its discoid, or disk-shaped, lesions—is by far the most common form of CCLE. • SLE, unlike CCLE, may lead to telogen effluvium, which typically presents as a diffuse nonscarring type of hair loss (see earlier discussion). Occasionally, the scarring alopecia of CCLE can be seen in a patient with SLE.

CLINICAL MANIFESTATIONS AND COURSE

CLINICAL MANIFESTATIONS

• The initial symptoms of scarring alopecia are caused by inflammation of the scalp. The patient may complain of an itching or burning sensation. In its early stages, there is no

• Typically, the patient with CCLE presents with patches of alopecia on the scalp that are red, atrophic, and mottled (representing areas of hypo- and hyperpigmentation) (FIG. 10.13). • Lesions may be quite pruritic. • Other similar lesions may be observed on the conchae of the external ears or elsewhere on the body.

SOME COMMON CAUSES OF SCARRING ALOPECIA • • • • • • • •

obvious hair loss or scarring noted. The diagnosis is often missed in this initial presentation, and the patient may be told by the clinician that he or she has “excessive dandruff” or “seborrheic dermatitis.” The patient may then be advised to shampoo more often with an antidandruff shampoo; this often results in exacerbation of symptoms. • As the disease progresses, the hair loss becomes more apparent. The loss of follicular orifices (ostia or pores) is a key feature of scarring alopecia, differentiating it from AA (see earlier discussion), a nonscarring inflammatory alopecia in which the follicular orifices remain intact and indicate that scarring has not taken place. • The process can further evolve into patches of alopecia that can coalesce into larger areas. The skin within the areas of hair loss may have a thin, shiny, atrophic appearance and may spread centrifugally, with an area of central scarring surrounded by an expanding periphery of erythema (inflammation).

Chronic cutaneous lupus erythem atosus Lichen planopilaris Central centrifugal cicatricial alopecia Traction alopecia Sarcoidosis Folliculitis decalvans Pseudofolliculitis barbae (see later in this chapter) Acne keloidalis (see later in this chapter)

DIAGNOSIS • A scalp biopsy for regular hematoxylin/eosin (H/E) staining demonstrates a lymphocytic infiltrate, and direct immunofluorescence may be helpful in making the diagnosis. • Serologic studies can be helpful; however, the vast majority of CCLE cases do not demonstrate the presence of antinuclear antibodies. Chap ter 10 • Hair and Scalp Disorders Resulting in Hair Loss

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Lich en Plan op ilaris BASICS • Lichen planopilaris (LPP) accounts for approximately another third of cases of scarring alopecia. Lichen planus (LP) is an idiopathic eruption with characteristic papules on the skin, nails, and mucous membranes (see Chapter 4, “Inflammatory Eruptions of Unknown Cause”); however, sometimes the scalp may be involved. • The inflammation may result in a scarring alopecia, which is then referred to as LPP to highlight the hair follicle involvement ( pilaris refers to hair). • In most cases of LPP, the inflammation is limited to the scalp, and typical LP lesions are not seen elsewhere on the skin. 10.13 Chronic cutaneous lupus erythematosus. Extensive scarring alopecia, as well as typical discoid lesions, are seen in this patient.

Et io lo g y • LPP and LP are considered to result from a cell-mediated immune response of unknown origin. CLINICAL MANIFESTATIONS

MANAGEMENT • Topical superpotent corticosteroids or intralesional corticosteroid injections are the first-line therapy for CCLE. Hydroxychloroquine (200 to 400 mg/day) is often effective, but glucose-6-phosphate dehydrogenase (G6PD) deficiency screening is required prior to treatment because patients with G6PD deficiency are more prone to the hematologic side effects of this drug. Patients taking hydroxychloroquine need to be monitored for anemia and require retinal examination prior and during treatment because of the potential retinopathy. • Other therapies that have been used include dapsone, isotretinoin, and thalidomide. The goal of treatment is to alleviate the scalp pruritus or discomfort, decrease inflammation, and prevent further destruction of the hair follicles.

• Patients who have LPP initially present with erythema and burning of the scalp; the condition progresses to the development of patchy alopecia, most commonly on the vertex of the scalp. Typically, there is perifollicular erythema and scale (FIG. 10.14). • Hair casts, which are white, sleevelike structures that encircle the hair shaft, can sometimes be noted in LPP. • Tufting or polytrichia, which are clumped hairs caused by surrounding scarring, are often seen. The condition tends to be progressive but “burns out” after several years.

HELPFUL HINT • When faced with a scarring alopecia in a woman of color, it is very important to rule out fungal infection of the scalp (tinea capitis), which can lead to a scarring alopecia.

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10.14 Lichen planopilaris. This woman has patchy areas of cicatricial alopecia. The affected skin is smooth, white, and devoid of erythema or pores, causing the so-called “footprints in the snow” appearance.

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• There is great variability in the severity of LPP. Frontal fibrosing alopecia (which affects the frontal area of the scalp) has recently been described and is believed to be a subtype of LPP. DIAGNOSIS • A scalp biopsy for regular H/E staining, demonstrating a lymphocytic infiltrate, may be helpful in making the diagnosis. • Serologic studies to help exclude connective tissue disease are recommended. Hepatitis C as well as certain medications (gold, atabrine, and quinacrine) have been associated with LPP. Fungal cultures and or periodic acid–Schiff (PAS) staining should be performed to rule out tinea capitis.

CLINICAL MANIFESTATIONS • Early hair loss is usually asymptomatic and gradual. Later, particularly if chemical relaxers and hot combs are used, scaling, pustules, and itching may occur and result in scarring alopecia. • Hypopigmentation and hyperpigmentation can be observed in affected scalp areas. • Tufting or polytrichia can also be noted. Patients often complain of burning or stinging in affected areas. • As the name CCCA implies, patches of scarring alopecia initially present on the central vertex of the scalp, and the alopecia progressively extends outward in a centrifugal pattern (FIG. 10.15). DIAGNOSIS Diagnosis is based on the following:

MANAGEMENT

• Clinical appearance • History of hair reshaping techniques • Scalp biopsy, if necessary

• Topical superpotent topical or intralesional corticosteroid injections are the first line of therapy for LPP. • Doxycycline or minocycline (100 to 200 mg/day) is often effective in mild cases of LPP. • Other therapies that have been used include cyclosporine, hydroxychloroquine, dapsone, and oral isotretinoin.

Cen tral Cen trifu gal Cicatricial Alop ecia BASICS • Central centrifugal cicatricial alopecia (CCCA) is the current terminology used to describe a type of scarring alopecia mostly seen in African-American women; it is believed to be caused by the use of various chemicals and/or heat to relax the hair. Previously, the traditional terms hot-comb alopecia and follicular degeneration syndrome were coined to describe this condition. • Chemicals such as thioglycolates, which are found in commercial styling products, create curls by destroying the disulfide bonds of keratin. These chemicals may also have irritant effects on the scalp that can result in hair shaft damage as well as inflammation of the scalp and loss of hair roots. • Hot-comb alopecia results from the excessive use of pomades with a hot comb or iron. (Hot combs or pomades alone do not cause permanent alopecia.) On contact with the hot comb or hot iron (i.e., marcelling iron), the pomade liquefies and drips down the hair shaft into the follicle; this results in a chronic inflammatory folliculitis that, in time, can lead to scarring alopecia and permanent hair loss.

10.15 Central centrifugal cicatricial alopecia. The continuous use of chemical relaxers resulted in permanent hair loss at the vertex of this woman’s scalp.

DIFFERENTIAL DIAGNOSIS • CCCA is not uncommon in black women. • However, it is important to rule out other causes of scarring alopecias, such as CCLE, LPP, tinea capitis, sarcoidosis, and traction alopecia, which are described in this chapter.

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MANAGEMENT • Treatment of CCCA consists of removing changing or eliminating the damaging hairstyle practices as well as reducing the inflammation. Encouraging the patient to change hairstyle practices requires sensitivity as well as a good understanding of the different hairstyles and practices of black women. • Natural hairstyles that do not place traction on the hair shaft are recommended.

• Use of mild, lye-free chemical relaxants once every 2 months is suggested, and the use of heat-relaxing devices such as hot combs and hood dryers should be discouraged. • Anti-inflammatory therapy with an oral tetracycline such as minocycline or doxycycline as well as topical or intralesional corticosteroids are helpful in the initial phases. • Once the inflammation is completely resolved, hair transplantation into scarred areas can be used to improve cosmesis.

Traction Alop ecia POINTS TO REMEMBER • Although a great majority of black women are using or have used chemical and thermal relaxers, a diagnosis of CCCA should not be made presumptively. A scalp biopsy for H/E staining and direct immunofluorescence, a negative PAS stain, as well as negative or nonreactive connective tissue serologies, helps rule out other causes of scarring alopecias. • The importance of early diagnosis and initiation of treatment of a scarring alopecia is of the utmost importance, because it can result in the complete destruction of the hair follicle. Once the follicle is replaced by scar tissue, the hair loss is irreversible.

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BASICS • Traction alopecia is seen almost exclusively in AfricanAmerican and African-Caribbean women of all ages, who are more likely to braid their hair. • The condition results from the prolonged trauma to the hair follicle by such hairstyles such as cornrows and braiding. • The persistent physical stress of traction injury caused by tight rollers and tight braiding or ponytails causes hair loss. • In addition, the use of hair dryers (with resultant overheating of hair shafts) and the practices of vigorous combing or brushing as well as bleaching can also contribute to hair breakage.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

• A combination of these patterns may be seen if both traction and hot combs or chemicals are used. DIAGNOSIS • The clinical presentation and history are usually sufficient to make the diagnosis.

MANAGEMENT A

• Early intervention and discontinuation of the damaging hairstyles are the mainstays of therapy, because delay may result in irreversible hair loss.

Sarcoid osis

B 10.16 A an d B Traction alopecia. A: This woman’s alopecia is the result of the use of tight curlers. Note the symmetric loss of hair in a frontotemporal distribution and the “relaxed” curl that was chemically straightened. B: Note the fringe of residual hairs at the distal margin of alopecia. These hairs were too short to be “grabbed” by the hair curlers.

• Hair loss may closely resemble that of traumatic alopecia. However, other signs and symptoms of sarcoidosis are usually apparent. A scalp biopsy of lesional skin may be necessary to distinguish sarcoidosis from traumatic alopecia. • Sarcoidosis of the scalp is seen most commonly in AfricanAmerican women. It is usually seen in patients who have other cutaneous or noncutaneous involvement, such as pulmonary sarcoidosis. • This contrasts with CCLE and LPP, where the scarring alopecia is less likely to be seen in conjunction with other cutaneous or systemic features of these diseases. Clinically, in sarcoidosis, atrophic patches of alopecia that mimic CCLE may be seen. DIAGNOSIS

CLINICAL MANIFESTATIONS • Traction alopecia is manifested by a symmetric pattern of hair loss, with broken hairs. • A characteristic border of residual hairs is often at the distal margin of the hair loss. • Follicular papules and pustules may be present and can result in permanent scarring alopecia. DISTRIBUTION OF LESIONS • Traction pattern: alopecia is evident at the temples and along the frontal hairline (FIGS. 10.16 A and B). Hair loss later extends to the vertex and occipital areas. • Chemical or hot-comb pattern: hair loss is more irregular (less symmetric) and reflects the areas where the chemicals or hot comb were applied.

• Indications that may be helpful: • Scalp biopsy for regular H/E staining demonstrating noncaseating granulomas • Evidence of cutaneous sarcoidosis elsewhere on the body or systemic involvement • Serologic studies to exclude connective tissue diseases are recommended.

MANAGEMENT • Potent topical, intralesional, or oral corticosteroids may be used to control sarcoidosis of the scalp. • Antimalarial agents such as hydroxychloroquine may be used in refractory cases. Chap ter 10 • Hair and Scalp Disorders Resulting in Hair Loss

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Follicu litis Decalvan s BASICS • Folliculitis decalvans presents as a scarring patch surrounded with follicular pustules. • Successive crops of peripheral pustules result in an expanding patch or patches of scarring alopecia (FIG. 10.17). DIAGNOSIS

10.17 Folliculitis decalvans. Extensive inflammation, pustules, and scarring are present.

Bacterial cultures from the follicular pustules often grow Staphylococcus aureus. This condition does not merely represent a bacterial folliculitis; rather, an abnormal immune response to possible staphylococcal antigens may be involved. • A scalp biopsy for H/E staining demonstrates a scarring alopecia with a neutrophilic infiltrate. • It is important to rule out tinea capitis, which can also present as a pustular scarring alopecia.

MANAGEMENT • Prolonged antistaphylococcal treatment is recommended, either monotherapy (erythromycin, tetracycline, cephalexin) or combination therapy (rifampin plus clindamycin or cephalexin). • Topical antibiotic agents and topical corticosteroids may be used in conjunction with systemic therapy. • Zinc sulfate (30 to 60 mg, three times daily) has been reported to be helpful in some cases.

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Pseu d o fo llicu lit is Ba rb a e a n d Acn e Kelo id a lis BASICS Hair follicle problems are very common in men and women of African-American, African-Caribbean, and Hispanic origin who have tightly curled hair. Postadolescent African-American men, in particular, experience “shaving bumps” (pseudofolliculitis barbae) and a characteristic acnelike, scarring condition located on the occiput referred to as acne keloidalis.

Pseu d ofollicu litis Barbae • Tightly coiled hairs emerge from curved hair follicles (ILL. 10.1) • When shaved, the hair becomes a sharp tip that curves downward as it grows and reenters the epidermis, or the sharpened hair may grow parallel to the skin and penetrate it. • Furthermore, newly erupting hairs from below may pierce and aggravate areas that are already inflamed. • Thus, growing hairs act as traumatic vehicles that produce an inflammatory foreign body–like reaction.

10.18 Pseudofolliculitis barbae. Tight, curly hairs that have been sharpened by shaving penetrate the skin. Inflammatory papules and pustules that resemble acne are evident. DISTRIBUTION OF LESIONS • Lesions are seen on the beard, particularly on the neck and the submental areas.

DESCRIPTION OF LESIONS • On close inspection, tight, curly hairs that have been sharpened by shaving and penetrate the skin are noted. • Inflammatory papules and pustules ensue (FIG. 10.18). • Ultimately, persistent flesh-colored papules that represent hypertrophic scars and postinflammatory pigmented lesions become prominent clinical features.

A

B

DIFFERENTIAL DIAGNOSIS • Acne vulgaris • Bacterial folliculitis

C

D

I10.1 Pseudofolliculitis barbae, or “razor bumps,” showing extrafollicular and transfollicular penetration. A: A curly hair grows from a sharply curved hair root. When shaved, the hair is left with a sharp point. As this hair grows, the sharp tip curves back and pierces the skin. B: The sharpened hair penetrates the skin. C and D: When hairs are cut too closely, they can penetrate the side of the hair root. Both types of follicular reentry cause a foreign body–like reaction (papule). (Modified from Crutchfield CE III. The causes and treatment of pseudofolliculitis barbae. CUTIS 1998;61:351–356, with permission.) Chap ter 10 • Hair and Scalp Disorders Resulting in Hair Loss

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MANAGEMENT

Pre ve n t ive Me asure s • Discontinuance of shaving is only partially helpful; however, this is generally not a choice desired by most patients. • Patients may avoid close shaving by using a guarded razor (e.g., PFB Bump Fighter). This razor is covered with a plastic coating that prevents the razor from contacting the skin directly. The use of an electric razor is another method that reduces the closeness of the shave. • Hairs may be lifted with a fine needle or a toothpick before they penetrate the skin (FIG. 10.19). • Patients should be advised not to pluck hairs because new hairs will again grow from below and penetrate a site that is already inflamed.

10.19 Pseudofolliculitis barbae. A curled hair is lifted with a fine needle after it had penetrated the skin.

Tre at m e n t • Treatment is difficult. • Nonfluorinated, class 5 or 6 topical steroids are used for inflammation and itching. • Used once daily, topical antibiotics such as erythromycin 2% (Akne-mycin) ointment or BenzaClin or Duac gel (these combine clindamycin and benzoyl peroxide) often reduce inflammation. • Systemic antibiotics such as minocycline are helpful when marked inflammation and pustulation are present. • Chemical depilatories such as Magic Shave and Royal Crown powders are effective in removing and softening

hairs; the main disadvantages are that they are irritating and they have an unpleasant odor. • Hair destruction using an extended-pulse width laser has been shown to be effective. • Eflornithine hydrochloride 13.9% (Vaniqa) is an enzyme inhibitor that slows hair growth (see Chapter 11, “Hirsutism”). • Electrolysis is difficult to use on inflammatory foci, but it can be partially effective as an adjunctive treatment method.

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Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Acn e Keloid alis (Follicu litis Keloid alis) BASICS • The name acne keloidalis is actually a misnomer. It has nothing to do with acne but is actually a type of folliculitis. • The pathogenesis of acne keloidalis is similar to that of pseudofolliculitis barbae (see previous section), in which coiled hairs produce a reentry phenomenon that results in characteristic features. DESCRIPTION OF LESIONS • Initially, inflammatory papules and pustules are noted. • Ultimately, hypertrophic scarring occurs, characterized by flesh-colored papules (FIG. 10.20) and possibly keloid formation.

10.20 Acne keloidalis. Hypertrophic scarring and fleshcolored papules are seen in this patient.

DISTRIBUTION OF LESIONS • This condition is characteristically seen in the lower occipital area, but it can extend to the adjacent or the entire scalp and thus may be indistinguishable from folliculitis decalvans (FIG. 10.21; see FIG. 10.17).

MANAGEMENT • Potent topical or intralesional steroids (5 to 10 mg/mL) help decrease itching and inflammation. • Topical antibiotics are used when papules and pustules are present. • A systemic antibiotic such as minocycline seems to be helpful because of its anti-inflammatory effect. • Surgical treatment is not without risk. It is reserved for extreme cases and may result in worse scarring.

10.21 Acne keloidalis and scalp folliculitis. Here the problem extends to the adjacent scalp.

POINTS TO REMEMBER SEE PATIENT HANDOUT “Pse ud o fo lliculit is Barb ae (Razo r Bum p s)” ON THE SOLUTION SITE

• When bacterial folliculitis is present, it is usually the result of secondary, not primary, pathogens. • Prevention of these disorders also depends on avoidance of close “clipper” shaves and haircuts.

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C H AP T ER

Hirsutism

11 OVERVIEW DISORDERS ASSOCIATED WITH HIRSUTISM • • • • • •

Polycystic ovary syndrom e (PCOS) Fam ilial hirsutism Drug-induced hirsutism Adrenal causes Other associated disorders Idiopathic hirsutism

Hirsutism is defined as the excessive growth of thick, dark hair in locations where hair growth in women is normally minimal or absent. Such male-pattern growth of terminal body hair usually occurs in androgen-stimulated locations, such as the face, chest, and areolae. Although the terms hirsutism and hypertrichosis are often used interchangeably, hypertrichosis actually refers to excess hair (terminal or vellus) in areas that are not predominantly androgen dependent. Whether a given patient is hirsute is often difficult to judge because hair growth varies among individual women and across ethnic groups. What is considered hirsutism in one culture may be considered normal in another. For example, women from the Mediterranean region and Indian subcontinent have more facial and body hair than do women from Asia, sub-Saharan Africa, and Northern Europe. Dark-haired, darkly pigmented individuals of either sex tend to be more hirsute than blond or fair-skinned persons. In women, hirsutism exceeding culturally normal levels can be as distressing an emotional problem as the loss of scalp hair. BASICS • Hirsutism, by itself, is a benign condition primarily of cosmetic concern. • However, when hirsutism in women is accompanied by masculinizing signs or symptoms, particularly when these arise well after puberty, it may be a manifestation of a more serious underlying disorder, such as an ovarian or adrenal neoplasm. Fortunately, such disorders are rare.

Pat h o g e n e sis • Hirsutism can be caused by abnormally high androgen levels or by hair follicles that are more sensitive to normal androgen levels. Therefore, increased hair growth is often seen in patients with endocrine disorders characterized by hyperandrogenism, which may be caused by abnormalities of either the ovaries or the adrenal glands.

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• The physiologic mechanism proposed for androgenic activity consists of three stages: (a) production of androgens by the adrenals and ovaries, (b) androgen transport in the blood on carrier proteins (principally sex hormone–binding globulin [SHBG]), and (c) intracellular modification and binding to the androgen receptor. • In short, central overproduction of androgen, increased peripheral conversion of androgen, decreased metabolism, and enhanced receptor binding are each potential causes of hirsutism. For circulating testosterone to exert its stimulatory effects on the hair follicle, it first must be converted into its more potent follicle-active metabolite, dihydrotestosterone. The enzyme 5- -reductase, which is found in the hair follicle, performs this conversion. • The severity of hirsutism does not correlate with the level of increased circulating androgens because of individual differences in androgen sensitivity of the hair follicles. • Testosterone stimulates growth, thereby increasing size and intensifying the pigmentation of hair. Estrogens act in an opposite manner by slowing growth and producing finer, lighter hairs. Progesterone has minimal effect on hair growth.

A

Cycle s o f Hair Gro wt h Hair grows in long cycles over many months: an anagen (active) phase (ILL. 11.1) is followed by a catagen (degenerative) phase, then a telogen (resting) phase, with different hairs alternating phases. The anagen and telogen phases are hormonally regulated. During the telogen phase, the hair shaft eventually separates from the follicle and falls out.

B Anagen Growth Stage

C Catogen Degeneration Stage

Telogen Resting Stage

I11.1 Cycles of hair growth. (Modified from Structure and function of the skin. Sams WM Jr, Lynch PJ, eds. In: Principles and Practice of Dermatology. New York: Churchill Livingstone, 1990:8, with permission.)

Chap ter 11 • Hirsutism

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The amount of free testosterone—the biologically active androgen that, after conversion to dihydrotestosterone, causes hair growth—is regulated by SHBG. Lower levels of SHBG increase the availability of free testosterone. SHBG decreases in response to the following:

11.1 Hirsutism. This patient has PCOS. This is the most common cause of androgen excess and hirsutism. Note the lesions of acne.

• Exogenous androgens • Certain disorders that affect androgen levels, such as polycystic ovary syndrome • Congenital or delayed-onset adrenal hyperplasia • Cushing’s syndrome • Obesity • Hyperinsulinemia • Hyperprolactinemia • Excess growth hormone • Hypothyroidism Conversely, SHBG increases with higher estrogen levels, such as those that occur during oral contraceptive therapy. The resulting increased SHBG levels lower the activity of circulating testosterone.

Disord ers Associated with Hirsu tism Po lycyst ic Ovary Syn d ro m e • The most common cause of androgen excess and hirsutism is polycystic ovary syndrome (PCOS). • Virilization is minimal, and hirsutism is often prominent. • Characteristic features include menstrual irregularities, dysmenorrhea, occasional glucose intolerance and hyperinsulinemia, and, often, obesity. • The hyperinsulinemia is believed to hyperstimulate the ovaries into producing excess androgens. • Women with PCOS may show other cutaneous manifestations of androgen excess in addition to hirsutism, such as recalcitrant acne (FIG. 11.1), acanthosis nigricans, and alopecia on the crown area of the scalp (a pattern that contrasts with the bitemporal and vertex androgenic alopecia seen in men) (see FIG. 10.2). • Hirsutism may also be seen in the following ovarian conditions, most of which are associated with virilization: • Luteoma of pregnancy • Arrhenoblastomas • Leydig cell tumors • Hilar cell tumors • Thecal cell tumors

11.2 Familial hirsutism. As seen in this Pakistani woman, familial hirsutism is both typical and natural in certain populations.

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Fam ilial Hirsut ism • This type of hirsutism is not associated with androgen excess. Familial hirsutism is both typical and natural in certain populations, such as in some women of Mediterranean or Middle Eastern ancestry (FIG. 11.2).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Drug -In d uce d Hirsut ism • Drugs that can induce hirsutism by their inherent androgenic effects include dehydroepiandrosterone sulfate (DHEA-S), testosterone, danazol, and anabolic steroids. • The current low-dose oral contraceptives are less likely to cause hirsutism than were previous formulations. Ad re n al Cause s • Children with congenital adrenal hyperplasia (CAH), the classic form of adrenal hyperplasia, may exhibit hirsutism. Such children may be born with ambiguous genitalia and symptoms of salt wasting and failure to thrive, and they may develop masculine features. • Late-onset CAH affects about 1% to 5% of hyperandrogenic women. Although these patients have clinical features that resemble PCOS, they manifest no salt-wasting symptoms and may not develop signs of virilization and menstrual irregularities until puberty or adulthood (FIG. 11.3). • Cushing’s syndrome is a noncongenital form of adrenal hyperplasia. It is characterized by an excess of adrenal cortisol production. • Androgen-producing adrenal tumors are extremely rare.

11.3 Hirsutism in late-onset congenital adrenal hyperplasia. An 18-year-old woman with clinical features that are similar to those of PCOS: acne, hirsutism, menstrual irregularities, and obesity.

Ot h e r Asso ciat e d Diso rd e rs • Other less common but potentially serious disorders associated with hirsutism include anorexia nervosa, acromegaly, hypothyroidism, porphyria, and cancer. Id io p at h ic Hirsut ism • The few hirsute women who do not have a familial form of hirsutism or any detectable hormonal abnormality are usually given a diagnosis of idiopathic, or end-organ, hirsutism. • Such patients have normal menses, normal-sized ovaries, no evidence of adrenal or ovarian tumors or dysfunction, and no significant elevations of plasma testosterone or androstenedione. • Antiandrogen therapy may improve hirsutism in some idiopathic cases. • This suggests that this form of hirsutism may be androgen induced. • It is believed that many of these women may have mild or early PCOS and androgen levels in the upper range of normal. CLINICAL MANIFESTATIONS The onset of hirsutism can take one of the following forms: • For example, in women with familial hirsutism, it often appears during puberty. • Excess growth of facial hair is seen in elderly postmenopausal women and may be caused by unopposed androgen. • It appears rather abruptly when an androgen-secreting tumor arises.

Chap ter 11 • Hirsutism

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DESCRIPTION OF LESIONS AND OTHER PHYSICAL FINDINGS • Excess terminal hair grows in a masculine pattern. • Other accompanying signs and symptoms to look for may include the following: • Acanthosis nigricans • Obesity • Pelvic mass • Signs or symptoms of virility • Signs or symptoms of Cushing’s syndrome • Acne • Alopecia DISTRIBUTION OF LESIONS A woman with hirsutism has excess terminal hair in a masculine pattern in key anatomic sites, including the following: • Face, particularly the moustache, beard, and temple areas • Chest, areolae, linea alba, upper back, lower back, buttocks, inner thighs, and external genitalia DIAGNOSIS • After familial and drug-induced causes for hirsutism have been excluded, hirsutism resulting from androgen excess should be considered. • Initial screening for total or free testosterone and DHEA-S often determines whether further testing is necessary. Testosterone and DHEA-S levels may provide clues to the source of excessive androgen production.

Se rum Te st o st e ro n e • Whether total testosterone is a better screening test than free testosterone is controversial. • The evaluation of total testosterone is less expensive and probably easier to interpret. • However, free testosterone may be a more sensitive indicator of hormonal level abnormality. • Testosterone levels vary during the different phases of the menstrual cycle by approximately 25%. • Early morning measurement of testosterone levels is advised. The upper limit of the reference range for total plasma testosterone levels is 70 to 90 ng/dL. • No direct correlation exists between the levels of testosterone and the degree of hirsutism, because hirsutism is caused by the action of dihydrotestosterone, which is the more potent testosterone metabolite. • Elevated free serum testosterone levels ( 80 ng/dL) are found in most women with anovulation and hirsutism.

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• In most patients in whom the total testosterone level is greater than 200 ng/dL ( 100 ng/dL in postmenopausal women), a tumor workup is indicated. This workup includes a pelvic examination and ultrasound, which usually are adequate to diagnose PCOS. If the test results are negative, an adrenal computed tomography scan is performed.

Se rum DHEA-S • In some patients who are hirsute, DHEA-S is elevated. Moderate elevations suggest an adrenal origin of the hirsutism. • Normal levels of DHEA-S accompanied by high levels of testosterone indicate that the ovaries, and not the adrenals, are producing the excess androgen. • A tumor workup is indicated in most patients in whom the DHEA-S level is greater than 700 g/dL (400 g/dL in postmenopausal women). An increase of this magnitude usually results from adrenal hyperplasia rather than the extremely rare adrenal carcinomas. Ot h e r Te st s If a woman shows severe or rapidly progressive hirsutism or signs or symptoms of virilism (e.g., infrequent or absent menses, acne, deepening of the voice, male-pattern balding, increased muscle mass, increased libido, clitoral hypertrophy), it may be necessary to perform additional tests. Ser u m An d ro st en ed io n e

• Androstenedione can originate in the adrenal glands or in the ovaries and often is elevated in patients with hyperandrogenism. • A serum androstenedione level above 100 ng/dL suggests an ovarian or adrenal neoplasm. Lu t ein izin g H o r m o n e a n d Fo llicle-St im u la t in g H o rm o n e

• Often, in women with PCOS, luteinizing hormone (LH) levels are elevated and follicle-stimulating hormone (FSH) levels are depressed, which results in elevated LH/FSH ratios ( 2 is common). • The evaluation of late-onset CAH and other types of adrenal abnormalities is beyond the scope of this chapter. If Cushing’s syndrome is suspected, a 24-hour urinary cortisol or an overnight dexamethasone suppression test should be performed.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

DIFFERENTIAL DIAGNOSIS • Drug-induced hypertrichosis should be distinguished from drug-induced hirsutism. In drug-induced hypertrichosis there is a uniform growth of fine hairs that appear over extensive areas of the trunk, hands, and face. This growth is not androgen dependent. • Precipitating drugs include phenytoin, minoxidil (FIG. 11.4), diazoxide, cyclosporine, penicillamine, high-dose corticosteroids, phenothiazines, acetazolamide, and hexachlorobenzene. The exact mode of action is not known, but presumably these agents also exert their effects independent of androgens. 11.4 Drug-induced hypertrichosis. Oral minoxidil was the cause of hypertrichosis in this patient.

MANAGEMENT

Ove rvie w • Treatment of hirsutism is unnecessary if no abnormal origin can be diagnosed and if the patient does not find the hirsutism cosmetically objectionable. Treatment should be offered, however, if an underlying disorder is identified or if the patient is troubled by the hair growth. • Management depends on the underlying cause. For example, non–androgen-dependent excess hair, such as hypertrichosis, is treated primarily with physical hair removal methods. In contrast, those patients who have androgendependent hirsutism may require a combination of physical hair removal and medical antiandrogen therapy. • As an alternative to hair removal, simple bleaching of hair is an inexpensive method that works well when hirsutism is not too excessive. Bleaches lighten the color of the hair so that it is less noticeable. Hair Re m o val Dep ila t io n

Depilatories remove hair from the surface of the skin. Depilatory methods include ordinary shaving and the use of chemicals, such as thioglycolic acid. • Shaving removes all hairs, but it is immediately followed by growth of hairs that were previously in anagen; as these hairs grow in, they produce rough stubble. There is no evidence that shaving increases the growth or coarseness of subsequent hair growth. However, most women prefer not to shave their facial hair. • Chemical depilation may be best suited for treatment of large hairy areas in patients who are unable to afford

more expensive treatments, such as electrolysis and laser epilation. Chemical depilatories separate the hair from its follicle by reducing the sulfide bonds that are found in abundance in hairs. Irritant reactions and folliculitis may result. Tem p o ra r y Ep ila t io n

• Epilation involves the removal of the intact hair with its root. Plucking or tweezing is widely performed. This method may result in irritation, damage to the hair follicle, folliculitis, hyperpigmentation, and scarring. • Waxing entails the melting of waxes that are then applied to the skin. When the wax cools and sets, it is abruptly peeled off the skin, and embedded hair is removed with it. This method is painful and sometimes results in folliculitis. Repetitive waxing may produce miniaturization of hairs, and, over the long run, it may permanently reduce the number of hairs. • Certain natural sugars, long used in parts of the Middle East, are becoming popular in place of waxes. They appear to epilate as effectively as, but less traumatically than, waxing. • Threading, a method used in some Arab countries, is a technique in which cotton threads are used to pull out hairs by their roots. Home epilating devices that remove hair by a rotary or frictional method are also available. Both methods may produce traumatic folliculitis. • Radiation therapy was a popular method of hair removal in the past. However, it has fallen out of favor and is no longer acceptable. continued on page 242

Chap ter 11 • Hirsutism

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MANAGEMENT Continued Per m a n en t Ep ila t io n Electrolysis and Therm olysis

• Hair destruction by electrolysis, thermolysis, or a combination of both is performed with a fine, flexible electrical wire that produces an electrical current after it is introduced into the hair shaft. Thermolysis (diathermy) uses a high-frequency alternating current and is much faster than the traditional electrolysis method, which uses a direct galvanic current. • Electrolysis and thermolysis are slow processes that can be used on all skin and hair colors, but multiple treatments are required. • Electrolysis and thermolysis can be uncomfortable and may produce folliculitis, pseudofolliculitis, and postinflammatory pigmentary changes in the skin. Laser Epilation

• Lasers can treat larger areas and can do so faster than electrolysis and thermolysis. They have skin-cooling mechanisms that minimize epidermal destruction during the procedure. • Skin and hair color often determine whether a laser should be used. Lasers are most effective on dark hairs on fair-skinned people. In such patients, lighter skin does not compete with darker hairs for the laser, which selectively targets the pigment (melanin). In dark-skinned people, a newer approach that delivers more energy to the hairs over a longer period may prove safe and effective. • As with electrolysis and thermolysis, multiple treatments are necessary for long-term hair destruction. • Folliculitis, pseudofolliculitis, discomfort, and pigmentary changes may result from laser therapy.

• It remains to be proven whether lasers are more effective in permanent hair removal than the more traditional methods. They are certainly more costly.

Ph arm aco lo g ic Tre at m e n t • In general, pharmacologic treatments for hirsutism are selected based on the underlying cause. • Medications (antiandrogens) are often administered while cosmetic hair removal techniques are being used. All these drugs must be given continuously, because when they are stopped, androgens will revert to their former levels. • The following medications are all absolutely contraindicated for use during pregnancy because of the risk of feminization of a male fetus: • Ovarian suppression (oral contraceptives) • Androgen receptor blockade and inhibition (spironolactone, flutamide, and cyproterone acetate) • Adrenal suppression (oral corticosteroids) • 5- -reductase inhibition (finasteride) • These agents can be used singly or in combination. Ne w Tre at m e n t s • Eflornithine hydrochloride cream 13.9% (Vaniqa) is a prescription topical cream that acts as a growth inhibitor, not a depilatory. The agent inhibits ornithine decarboxylase, an enzyme required for hair growth. It is indicated for the reduction of unwanted facial hair in women. Twice-daily use for at least 4 to 8 weeks is necessary before effectiveness is noted. • Metformin (Glucophage) reduces insulin levels, and this change in turn reduces the ovarian testosterone levels by competitive inhibition of the ovarian insulin receptors. This drug is effective in treating hirsutism in women with PCOS.

POINTS TO REMEMBER • Androgen-stimulated hirsutism may be a marker for androgen excess and may occasionally signal a potentially serious underlying metabolic disorder or potentially fatal neoplasm. • Expensive hormonal laboratory tests for a woman with simple hirsutism are usually not cost-effective. However, if a woman shows a constellation of virilizing signs or symptoms, such as infrequent or absent menses, acne, deepening of the voice, male-pattern balding, increased muscle mass, increased libido, and clitoral hypertrophy, she should be referred to an endocrinologist.

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C H AP T ER

12

Disorders of the Mouth, Lips, and Tongue

OVERVIEW Oral mucous membrane lesions are often clues to the presence of systemic illnesses, such as acquired immunodeficiency syndrome (AIDS), syphilis, and systemic lupus erythematosus. They may also be helpful in diagnosing dermatologic conditions, including lichen planus and pemphigus. Lesions such as “canker sores” are often seen as isolated phenomena but may also be an accompaniment or a precursor to a symptom complex, such as that seen in Behçet’s syndrome or ulcerative colitis. It is often difficult to make a clinical diagnosis in the oral cavity. Lesions may resemble normal variants, or they may look like each other. Inflammatory oral lesions—particularly those that are vesicobullous—rarely remain intact and unruptured. Instead, such lesions usually become erosions and ulcers by the time clinicians see them, adding to the difficulty of diagnosis.

COMMON MANIFESTATIONS INCLUDE: • • • • • • •

Erosions, blisters, fissures, and ulcers Erosions and ulcers of the tongue Whitish plaques Pigm entary changes Neoplasm s Cystic lesions Norm al variants

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Ero sio n s, Blist ers, Fissu res, a n d Ulcers Ap h th ou s Stom atitis BASICS

12.1 Aphthous stomatitis. A small punched-out erosion has a bright red margin surrounding a gray-white or yellowish center.

• Commonly known as “canker sores,” aphthous stomatitis lesions (aphthous ulcers) are a common, recurrent problem consisting of shallow erosions of the mucous membranes. • They are seen in children and adults and appear to be more common in women than men. • Aphthous stomatitis has no known cause, but an immune mechanism is considered the most likely contributory factor. • Patients often ascribe recurrences to psychologic stress or local trauma. • Women may correlate them with their menstrual cycle. • Most cases heal spontaneously, only to recur unexpectedly. • Oral erosions that are indistinguishable from aphthous stomatitis are sometimes seen in primary herpes simplex virus (HSV) infections. DESCRIPTION OF LESIONS • The lesions of aphthous stomatitis are small (2 to 5 mm), shallow, well-demarcated, punched-out erosions. • Lesions typically have a ring of erythema, with a gray or yellowish center (FIG. 12.1). DISTRIBUTION OF LESIONS • Lesions may be seen on the buccal, labial, and gingival mucosa, as well as on the tongue (see FIG. 6.27).

12.2 Aphthous stomatitis in Behçet’s syndrome. Large, painful erosions and extensive aphthae are evident on the lips and tongue of this woman.

CLINICAL MANIFESTATIONS • The lesions are usually painful. • They tend to heal in 4 to 14 days, a duration similar to that of HSV lesions. • Patients with human immunodeficiency virus (HIV) or Behçet’s disease may develop aphthous stomatitis lesions that are larger and more persistent, painful, and extensive than those seen in other patients (FIG. 12.2).

DIFFERENTIAL DIAGNOSIS The presence of persistent or large painful aphthae broadens the differential diagnosis to include: • Primary HSV infection • Autoimmune bullous diseases such as pemphigus vulgaris and bullous pemphigoid • Recurrent erythema multiforme • Systemic lupus erythematosus • Cyclic neutropenia • Erosive oral lichen planus • Ulcerative colitis • Behçet’s disease 244

DIAGNOSIS • The diagnosis is made clinically. • Most intraoral ulcers in immunocompetent patients are canker sores, not HSV lesions.

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MANAGEMENT Therapeutic options for aphthous stomatitis lesions include: • Symptomatic therapy with topical anesthetic viscous lidocaine (Xylocaine) may help. • Vanceril (beclomethasone dipropionate) aerosol can be sprayed directly on lesions. • Superpotent topical steroids are applied directly to lesions and held there by pressure with a finger. • Tetracycline suspension (250 mg/tsp); patients should “swish and swallow.” • Diphenhydramine (Benadryl) suspension; patients are to “gargle and spit.” • Tacrolimus ointment (Protopic) 0.1% and (Elidel) pimecrolimus cream 1% applied at bedtime may accelerate healing.

• Silver nitrate, applied directly to lesions, also can promote healing. • Intralesional corticosteroid injections or a brief course of systemic corticosteroids are effective in reducing pain and healing lesions in patients with large, persistent, painful ulcers. • Recently, thalidomide has been used with some success in healing large, painful, persistent aphthae in persons with HIV infection. • However, even a single dose of thalidomide has been known to cause fetal malformation. • Consequently, women of childbearing potential should use thalidomide only if they receive counseling and use effective contraception.

POINT TO REMEMBER • Most intraoral ulcers in immunocompetent patients are canker sores, not HSV lesions; recurrent HSV infection rarely occurs inside the mouth.

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HELPFUL HINT • A single, nonhealing ulcer (lasting more than 2 months) should undergo biopsy to rule out squamous cell carcinoma (FIG. 12.3).

12.3 Squamous cell carcinoma. This persistent, nonhealing ulceration proved to be a squamous cell carcinoma. (Image courtesy of Ashit Marwah, M.D.)

Eryth em a Mu ltiform e See also Chapter 18, “Diseases of Vasculature.”

12.4 Erythema multiforme caused by herpes simplex virus. This patient has a recurrent HSV infection. Note the drying crust of the herpetic “cold sore” on his lower lip and the targetlike lesions on his palm.

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Eryt h e m a Mult ifo rm e Min o r • Erythema multiforme minor is a self-limited eruption characterized by symmetrically distributed erythematous macules or papules, which develop into the characteristic targetlike lesions consisting of concentric color changes with a dusky central zone that may become bullous. This is not a disease but a syndrome with multiple underlying causes and associations such as drug reactions, poison ivy contact dermatitis, and, most often, recurrent herpes virus infection. • A crusted lesion of recurrent HSV may be present on the vermilion border of the lip during an outbreak of erythema multiforme (FIG. 12.4).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Eryt h e m a Mult ifo rm e Majo r (St e ve n s-Jo h n so n Syn d ro m e ) • This is the more serious variant of erythema multiforme. It has extensive mucous membrane involvement, systemic symptoms, and widespread lesions. • Erythema multiforme major is often accompanied by fever, malaise, myalgias, and severe, painful mucous membrane involvement. • Hemorrhagic crusts on lips and other mucous membranes are seen in addition to the extensive targetoid lesions elsewhere (FIG. 12.5). Syst e m ic Lup us Eryt h e m at o sus • Erosions or ulcerations can be seen on the oral mucosa. • See also Chapter 25, “Cutaneous Manifestations of Systemic Disease.” 12.5 Erythema multiforme major (Stevens-Johnson Syndrome). Bullae and hemorrhagic crusts are noted on the lips of this patient. He has targetoid lesions elsewhere on his body.

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Perlèch e

12.6 Perlèche (angular cheilitis) and atopic cheilitis. This child has scaling, fissuring, and crusting at the corners of her mouth, as well as eczema of her lips. She also has eczema on other areas of her skin.

• Perlèche (derived from the French word meaning “to lick”) is an erythematous eruption that occurs at the corners of the mouth. It is also known as angular cheilitis. • It is sometimes seen in young patients who have atopic dermatitis, specifically atopic cheilitis (FIG. 12.6). • It also appears in the elderly and may be caused by aging and atrophy of the muscles of facial expression that surround the mouth, which results in “pocketing” at the corners of the mouth (FIG. 12.7). These pockets become macerated and serve as nidi for the retention of saliva, resulting in the secondary overgrowth of microorganisms such as yeasts and/or bacteria. • In many instances, perlèche is often simply a form of intertrigo, a common inflammatory condition of skin folds that occurs when opposing moist skin surfaces are in constant contact with each other (see Chapter 3, “Psoriasis”). • Other factors such as poor-fitting dentures, malocclusion, anodontia, and bone resorption may lead to drooling or vertical shortening of the face, thus accentuating the melolabial crease. • Lip licking in children, mouth breathing, and orthodontic devices are also risk factors. • Vitamin deficiency is often blamed but rarely proved as a cause of perlèche. CLINICAL MANIFESTATIONS • Redness, scaling, fissuring, and crusting occur at the corners of the mouth. • Patients may also have evidence of atopic cheilitis and/or atopic dermatitis elsewhere on the body.

12.7 Perlèche (angular cheilitis). This patient’s problem was believed to be caused by a problem with her dentures.

MANAGEMENT • A mild topical steroid such as desonide (DesOwen) 0.05% ointment, Elocon ointment, or over-thecounter hydrocortisone 1% cream or ointment often helps resolve the inflammation. • Petrolatum or other ointments are used to protect and moisturize the area. • Topical anticandidal (ketoconazole, clotrimazole, nystatin) and antibacterial agents (mupirocin), either alone or in combination with a class 6 topical hydrocortisone ointment, are often effective. • Topical immunomodulators such as Protopic ointment 0.1% or Elidel 1% cream may also be tried. • If necessary, a dental referral is suggested to correct potential causative factors mentioned earlier. • Injection of collagen into the responsible overlapping skin folds has been beneficial in some selected patients.

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Ero sio n s a n d Ulcers o f t h e To n gu e Mu cou s Patch es of Secon d ary Syp h ilis • The lesions of secondary syphilis on the tongue are known as mucous patches (FIG. 12.8). (For a full discussion of this condition, see Chapter 19, “Sexually Transmitted Diseases,” and FIG. 19.18.) • This condition is characterized by asymptomatic, round or oval, eroded lesions or papules that are devoid of epithelium. The lesions teem with spirochetes. • A Venereal Disease Research Laboratory test is reactive.

Geograp h ic Ton gu e • Geographic tongue, or benign migratory glossitis, is a common idiopathic finding (FIG. 12.9). • The lesions are areas that are shiny, red, and devoid of papillae and resemble mucous patches. These lesions seem to move about on the surface of the tongue and change configurations from one day to the next, thus accounting for the bizarre, shifting patterns. • Reports have suggested an association of geographic tongue with psoriasis; however, its 2% incidence in patients with psoriasis is no greater than would be expected in the otherwise healthy population. • No treatment is necessary.

12.8 Mucous patches of secondary syphilis. These mucous patches result from eroded epithelium of the tongue.

12.9 Geographic tongue. Shiny, red patches are devoid of papillae (note the resemblance to the mucous patches shown in FIG. 12.8).

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W h it ish Pla q u es Lich en Plan u s • For a full discussion of this condition, see Chapter 4, “Inflammatory Eruptions of Unknown Cause.” DESCRIPTION OF LESIONS • A white, lacy network of lesions is present on the buccal mucosa (FIG. 12.10), tongue, or gums. • The lesions may be erosive, ulcerative, and painful. • Typical lesions of lichen planus may or may not be present elsewhere on the body.

12.10 Oral lichen planus. A white, lacy network of lesions and erosions is present on the buccal mucosa. Note the erosions.

DIFFERENTIAL DIAGNOSIS • White oral lichen planus lesions are often confused with oral candidiasis, oral leukoplakia, and a normal bite line (see FIG. 4.23).

Oral Leu kop lakia

12.11 M.D.)

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Leukoplakia. (Image courtesy of Ashit Marwah,

• This white macular or plaquelike lesion is considered a precursor to squamous cell carcinoma of the mucous membranes. • Smoking, chewing tobacco, and ethanol abuse are all contributing factors. • White adherent plaques are present. • Lesions occur on the tongue (FIG. 12.11), buccal mucosa, hard palate, and gums. • Oral leukoplakia may resemble oral lichen planus, oral hairy leukoplakia (see FIG. 12.12), or white plaques caused by trauma. • Less than 5% of lesions have been reported to develop into squamous cell carcinoma.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Oral Hairy Leu kop lakia • Oral hairy leukoplakia is associated with the Epstein-Barr virus (FIG. 12.12). • It is seen in patients with HIV infection (see Chapter 24, “Cutaneous Manifestations of HIV Infection”) and in transplant recipients. • Filiform papules that resemble white hairs are seen on the sides of the tongue. • Lesions are usually asymptomatic.

Can d id iasis (“Th ru sh ”) • Oral candidiasis is seen in immunocompromised patients (see Chapter 24, “Cutaneous Manifestations of HIV Infection”) and in neonates. • Curdlike or erosive lesions are easily removed with gauze. • Lesions may involve the tongue, the oropharynx, and the angles of mouth (angular cheilitis). • A potassium hydroxide examination or fungal culture is positive.

12.12 Oral hairy leukoplakia. This patient has AIDS. Note the papules on the sides of the tongue that resemble white hairs.

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Pigm en t a r y Ch a n ges Labial Melan otic Macu le • This is a common, benign, pigmented macule on the lower lip of adults. • It is probably caused by sun exposure (FIG. 12.13).

Black Hairy Ton gu e

12.13 Labial melanotic macule. This is a common, benign, pigmented macule on the lower lip of adults. It is probably caused by sun exposure.

• Black hairy tongue is more than just a pigmentary change. Actually, it represents benign, asymptomatic hyperplasia (an accumulation of keratin) or hypertrophy of the filiform papillae of the tongue. The pigmentation results from the normal pigment-producing bacterial flora that colonize the keratin. • It has been debatably associated with smoking, excessive coffee or tea drinking, and the prolonged use of oral antibiotics, and it is considered by some clinicians as a possible marker for AIDS. CLINICAL MANIFESTATIONS • A velvety, hairlike thickening of the tongue’s surface is apparent (FIG. 12.14). • The color can range from a yellowish brown or green to jet black.

MANAGEMENT

12.14 Black hairy tongue. A velvety, hairlike thickening of the tongue’s surface is noted. The color can range from a yellowish-brown or -green to jet black.

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• Brushing with a dilute hydrogen peroxide solution may bleach the pigmented tissue. • A toothbrush can be used to scrape off the excess keratin. • Tretinoin 0.05% gel or lotion has also been used.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Pigm en tation from Dru gs • A black discoloration of the tongue should be distinguished from black hairy tongue (described earlier). In these cases, there is no hyperkeratosis or hypertrophy of papillae. Oral mucous membrane pigmentation has been noted to result from the following agents: • Antimalarials (FIG. 12.15), bismuth (FIG. 12.16), chlorhexidine mouth rinses, doxorubicin, fluoxetine, inhalation of heroin smoke, ketoconazole, lomefloxacin, propranolol, risperidone, sulfonamides, terbinafine, tobacco, zidovudine, and all tetracyclines have been associated with pigmentation. • Artifactual pigmentation has been noted to result from amalgam tattoos and dental fillings. 12.15 Antimalarial hyperpigmentation. Pigmentation of this patient’s tongue is secondary to antimalarial therapy with hydroxychloroquine (Plaquenil).

12.16 Pigment artifact. The black pigmentation on this patient’s tongue was caused by the deposition of bismuth, the active ingredient in Pepto-Bismol. It was easily removed.

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Neo p la sm s Pyogen ic Gran u lom a • Pyogenic granuloma is a benign neoplasm (FIG. 12.17) seen on the lips and gums, particularly in pregnant women (see Chapter 21, “Benign Skin Neoplasms”).

Ven ou s Lake • A venous lake (venous varix) is another common benign vascular neoplasm; it usually occurs in patients older than 60 years of age. • This neoplasm is generally characterized by dark blue to purple macules or papules that may be seen on the lower lip (FIG. 12.18), face, ears, and eyelids. 12.17 Pyogenic granuloma. This angiomatous-appearing lesion proved to be a pyogenic granuloma after it was biopsied.

Oral Fibrom a • Most often observed in adults, oral fibromas are the most common oral neoplasm. Most represent reactive fibrous hyperplasia caused by trauma or local irritation. • They are seen most often on the buccal mucosa along the plane of occlusion of the maxillary and mandibular teeth. Oral fibromas present as asymptomatic, smooth-surfaced, firm, solitary papules. The diameter may vary from 1 mm to 2 cm. Ulceration caused by repeated trauma may occur (FIG. 12.19).

12.18 Venous lake. These soft, compressible blebs are common findings on the lips of the elderly.

12.19 Oral fibroma. This firm nodule may appear on the lip, tongue, or buccal mucosa. 254

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

• The clinical differential diagnosis of a fibroma includes giant cell fibroma, neurofibroma, peripheral giant cell granuloma, mucocele, benign and malignant salivary gland tumors, as well as squamous cell carcinoma (FIG. 12.20).

Solar Keratosis • For a full discussion, see Chapter 22, “Premalignant and Malignant Skin Neoplasms.” • These lesions are most often seen in elderly men with fair complexions. • Generally, the lesion is a slow-growing, firm papule or ulcer. • Initially, it may appear as a nonhealing erosion. • Solar keratoses are seen most often on the lower lip, where there is maximal sun exposure (FIG. 12.21). SEE PATIENT HANDOUT “So lar Ke rat o sis (Act in ic Ke rat o sis)” ON THE SOLUTION SITE

12.20 Squamous cell carcinoma. This patient has a nodular squamous cell carcinoma on the buccal mucosa. (Image courtesy of Ashit Marwah, M.D.)

Sq u am ou s Cell Carcin om a • A squamous cell carcinoma may evolve from a solar keratosis in this area (FIG. 12.22), or it may arise de novo inside the oral cavity.

12.21 Solar keratosis. Note the erosions and crusting on the lower lip of this elderly patient.

12.22 Squamous cell carcinoma. This patient has a squamous cell carcinoma of the lower lip. Chapter 12 • Disorders of the Mouth, Lips, and Tongue

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Cyst ic Lesio n s Mu cou s Cyst • A mucous cyst (mucocele) (FIG. 12.23) is a common, mucus-filled, blisterlike lesion of the minor salivary glands in the oral cavity. Some authors prefer the term mucocele since most of these lesions are not true cysts because of the absence of an epithelial lining. The lesions are considered to be caused by trauma to the openings of salivary glands. • This condition is seen most commonly in infants, young children, and young adults. CLINICAL MANIFESTATIONS 12.23

Mucocele. Cystic lesion on the lingual mucosa.

• A bluish or clear papule contains mucoid material. • It is easily ruptured and sometimes recurrent. • Eventually, the surface of the lesion turns irregular and whitish because of multiple cycles of rupture and healing caused by trauma or puncture. • The most frequent locations are in the lower lip, floor of the mouth, cheek, palate, retromolar fossa, and dorsal surface of the tongue. These lesions spare the upper lip. • They may spontaneously disappear, particularly in infants.

MANAGEMENT • Patients with a superficial mucous cyst require reassurance only. • Cryosurgery with liquid nitrogen spray may be performed. After 4 to 7 days, a necrotic surface is observed in the treated area. The treated area separates from the surrounding mucosa in 1 to 2 weeks to expose a new epithelialized surface. • The advantages of the procedure include simple application, minor discomfort during the procedure, and

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• • •

•

low incidence of complications (e.g., secondary infection, hemorrhage). • However, the possibility of recurrence exists. Another therapeutic strategy is argon laser treatment. Partial or total electrodesiccation is also performed. Intralesional injections of triamcinolone acetonide also have been reported as treatments for mucous cysts; however, these are not used routinely. Oral surgery is the treatment of choice for deeper, recalcitrant lesions. Surgical excision should include the immediate adjacent glandular tissue.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Od on togen ic Sin u s (Cu tan eou s Den tal Sin u s Tract) • Most often, these lesions appear on the chin or lower jaw. The lesion often has a small indentation that results from scarring (FIG. 12.24). • The pathologic process evolves from an intraoral abscess that forms a sinus tract that dissects subcutaneously and exits through the face or neck. The patient is usually unaware of the underlying dental etiology. • Often diagnosed incorrectly, this lesion of dental origin often resembles a furuncle, a cyst, a pyogenic granuloma, or an ulceration. 12.24 Odontogenic sinus (cutaneous dental sinus tract). Often misdiagnosed, this lesion of the mandibular skin originated in a subjacent dental abscess. MANAGEMENT • Panoramic or apical radiographic examinations help make the diagnosis. • Treatment may require oral antibiotics, tooth extraction, and/or root canal therapy.

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No rm a l Va ria n t s Ford yce Sp ots • Fordyce spots (FIG. 12.25) are normal findings that represent ectopic mucous glands. They are brought to medical attention when they are noted by the patient. • The yellow papules occur on the lips or buccal mucosa. • The lesions are more obvious when the skin is stretched. • They are incidental findings that require no treatment.

Toru s

12.25 Fordyce spots. Yellow papules on the labial mucosa. These papules are normal variants.

• Tori are developmental abnormalities that result in overgrowth of mature bone (FIG. 12.26); they differ only by their location. • These findings have been known to occur more commonly in certain ethnic groups (e.g., Native Americans, Inuit, African Americans, and certain Asian populations). In these groups, the conditions show an autosomal dominant inheritance pattern. • Treatment is not necessary.

12.26 Torus palatinus. This woman has an asymptomatic bony hard swelling located on the midline of her hard palate. The location, clinical appearance, and texture of tori and exostoses are so characteristic that the diagnosis can be made without resorting to biopsy.

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C H AP T ER

13

Diseases and Abnorm alities of Nails Herbert P. Goodheart and Hendrick Uyttendaele

OVERVIEW Mammals use their nails as weapons, as primitive tools, for grooming purposes, for scratching, and for the removal of infestations. Similarly, humans use their fingernails to help pick up small objects and to scratch itchy areas. Fingernails protect vulnerable fingertips; toenails protect toes from the impact of footwear and external trauma. Nails also are important contributors to the aesthetic appearance of the hands and feet. For the health care provider, nail abnormalities may be the first signal that a systemic disease is present.

COMMON NAIL PROBLEMS • • • •

Longitudinal ridging (onychorrhexis) Brittle nails (onychoschizia) Onycholysis Green nail syndrom e TRAUMATIC LESIONS

• Subungual hem atom a • Median nail dystrophy INFLAMMATORY DISORDERS • Psoriasis INFECTIONS OF THE NAIL AND SURROUNDING TISSUES • • • •

Acute paronychia Chronic paronychia Onychom ycosis Digital m ucous (m yxoid) cyst NAIL PROBLEMS: MISCELLANEOUS DISORDERS

• • • • • • • • •

Leukonychia striata Yellow nail syndrom e Koilonychia Derm atom yositis Subungual verruca Junctional nevus Terry’s nails Half-and-half nails Dystrophy from preform ed artificial nails

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Co m m o n Na il Pro b lem s Lon gitu d in al Rid gin g (On ych orrh exis) Longitudinal ridging is a very common and normal variant in elderly persons. It consists of parallel ridges that run lengthwise along the nail plates (FIG. 13.1). Such ridges are more commonly observed in fingernails than in toenails. Occasionally, longitudinal ridging is seen in younger persons. The etiology is unknown and the condition is not indicative of any trauma, infection, or nutritional deficiency.

MANAGEMENT 13.1 Longitudinal ridging. Parallel elevated ridges are characteristic of this normal variant. The ridges may have a beaded appearance.

• There is no treatment available to decrease longitudinal ridging, except for filing and buffing the ridges down with a soft file.

Brittle Nails (On ych osch izia)

13.2 Onychoschizia. The distal nail splits into layers parallel to the nail’s surface.

MANAGEMENT Traditionally, distal nail splitting has been compared to scaly, dry skin elsewhere on the body. Thus, many treatment recommendations are similar to those for dry skin: • Avoid excessive contact with water soaps, and other detergents. Wear gloves when washing dishes. • Gloves should be worn in cold weather. • Apply moisturizing creams or ointments (e.g., lactic acid creams in 5% to 12% concentrations) at bedtime or after bathing or washing. 260

Brittle and split (onychoschizia) nails are common in adults (FIG. 13.2). In some people, nails become fragile and easily break off at the free edge. This has traditionally been considered a sign of nail plate dehydration; however, a recent study has indicated that the water content of brittle nails is not significantly different from that of normal nails. Brittle nails are a common complaint in adult and elderly women and can also be observed in people with iron deficiency and thyroid disease. Elderly men are less apt to present with this problem. The increased incidence in women may be a result of their higher cosmetic awareness, their frequent use of nail products, menopausal status, or frequent exposure to harmful extrinsic factors (e.g., detergents or water).

• Keep the nails short; trim them when they are well hydrated and less likely to be frayed and use a soft file to keep the distal nail edge smooth. • Consider taking the B2-complex vitamin supplement biotin (2.5 mg/day). Some observers claim to have had some success in increasing nail integrity and thickness with this regimen.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

On ych olysis This finding represents a separation of the nail plate from its underlying attachment to the pink nail bed (FIG. 13.3). The separated portion is white and opaque, in contrast to the pink translucence of the attached portion. Normal physiologic onycholysis is seen at the distal free margin of healthy nails as they grow. It usually starts distally and progresses proximally, causing an uplifting of the distal nail plate. When separation is more proximal, the onycholysis becomes more obvious and becomes cosmetically objectionable. In some patients, the nail takes on a green or yellow tinge (see the discussion of green nail syndrome later in the next section). Onycholysis is most frequently seen in women, particularly in those with long fingernails. It may become painful and may interfere with routine function of the nails (e.g., picking up small objects, such as coins and paper clips).

Pat h o g e n e sis Whereas onycholysis may sometimes result from onychomycosis (tinea unguium), fungal nail infection is only one cause of onycholysis. The causes of this disorder can be divided into two main types, external and internal. Ex t er n a l Ca u ses

• Irritants such as nail polish, nail wraps, nail hardeners, and artificial nails can cause the problem. Onycholysis may also be seen in persons who frequently come into contact with water, such as bartenders, hairdressers, manicurists, citrus fruit handlers, and domestic workers. • Trauma, especially habitual finger sucking, athletic injuries to the toes, wearing of tight shoes, and the use of fingernails as a tool, can all cause the disorder. • Traumatic onycholysis of the toenails can be caused by a lack of appropriate nail care. It is often difficult for elderly patients to trim toenails frequently. This may be a result of arthritis, decreases in fine motor control, or a decline in flexibility. Such difficulties may result in long nails that interfere with shoes fitting properly. • Fungal infections (e.g., chronic paronychia or onychomycosis) are another cause. • Some drugs can act as phototoxic agents to induce fingernail onycholysis. Photo-onycholysis usually occurs abruptly on multiple nails at the same time (rather than slowly progressing). Such drugs include diuretics, sulfa drugs, tetracycline, doxycycline, and, particularly, demethylchlortetracycline.

13.3 Onycholysis. The separated portion of the nail is white and opaque; the attached portion is pink and translucent. In t ern a l Ca u ses

• Psoriasis is the most common cause. Patients generally have evidence of psoriasis elsewhere on the body, or there may be other psoriatic nail findings, such as pitting. • Inflammatory skin diseases of the nail matrix (root), such as eczematous dermatitis or lichen planus, can cause onycholysis. • Neoplasms and subungual warts are possible causes, especially if only one nail is involved (See FIG. 13.20). • Other possible internal causes include thyroid disease, pregnancy, and anemia.

MANAGEMENT The goal of management is to keep the newly growing nail attached by: • Keeping nails dry and cut closely; proper trimming (along the contour) on a regular basis can protect the nails from injury • Using nail polish sparingly • Avoiding unnecessary manipulation of nails • Treating or avoiding the underlying cause of the problem, if known

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Green Nail Syn d rom e This is a consequence of onycholysis. Green nail syndrome is a painless discoloration under the nail and should not be confused with a subungual fungal infection (FIG. 13.4).

Pat h o g e n e sis • The “dead space” under the onycholytic nail serves as an excellent breeding ground for microbes. • Often, Pseudomonas species are present; their presence usually accounts for the green or green-black nail color.

MANAGEMENT 13.4 Green nail syndrome. The “dead space” under the nail often harbors Pseudomonas species. The green color is virtually pathognomonic for Pseudomonas.

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• Soak the affected nail twice daily in a mixture either of one part chlorine bleach and four parts water or of equal parts acetic acid (vinegar) and water. This generally eliminates the discoloration. • If possible, avoid or minimize the underlying cause (i.e., the factor that led to onycholysis, as described in the previous section).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Tra u m a a n d In fl a m m a t io n BASICS • Injuries to the nail root (the matrix that directly underlies the proximal nail fold) may be caused by direct trauma, microbes (e.g., fungi, bacteria), inflammatory conditions (e.g., eczema), or a digital myxoid cyst. • These disorders sometimes result in characteristic deformities; for example, nail pitting, “oil spots,” and onycholysis may be seen in patients with psoriasis. • At other times, deformities result from eczema in the proximal nail fold.

Trau m atic Lesion s Trauma is the most common cause of nail disorders.

Sub un g ual He m at o m a This condition results from trauma to the nail matrix or nail bed, such as repeated minor injuries (e.g., tight shoes, sports injuries) or substantial impact (as from a hammer). • An acute subungual hematoma that results from rapid accumulation of blood under the nail plate can be very painful (FIG. 13.5), whereas small lesions may be painless and may go unnoticed for some time. • Chronic, painless subungual hematomas that are clearly not the result of trauma may appear similar to a neoplasm, such as an acral lentiginous melanoma (which is very rare). Because the coagulated bloodstains remain until the nail grows out (for 6 to 12 months), the diagnosis may be in doubt for some time.

DIFFERENTIAL DIAGNOSIS • Junctional nevus is a possibility (see FIG. 13.21; see FIG. 22.51). • Acral lentiginous melanoma should be considered (see FIG. 22.52).

POINT TO REMEMBER • If there is a strong suspicion of melanoma, the nail bed should undergo biopsy.

13.5 Acute subungual hematoma. This results from the rapid accumulation of blood.

MANAGEMENT • An acute, painful, swollen subungual hematoma may be incised and drained by placing the red-hot end of a heated paper clip on the area elevated by the hematoma. The small hole created with this procedure allows the blood to drain and thus quickly relieves the pain. (Note: This technique is best left to a health professional. Patients with hematomas should not be encouraged to try it themselves.) • Twirling a 27-gauge needle to create a similar hole is an alternative method for draining the blood.

HELPFUL HINT • A rapid method to substantiate the presence of a hematoma is to pare the nail plate gently with a no. 15 scalpel blade or to file it down until the coagulated blood can be visualized.

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Me d ian Nail Dyst ro p h y • This condition results from a compulsive habit—repeated trauma to the proximal nail fold of the thumb, usually inflicted by the nail of the adjacent index finger (FIG. 13.6). Some patients may do this with both hands, and this causes bilateral damage. • The resultant nail deformity is analogous to an injury to the root of a tree that deforms the growing tree trunk. Dia gn o sis

• The patient can sometimes be observed performing the repeated action without being aware of it. (This is particularly true in children.)

MANAGEMENT • Treatment of any habit is difficult; the habit and resultant nail deformity are usually chronic by the time medical attention is sought. • It can be suggested to patients that breaking this habit may be aided by an alternative activity, such as knitting or needlepoint. Parents may be advised to have children keep tape or another dressing on the affected nails.

A

B 13.6 A an d B Median nail dystrophy. A: Note the vertical ridging (“washboard” appearance) in the nails caused by a habitual tic. After repeated trauma to the proximal nail fold, median nail dystrophy can result. B: Most often, the patient habitually presses the nail of the adjacent finger against the proximal nail fold.

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In flam m atory Disord ers Inflammatory disorders that involve the nail matrix, such as psoriasis, can result in distinctive deformities of the nails, whereas other conditions, such as eczema of the proximal nail fold, result in nonspecific deformities.

Pso riasis • The typical nail changes are pitting (FIG. 13.7), onycholysis, thickening (subungual hyperkeratosis), and “oil spots.” • For a more comprehensive discussion, see Chapter 3, “Psoriasis.” Ecze m at o us De rm at it is wit h Se co n d ary Nail Dyst ro p h y • Nail deformity secondary to eczematous dermatitis is a problem that is often overlooked in patients with severe atopic dermatitis (FIG. 13.8). • It results when eczematous dermatitis involves the distal extensor surface of the fingers, and the associated inflammation also involves the matrix, or “root,” of the nail. The inflamed matrix, which underlies the proximal nail fold, consequently gives rise to a dystrophic nail plate.

13.7 Psoriasis. Pitting, onycholysis, and “oil spots” are evident in this nail.

DESCRIPTION OF LESIONS • Eczematous dermatitis that involves the nail plate is located on the dorsum of the distal part of the finger (the proximal nail fold). • The nails generally have a ripplelike deformity that corresponds to the time of activity of the inflammation.

MANAGEMENT • Improvement of the appearance of the nail plate follows control of inflammation of the proximal nail fold skin with the use of topical steroids.

13.8 Eczematous dermatitis. The eczema of the proximal skin also affects the matrix (root) of the nail; this results in nail dystrophy.

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In fect io n s o f t h e Na il a n d Su r ro u n d in g Tissu es The term paronychia refers to inflammation of the nail folds surrounding the nail plate. The condition can be either acute or chronic.

Acu te Paron ych ia

13.9 Acute paronychia. Acutely red, tender, unilateral involvement of the proximal nail fold. Often, pus is visible through the proximal or lateral nail fold.

Pat h o g e n e sis • Acute paronychia usually results from an infection caused by Staphylococcus aureus; less commonly, it may be caused by streptococci or Pseudomonas species. • Generally, only one nail is involved. • The condition may occur spontaneously, or it may follow trauma or manipulation, such as nail biting, a manicure, or removal of a hangnail. CLINICAL MANIFESTATIONS • Acute paronychia is heralded by the rapid onset of bright red swelling of the proximal or lateral nail fold behind the cuticle. • A throbbing, tender, and intensely painful lesion often results (FIG. 13.9).

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS • Acute bacterial paronychia can be confused with herpetic whitlow. • A Tzanck preparation (see FIG. 6.26), bacterial culture, or both must be performed when the diagnosis is in doubt.

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MANAGEMENT • Mild cases may require only warm saline or aluminum acetate (Domeboro 1:40) soaks for 10 to 15 minutes two to four times daily. • In more severe cases, simple incision and drainage (with a no. 11 surgical blade) usually afford rapid relief of pain. • Occasionally, systemic therapy with antistaphylococcal antibiotics, such as dicloxacillin, or a cephalosporin, may be needed.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ch ron ic Paron ych ia This condition primarily results from a combination of chronic moisture, irritation, and trauma to the cuticle and proximal nail fold (FIG. 13.10). It occurs much more often in women than in men, and it is particularly common in persons whose hands are frequently exposed to a wet environment, such as housewives, domestic workers, bartenders, janitors, bakers, dishwashers, dentists, dental hygienists, and children who habitually suck their thumbs. It is also seen more often in patients with diabetes and in persons who manicure their cuticles. The predisposing factor is usually trauma or maceration that produces a break in the barrier (cuticle) between the nail fold and nail plate. This allows moisture to accumulate and microbial colonization to follow.

Pat h o g e n e sis • Although Candida is frequently isolated from the proximal nail fold of patients with chronic paronychia, a primary pathogenesis for this organism has never been proven. • In fact, evidence indicates that this condition is not a fungal infection at all but is actually an eczematous process. • Instances in which Candida may play a primary pathogenic role include patients who are diabetic and those with primary mucocutaneous candidiasis. • For this reason, topical steroids are often a more effective therapy than topical or even systemic antifungal agents. CLINICAL MANIFESTATIONS • Chronic paronychia usually develops slowly and asymptomatically. • Secondary nail plate changes often occur, including onycholysis (see earlier discussion). A greenish or brown discoloration along the lateral borders and transverse ridging of the nails may appear. • One or more fingers can be involved.

13.10 Chronic paronychia. In addition to erythema and edema of the proximal nail fold, nail dystrophy and the absence of a cuticle is noted here.

DIFFERENTIAL DIAGNOSIS • The diagnosis can generally be established based on the typical clinical appearance of the fingers and the patient’s history. The presence of a candidal infection can be confirmed with a potassium hydroxide preparation or fungal culture, if necessary. • Various pathogens and contaminants—including Candida species, gram-positive or gram-negative organisms, or mixed flora—may be cultured from the pus obtained from under the proximal nail fold. Bacterial culture often grows a mixed flora.

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MANAGEMENT • Avoid prolonged exposure to moisture and trauma, especially frequent hand washing and manicures. • Wear gloves (the cotton-under-vinyl variety is best) when performing tasks such as washing dishes. In addition, one or more of the following treatments should be considered: • A superpotent topical steroid such as clobetasol cream 0.05% can be applied once or twice daily to the proximal nail fold. Alternatively, Cordran tape may be applied nightly to this area.

• One to two drops daily of 3% thymol in 70% ethanol (compounded by a pharmacist) can be placed under the proximal nail fold. • A topical broad-spectrum antifungal agent, such as clotrimazole, ketoconazole, econazole, or miconazole, is often combined with a potent topical corticosteroid (see earlier discussion) to provide antifungal as well as anti-inflammatory effects. • If topical therapy is ineffective, oral broad-spectrum antiyeast therapy such as itraconazole (Sporanox) or ketoconazole (Nizoral) may be prescribed if clinically indicated and there are no contraindications to their use.

POINTS TO REMEMBER • Chronic paronychia is frequently misdiagnosed—and treated—as an acute staphylococcal paronychia. • Chronic paronychia is distinct from onychomycosis, which is a fungal infection of the nail itself.

On ych om ycosis For a complete discussion, see Chapter 7, “Superficial Fungal Infections.” SEE PATIENT HANDOUT “Fun g al Nails (On ych o m yco sis)” ON THE SOLUTION SITE 13.11 Digital mucous (myxoid) cyst. Note the longitudinal groove in the nail plate.

Digital Mu cou s (Myxoid ) Cyst This is not a true cyst, because it lacks an epidermal lining. It is actually a focal collection of clear, gelatinous, viscous mucin (focal mucinosis) that occurs over the distal interphalangeal joint or, more commonly, at the base of the nail. DESCRIPTION OF LESIONS

13.12 Digital mucous (myxoid) cyst over the distal interphalangeal joint. Notice the absence of the longitudinal groove. 268

• Pressure from the lesion on the nail matrix (root) often results in a characteristic longitudinal groove in the nail plate (FIG. 13.11). • When the lesion occurs more proximally, such as over the distal interphalangeal joint, there is no longitudinal groove (FIG. 13.12). • This dome-shaped, rubbery lesion occurs exclusively in adults, particularly in women older than 50 years of age. Some myxoid cysts are believed to be a consequence of osteoarthritis, rather than trauma.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

MANAGEMENT This benign lesion may be treated as follows: • It may be ignored, particularly if it is asymptomatic. • Lesions have reportedly resolved after several weeks of daily firm compression. • Incision and drainage (FIG. 13.13 ), cryosurgery with liquid nitrogen, and intralesional triamcinolone injections may be performed, with varying results. • Surgical excision is reserved for the occasional painful or otherwise troublesome lesion. A

B

13.13 A an d B Digital mucous (myxoid) cyst. Incision and drainage. Blood-tinged, viscous, jellylike mucoid material is expressed.

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Miscella n eo u s Na il Diso rd ers • In addition to the disorders already described, various other conditions can affect the nails. • Some of these disorders produce characteristic nail findings that may serve as clues to unrecognized systemic disease.

Le uko n ych ia St riat a FIGURE 13.14. • Leukonychia striata, which is also called transverse striate leukonychia, is often mistaken for a fungal nail infection. • These white lines result from an injury to the nail matrix that occurred about 2 to 3 months earlier. The underlying injury is often an antecedent illness or the repeated trauma of manicuring; occasionally, it develops after liquid nitrogen therapy for warts. 13.14 Leukonychia striata. These white spots caused by trauma are extremely common.

Ye llo w Nail Syn d ro m e FIGURE 13.15. • The nails are yellow, curved, and grow slowly. Yellow nail discoloration also has been reported in patients with acquired immunodeficiency syndrome. • This syndrome is associated with certain respiratory disorders (e.g., bronchiectasis, chronic respiratory infections, lymphedema, pleural effusion, ascites).

In cre ase d Tran sve rse Nail Curvat ure (Pin ce r Nails) FIGURE 13.16.

13.15 Yellow nail syndrome. These are thickened, slowgrowing nails.

• Increased transverse curvature is often manifested as a pincer nail deformity. • In this deformity, the nails’ normal transverse curvature increases along the longitudinal axis and becomes more pronounced at the distal edge, which results in “pinching” of the underlying skin. This condition can become quite painful and may predispose the patient to infections and ingrown nails. • Pincer nails are often congenital and may be seen in persons with the yellow nail syndrome or as a normal variant. They are also seen in women who wear ill-fitted shoes as well as those who also have inflammatory osteoarthritis.

13.16 Pincer nails. The nails curve inward and pinch the nail bed.

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Ko ilo n ych ia FIGURE 13.17. • Acquired koilonychia, also known as spoon nails, may be seen in association with trauma to the cuticle and proximal nail folds, iron-deficiency anemia, hemochromatosis, or endocrine or cardiac disease. Spoon-shaped or concave nails may also be seen in early infancy and may be self-limited.

Sarco id o sis FIGURE 13.18. • Dystrophic, thickened nail plates result from infiltration of the proximal nail folds by sarcoidal plaques. • Note that only those nail folds with sarcoidal infiltrates of the proximal nail folds are associated with nail plate dystrophy.

13.17 nail.

Koilonychia. Note the spoon-shaped curve of the

De rm at o m yo sit is FIGURE 13.19. • The proximal nail fold demonstrates periungual erythema, telangiectasias, thickening of the cuticles (“ragged cuticles”), and distal nail plate thinning.

13.18 Sarcoidosis. Note that the dystrophic changes affect only nail plates that have involvement (sarcoidal lesions) of proximal nail folds.

13.19 Dermatomyositis. Periungual telangiectasias as well as nail dystrophy are apparent in this patient.

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Sub un g ual Ve rruca FIGURE 13.20. • A solitary wart of the nail bed lifting the nail plate is often mistaken for a fungal infection. • The possibility of subungual squamous cell carcinoma, basal cell carcinoma, or other neoplasm should always be considered if only one nail or periungual area is involved. Squamous cell carcinoma usually presents in the elderly and has a male predominance.

Jun ct io n al Ne vus FIGURE 13.21.

13.20 Subungual verruca. Rarely, in the proper clinical context, a solitary lesion such as this can be a squamous cell carcinoma.

• This evenly pigmented linear nevus emanates from nests of nevus cells in the nail matrix. • These lesions are quite common in blacks and may be multiple. They are much less common in whites. • Any smudging or leaching of pigment or variation from the original black band should prompt an immediate biopsy to rule out malignant melanoma (see FIG. 22.51).

Te rry’s Nails FIGURE 13.22. • Terry’s nails are associated with cirrhosis, congestive heart failure, and adult-onset diabetes mellitus. This condition also may be seen as a normal finding associated with age. • The patient shown in Figure 13.22 had a liver transplant for cirrhosis. His nail beds are white with a narrow zone of pink under the distal end of the plate.

13.21 Junctional nevus. A brown linear band of longitudinal melanonychia in a child.

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Terry’s nails. This patient had cirrhosis of the liver. Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Half-an d -Half Nails FIGURE 13.23. • The proximal half of the nail is white and the distal portion retains the normal pink color. • These characteristic color changes may be seen in chronic renal failure.

Dyst ro p h y fro m Pre fo rm e d Art ificial Nails FIGURE 13.24. • Acrylic sculptured nails and the less expensive preformed plastic artificial nails are used for nail elongation. They are attached directly to the natural nail plate, which they cover entirely. The artificial nails are glued to the natural nail plate with an acrylate-based adhesive. • Minor upward pressure on the distal tip of the artificial nail can result in significant distal onycholysis; complete nail avulsion can even result. Any space between the natural nail plate and the artificial nail may become infected (bacterial or fungal) or deformed, and this will often not be noticed until removal of the artificial nail.

13.23 Half-and-half nails. Note that the proximal half is white and the distal half is pink. This patient had renal failure.

13.24 Nail dystrophy from artificial nails. The nail deformity in this woman was noticed when her artificial nails were removed.

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C H AP T ER

Pigmentary Disorders

14 OVERVIEW DISORDERS OF HYPOPIGMENTATION • • • • •

Vitiligo vulgaris Other form s of hypopigm entation Postinflam m atory hypopigm entation Idiopathic guttate hypom elanosis Other types of hypom elanosis DISORDERS OF HYPERPIGMENTATION

• • • • •

Melasm a Postinflam m atory hyperpigm entation Phyto-photoderm atitis and berloque derm atitis Poikiloderm a of Civatte Confluent and reticulated papillom atosis (GougerotCarteaud disease) • Acanthosis nigricans • Carotinem ia

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Skin color is mainly due to melanin. The amount of melanin is determined primarily by hereditary factors and by the result of exposure to ultraviolet radiation (tanning).

Me lan o g e n e sis Melanocytes in the basal layer of the epidermis produce melanin. The melanin pigment is manufactured on melanosomes (intracytoplasmic organelles). Once made, the melanosomes are carried along dendrites and delivered to neighboring keratinocytes of the epidermis. Darkly pigmented skin has melanosomes that contain more melanin and are larger in diameter than in light skinned individuals, and when those melanosomes are transferred to keratinocytes, they are singly dispersed and degrade more slowly. Increase in melanin (hyperpigmentation or hypermelanosis) can be due to an increased number melanocytes or from increased production of melanin. Reduction in melanin production or a loss of melanocytes results in pale patches (hypopigmentation or hypomelanosis) or white patches (leukoderma). Vitiligo is a specific type of leukoderma characterized by depigmentation of the epidermis due to a partial or complete loss of melanocytes.

Diso rd ers o f H yp o p igm en t a t io n Vitiligo Vu lgaris BASICS • An acquired disorder of skin depigmentation, vitiligo vulgaris (common vitiligo) affects 1% to 2% of the world’s population. • Thirty percent of patients with vitiligo report a positive family history of the disorder. • A distinct form of vitiligo occurs in children, and this form is often segmental or dermatomal in its distribution. Some children may develop halo nevi, which are melanocytic nevi encircled by a white halo of depigmentation (see Chapter 21, “Benign Skin Neoplasms”).

Pat h o g e n e sis • Although the cause of vitiligo vulgaris is still unknown, the condition is thought to result from an autoimmune process that prompts the loss of melanocytes. Vitiligo may develop in patients with other diseases that are believed to have an autoimmune basis (e.g., thyroid dysfunction, Addison’s disease, alopecia areata, diabetes mellitus, and pernicious anemia), and this finding supports the hypothesis that an immune mechanism may be involved in its pathogenesis. • Another theory proposes that vitiligo is caused by an abnormality of nerve endings adjacent to skin pigment cells.

14.1 Vitiligo. Depigmented macules are characteristic of vitiligo vulgaris. Note the characteristic periorificial distribution in this patient.

DESCRIPTION OF LESIONS • Physical examination of a patient with vitiligo reveals hypopigmented (FIG. 14.1) or depigmented, chalk-white macules. • Occasionally, the lesions may have various shades of color and may include islands of repigmentation (FIG. 14.2). • In dark-skinned people, pigmentary loss may be observed at any time of year, whereas in light-skinned people, the lesions may be most obvious in the summer, because the tanning effects of the summer sun can accentuate the contrast between the light and dark skin.

14.2 Vitiligo. Various shades of hypopigmentation, depigmentation, and islands of spontaneous repigmentation can be seen in this patient. Note the white eyelashes.

DISTRIBUTION OF LESIONS • Vitiliginous lesions tend to have a bilateral, symmetric distribution. • They frequently occur on acral areas (e.g., the hands and feet), body folds, bony prominences, and external genitals. • Lesions characteristically appear around orifices (e.g., the mouth, eyes, nose, and anus), but they may also involve the eyebrows, eyelashes, and scalp hair, resulting in white hairs (leukotrichia). • In severe cases, vitiligo may be more widespread (FIG. 14.3) or even total (vitiligo universalis). 14.3 Vitiligo. Extensive depigmentation is evident in this patient.

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CLINICAL MANIFESTATIONS • Clinical manifestations often develop cyclically. A rapid loss of pigment is followed by a stable period (during which some repigmentation may occur), and then generally by recurrence. • Some patients spontaneously experience partial repigmentation; total repigmentation is unusual. • Patients with severe vitiligo may experience embarrassment and lowered self-esteem. DIAGNOSIS • A clinical diagnosis of vitiligo is usually based on the characteristic appearance of the skin lesions. • The diagnosis can be aided by Wood’s lamp examination; this should reveal a milk-white fluorescence. Wood’s lamp is a handheld black light that makes hypopigmented areas appear lighter and depigmented areas (e.g., those produced by vitiligo) appear as a pure white or bluish white fluorescence (FIG. 14.4).

A

B 14.4 A an d B Vitiligo. Wood’s lamp examination reveals a “milk-white” fluorescence in areas depigmented by vitiligo. Note the depigmented eyebrows and eyelashes.

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DIFFERENTIAL DIAGNOSIS

Po st in flam m at o ry Hyp o p ig m e n t at io n See also later discussion. • Because the lesions of this disorder are not totally depigmented, they are generally off-white in color. • Often, patients who have postinflammatory hypopigmentation reveal a history of preexisting inflammatory dermatitis, such as eczema or tinea versicolor.

Le p ro sy • Cutaneous leprosy often manifests with areas of hypopigmentation. The lesions may appear as hypopigmented macules, plaques, or nodules that become insensitive to touch. • Leprosy is extremely rare in the United States, but it may be seen occasionally in patients who emigrate from endemic areas, such as India or parts of South and Central America.

Hyp o p ig m e n t e d Tin e a Ve rsico lo r • This disorder is frequently mistaken for vitiligo vulgaris. Patients with active, untreated tinea versicolor have a whitish scale. • In addition, under Wood’s lamp examination, the lesions may appear as a yellow-orange fluorescence, and skin scrapings tested with potassium hydroxide are positive for the hyphae and spores of the responsible yeast. Inactive, or postinflammatory, spots of tinea versicolor lack scale and are hypopigmented (see Chapter 7, “Superficial Fungal Infections”). Ch e m ical Le uko d e rm a • This develops on the hands of persons who work with germicidal detergents or with certain rubber-containing compounds that destroy melanocytes. • The diagnosis is established based on the location of the lesions (e.g., only on the hands) and a history of exposure (FIG. 14.5).

MANAGEMENT • Treatment options for vitiligo include repigmentation therapies for the macules and depigmentation of the remaining healthy skin in patients with extensive disease. • If administered early to patients with limited disease, potent (class 2) and superpotent (class 1) topical corticosteroids are occasionally helpful in promoting repigmentation. • The hands and feet respond poorly to this treatment as well as other therapies mentioned in this section. • Less potent topical steroids such as 1% hydrocortisone should be used on eyelid skin. • Reports of repigmentation have been noted in some patients who applied tacrolimus (Protopic) 0.1% ointment or picrolimus (Elidel) 1% cream twice daily for 2 to 3 months.

14.5 Chemical leukoderma. Chemically induced depigmentation is limited to this patient’s hands. Exposure to a cleaning product containing phenol caused the areas of depigmentation in this patient, who routinely used the product at work.

• Photochemotherapy (see Chapter 3, “Psoriasis”), using psoralens and natural sunlight or psoralens and ultraviolet A light (PUVA) in a phototherapy light box, is sometimes tried. However, this treatment is time-consuming and often ineffective. It should generally not be used for children younger than 9 years. • The treatments are 50% to 70% successful in restoring some color on the face, trunk, and upper arms and legs. • Again, the hands and feet respond poorly to this method. • Narrow-band UVB and excimer laser therapy are expensive and not readily available. • Surgical transplants may be attempted. The following methods may be tried for small, stable areas of vitiligo. • Punch grafts: Punch biopsy specimens from a pigmented donor site are transplanted into depigmented continued on page 278

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MANAGEMENT Continued

sites, however, a residual, pebbled pigmentary pattern may result. • Minigrafting: Small donor grafts are inserted into incisional recipient areas of vitiligo and held in place with pressure dressings. As with punch grafting, this procedure does not result in total return of normal pigment, and a mottled pigmentation may result. • Special cosmetic makeup that is formulated to match the patient’s normal skin color (e.g., Dermablend or Covermark) or self-tanning compounds that contain dihydroxyacetone may effectively hide the white patches. • Sunscreens can be used to avoid exacerbating the contrast between normal skin and lesions and to protect the lesions, which are sensitive to the sun. • If attempts at repigmentation do not produce satisfactory results, depigmentation may be attempted in selected patients. Those with extensive vitiligo (more than 50% loss of pigment) may elect to have the remaining skin “bleached” with Benoquin (20% monobenzyl ether of hydroquinone). The results are permanent (FIG. 14.6).

14.6 Vitiligo. Extensive depigmentation. The residual normal pigmentation was treated with Benoquin.

HELPFUL HINTS

POINTS TO REMEMBER • Health care professionals should resist the tendency to trivialize vitiligo by referring to it as simply a cosmetic disorder. • Patients should be urged to use sunscreens whenever they are exposed to the sun. By minimizing tanning, sunscreens lessen the contrast between healthy skin and lesions; they also protect the vitiliginous skin, which is sensitive to the sun. • If indicated by positive findings in the patient’s history or physical examination, screening of vitiligo patients for autoimmune diseases should be done; however, the frequency of these associations is not sufficiently high to warrant routine blood tests. • Response rates to treatments for vitiligo often are disappointing, and lesions on the backs of the hands and feet are very resistant to therapy.

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• Clinicians should be sensitive to patients who have emigrated from countries in which leprosy is endemic—and generally dreaded. Such patients may feel particularly embarrassed and stigmatized by focal areas of lightened skin color, regardless of the cause of the hypopigmentation. • For children who have light skin tones, sunscreens and observation may be the best course.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

SEE PATIENT HANDOUT “Vit ilig o ” ON THE SOLUTION SITE

Oth er Form s of Hyp op igm en tation BASICS • Although hypopigmentation and depigmentation are more obvious in dark-skinned persons, they can cause problems even in light-skinned persons, particularly those who tan. • Persons with dark complexions appear to be at an increased risk of developing these pigmentary changes. • Postinflammatory reactions are the most common cause of hypopigmentation. Localized alterations in skin color are not uncommon after many cutaneous inflammatory conditions. In addition, neonates and toddlers may exhibit congenital areas of hypopigmentation. • Occasionally, a combination of light and dark patches may develop. • Often, the pigmentary changes are self-limited; they require only time for resolution. Nevertheless, they can be a source of embarrassment for many patients. Providing reassurance and practical advice on how best to conceal the areas of altered skin color can help patients cope better with these disorders.

14.7 Atopic dermatitis. Postinflammatory hypopigmented macules can be seen in this infant who has atopic dermatitis. Note active areas of inflammation on the neck and axillary areas.

Po st in flam m at o ry Hyp o p ig m e n t at io n • Lightening of the skin may follow nearly any inflammatory cutaneous eruption (e.g., eczema or psoriasis; FIG. 14.7). • In pityriasis alba, hypopigmented round spots are commonly seen on the face and other areas of the skin in children with atopic dermatitis. Occasionally, the slightly scaly patches that precede the hypopigmentation may be seen (FIG. 14.8). • Postinflammatory hypopigmentation may also develop after an injury to the skin, such as a burn or surgical scar. The areas of hypopigmentation roughly correspond to the location and shape of the antecedent eruption (“footprints”). 14.8 Pityriasis alba. Hypopigmented round spots are commonly seen on the faces in children who have atopic dermatitis.

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MANAGEMENT • In general, the pigmentary changes that follow mild inflammatory dermatoses slowly revert to normal over several months. However, those that follow more severe inflammation or injury may be permanent. • For facial lesions, if there is any scale or erythema, treatment with a mild class 6 topical steroid such as over-the-counter 1% hydrocortisone cream twice daily may be helpful. • The passage of time often improves the cosmetic abnormality. • In the interim, makeup products such as Covermark and Dermablend can be used to conceal the areas of hypopigmentation. • Artificial tanning lotions can also be useful.

Id iop ath ic Gu ttate Hyp om elan osis 14.9 Idiopathic guttate hypomelanosis. Note the white spots on this elderly woman’s shin.

HELPFUL HINTS • Postinflammatory hypopigmentation is of greater concern to patients with darker skin; in fact, the hypopigmentation is more often more troubling than the preceding inflammatory condition that brought it on. • Pityriasis alba and tinea versicolor are the most common causes of postinflammatory hypopigmentation, and both are commonly misdiagnosed as vitiligo.

Idiopathic guttate hypomelanosis (IGH) is the formal name for the idiopathic white spots that often appear on the arms and lower legs of middle-aged and elderly people. This condition occurs in all races, but as with vitiligo, it is more apparent in persons with darker skin. Typically, IGH develops first on the legs of women in early adult life (FIG. 14.9). Later, it may spread to other sun-exposed areas, such as the arms and the upper part of the back. • The characteristic discrete, angular, or circular macules are 1 to 3 mm in diameter. However, lesions may measure up to 10 mm in diameter. • These spots tend to develop more commonly in areas of chronic sun damage, particularly on the anterior lower legs and forearms. Inexplicably, the face is not involved. • They produce no symptoms other than skin discoloration. • There is no effective treatment.

HELPFUL HINT • Patients should be reassured that this condition is not vitiligo.

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Oth er Typ es of Hyp om elan osis Numerous systemic and congenital conditions may cause hypopigmentation. They include the following: • Endocrine diseases, such as Addison’s disease and hypothyroidism, may cause hypopigmentation. • Genetic conditions, such as congenital vitiligo, tuberous sclerosis, and albinism, may also cause this condition. • Congenital areas of hypopigmentation (FIG. 14.10). • Infectious diseases, such as leprosy, pinta, and yaws, may be causes. • In addition, hypomelanosis may result from the use of topical therapeutic agents, such as corticosteroids, hydroquinone, and retinoids. Nutritional deficiencies (especially vitamin B12 deficiency and kwashiorkor) may also cause a loss of pigmentation. These disorders should be considered in the appropriate clinical or environmental context.

POINT TO REMEMBER • The likelihood that normal pigmentation will return depends on the degree and type of injury.

14.10 Nevus depigmentosus. This off-white linear hypomelanosis has been present since birth. It has enlarged commensurate with the patient’s growth.

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Diso rd ers o f H yp erp igm en t a t io n Melasm a BASICS

14.11 Melasma of cheeks. Melasma may result from pregnancy, oral contraceptive use, or menopause, or it may arise de novo for no apparent reason.

• Formerly known as chloasma, melasma, or the “mask of pregnancy,” is an acquired form of hyperpigmentation that is seen most commonly on the face. • It may result from pregnancy, oral contraceptive use, or menopause, or it may arise de novo for no apparent reason. It is exacerbated by exposure to sunlight. Melasma is rare before puberty and most commonly occurs in women during their reproductive years. • When men are affected, the clinical and histologic picture is identical; however, the explanation for this condition is unknown. • Melasma is seen most frequently in young women of childbearing age, particularly those who have darker complexions and live in sunny climates. It is seen in Asia, the Middle East, South America, Africa, and the Indian subcontinent. In North America, melasma is most prevalent among Hispanics, African-Americans, and immigrants from countries in which it is common. CLINICAL MANIFESTATIONS AND DESCRIPTION OF LESIONS

14.12 Melasma of the “moustache” area. Note the darkening above the patient’s upper lip.

• Clinically, melasma is primarily a cosmetic problem. • It consists of asymptomatic, blotchy darkening of the facial skin. • Lesions are tan to brown, hyperpigmented macules that may coalesce into symmetric, well-demarcated patches (FIG. 14.11). • During pregnancy, the darkening of the skin often occurs in the second and third trimesters and spontaneously fades after termination of pregnancy. • Melasma also tends to fade on discontinuance of oral contraceptives or avoidance of sunlight; however, it may persist indefinitely. DISTRIBUTION OF LESIONS • Lesions are found mainly on the cheeks, angles of the jaw, forehead, nose, chin, and above the upper lip (FIG. 14.12).

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DIFFERENTIAL DIAGNOSIS

Po st in flam m at o ry Hyp e rp ig m e n t at io n See also the discussion in the subsequent section. • This may often be explained by a previous inflammatory eruption or injury. In general, lesions roughly correspond to the location of inflammation or injury, and they have less clearly defined margins than are seen in melasma.

MANAGEMENT • Treatment of melasma involves a combination approach using one or more bleaching agents and cosmetic camouflage. In addition, sun avoidance and the use of sunblocks are essential. • Bleaching creams that contain the tyrosinase inhibitor hydroquinone are readily available. Over-the-counter preparations such as Ambi and Esoterica contain 2% hydroquinone. • Preparations of 3% hydroquinone (Melanex) and 4% hydroquinone (Eldoquin Forte) are available by prescription only. Some products such as Eldopaque contain a sunblock; Lustra, a 4% hydroquinone agent, also contains vitamins C and E and glycolic acid. • Hydroquinone preparations are applied twice daily to areas of darkening only.

POINTS TO REMEMBER • Treatment requires patience during the many months in which lightening agents must be applied. • Without the strict avoidance of sunlight, potentially successful treatments for melasma are doomed to failure.

So lar Le n t ig in e s (“Live r Sp o t s”) • These lesions (referred to in the singular as lentigo) have uniform coloration and are acquired during middle age on sun-exposed areas, such as the face and backs of the hands (see also Chapter 21, “Benign Skin Neoplasms”).

• Other lightening agents include the tyrosinase inhibitor azelaic acid (Azelex 20% cream), which may be used in addition to hydroquinone. • Topical tretinoin can also be used in combination with both hydroquinone and a topical steroid (Tri-Luma cream). • Alpha-hydroxy acid products, such as mild glycolic acid peels, may also be used to hasten the effect of other topical lightening agents. They should be used cautiously in darkly pigmented Hispanics, Asians, and blacks because of the risk for postinflammatory pigmentary hyperpigmentation (see next section). • Kojic acid, a tyrosinase inhibitor, is used in Japan and the Middle East, and it seems to have an efficacy similar to that of hydroquinone.

HELPFUL HINTS • Patients receiving treatment should be cautioned to expect slow but gradual lightening. • Destructive modalities (e.g., cryotherapy, mediumdepth chemical peels, lasers) yield unpredictable results and are associated with numerous potential adverse effects. • Sunscreens that contain opaque physical blockers such as titanium dioxide and zinc oxide are preferred over chemical sunscreens because of their broader protection.

SEE PATIENT HANDOUT “Me lasm a” ON THE SOLUTION SITE

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Postin flam m atory Hyp erp igm en tation BASICS • Darkening of the skin may occur after nearly any inflammatory eruption, including eczema, lichen planus (FIG. 14.13), or acne (FIG. 14.14), or after an injury such as a burn. Elective skin treatments (e.g., chemical peels, laser resurfacing, or dermabrasion) may also precipitate it. • The hyperpigmentation stems from the melanocytes’ exaggerated response to cutaneous insult, which results in an increased or abnormal distribution of the pigment melanin. • Like melasma, postinflammatory hyperpigmentation tends to develop more often in people with dark complexions. 14.13 Lichen planus, postinflammatory hyperpigmentation. Hyperpigmentation is quite characteristic of healing lesions of lichen planus.

14.14 Postinflammatory hyperpigmentation. In this patient, healing acne lesions resulted in hyperpigmentation.

DESCRIPTION AND DISTRIBUTION OF LESIONS • Lesions tend to conform in location and shape to the preceding eruption or injury. • On occasion, lesions may mimic the exact shape of the inciting insult (FIG. 14.15).

A

MANAGEMENT • Often, the passage of time, coupled with sun protection, affords a gradual lightening of darkened areas. • Avoidance of the inciting event may prevent future lesions. Treatment of acne, for example, prevents the formation of new inflammatory lesions and allows old pigmented lesions to fade. • When lesions persist, many of the measures used to treat melasma (see earlier discussion) may be tried. However, persistent postinflammatory hyperpigmentation tends to be much more recalcitrant than is melasma to therapeutic measures, and cosmetic cover-ups may be used.

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B

14.15 A an d B Postinflammatory hyperpigmentation. In this patient, the cause was contact dermatitis from his eyeglasses. Note how the lesions conform to the shape of the frames.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ph ytop h otod erm atitis an d Berloq u e Derm atitis BASICS • A botanical cause for dermatitis is suspected when the pattern of the eruption is linear or streaky, such as that noted in the contact dermatitis caused by poison ivy (see Chapter 2, “Eczema”). The pattern is nearly always asymmetric. Some plants cause an eruption only after the skin is exposed to the sun; this is referred to as photocontact dermatitis or phytophotodermatitis. • When the phytophotodermatitis is caused by perfume or other agents such as oil from the bergamot lime (Citrus bergamia), an ingredient in perfumes and fragrances, it is referred to as berloque dermatitis. Bergapten is also a naturally occurring component of the following: • Various other fruits, such as lemon oil • Plants such as false Queen Anne’s lace (Ammi majus) and the giant Russian hogweed (Heracleum mantegazzianum) • The initial skin response on exposed parts that have been in contact with the plant or perfume and then exposed to the sun resembles an exaggerated sunburn with (FIG. 14.16A) or without blistering. • Ultimately, postinflammatory hyperpigmentation that may last several weeks (FIG. 14.16B) or months occurs. • The reaction is a chemically induced, nonimmunologic, acute skin irritation requiring light (usually within the UVA spectrum; i.e., 320 to 400 nm) on bergapten, or 5-methoxypsoralens, a furocoumarin, the photoactive component of bergamot oil.

Poikilod erm a of Civatte BASICS • This common condition occurs primarily in middle-aged, fair-skinned women. • It is primarily of cosmetic concern to patients. Hormonal changes related to menopause or low estrogen levels may be a causal factor. • Lesions consist of erythema associated with a mottled pigmentation located on the sides of the neck and other sunexposed areas. • The distribution of skin changes—the sparing of the shaded submental and submandibular areas—supports chronic sunlight exposure as the apparent cause of this condition (FIG. 14.17).

A

B 14.16 A an d B Berloque dermatitis. A: This woman was squeezing limes for an outdoor barbecue 2 days before this blistering, hyperpigmented eruption began. B: This is the same patient 2 weeks later. Note the postinflammatory hyperpigmentation.

MANAGEMENT • There is no very effective medical treatment; however, the patient should be advised about avoidance of sun exposure and the proper use of sunscreens to prevent further skin involvement. • The pulsed-dye laser has been noted to decrease the redness of this condition.

14.17 Poikiloderma of Civatte. The persistent erythema in this patient is characteristic. Note the sparing of the shaded areas under the chin and jawline.

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Con flu en t an d Reticu lated Pap illom atosis (Gou gerot-Carteau d Disease) BASICS

14.18 Confluent and reticulated papillomatosis. The darkly pigmented, coalescing papules are shown here in a typical distribution. Note that this patient also has evidence of acanthosis nigricans on her neck and axillae.

• Confluent and reticulated papillomatosis (CRP) is an uncommon condition of unknown etiology. Causal theories include an endocrine disruption, a disorder of keratinization, and an abnormal host reaction to Pityrosporum organisms or bacteria. • It usually has its onset shortly after puberty. • CRP is characterized by hyperkeratotic papules, usually located on the trunk. The lesions coalesce to form hyperpigmented, confluent plaques centrally and a reticular pattern peripherally (FIG. 14.18).

MANAGEMENT DIFFERENTIAL DIAGNOSIS • Acanthosis nigricans (see following section), which CRP resembles histopathologically, and darkly pigmented tinea versicolor are the most common conditions that may be confused with CRP.

• CRP responds to oral tetracycline, such as minocycline 100 mg twice a day.

Acan th osis Nigrican s BASICS • A characteristic hyperpigmented skin pattern, acanthosis nigricans occurs primarily in flexural folds. The skin is thought to darken and thicken in reaction to circulating growth factors. • Most cases of acanthosis nigricans, including idiopathic cases and those associated with obesity, are referred to as benign acanthosis nigricans. Other benign forms of acanthosis nigricans are associated with endocrine disorders, such as insulin-resistant diabetes, polycystic ovary syndrome, Cushing’s disease, Addison’s disease, pituitary tumors, pinealomas, and hyperandrogenic syndromes with insulin resistance (FIG. 14.19). Acanthosis nigricans is sometimes related to drug use, most commonly secondary

14.19 Acanthosis nigricans. This patient has diabetes. Note the marked hyperpigmentation.

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to glucocorticoids, nicotinic acid, diethylstilbestrol, or growth hormone therapy. Acanthosis nigricans may also be inherited without any disease associations. • The rare, so-called malignant acanthosis nigricans is associated with an internal malignant disease, usually an intraabdominal adenocarcinoma. Affected patients generally have a poor prognosis. The skin condition is sometimes seen before the cancer is recognized; it can also be associated with recurrences and metastases. DESCRIPTION OF LESIONS • Acanthosis nigricans generally presents with a gradual evolution of symmetric, asymptomatic, tan or brown to black, leathery or velvety plaques. The plaques are sometimes “warty” (papillomatous) and studded with skin tags. They have linear, alternating, dark and light pigmentation that becomes more apparent when the skin is stretched (FIG. 14.20). DISTRIBUTION OF LESIONS • The most common sites of involvement are the axillae, the base of the neck, the inframammary folds, the inguinal areas, and the antecubital fossae. • The dorsa of the hands (especially the knuckles), the elbows, and the knees are also common locations. • Less commonly, mucous membranes, the vermilion border of the lips, and the eyelids are involved.

14.20 Acanthosis nigricans. Linear, alternating dark and light pigmentation becomes more apparent when the skin is stretched.

POINTS TO REMEMBER • Malignant acanthosis nigricans generally has a sudden onset, but otherwise it clinically resembles the benign form of the disorder. • Concern is greatest when acanthosis nigricans suddenly arises in a nonobese adult who has no family history of the condition.

MANAGEMENT • Acanthosis nigricans is primarily a cosmetic concern. • Treatment is generally not effective

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Caroten em ia BASICS • Carotenemia is characterized by yellow pigmentation of the skin caused by an increased level of beta-carotene in the blood. Most cases result from prolonged and excessive consumption of carotene-rich foods, such as carrots, squash, and yams (sweet potatoes). • Less commonly, carotenemia has been associated with diabetes mellitus and hypothyroidism. DESCRIPTION OF LESIONS

14.21 Carotenemia. The yellow-orange palms in this patient from West Africa were attributed to his diet, which consisted of an abundance of yams.

• The yellow-orange pigmentation often appears on the palms and soles (FIG. 14.21). • The tip of the nose, the nasolabial folds, the palate, and other areas of the skin may become involved. • The sclerae are spared, which distinguishes carotenemia from jaundice.

MANAGEMENT • Diet-induced carotenemia is a benign condition. The yellow pigmentation generally resolves with dietary changes.

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C H AP T ER

Pruritus: The “Itchy” Patient

15 OVERVIEW Pruritus, the most common symptom of all skin diseases, can be simply defined as an unpleasant sensation that elicits the urge to scratch. Pruritus may result from the following: • Common primary skin disorders such as eczema, lichen simplex chronicus, xerosis, psoriasis, lichen planus, or, rarely, dermatitis herpetiformis • Exogenous causes such as drugs, contact dermatitis (e.g., poison ivy), scabies, lice, fiberglass, and aquagenic pruritus • Internal disorders such as chronic renal failure, acquired immunodeficiency syndrome, polycythemia vera, cholestasis, pregnancy-related disorders, primary biliary cirrhosis, diabetes mellitus, thyroid disease, and carcinoid syndrome • Psychogenic causes such as delusions of parasitosis, neurotic excoriations, pruritus ani, and obsessive-compulsive disorder • Associated malignant diseases such as Hodgkin’s disease, leukemia, and multiple myeloma

PRURITUS OF UNKNOWN ORIGIN (PUO) • • • • • •

Neurotic excoriations (factitia) Pruritus of chronic renal disease Pruritus caused by liver disease Pruritus resulting from hypothyroidism Pruritus resulting from hyperthyroidism Pruritus resulting from Hodgkin’s disease CLINICAL VARIANTS

• Aquagenic pruritus • Notalgia paraesthetica • Brachioradial pruritus

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Pru rit is o f Un k n o w n Origin BASICS Pruritus of unknown origin (PUO) is itching for more than 2 to 6 weeks with no determined cause. DESCRIPTION OF LESIONS • Linear excoriations, crusts, lichenified plaques, and wheals may be present. • Pruritus with no lesions is also quite common. • When lesions have bizarre appearances, facticia or “neurotic excoriations” should be suspected. (FIG. 15.1) (see also Chapter 2, “Eczema”).

15.1 Neurotic excoriations ( factitia). These self-induced ulcers convinced the patient that she was infested with lice.

DISTRIBUTION OF LESIONS • Symptoms or clinical lesions may be localized (FIG. 15.2) or widespread. DIAGNOSIS • A search for the cause of the pruritus is based on the following: • A careful history • Physical evidence (linear excoriations, crusts) • The workup for PUO includes the following: • Rectal and pelvic examinations, if indicated • Complete blood count • Stool examination for parasites and occult blood • Chest radiograph • Thyroid, renal, and liver function tests • Follow-up of the patient for as long as necessary to make a diagnosis

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MANAGEMENT • Whenever possible, treatment of the underlying systemic disease that causes the pruritus may bring relief. • Antihistamines are of more benefit in the treatment of allergic conditions, urticaria, and drug reactions than they are for the treatment of itching and may be no more effective than placebo. Despite this finding, the powerful effect of antihistamines as placebos should not be overlooked. • Topical therapy that can be soothing and helpful in some patients includes the following: • Menthol, phenol, camphor, and calamine lotions (e.g., Sarna, Prax, PrameGel) may be used. • Topical steroids are generally not very helpful when no lesions are apparent. • Cold applications of frozen vegetable packets may be useful.

Fo r Prurit us o f Ch ro n ic Re n al Dise ase • Renal pruritus occurs most often in those receiving hemodialysis. • Ultraviolet B (UVB) therapy is often effective. Narrow-band UVB is particularly effective. • Oral ingestion of activated charcoal may be helpful. It is inexpensive and generally well tolerated; therefore, it is considered a reasonable treatment when UV therapy has failed.

POINTS TO REMEMBER • Antihistamines often exert their antipruritic action by inducing sleep (soporific effect). • Topical emollients are an essential component of the therapy of pruritus when xerosis is present.

• Successful kidney transplantation is the only definitive treatment for chronic renal pruritus.

Fo r Prurit us Cause d b y Live r Dise ase • Cholestyramine (Questran), a bile acid sequestrant, can be used to treat the pruritus that often occurs during liver failure because of the liver’s inability to eliminate bile. Cholestyramine binds bile in the gastrointestinal tract to prevent its reabsorption. • Pruritus associated with obstructive malignancy of the biliary tract (e.g., primary sclerosing cholangitis) may be relieved by placing a stent to relieve the obstruction. Fo r Prurit us Re sult in g fro m Hyp o t h yro id ism • The pruritus of hypothyroidism is primarily secondary to xerosis and should be treated with emollients and thyroid hormone replacement. Fo r Prurit us Re sult in g fro m Hyp e rt h yro id ism • Pruritus secondary to hyperthyroidism generally improves with correction of thyroid function. Fo r Prurit us Re sult in g fro m Ho d g kin ’s Dise ase • Pruritus caused by lymphoma may precede the diagnosis. • Systemic corticosteroids with palliative chemotherapy in late-stage Hodgkin’s disease often provide relief.

HELPFUL HINTS • The dosage of antihistamines should be titrated gradually upward using nonsedating agents during the daytime and sedating agents at bedtime. • Scabies should be considered if more than one family member itches. • Hodgkin’s disease may present with pruritus that precedes the diagnosis by up to 5 years.

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Clin ical Varian ts • A patient may complain of itching caused by reasons that seem totally inexplicable or bizarre. Many histories have various twists and turns, such as the following. AQUAGENIC PRURITUS • The person with aquagenic pruritus experiences intense itching only after exposure to water. NOTALGIA PARESTHETICA • This not uncommon condition is seen most often in middleaged and elderly patients. Notalgia paresthetica is thought to represent a sensory neuropathy that is caused by nerve impingement for spinal arthritis. • It most often consists of a localized, very focal, often unilateral area of recurrent itching that characteristically occurs on the lower or mid-scapula. The postinflammatory hyperpigmentation that sometimes results from the chronic rubbing and scratching reveals the diagnosis (see FIG. 15.2). • Treatment is often futile. Capsaicin (Zostrix) cream, which depletes nerve endings of their chemical transmitters, may be tried. 15.2 Notalgia paraesthetica. Note the typical location on the lower scapula. The postinflammatory hyperpigmentation resulted from the chronic rubbing and scratching of this itchy area.

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BRACHIORADIAL PRURITUS • Brachioradial pruritus (BRP) is an intense itching sensation of the arm, usually between the shoulder and elbow of either or both arms. • There is ongoing debate regarding whether BRP is caused by a nerve entrapment in the cervical spine or a prolonged exposure to sunlight, because the outer, sun-exposed aspects of the arms are most often affected. • Measures to treat BRP include the following: • Sun protection; wearing clothing with long sleeves is more effective than use of sunscreens alone • Capsaicin (Zostrix) cream • Ice packs • Amitriptyline tablets at night • Anticonvulsant agents, including gabapentin 300 mg three times daily • Electrical cutaneous nerve field stimulation

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C H AP T ER

Xerosis: The “Dry” Patient

16 OVERVIEW Xerosis, or dry skin, is a common occurrence in winter climates, particularly in conditions of cold air, low relative humidity, and indoor heating. Xerosis can affect anyone, but it tends to be more severe in certain persons, especially those with a hereditary predisposition. Modern lifestyles are also contributing factors. In Western societies, people tend to overbathe, and they often live and work in overheated spaces. The word “dry” is sometimes misapplied. Skin that appears to be dry (i.e., that shows a buildup of scale) may not always be suffering from a lack of water but rather from an overadherence or hyperproliferation of scale. Overadherence of scale may occur in patients with ichthyosis (see Chapter 2, “Eczema”). Hyperproliferation of scale is noted in atopic dermatitis, psoriasis, seborrheic dermatitis, and common dandruff.

XEROSIS ASTEATOTIC ECZEMA ATOPIC DERMATITIS

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XEROSIS • Xerosis, or dry skin, tends to be most apparent on the hands and lower legs. • It becomes especially common in persons who are older than 65 years of age (FIG. 16.1).

Pat h o g e n e sis • The reasons why the skin becomes—or appears to become—dry are not well understood. It has been proposed that xerosis may be secondary to diminished production of sebum (asteatosis), as well as to reduced eccrine gland activity. However, other biochemical factors related to aging skin have also been implicated. • Popular folklore and the lay literature often blame xerosis on inadequate water ingestion, but there is no scientific basis for this claim. Ast e at o t ic Ecze m a See also FIGURE 2.52.

16.1 Xerosis. Dry skin tends to be most apparent on the hands and lower legs. This elderly patient’s legs are dry and scaly.

• Asteatotic eczema (winter eczema) is caused by a relative loss of water from the skin through evaporation, a lack of normal desquamation, and, possibly, a decline in the production of sebum (the skin’s natural lubricant and sealant). • Most often seen on the shins, with seasonal recurrences during the winter months, this form of eczema is a common, sometimes pruritic, low-grade dermatitis. Early on, the affected skin feels and looks dry (FIG. 16.2); later, an inflammatory dermatitis may evolve.

16.2 Asteatotic eczema. Xerosis and subtle changes consisting of exaggerated skin markings are seen in this patient. 294

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• Occurring exclusively in adults, lesions most commonly appear on the shins, arms, hands, and trunk (see Chapter 2, “Eczema”). Because the eruption often resembles the surface of a cracked porcelain vase, it is often referred to as erythema craquelé. It is also likened to the appearance of a dry riverbed (FIG. 16.3). • A clinical variant consists of small, square, scaly plaques that are often mistaken for tinea corporis (ringworm) or psoriasis and treated as such (FIG. 16.4).

At o p ic De rm at it is • Dry, xerotic, exquisitely sensitive, itchy skin is the major feature of atopic dermatitis (eczema) (see Chapter 2, “Eczema,” for management of this condition). Atopic skin is often characterized by decreased water content, increased water loss, and reduced water-binding capacity, as well as epidermal hyperproliferation, resulting in lichenification (an exaggeration of normal skin markings) and buildup of scale. • Patients usually have a personal or family history of allergies, asthma, or hay fever. In addition to scaly eczematous plaques, such patients may develop painful linear cracks or fissures from xerosis, particularly on the palms, soles, and fingertips (FIG. 16.5).

16.4 Asteatotic eczema. In this patient there are small, squarish plaques that resemble ringworm.

16.5 Atopic dermatitis, hand eczema. Dry, sensitive, itchy, lichenified skin is characteristic of this condition. This patient has painful fissures of the distal fingers.

16.3 Asteatotic eczema. Here the skin resembles a cracked porcelain vase (erythema craquelé).

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DIFFERENTIAL DIAGNOSIS

Ich t h yo sis Vulg aris See FIGURE 2.21. • Ichthyosis vulgaris (the most commonly seen variant of ichthyosis) resembles dry skin; however, it is actually caused by overadherence of scale. • It is frequently associated with atopy. • Skin with ichthyosis vulgaris resembles fine fish scales and tends to be most clinically obvious on the shins. • Ichthyosis vulgaris is inherited in an autosomal dominant fashion and tends to improve with age.

MANAGEMENT

Mo ist urize rs • Moisturizers do not add water to the skin, but they help retain or “lock in” water that is absorbed while bathing. Therefore, moisturizers should be applied while the skin is still damp. • There are numerous over-the-counter moisture preparations in ointment bases, cream bases, and lotions. Some moisturizers contain alpha-hydroxy acids. The choice of product is based on personal preference, ease of application, cost, and effectiveness. • Ammonium lactate 12% (Lac-Hydrin) lotion or cream is a prescription alpha-hydroxy acid preparation that may be applied after bathing. It is very effective and is used for more severe cases of xerosis. The 12% ammonium lactate preparation may be purchased over the counter as AmLactin. • A 40% urea lotion (Carmol 40) is useful for moderate to severe dryness.

Dry Skin Th at ’s No t “Dry” • Many patients complain of “dry skin” from the use of topical retinoids such as Retin-A for the treatment of acne. Actually, the “dryness” is scaling that results from the exfoliative effect of the topical retinoid. • Another common complaint is that of scaling and “dryness” from seborrheic dermatitis of the face and scalp. In such cases, the skin is not dry and deprived of moisture; rather, it scales and flakes from the inflammatory process.

Ot h e r St rat e g ie s • For the dermatitis, itching, and erythema of atopic dermatitis or asteatotic eczema, low- to medium-potency (class 4 to 6) topical corticosteroids are valuable. In severe cases, more potent topical corticosteroids (class 1 to 3) may be applied for brief periods when necessary. • Showers and baths that are less frequent and shorter may be helpful. Only tepid water should be used. • Soap avoidance (on affected areas) or mild soaps (e.g., Dove, Basis) or a soap substitute (e.g., Cetaphil lotion) may be tried. However, excessive use of any soap or substitute should be avoided, especially on affected areas. • Adhesive dressings (Band-Aids) are effective in promoting healing of fissures. • Lined gloves, worn while washing dishes, can keep hands dry. • Scarves, gloves, and other apparel can help to provide adequate protection from exposure to outdoor cold. • The use of room humidifiers and the ingestion of copious amounts of water are of questionable value.

HELPFUL HINTS

POINTS TO REMEMBER • Dry skin and persistent pruritus—especially in elderly patients—may be evidence of a systemic condition (e.g., hypothyroidism or hypoparathyroidism), renal disease, or an underlying malignant disease. • Dry or scaly skin may be associated with the use of cholesterol-lowering agents, in particular nicotinic acid. • A genetically determined ichthyosis should be distinguished from simple xerosis, although the management of both conditions is similar.

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• Cocoa butter, petroleum jelly, or even vegetable shortening (e.g., Crisco) can be used as inexpensive moisturizers when cost is a consideration. These are very effective and do not contain many additives that may be sensitizing. • For fissures, Krazy Glue, a cyanoacrylate glue that is carefully applied to “seal the cracks,” is a nontoxic dressing that is reported to promote healing.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

SEE PATIENT HANDOUT “Dry Skin (Xe ro sis)” ON THE SOLUTION SITE

C H AP T ER

Drug Eruptions

17 OVERVIEW An adverse drug reaction is any nontherapeutic deleterious effect of a prescribed or over-the-counter medication. Drug eruptions can mimic almost any dermatosis. Drug reactions may be allergic (immunologic) or nonallergic (toxic). Allergictype drug reactions are not dose dependent. They are classified as the four following types of immunologic reactions: • Type I: classic immediate hypersensitivity (urticaria, angioedema, anaphylaxis) • Type II: cytotoxic (hemolysis, purpura) • Type III: immune complex (vasculitis, serum sickness, urticaria, angioedema) • Type IV: delayed hypersensitivity (contact dermatitis, exanthematous reactions, photoallergic reactions) Nonallergic drug eruptions are more common than allergic-type eruptions; they may be dose related or idiosyncratic. Vertigo caused by high-dose minocycline, demethylchlortetracycline-related photosensitivity reactions, and irritant reactions from topical retinoids are examples.

EXANTHEMATOUS DRUG ERUPTION URTICARIAL DRUG ERUPTION DRUG PHOTOSENSITIVE OR PHOTOTOXIC ERUPTION FIXED DRUG ERUPTION ERYTHRODERMA HYPERSENSITIVITY SYNDROME LEUKOCYTOCLASTIC VASCULITIS ERYTHEMA MULTIFORME MAJOR TOXIC EPIDERMAL NECROLYSIS LICHENOID DRUG ERUPTION LUPUS-LIKE DRUG ERUPTION ACNEIFORM DRUG ERUPTION

BASICS • Most drug eruptions are exanthematous (red rashes) and usually fade in a few days. • More serious reactions include erythema multiforme major (Stevens-Johnson syndrome), toxic epidermal necrolysis, and serum sickness. The presence of urticaria, mucosal involvement, extensive or palpable purpura, or blisters almost always requires discontinuation of the responsible drug. Certain classes of systemic medications, such as antimicrobial agents, nonsteroidal antiinflammatory drugs (NSAIDs), cytokines, chemotherapeutic agents, and psychotropic agents, are associated with a high rate of cutaneous reactions. Risk factors include the following: • Age: Drug eruptions are more commonly seen in elderly persons because they often take more drugs than younger people and they often take more than one drug at a time; consequently, they are more likely to have been previously sensitized. 297

• A history of previous drug reactions is a risk factor. • A family history of drug eruptions is another factor. • Prolonged use of a drug can predispose patients to drug eruptions. • Paradoxically, although human immunodeficiency virus (HIV) infection causes profound anergy to other immune stimuli, the frequency of drug hypersensitivity reactions is increased markedly compared with both immunocompetent and HIV-negative immunocompromised populations.

Ch aract e rist ic Skin Re act io n s Pro d uce d b y Drug s Adverse cutaneous drug reactions can mimic many common non-drug-related skin eruptions, and certain drugs are more likely to cause characteristic reactions in the skin, as follows:

17.1 Drug eruption. Exanthematous reaction to a sulfa drug.

17.2 Drug eruption. Note the “drug red” color of this confluent eruption caused by a penicillin derivative.

• Exanthems and urticarial reactions: sulfonamides, penicillins, hydantoins, allopurinol, quinidine, angiotensinconverting enzyme inhibitors, barbiturates, carbamazepine, isoniazid, NSAIDs, and phenothiazine, as well as thiazide diuretics, aspirin, blood products, cephalosporins, dextran, opiates, radiocontrast dye, ranitidine, and vaccines • Acneiform eruptions: systemic steroids, topical steroids, lithium, oral contraceptives, and androgenic hormones • Photo-induced: tetracyclines, particularly demethylchlortetracycline and doxycycline; griseofulvin; certain diuretics; sulfonylurea agents used to treat diabetes; NSAIDs; and phenothiazines • Erythema nodosum: iodides, oral contraceptives, penicillin, gold, amiodarone, sulfonamides, and opiates • Bullous eruptions: penicillin, sulfonamides, captopril, iodides, gold, and furosemide • Purpura: anticoagulants and thiazides • Vasculitic eruptions: allopurinol, aspirin or other NSAIDs, cimetidine, gold, hydralazine, penicillin, phenytoin, propylthiouracil, quinolones, sulfonamide, tetracycline, and thiazides • Erythema multiforme major (Stevens-Johnson syndrome) and erythema multiforme minor: sulfonamides, penicillins, tetracyclines, hydantoins, and barbiturates • Fixed drug eruptions: tetracyclines, sulfonamides, griseofulvin, barbiturates, phenolphthalein, and NSAIDs • Contact dermatitis: neomycin and preservatives in topical medications DESCRIPTION OF LESIONS • The morphology of a drug eruption can often provide clues to the most likely responsible agent.

Exan t h e m at o us Drug Erup t io n • Lesions are morbilliform (resembling measles) (FIG. 17.1). • There may be areas of confluence. • Lesions are pink, “drug red,” or purple (FIG. 17.2). 17.3 Urticarial drug eruption. Note the bizarre shapes of the urticarial plaques. 298

Urt icarial Drug Erup t io n • Urticarial drug eruptions usually occur as wheals that may coalesce or take cyclic or gyrate forms (FIG. 17.3).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

• Lesions usually appear shortly after the start of drug therapy and resolve rapidly when the drug is withdrawn (see also Chapter 18, “Diseases of Vasculature”).

Drug Ph o t o se n sit ivit y o r Ph o t o t o xic Erup t io n • This may appear as erythematous (an exaggerated sunburn; FIG. 17.4), eczematous, or lichenoid (resembling lichen planus). • Lesions generally occur on sun-exposed areas such as the “V” of the neck, extensor forearms, and the face (FIG. 17.5). Fixe d Drug Erup t io n • This is a reaction of circular red plaques or blisters that recurs at the same cutaneous site each time the drug is ingested. In other words, a rechallenge of the drug results in an identical eruption at the same site or sites. • Lesions may be round or oval, single (FIG. 17.6), or multiple (FIG. 17.7).

17.5 Phototoxic drug eruption. This is a phototoxic eruption caused by hydrochlorothiazide. The eruption appears in a photo distribution—the “V” of the neck and the extensor forearms.

17.6 Fixed drug eruption. An oval lesion occurred at the identical site where it had occurred previously. In both episodes, the rash emerged after this patient ingested a sulfonamide antibiotic. Note the eroded blister in the center of the lesion.

17.4 Drug photosensitivity eruption. Erythematous (exaggerated sunburn) reaction in a person who was taking demeclocycline (Declomycin) and fell asleep on the beach. (Courtesy of the Albert Einstein College of Medicine, Division of Dermatology, Bronx, New York.)

17.7 Fixed drug eruption, multiple lesions. These lesions are postinflammatory and were caused by phenytoin (Dilantin). Chap ter 17 • Drug Eruptions

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• A lesion on the glans penis is not unusual (FIG. 17.8). • Lesions initially are erythematous; later they become violaceous. • Lesions often blister and erode. • The eruption often heals with characteristic postinflammatory hyperpigmentation.

17.8 Fixed drug eruption. An oval erosion on the glans penis occurred in this patient who was taking minocycline. According to the patient, an identical lesion—in the same location—appeared when he was given minocycline previously.

Eryt h ro d e rm a (Exfo liat ive De rm at it is) • This is widespread inflammation of the skin (see Chapter 25, “Cutaneous Manifestations of Systemic Disease”), and it may result from an underlying skin condition, drug eruption, internal malignancy, or immunodeficiency syndrome. • Lymphadenopathy is often noted, and hepatosplenomegaly, leukocytosis, eosinophilia, and anemia may be present. Hyp e rse n sit ivit y Syn d ro m e • This is a potentially life-threatening complex of symptoms often caused by anticonvulsants. It usually begins within 1 to 3 weeks after a new drug is started, but it may develop 3 months or later into therapy. • Patients have fever, sore throat, rash, lymphadenopathy, hepatitis, nephritis, and leukocytosis with eosinophilia. • Aromatic anticonvulsant drugs cross-react (i.e., phenytoin, phenobarbital, carbamazepine); valproic acid is a safe alternative. Le uko cyt o clast ic Vasculit is • This is a common drug eruption. • It is characterized by palpable purpura. Fever, myalgias, arthritis, and abdominal pain may be present. • A laboratory evaluation to exclude internal involvement is mandatory (see Chapter 18, “Diseases of Vasculature”). Eryt h e m a Mult ifo rm e Majo r • Stevens-Johnson syndrome can be caused by drugs and infections (see Chapter 18, “Diseases of Vasculature”). • It is characterized by widespread skin involvement, large and atypical targetoid lesions, significant mucous membrane involvement, constitutional symptoms, and sloughing of the skin (see Chapter 18, “Diseases of Vasculature”).

17.9 Toxic epidermal necrolysis. A child with a severe, generalized eruption with epidermal necrosis and denuded erosive areas. (Image courtesy of Ashit Marwah, M.D.)

To xic Ep id e rm al Ne cro lysis • This is a severe skin reaction that involves a prodrome of painful skin, followed by rapid, widespread, skin sloughing (FIG. 17.9). • Most cases are the result of drugs (see also Chapter 24, “Cutaneous Manifestations of HIV Infection”). • Secondary infection and sepsis are major concerns. Eryt h e m a No d o sum • This is characterized by tender, red, subcutaneous nodules that typically appear on the anterior aspect of the legs. • Erythema nodosum is a reactive process often secondary to infection, but it may be caused by medications, especially oral contraceptives and sulfonamides (see Chapter 18, “Diseases of Vasculature”).

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Lich e n o id Drug Erup t io n • This reaction appears similar to lichen planus (see Chapter 4, “Inflammatory Eruptions of Unknown Cause”). Lup uslike Drug Erup t io n • Symptoms are identical to those of systemic lupus erythematosus, but skin findings are uncommon. • Lesions are also identical to drug-induced subacute cutaneous lupus erythematosus, which is characterized by annular, psoriasiform, nonscarring lesions in a photodistributed pattern (see Chapter 25, “Cutaneous Manifestations of Systemic Disease”). Acn e ifo rm Drug Erup t io n s • The usual responsible agents are systemic steroids. • Lesions generally appear on the trunk as monomorphic papules and pustules (FIG. 17.10).

17.10 Acneiform eruption caused by oral steroids. This patient developed multiple papules and pustules in a characteristic distribution.

DISTRIBUTION OF LESIONS Drug eruptions have specific regional predilections. For example: • Exanthems tend to be symmetric and occasionally generalized in distribution; they are noted particularly on the trunk, thighs, upper arms, and face. • The distribution of a contact dermatitis most often corresponds the area of initial insult to the skin (FIG. 17.11). • A fixed drug eruption may present as a solitary isolated lesion occurring most often on the hands, feet, and genitalia; multiple lesions may occur on the trunk and extremities. • A photo-induced drug eruption occurs on the face, dorsal forearms, and “V” of the neck and upper sternum. • Erythema nodosum occurs characteristically in the pretibial area. • Purpura and vasculitic drug eruptions also tend to occur on the lower extremities. • Topical steroid-induced rosacea occurs on the face. • Steroid atrophy most often occurs in body folds (axillae and inguinal creases). • Urticaria can be seen anywhere on the body. • Angioedema occurs in a periorbital, labial, and perioral distribution. • Erythema multiforme lesions commonly manifest on mucous membranes as well as on the palms and soles; they can also be widespread (see Chapter 18, “Diseases of Vasculature”).

17.11 Contact dermatitis. The geometric, erythematous lesions in this patient were caused by a reaction to leads used for a cardiac stress test.

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CLINICAL MANIFESTATIONS MANAGEMENT • The drug should be discontinued, if feasible. However, the decision to discontinue a potentially vital drug presents a dilemma. • Oral antihistamines, such as diphenhydramine (Benadryl), hydroxyzine (Atarax), or the nonsedating agents cetirizine (Zyrtec) and loratadine (Claritin), may be helpful. • Systemic steroids are given only in severe cases in which an infectious cause has been excluded.

POINTS TO REMEMBER • Prompt recognition and withdrawal of an offending drug are important, particularly in patients with severe reactions. • If it is necessary to continue the drug (i.e., there is no alternative medication) and the adverse reaction is mild or tolerable, the difficulty may be minimized by decreasing the dosage or treating the adverse reaction. • Persons who are immunocompromised have a greater risk of developing a drug eruption than the general population.

HELPFUL HINTS • Drug reactions can occur even after years of continuous therapy with the same drug. • Drug reactions can occur days after a drug has been discontinued. • A drug eruption may easily be confused with a feature of the condition that it is intended to treat (e.g., a viral exanthem treated with an antibiotic). • Patients with infectious mononucleosis are likely to develop a morbilliform rash when they are given ampicillin. • Exanthematous eruptions in adults are mostly the result of medications; in children, however, they are more likely to be a result of a viral infection.

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• Pruritus is a common complaint; however, adverse drug reactions also can cause pruritus unaccompanied by a rash. • Acute urticarial lesions usually appear shortly after the onset of drug therapy and resolve rapidly when the drug is withdrawn. • Mucous membrane lesions are often painful (e.g., erosions, ulcers). • Drug eruptions may be associated with systemic anaphylaxis or with extensive mucocutaneous exfoliation and multisystemic involvement; however, most drug eruptions are mild and self-limited, resolving after the offending agent is discontinued. • In drug eruptions with vasculitis, fever, myalgias, arthritis, and abdominal pain may be present. Vasculitis typically begins 7 to 21 days after the onset of drug therapy. The vasculitic process also may include other organ systems. DIAGNOSIS • Obtaining a detailed, careful history from the patient or family is paramount. • A handy reference to drug eruptions and interactions should always be available. • Patients occasionally have eosinophilia. • Skin biopsy of an exanthem showing perivascular lymphocytes and eosinophils may be helpful, but it is not diagnostic. Characteristic histopathologic changes may occur in some cases, such as leukocytoclastic vasculitis in palpable purpura and panniculitis in erythema nodosum; however, these findings are not necessarily diagnostic of a drugrelated origin. • Rechallenging with a suspected drug as a diagnostic tool is generally discouraged, unless: • Alternative agents are not available and the drug is indispensable to the patient. • The reaction is minor.

DIFFERENTIAL DIAGNOSIS • Viral or bacterial exanthems generally occur with fever and other symptoms; however, they are often indistinguishable from a drug eruption. • Pityriasis rosea should be considered. • Acute urticaria (not drug-induced) is another possible diagnosis. • Chronic urticaria (not drug-induced) should be considered.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

C H AP T ER

Diseases of Vasculature

18 OVERVIEW Cutaneous manifestations of vascular disorders range from a mild rash, urticaria, or angioedema to severe, life threatening vasculitis or anaphylaxis. Diseases featuring inflammation of the wall of blood vessels due to leukocyte migration and resultant damage can affect various organ systems. Large, medium, and/or small vessels may be involved.

URTICARIA AND ANGIOEDEMA • • • • • • •

Acute urticaria Chronic urticaria Derm atographism Cold urticaria Light-induced (solar) urticaria Cholinergic urticaria Other physical urticarias ERYTHEMA MULTIFORME NON-PALPABLE PURPURA AND BENIGN SMALL VESSEL VASCULITIS

• Actinic (senile purpura) • Scham berg’s purpura • Majocchi’s purpura (purpura annularis telangiectodes). HYPERSENSITIVITY VASCULITIS • Palpable purpura

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Urt ica ria a n d An gio ed em a BASICS

CLASSIFICATION

• Urticaria, commonly known as hives, is a reaction of cutaneous blood vessels that produces a transient dermal edema consisting of papules or plaques of different shapes and sizes. • Angioedema refers to edema that is deeper than urticaria and involves the dermis and subcutaneous tissue. • By definition, an individual urticarial lesion lasts less than 24 hours. • A total of 10% to 20% of the population has at least one episode of urticaria or angioedema at some point in his or her lifetime.

• Urticaria may be classified as acute or chronic urticaria, physical urticaria, urticarial vasculitis, and hereditary angioedema (rare).

Pat h o p h ysio lo g y • Release of histamine and other compounds by mast cells and basophils causes the appearance of urticaria. Mast cell activation causes degranulation of intracellular vesicles that contain histamine, leukotriene C4, prostaglandin D2, and other chemotactic mediators that recruit eosinophils and neutrophils into the dermis. Histamine and chemokine release lead to extravasation of fluid into the dermis (edema). Histamine effects account for many of the clinical and histologic findings of urticaria. • As with drug reactions, urticaria may be immune mediated or nonimmune mediated (see Chapter 17, “Drug Eruptions”). Causes of urticaria and angioedema include the following: • Immunologic causes, mediated by immunoglobulin E (IgE), include food, drugs, and parasites. • Complement-mediated causes include serum sickness and whole blood transfusions. • Physical stimuli that are non–IgE-mediated include cold, sunlight, and pressure (e.g., dermatographism). • Occult infections include sinusitis, dental abscesses, and tinea pedis. However, such problems are rarely associated with chronic urticaria. • In 85% to 90% of patients with chronic urticaria, the origin is unknown (i.e., chronic idiopathic urticaria).

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Acut e Urt icaria Acute urticaria, by definition, lasts less than 6 weeks. • Outbreaks are often IgE-mediated. • Many patients have an atopic history. • There may be an obvious precipitant such as an acute upper respiratory infection, drug, parasitic infection, or bee sting. • The most common drugs that may cause acute hives are antibiotics (especially penicillin and sulfonamides), pain medications such as aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), narcotics, radiocontrast dyes, diuretics, and opiates such as codeine. • The most common foods associated with acute urticaria are milk, wheat, eggs, chocolate, shellfish, nuts, fish, and strawberries. Food additives and preservatives such as salicylates and benzoates may also be responsible. • Systemic diseases such as lymphomas and collagen vascular diseases may have an associated urticaria. • Acute urticaria also may be caused by physical stimuli such as pressure, cold, sunlight, or exercise. Such hives are called physical urticarias (see later discussion). • Anaphylaxis or an anaphylactoid reaction can occur.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ch ro n ic Urt icaria Chronic urticaria is, by definition, urticaria that lasts longer than 6 weeks, although the cutoff point is an arbitrary one. • Chronic urticaria occurs in a 2:1 female-to-male ratio. • It is seen predominantly in adults. • The cause is usually unknown; however, chronic urticaria may, very infrequently, be a sign of one of the following systemic diseases: systemic lupus erythematosus (SLE), serum hepatitis, lymphoma, polycythemia, macroglobulinemia, or thyroid disease. DESCRIPTION OF LESIONS • Papules and plaques are of varying sizes. • Wheals are the color of the patient’s skin or pale red; a white halo may be noted at the periphery of the lesions (FIG. 18.1). • Lesions have various shapes; they can be annular, linear, arciform, or polycyclic, and frequently they are multiple, with bizarre shapes (FIGS. 18.2 and 18.3). • Individual lesions disappear within 24 hours (evanescent wheals). • Lesions may be accompanied by a deep swelling (angioedema) around the eyes, lips, and tongue that often looks frightening. Fortunately, angioedema usually lasts less than 24 hours.

18.2 Urticaria. Multiple lesions have various shapes and sizes.

18.3 Acute urticaria. Lesions are annular, arciform, and polycyclic, with bizarre shapes.

18.1

Urticaria. Skin-colored wheals are present.

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DISTRIBUTION OF LESIONS • Angioedema is noted primarily in the periorbital area (FIG. 18.4), lips, and tongue. • Urticarial lesions may occur anywhere on the body and may be localized or generalized. CLINICAL MANIFESTATIONS

18.4

Urticaria. Marked angioedema is noted.

• Lesions generally itch. • Arthralgia, fever, malaise, and other symptoms may accompany urticaria when it is the result of hepatitis or serum sickness, for example. • Scratching and rubbing of lesions generally do not produce scabs or crusts similar to those seen in atopic dermatitis. • Episodes of acute urticaria lasts for hours to days (generally less than 30 days). • Approximately 50% of patients with chronic urticaria are free of lesions in 1 year; in other patients, lesions may recur for many years. • Emotional stress may trigger recurrences. DIAGNOSIS OF CHRONIC URTICARIA The diagnosis of acute and chronic urticarias is usually made on clinical observation and history. If a complete review of systems is normal, and a physical urticaria is ruled out, it is often futile to perform multiple laboratory tests to determine a cause for chronic urticaria. Nonetheless, a positive symptomdirected search for underlying illness (e.g., SLE, thyroid disease, lymphoma, and necrotizing vasculitis) may warrant evaluations such as: • • • • • • • •

Complete blood count Erythrocyte sedimentation rate Fluorescent antinuclear antibody test Thyroid function studies Hepatitis-associated antigen test Assessment of the complement system Radioallergosorbent test for IgE antibodies In the presence of eosinophilia, stool examination for ova and parasites • CD203c assay, a new in vitro diagnostic test that is used to detect autoimmune urticaria and identifies antibodies that are responsible for many cases of chronic idiopathic urticaria

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Clin ical Varian ts SOME PHYSICAL URTICARIAS AND THEIR CAUSES

Ph ysical Urt icarias Physical factors are the most commonly identified causes of chronic urticaria. Physical urticarias are diagnosed by challenge testing.

• • • • •

Derm atographism results from firm stroking or scratching. Cold urticaria is caused by exposure to cold. Aquagenic urticaria results from contact with water. Cholinergic urticaria is caused by heat or exercise. Solar urticaria results from sun exposure.

De rm at o g rap h ism (“Skin Writ in g ”) FIGURE 18.5. • Dermatographism affects more than 4% of the general population, in whom it is physiologic and asymptomatic. • Linear erythematous wheals occur 3 to 4 minutes after firmly stroking the skin with the wooden handle of a cotton swab; they fade within 30 minutes. A delayed form also exists. • Lesions are seen under constrictive garments, such as belts and bras, or after a person scratches. • In some persons, itching is the primary symptom. • Episodes of dermatographism may persist for years.

Co ld Urt icaria FIGURES 18.6 A and B. • Cold urticaria occurs mainly in young adults and children. A

B

18.5 Dermatographism (“skin writing”). These lesions occurred 3 minutes after stroking with the wooden tip of a cotton swab.

18.6 an d B Cold urticaria. The “ice cube test.” Before (A) and 5 minutes after (B) application of an ice cube. A large wheal and surrounding erythema have appeared.

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• Itchy hives occur at sites of cold exposure, such as areas exposed to cold winds or immersion in cold water. • In the “ice cube test,” a wheal arises on the skin after application of an ice cube.

Lig h t -In d uce d (So lar) Urt icaria FIGURES 18.7 A and B. • Solar urticaria occurs in sun-exposed areas of the skin and is triggered by different wavelengths of light.

Ch o lin e rg ic Urt icaria • This type of urticaria is induced by exercise or a hot shower. • The patient exercises to the point of sweating, which provokes lesions and establishes the diagnosis. • Typical lesions are multiple, small, monomorphic wheals.

A

Ot h e r Ph ysical Urt icarias • These include those induced by pressure, heat, vibration, and water (aquagenic urticaria).

B 18.7 A an d B Solar urticaria induced by ultraviolet A light. Before sun exposure (A) and after 15 minutes of sun exposure through a glass window (B). The glass window filters out ultraviolet B light.

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DIFFERENTIAL DIAGNOSIS

In se ct Bit e Re act io n s These reactions are also known as papular urticaria. For a full discussion of insect bite reactions, see Chapter 20, “Bites, Stings, and Infestations.” • Reactions to insect bites may be indistinguishable from ordinary hives. • Bites are generally seen on exposed areas. • They may have a central punctum and crust; they also may blister. • Individual lesions may last more than 24 hours.

Eryt h e m a Mult ifo rm e Min o r See also subsequent detailed discussion. • Lesions are targetoid. • Lesions last more than 24 hours. • Lesions are generally nonpruritic.

• Lesions are usually solitary, annular, and targetlike. • Lesions may last more than 24 hours. • Lesions are generally nonpruritic.

Urt icarial Vasculit is This condition is rare and is probably related to circulating immune complexes. • Persistent hivelike lesions last more than 24 hours. • Lesions may be tender rather than itchy. • Residual purpura or hyperpigmentation often ensues on resolution of lesions. • Evidence of vasculitis (e.g., purpura) is occasionally seen in the lesions. • The diagnosis is confirmed by skin biopsy. • Patients may have hypocomplementemia and an elevated erythrocyte sedimentation rate. • Urticarial vasculitis may be associated with collagen vascular diseases.

Eryt h e m a Mig ran s (Acut e Lym e Dise ase ) For a full discussion of this condition, see Chapter 20, “Bites, Stings, and Infestations.” • Erythema migrans may be indistinguishable from urticaria.

MANAGEMENT • If possible, the cause of the hives should be eliminated, and tight clothing and hot baths and showers should be avoided, particularly in people who have physical urticaria. • Salicylates, NSAIDs, and narcotics, which are all histamine-releasing agents, may aggravate both acute and chronic urticaria and should be avoided. • Histamine H1 blockers include hydroxyzine (Atarax), diphenhydramine (Benadryl), and cyproheptadine (Periactin); H1 and H2 blockers may be used in combination, such as cimetidine (Tagamet) plus hydroxyzine. These first-generation antihistamines compete with histamine at the tissue receptor level. Patients with chronic urticaria often require much higher than the usual doses of antihistamines. • Nonsedating antihistamines, such as loratadine (Claritin) 10 mg, desloratadine (Clarinex) 5 mg, fexofenadine (Allegra) 60/180 mg, and cetirizine (Zyrtec)

10 mg, may be used during the day, and a more sedating H1 blocker or a tricyclic antidepressant drug, such as doxepin (Sinequan), may be tried at bedtime. Doxepin can be given at much lower dosages than when it is used as an antidepressant (e.g., from 5 mg two times daily to 50 mg three times daily). • For the pediatric age group: • Fexofenadine (Allegra) is approved for use in children as young as 6 months of age in a liquid form dosed at 15 mg twice a day and 30 mg twice a day for children aged 2 to 11 years. • A sedating antihistamine such as diphenhydramine or hydroxyzine may be added at bedtime. • Systemic steroids are sometimes used for short periods to break the cycle of chronic urticaria; however, they are not indicated for long-term use in the treatment of chronic idiopathic urticaria. • If all else fails, a diary of daily foods eaten may be kept, with subsequent food elimination. However, this approach is rarely successful.

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HELPFUL HINTS

POINTS TO REMEMBER • Except for the physical urticarias and urticaria that is obviously associated with drugs and systemic disease, determining the cause of chronic urticaria is generally a fruitless task. • Most often, routine blood tests are of little or no value in determining the cause of acute or chronic urticaria. • Antihistamines remain the mainstay for treating chronic urticaria; a combination of these agents may be necessary for control. • Allergies are almost never the cause of chronic urticaria. Allergy testing is expensive and often tests that are positive for allergies have no relation to the patient’s urticaria. • When individual wheals persist for more than 24 hours, the process is unlikely to be urticaria.

• Epinephrine, which is often administered by intramuscular or subcutaneous injection for acute urticaria, should not be used for routine cases of hives. It should be reserved for cases of acute anaphylaxis. • Patients with documented cold urticaria should be advised not to immerse themselves abruptly in cold water. • Patients with severe reactions should consider wearing a medical alert bracelet that describes their problem. • Montelukast (Singulair), a leukotriene receptor antagonist used to treat asthma, has been found to be effective in some cases of chronic idiopathic urticaria that are refractory to antihistamines. • Immunotherapies using prednisone, plasmapheresis, intravenous immunoglobulin, low-dose methotrexate, oral psoralens plus ultraviolet A treatment, oral tacrolimus, azathioprine, and cyclosporine have been used in severe, recalcitrant cases. • Children with chronic urticaria occasionally have an underlying autoimmune disease; thyroid antibodies are the most common positive finding.

SEE PATIENT HANDOUT “Hive s (Urt icaria)” ON THE SOLUTION SITE

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Er yt h em a Mu lt ifo rm e BASICS • Erythema multiforme (EM) is a confusing condition for many health care providers. The classic description of EM made by Ferdinand von Hebra in the late 19th century was very specific and is still currently used. He described “a selflimited eruption characterized by symmetrically distributed erythematous papules, which develop into characteristic targetlike lesions consisting of concentric color changes with a dusky central zone that may become bullous” (FIG. 18.8). This classic form of EM is currently defined as EM minor. • The more serious variant, with extensive mucous membrane involvement, systemic symptoms, and more widespread lesions, is called EM major (Stevens-Johnson syndrome). • EM is a reaction pattern of dermal blood vessels with secondary changes noted in the epidermis that results clinically in curious targetlike shapes. • EM is most commonly seen in late adolescence and in young adulthood. Affected persons are generally in good health.

18.8 Erythema multiforme. Characteristic targetlike lesions are noted here.

Cause s The list of causes of EM is long and is, in many, a duplication of the list of causes of urticaria (see previous section). Most instances of both EM major and minor are idiopathic; however, the following are the most well-documented associations. • The most common precipitating cause of EM minor is recurrent labial herpes simplex virus infection (FIG. 18.9); recurrences of herpes progenitalis also have been reported to precede or sometimes occur simultaneously with episodes of recurrent EM minor. EM minor is unlikely related to drugs. • Precipitating factors in EM major are drugs (sulfonamides, penicillin, hydantoins, barbiturates, allopurinol, NSAIDs); Mycoplasma infection; pregnancy; Streptococcus infection; hepatitis A and B; coccidioidomycosis; and Epstein-Barr virus infection. • Poison ivy (rhus dermatitis) has also been reported to be associated with erythema multiforme.

18.9 Erythema multiforme minor. This patient has a recurrent herpes simplex virus infection. Note the drying crust of the herpetic “cold sore” on her upper lip and the targetlike lesions on her palm (see also FIG. 12.4).

DESCRIPTION OF LESIONS • Lesions begin as round, erythematous macules. • Some lesions evolve to form targetoid plaques (iris lesions) with a dark center that may become vesicobullous. • Lesions persist (are “fixed”) for at least 1 week. • Erosions and crusts form. DISTRIBUTION OF LESIONS • Lesions are bilateral and symmetric. • The palms and soles, dorsa of hands and feet, extensor forearms and legs, face, and genitalia are affected. • Mucous membrane lesions are limited to the mouth in EM minor. • Extensive mucous membrane lesions in EM major may be located in multiple sites, including the mouth, pharynx, eyes, and genitalia (FIG. 18.10).

18.10 Erythema multiforme major. Extensive hemorrhagic crusting on mucous membranes is noted in a patient with fever and extensive erythematous lesions (see also FIG. 12.5). Chap ter 18 • Diseases of Vasculature

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CLINICAL MANIFESTATIONS MANAGEMENT • If known, the precipitating cause should be eliminated or treated. • Suspected etiologic drugs should be discontinued. • Empiric treatment with oral acyclovir, famciclovir (Famvir), or valacyclovir (Valtrex) may prevent or mitigate recurrences if EM is a result of herpes simplex virus infection (see Chapter 6, “Superficial Viral Infections,” for dosages). • Wet dressings (e.g., Burow’s solution) and topical steroids may be applied to oozing lesions. • In life-threatening situations, such as may occur in EM major, hospitalization is often essential. The use of systemic steroids in such severe cases is controversial, and their effectiveness has not been established. • The use of intravenous gamma globulin and cyclosporine is also controversial, and the effectiveness of these treatments has not been confirmed by double-blind studies.

POINTS TO REMEMBER • EM is not a disease but a syndrome, a reaction to underlying stimuli, with multiple causes and various degrees of severity. • Even in the clinical absence of herpes simplex virus infection, recurrent EM may be suppressed with oral acyclovir, famciclovir, or valacyclovir.

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Eryt h e m a Mult ifo rm e Min o r • The eruption is acute, self-limited, and often recurrent. • Evidence of herpes labialis may be present. • Little or no mucous membrane involvement is noted. Eryt h e m a Mult ifo rm e Majo r • EM major is often accompanied by symptoms of fever, malaise, and myalgias. • Severe, painful mucous membrane involvement occurs. • Possible complications include keratitis, corneal ulcers, upper airway damage, and pneumonia. DIAGNOSIS • Typical target lesions are present. • Skin biopsy is performed, if necessary.

DIFFERENTIAL DIAGNOSIS

Urt icaria • Lesions are transient, not “fixed.” • Lesions are pruritic. • The center of annular lesions is not dusky in color. Prim ary He rp e s Gin g ivo st o m at it is an d Prim ary Bullo us Dise ase s o f t h e Oral Cavit y • In the absence of nonmucous membrane skin lesions, other diseases of the mucous membranes may be clinically indistinguishable from those of EM. • Mucous membrane biopsy may be necessary to distinguish oral bullous EM from primary bullous diseases such as pemphigus vulgaris or bullous pemphigoid (see also Chapter 12, “Disorders of the Mouth, Lips, and Tongue”).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Pu rp u ra BASICS Purpura is defined as a hemorrhage of blood into the skin or mucous membranes (FIG. 18.11). It is most commonly seen on dependent areas (i.e., the lower legs and ankles). Purpuric skin is purple, violaceous, or dark red in color and is nonblanchable because blood is present outside of vessel walls. In contrast, erythema is red in color and blanches on compression because blood remains within the vessels. Nonpalpable purpuric lesions that are smaller than 3 mm in size are referred to as petechiae; those larger than 3 mm are called ecchymoses. Purpura is further subdivided into nonpalpable (macular) and palpable (papular) categories. The lower legs are the most common location for purpuras as well as the primary site of peripheral venous disease such as stasis dermatitis (see Chapter 2, “Eczema”). Purpuric lesions can be a sign or symptom of other vascular disorders such as coagulopathies or vasculitis and may serve as clues to systemic diseases such as SLE. Of lesser concern are the socalled “benign” variants—the benign pigmented purpuras (BPPs) that are caused by capillaritis, which allows blood to exit small vessels (extravasation) and create petechiae. As their name implies, BPPs are not associated with any systemic disease.

18.11 Purpura. Petechiae and ecchymoses combine and form areas of nonblanching purpura.

Non p alp able Pu rp u ra an d Sm all Vessel Vascu litis BASICS • Nonpalpable purpura may be seen after the following: • Minor trauma to the skin. This may precipitate purpura, particularly when a patient is taking drugs such as aspirin, clopidogrel (Plavix), NSAIDs, and warfarin (Coumadin), all of which increase clotting time. • Long-term application of potent topical steroids on the skin of elderly patients. • It also may be seen in association with: • BPP (see subsequent discussion). • Blood dyscrasias and coagulopathies, such as thrombocytopenia, leukemia, and disseminated intravascular coagulopathy. Lesions are more commonly on dependent areas (i.e., lower legs and ankles; buttocks in bedridden patients). • Actinic purpura (formerly known as senile purpura), which is a prevalent finding on the dorsal forearms in elderly persons. Such ecchymoses are believed to result from minor trauma to an area of chronic sun exposure. Thinning of skin and “fragile capillaries” are considered the cause (FIG. 18.12). • Chronic venous insufficiency of the lower extremities.

18.12 Senile, or actinic, purpura. Ecchymoses are present on the dorsal forearms in an elderly person.

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DESCRIPTION OF LESIONS • Lesions begin as nonblanching, red, pinpoint-size macules (petechiae) or bruises (ecchymoses) that may coalesce. • Older lesions become purple, then brown as hemosiderin forms. CLINICAL MANIFESTATIONS • Lesions are generally asymptomatic, but they may be mildly pruritic. • BPP may be of cosmetic concern to patients; other patients wish to be reassured that purpura is not a sign of a serious disease. • Lesions may persist for months to years or indefinitely.

Varian ts of Ben ign Pigm en ted Pu rp u ra Sch am b e rg ’s Purp ura • This is most commonly seen on the lower extremities. • It is the most common of the BPPs and occurs primarily in adults, especially in the elderly. It is characterized by socalled “cayenne pepper” purpura (FIGS. 18.13 and 18.14). 18.13 Schamberg’s purpura. “Cayenne pepper” petechiae are seen on the lower extremities.

18.14 Schamberg’s purpura. In this patient, the lesions are more extensive. Coalescence of petechiae has created large areas of nonpalpable purpura. Note the hyperpigmented macules indicating the presence of hemosiderin in the skin. (Image courtesy of Art Huntley, M.D.) 314

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Majo cch i’s Purp ura (Purp ura An n ularis Te lan g ie ct o d e s) • Also a capillaritis, these asymptomatic annular lesions may be seen especially in adolescents and young adults and may appear at any site. • Lesions consist of pigmentation that is annular in configuration, often with a central clearing. The purple, yellow, or brown patches consist of telangiectases and hemosiderin deposition (FIG. 18.15). DIAGNOSIS • The diagnosis is made on clinical presentation. • Lesions are not palpable and are nonblanching on diascopy (direct pressure).

18.15 Majocchi’s purpura (purpura annularis telangiectodes). This is the characteristic ring-shaped nonblanching purpuric lesion that has become hyperpigmented because of the presence of hemosiderin. (Image courtesy of Art Huntley, M.D.)

DIFFERENTIAL DIAGNOSIS • Biopsy may be necessary at times to distinguish benign purpura from leukocytoclastic vasculitis, the histopathologic finding in palpable purpura (see next section).

MANAGEMENT • BPP generally requires no workup; however, if a blood dyscrasia or coagulopathy is suspected, appropriate laboratory tests should be ordered. • Possible offending drugs should be evaluated regarding their risk-to-benefit ratio. • A coagulopathy or blood dyscrasia should be ruled out, if it is clinically suspected.

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Palp able Pu rp u ra BASICS • Palpable purpura (PP) is a vasculitis of the skin. It involves a group of conditions that affect the vessels that lie within the middle to upper dermis. When the vasculitis is more extensive and affects internal organs—most commonly the gastrointestinal tract, kidneys, central nervous system, and joints—it may then be referred to as hypersensitivity vasculitis (HV). • The prognosis is good when no internal involvement is present. PP and HV may be acute or chronic. Common to all forms of vasculitis are the inflammation and destruction of blood vessel walls by inflammatory cells. Palpability of lesions is caused by the accumulation of inflammatory cells and the leakage of blood from the vessels.

18.16 Palpable purpura. Nonblanching papules suggest vasculitis. Hemorrhagic blisters and coalescence of lesions arise from purpuric areas and are indicative of more severe vessel involvement.

Pat h o p h ysio lo g y • It is believed that the deposition of circulating immune complexes in the postcapillary venules is the cause of vasculitis. The circulating immune complexes may also deposit in organs, causing a vasculitis with resultant gastrointestinal bleeding, hematuria, and arthralgias. • Leukocytoclastic vasculitis is the characteristic histopathologic finding of PP and HV. Biopsy of lesions shows characteristic leukocytoclastic vasculitis (“nuclear dust”). • The cutaneous vasculitis may be associated with a hypersensitivity to antigens from drugs (most often antibiotics), NSAIDs, allopurinol, thiazide diuretics, and hydantoins. Conditions that may be associated with HV include malignancies; infectious diseases; cryoglobulinemias; other underlying diseases such as SLE, Sjögren’s syndrome, rheumatoid arthritis, and inflammatory bowel diseases; paraproteinemia; ingestants and infections such as beta-hemolytic streptococcal infection; viral hepatitis, particularly hepatitis C; and human immunodeficiency virus infection. • More than 50% of cases are idiopathic and may occur in the absence of any systemic disease. DESCRIPTION OF LESIONS • Lesions tend to appear in crops; they are red to violaceous to purple in color and are nonblanching (FIG. 18.16). • Infrequently, hemorrhagic vesicles or bullae may occur and develop into painful ulcerations (FIG. 18.17). • Healing takes place within 1 to 2 weeks and may result in postinflammatory hyperpigmentation and/or scarring. DISTRIBUTION OF LESIONS

18.17 Vasculitis. This patient has cryoglobulinemic vasculitis. Hemorrhagic blisters are forming a large ulceration on her ankle. 316

• The lesions are characteristically symmetric in distribution. They are most often seen in dependent areas such as the lower legs and ankles and on the buttocks in bedridden patients, but any area of the skin can be involved. • In severe forms, lesions can become generalized.

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CLINICAL MANIFESTATIONS • Lesions may be asymptomatic, mildly pruritic, slightly painful, or very painful (ulcers) and may occur in the absence of any systemic disease. • Lesions can be recurrent; however, the majority of patients (90%) have only a single episode. • There may be associated malaise and possible fever. • In systemic vasculitis, symptoms are referable to the organ involved.

chemistry panel, erythrocyte sedimentation rate, urinalysis, and stool examination for occult blood. Further studies (e.g., serum complement, antinuclear antibodies) should be directed by the patient’s symptoms. Other testing may include serum protein electrophoresis, cryoglobulins, and hepatitis C antibody for patients who have no identifiable disease. • Biopsy of fresh lesions shows characteristic leukocytoclastic vasculitis (“nuclear dust”). A biopsy performed too early or too late in its evolution may not reveal these findings.

DIAGNOSIS • Laboratory investigations that are useful for identifying any underlying disease include complete blood count, a blood

DIFFERENTIAL DIAGNOSIS

He n o ch -Sch ö n le in Purp ura • Henoch-Schönlein purpura (HSP) is a term that should be reserved for disease that follows an upper respiratory infection, generally in children. It is a type of HV caused by group A streptococci. • HSP generally occurs in persons 20 or younger but may also be seen in adults. • Clinical and histopathologic findings are similar to those of HV. Abdominal pain, arthralgia, hematuria, and proteinuria may be present. • Patients with HSP caused by group A streptococci have a perivascular IgA immunofluorescent deposition in the skin and kidneys. In children and in some adults, serologic testing for a possible streptococcal infection should be considered (streptozyme or antistreptolysin O titer). Art h ro p o d Bit e Re act io n s • When these appear on the lower extremities, they can mimic PP. • The history of exposure to bites is often obtainable (FIG. 18.18). 18.18 Arthropod bite reaction. These intensely pruritic discrete and confluent nonblanching purpuric lesions occurred several days after this patient walked in tall grass, where he was bitten by chigger mites. continued on page 318

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DIFFERENTIAL DIAGNOSIS Continued

Se p t ic Vasculit is • Palpable and nonpalpable purpura may also be seen in septic vasculitis, in which lesions are more often acral (i.e., distal on toes or fingertips) and tend to be few in number (e.g., gonococcemia) (FIG. 18.19). • Lesions also tend to lack the characteristic symmetry of HV. • Patients who have septic vasculitis may also be febrile and show other signs and symptoms of their underlying infection. Ot h e r Vasculit id e s • It should be kept in mind that cutaneous vasculitis, and thus PP, may be seen in patients with rare diseases such as Wegener’s granulomatosis, polyarteritis nodosa, cryoglobulinemic vasculitis, antiphospholipid syndrome, microscopic polyangiitis, and Churg-Strauss syndrome (allergic granulomatosis). • Many of these conditions involve larger vessels than are typically involved in HV. At ro p h ie Blan ch e (Live d o id Vasculo p at h y) • Patients present with small, porcelain-white, stellate (star-shaped) scars with surrounding telangiectasias (FIG. 18.20). The initial lesions are typically painful purpuric macules or papules on the malleoli and the adjacent dorsa of the feet that often appear in clusters and form irregular patterns of superficial punched-out ulcers. • The white scars result from the healing of such ulcerations and represent an end-stage feature of chronic venous insufficiency. • Livedoid vasculopathy has become the more dynamic, more inclusive term because it better explains the pathogenic process that leads to the condition. • In addition to chronic venous hypertension, atrophie blanche has been associated with conditions that have a vascular occlusive component to them, such as deficiencies in a variety of blood factors, a history of increased plasma homocysteine levels, the presence of antiphospholipid antibodies, and abnormalities in fibrinolysis and platelet function. There is also a primary or idiopathic type of atrophie blanche that is a distinct condition and is not usually the result of other diseases. As with secondary atrophie blanche, women are affected more often than men.

18.19 Disseminated gonococcemia. This is an example of septic vasculitis. Note the two palpable purpuric hemorrhagic vesicles.

18.20 Atrophie blanche (livedoid vasculopathy). White, stellate scars are present. The proximal erythema and the superficial varicosities that surround the affected area (corona phlebectasia) suggest that stasis dermatitis is the cause of her vasculitis.

Pyo d e rm a Gan g re n o sum • Ulcerative lesions that evolve from PP may resemble the chronic ulcers of this disease.

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POINTS TO REMEMBER MANAGEMENT • PP may be a sign of systemic vasculitis, sepsis, drug allergy, underlying disease, or an idiopathic benign reaction pattern. • Patients with PP that primarily affects the skin, and not the internal organs, have a good prognosis. • When evaluating purpura (both palpable and nonpalpable, septic and nonseptic) of the lower extremities, other, often rare, entities must also be considered as diagnostic possibilities in the proper clinical context. • The diagnosis of BPP is generally made on clinical grounds, and the patient should be reassured about the benign nature of these lesions.

HELPFUL HINT • Vasculitis in patients with Wegener’s granulomatosis, polyarteritis nodosa, or Churg-Strauss syndrome can be considered a potentially fatal disease. Treatment with systemic corticosteroids and/or immunosuppressive/cytotoxic agents is necessary.

• If known, the precipitating cause (e.g., drug) should be eliminated or the responsible underlying disease (e.g., SLE) should be treated. • Elevation of the legs (above the level of the heart) and/or compression stockings may be useful because the disease often affects dependent areas. • In general, no treatment is necessary for mild, selflimited episodes. • For painful cutaneous lesions or arthralgias, NSAIDs may be used (e.g., ibuprofen, indomethacin, or naproxen). • For severe, extensive or recalcitrant cases, oral corticosteroids are indicated. The dose is slowly reduced over the course of several weeks. • For recurrent or persistent lesions, dapsone and colchicine have also been reported to be effective. • In cases of rapid progression or systemic involvement, immunosuppressants such as cyclophosphamide (Cytoxan), azathioprine (Imuran), methotrexate (Rheumatrex), and mycophenolate mofetil (CellCept) have been used in conjunction with systemic steroids as steroid-sparing agents. • Recently the use of rituximab (Rituxan) has been reported to be helpful in some cases of vasculitis.

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C H AP T ER

19

Sexually Transm itted Diseases Mary Ruth Buchness and Herbert P. Goodheart

OVERVIEW ANOGENITAL WARTS HERPES SIMPLEX GENITALIS SYPHILIS • • • •

Secondary syphilis Latent syphilis Tertiary syphilis Congenital syphilis CHANCROID LYMPHOGRANULOMA VENEREUM GRANULOMA INGUINALE (DONOVANOSIS)

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• Until the 1990s, sexually transmitted diseases (STDs) were commonly known as venereal diseases. Veneris is the Latin form of the name Venus, the Roman goddess of love. • Syphilis is common worldwide, and since the late 1990s infectious early syphilis has re-emerged as an important disease in western Europe and the United States and is an important facilitator of human immunodeficiency virus (HIV) transmission. • An estimated 1% of the population of the United States has clinically evident lesions of the human papilloma virus (HPV), and 15% have latent HPV infection. HPV is thought to be one of the main causes of cervical cancer, and it has also been linked with other types of cancers of the female and male reproductive system. • Herpes simplex virus (HSV) infection is another STD that presently has no cure. The incidence of HSV-2 infection is also one of the most rapidly increasing among STDs in the United States. • Chancroid is rare in the United States and Western Europe. In the United States, it is associated with the use of crack cocaine. • Lymphogranuloma venereum and granuloma inguinale are also reported rarely in the United States and Western Europe and are more frequently seen in tropical and subtropical regions.

An o gen it a l Wa rt s BASICS • Anogenital warts, for the most part, are sexually transmitted viral warts caused by infection with specific types of HPV. Despite the generally benign nature of the proliferations, certain types of HPV can place patients at a high risk for anogenital cancers. • Treatment of genital warts can be difficult and lengthy. Patients should be counseled about their risk of infectivity to others. They also should be advised of their increased risk of having other STDs. • The incubation period is variable, ranging from 3 weeks to 8 months, with a reported average, in one study, of 2.8 months. • HPV has been identified in the skin of infected persons at a distance of up to 1 cm from the actual lesion; this feature may explain the high recurrence rate. HPV types 16, 18, 31 to 35, 39, 42, 48, and 51 to 54 have been identified in cervical and anogenital cancers. • The median duration of infection is 8 months. In a study of college women, only 9% had persistence of infection after 2 years, even among those infected with oncogenic subtypes. • Lesions tend to be more extensive and recalcitrant to treatment in immunocompromised persons; they also tend to grow larger and more numerous during pregnancy. • Women with HPV infection who are pregnant or who are considering pregnancy pose specific challenges. In addition to the potential for rapid proliferation of external genital warts during pregnancy, the presence of HPV infection raises concerns regarding the risk of laryngeal papillomatosis or genital HPV infections in the newborn; however, cesarean section does not eliminate the risk of transmission. • More than half of children with anogenital warts have a manifestation of viral inoculation at birth or incidental spread of cutaneous warts. Such cases often are caused by nongenital HPV infections.

19.1 Condyloma acuminatum. Lesions resemble small cauliflowers.

Risk Fact o rs • Transmission of anogenital HPV infection occurs largely by sexual intercourse. • Other risk factors for infection include cigarette smoking, participating in sexual activity at an early age, having a high number of sexual partners, having another STD, immunosuppression, and having an abnormal Pap smear result. DESCRIPTION OF LESIONS There are five morphologic types of anogenital warts, and a patient may manifest more than one type. The appearance of warts depends on its location; for example, the condyloma acuminatum type tends to occur on moist surfaces. • Condyloma acuminatum may resemble small cauliflowers (FIG. 19.1). • Warts may appear as smooth, dome-shaped, papular lesions (FIG. 19.2).

19.2 Condyloma acuminatum. Smooth, dome-shaped papular lesions are present. Chap ter 19 • Sexually Transm itted Diseases

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• They can look like typical verrucous papules or plaques that resemble common warts (FIG. 19.3). • Occasionally, they present as flat papules that may be hyperpigmented. DISTRIBUTION OF LESIONS

19.3 Condyloma acuminatum. These papules have the appearance of common warts.

An o g e n it al Le sio n s • In men, lesions occur on the penis, scrotum, mons pubis, inguinal crease, and perianal area (FIG. 19.4). • In women, the vagina, labia (FIG. 19.5), mons pubis, perianal area, and uterine cervix are the most common locations. • Intra-anal warts are seen predominantly in patients who have engaged in receptive anal intercourse. • Warts may also be found in the peri- and intraurethral areas in men. Out sid e t h e Ge n it al Are a • HPV has been associated with conjunctival, nasal, oral, and laryngeal warts.

19.4 Condyloma acuminatum. Perianal warts are seen in this patient.

19.5 Condyloma acuminatum. Note the labial warts in this patient. Compare to FIGURE 19.7. 322

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CLINICAL MANIFESTATIONS • Genital warts are usually asymptomatic. • Lesions may become pruritic, particularly perianal and inguinal lesions. • They may be painful or bleed if traumatized. • Genital warts may resolve spontaneously or, rarely, progress to invasive squamous cell carcinoma. DIAGNOSIS • The diagnosis of anogenital warts is generally straightforward when the patient presents with the typical cauliflowerlike lesions of condyloma acuminatum or with characteristic verrucous or filiform warts. • However, when lesions are papular (flat-topped), pigmented, moist, or erosive, the diagnosis may not be as clinically obvious.

19.6 Cervical warts. Acetowhitening of subclinical lesions on the cervical mucosa is shown here.

Ace t o wh it e Te st o n Muco us Me m b ran e s • In women, colposcopy is performed using 35% acetic acid, which produces an acetowhitening of subclinical lesions on the vaginal and cervical mucosa (FIG. 19.6). • Atypia or koilocytosis found on Pap smears represents early changes resulting from HPV infection. Ace t o wh it e Te st o n No n -Muco us Me m b ran e Are as • Application of a 5% concentration of acetic acid for 15 to 20 minutes makes subclinical lesions turn white. • Any lesion with epidermal hyperkeratosis appears white. Thus, this method often produces false-positive results and is no longer recommended for routine screening for genital warts. Bio p sy A biopsy may be needed to identify confusing anogenital lesions. • After local anesthesia with lidocaine, curved iris scissors are used to obtain a small specimen (snip biopsy) from the labia minora or perianal area. A punch biopsy or, more simply, a shave biopsy may be obtained from non-mucous membrane skin (see Chapter 26, “Diagnostic and Therapeutic Procedures”). If an ulcer or an indurated nodule is present— particularly if carcinoma is suspected—a punch or excisional biopsy should be performed. • A biopsy is used to rule out anogenital bowenoid papulosis or frank squamous cell carcinoma in atypical or recalcitrant lesions. (text continued on page 327)

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DIFFERENTIAL DIAGNOSIS

No rm al An at o m ic St ruct ure s • In women, vestibular papillae are normal anatomic structures. Unlike warts, vestibular papillae (vulvar papillomatosis) occur near the vaginal vestibule in symmetric clusters or in a linear pattern. They often appear as monotonous, small, smooth projections that resemble cobblestones (FIG. 19.7). • In men, pearly penile papules are frequently mistaken for warts. They are small, skin-colored to shiny, pearly papules that are located around the rim of the corona of the glans penis (FIGS. 19.8 and 19.9). • Fordyce spots are angiokeratomas. They occur on the medial labia minora in many women (see FIG. 21.47). Be n ig n Le sio n s • Common benign skin lesions, such as skin tags, seborrheic keratoses, and melanocytic nevi, may also be easily mistaken for warts. • Skin tags are smooth and may be pigmented or skincolored. Seborrheic keratoses and melanocytic nevi often have a verrucous (keratotic) appearance and may be pigmented. Ot h e r Co n d it io n s • Hemorrhoids. Not infrequently, anal hemorrhoids are mistaken for warts. Hemorrhoids are smooth and compressible. • Molluscum contagiosum. This pox virus infection can easily be confused with, and may coexist with, genital warts. It is seen most often in young children and in patients with HIV infection and in sexually active young

19.7 Vestibular papillae (vulvar papillomatosis). These normal anatomic structures occur near the vaginal vestibule in symmetric clusters or in a linear pattern. They are frequently mistaken for warts.

19.8 Pearly penile papules. These normal anatomic structures occur as shiny papules that are present around the corona of the glans penis and the frenum of the penis.

19.9 Pearly penile papules. These hairlike papules are sometimes referred to as “hirsutoid papules.” They are also frequently misdiagnosed and treated as warts. continued on page 325

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DIFFERENTIAL DIAGNOSIS Continued adults (see Chapter 6, “Superficial Viral Infections,” and Chapter 24, “Cutaneous Manifestations of HIV Infection”). The lesions are dome-shaped, waxy or pearly white papules with a central white core, which is often revealed by inspection with a handheld magnifier. • Condyloma latum of secondary syphilis. Lesions are moist, smooth-surfaced, and, usually, whitish and flattopped. Serologic tests for syphilis are positive (see FIG. 19.20).

from and appear as a fungating condyloma (FIG. 19.10). It is associated with HPV types 6 and 11 and should be considered in the differential of lesions measuring greater than 1 cm in diameter. Only radical surgical extirpation is considered appropriate treatment. • Squamous cell carcinoma. These lesions are rapidly growing nodules or tumors, and they may be erosive or ulcerative.

Malig n an t Ne o p lasm s When any of the following conditions are suspected, a biopsy should be performed. • Bowenoid papulosis. These lesions are clinically similar to, and often indistinguishable from, flat or dome-shaped genital warts. They are associated with HPV type 16 or 18. Histologically, bowenoid papulosis demonstrates squamous cell carcinoma in situ; however, it follows a largely benign clinical course. • Giant condyloma acuminatum. Also known as a Buschke-Löwenstein tumor, this lesion is a low-grade, locally invasive squamous cell carcinoma that can arise

MANAGEMENT

Co un se lin g • Patients should be advised about the long latency period of HPV; thus, a patient may not have contracted condyloma from his or her current partner. • Male patients should use condoms at least 1 year after clinical infection is treated; however, condoms are not perfect protection because warts can occur on genital areas other than the penis or vagina. • In affected women, there is a risk of malignant degeneration to cervical intraepithelial neoplasia or squamous cell carcinoma. If cervical warts are found during examination or if vulvar neoplasia is confirmed by biopsy, referral for colposcopic evaluation is indicated. • It is recommended that anogenital warts be treated in pregnant women during the second and third trimesters and that vaginal delivery be performed if possible. • In affected men with perianal warts, there is a risk of malignant degeneration to anal intraepithelial neoplasia or anal carcinoma. Atypical lesions should be biopsied. • The U.S. Centers for Disease Control and Prevention (CDC) recommends cesarean section only when the vaginal outlet is obstructed by extensive condylomata or if vaginal delivery would cause excessive bleeding.

19.10 Giant condyloma acuminatum. This low-grade, locally invasive malignant tumor can arise from and appear as a fungating condyloma.

• Patients who have internal anal or rectal warts tend to have continual recurrences of external warts and should be referred to a rectal surgeon. • Diagnosis of genital warts in a child requires that the clinician report suspected abuse to begin an evaluation process that may or may not confirm sexual abuse (FIG. 19.11).

19.11 Perianal warts in an infant. The possibility of child abuse should always be considered in these cases. continued on page 326

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MANAGEMENT Continued

Surg ical Th e rap y • Cryosurgery with liquid nitrogen. Cryosurgery is very effective for treating multiple, small warts (e.g., lesions on the shaft of the penis and vulva). Cryotherapy is also safe for the mother and fetus when used during the second and third trimesters of pregnancy. • Electrodesiccation and curettage. This is quite effective for a limited number of lesions on the shaft of the penis. • Carbon dioxide laser treatment. This is more expensive and includes a danger of the operator developing laryngeal lesions from virus in the laser plume. • Surgical excision (useful for debulking large “cauliflower” lesions). Large, unresponsive lesions around the rectum or vulva can be treated with scissor excision of the bulk of the mass followed by electrocautery of the remaining tissue down to the skin surface. In t rale sio n al Th e rap y • Interferon- 2b (11.5 units three times weekly for 3 weeks). This is not recommended by the CDC because of high expense and a lack of increased efficacy over other treatments. It may also cause flulike symptoms. To p ical Th e rap y See TABLE 19.1. Vaccin e • Quadrivalent vaccine (Gardasil) protects against HPV subtypes 6, 11, 16, and 18. • A bivalent vaccine protects against subtypes 16 and 18. Approval is pending.

• The Advisory Committee on Immunization Practices of the CDC recommends routine immunization of girls at 11 and 12 years of age, with the vaccine being made available to girls as young as 9 and women as old as 26. Efficacy has not been studied in women older than 26 or in males. • Women younger than 26 years of age with abnormal or equivocal Pap smears, known HPV infection, or genital warts can be vaccinated. However, the vaccine does not protect against HPV subtypes that the vaccine recipient already has. • Gardasil can be used in women younger than 26 years of age who are breastfeeding or are immunocompromised; however, those women who are immunodeficient may not produce an adequate number of antibodies in response to the vaccine. • Pregnant women should not be vaccinated. • The goal is to reduce the incidence of anogenital cancers by immunizing against the most common oncogenic subtypes. • Postmarket research has shown the quadrivalent vaccine to be almost 100% effective in preventing infection with HPV 16 and 18. It is also effective, to a lesser extent, in preventing infection with an additional 10 subtypes of HPV, including oncogenic subtypes responsible for 20% of cervical cancers. • Refer to the CDC Web site (www.cdc.gov/std/) for the most current updates.

Tre at m e n t fo r Pre g n an t Wo m e n • In the ambulatory setting, appropriate treatment choices include trichloroacetic or bichloracetic acid and ablative procedures, such as cryosurgery.

HELPFUL HINTS

POINTS TO REMEMBER • Immunosuppressed patients, such as those with acquired immunodeficiency syndrome (AIDS) and those taking immunosuppressive therapy (e.g., renal transplant recipients), are more likely than others to develop persistent HPV infection and subsequent dysplasia and malignant disease. • Malignant degeneration may be indicated by increases in size, pain, or bleeding. • Pearly penile papules, vestibular papillae, and other normal anatomic structures are often mistaken for condyloma acuminatum.

SEE PATIENT HANDOUT “Ge n it al Wart s” ON THE SOLUTION SITE

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• Although skin warts are common in the general pediatric population, genital warts are uncommon in children. Consequently, the diagnosis of genital warts in children should alert the health care provider to the possibility of sexual abuse. • Confusing condyloma lata for genital warts misses the diagnosis of highly infectious secondary syphilis and leads to inappropriate therapy and potentially disastrous sequelae for the patient. • Confusing pearly penile papules, vestibular papillae, or Fordyce spots with genital warts results in unnecessary treatment and unwarranted psychosocial stress. • Cesarean delivery should not be performed solely to prevent transmission of HPV infection to the newborn; however, it is advisable to remove visible lesions during pregnancy.

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Tab le 19.1 TOPICAL THERAPIES FOR ANOGENITAL WARTS TREATMENT Patient-applied therapies Imiquimod 5% (Aldara) cream

Podofilox (Condylox) 0.5% solution or gel

Provider-applied therapies Podophyllin resin 10% to 25% in tincture of benzoin

Trichloroacetic or bichloracetic acid 80% to 90%

APPLICATION It is used three times weekly at bedtime for up to 16 weeks. It enhances a patient’s immunity to HPV by increasing local production of interferon. Efficacy in immunocompromised patients is unknown. Safety for use in pregnancy is not known. It is used twice daily (morning and evening) for 3 days, then followed by 4 days without therapy. This 1-week cycle of treatment may be repeated up to four times until no wart remains. Safety for use in pregnancy is not known. It is carefully applied to the wart surface. The patient is instructed to wash the area in 4 to 6 hours, and the interval is increased for subsequent treatments. It is most effective on warts on moist surfaces (perianal, labial, under the prepuce). Podophyllin is an antimitotic agent that causes local tissue destruction. It should not be used in pregnant women or on extensive mucosal surfaces. First, the surrounding normal epithelium is coated with a protective substance, such as 2% lidocaine jelly or Vaseline petroleum jelly, and then a small, cottontipped applicator is used to apply the medication carefully to the wart surface. These agents can cause intense burning of mucosal surfaces. They are most effective on small warts and on nonmucosal surfaces. They may be followed by the use of podophyllin on nonmucosal surfaces.

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H erp es Sim p lex Gen it a lis BASICS

19.12 Herpes simplex genitalis. Grouped vesicles on an erythematous base are evident in this patient.

• Herpes simplex genitalis is a genital disease caused most commonly by HSV-2, although HSV-1 can also infect genital skin. It is most commonly, but not invariably, sexually transmitted. • HSV is the most common cause of ulcerative genital lesions. The disease is highly contagious during the prodrome and while the lesions are active. • HSV establishes latency in the dorsal root ganglia and reappears after different triggers in individual patients. Triggers include psychologic or physiologic stress, physical trauma such as from sexual intercourse, menses, and immunosuppression. • Affected patients may have recurrences that are infrequent or as common as once monthly. Patients who have six or more episodes per year are candidates for long-term suppressive therapy.

Risk Fact o rs • Women have higher acquisition rates and more recurrences than do men. • People between 15 and 35 years of age have a greater chance to contract HSV-2. • For those individuals who are infected with HPV (see earlier discussion) and HSV, those who have a greater number of sexual partners are also more likely to develop HSV. DESCRIPTION OF LESIONS

19.13 Herpes simplex genitalis. Vesicles have become grouped erosions in this patient.

• Initially, lesions appear as grouped vesicles on an erythematous base (FIG. 19.12). • Lesions may then become pustular, crusted, and eroded (FIG. 19.13). • Crusting of the lesions occurs over 15 to 20 days, before reepithelialization begins. • Chronic ulcerations or crusted or verrucous papules may develop in immunocompromised patients (see FIGS. 24.3 and 24.4). DISTRIBUTION OF LESIONS • In women, the vulvae, perineum, inner thighs, buttocks, and sacral area (FIG. 19.14) are the most common sites of involvement. • In men, the penis, scrotum, thigh, and buttocks are the typical locations.

19.14 Herpes simplex. This is a common site of HSV-2 in women.

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CLINICAL MANIFESTATIONS

Prim ary He rp e s Sim p le x • As with HSV-1, this may be more severe than recurrent infections (see Chapter 6, “Superficial Viral Infections”). • The duration is generally from 10 to 14 days. • Regional adenopathy may be present. • Fever, dysuria, urinary retention, and constipation may also occur. • Alternatively, the initial outbreak may be mild or asymptomatic, so that the patient sheds virus intermittently without realizing that he or she is infected. Re curre n t He rp e s Sim p le x • There is often a prodrome of itching, burning, numbness, tingling, or pain 1 to 2 days before a clinical outbreak. • Lesions are localized and recur at the same site or in close proximity each time. • Regional adenopathy may be present. • Vulvar involvement may cause dysuria. • The duration is generally from 3 to 5 days. • Chronic ulcerative lesions are indicative of immunosuppression. • The risk of neonatal transmission is less than 3% and is greatest in patients with primary HSV at the time of delivery. COMPLICATIONS • Genital ulcer disease puts the patient at an increased risk of HIV infection.

• The risk of neonatal transmission depends on when the maternal infection is acquired. The risk to the neonate is less than 1% if the maternal infection is recurrent or is acquired at the beginning of pregnancy and is 30% to 50% if the maternal infection is acquired near term. • If maternal HSV is acquired near the time of delivery, cesarean section is usually advised. • Patients with certain skin diseases, such as atopic dermatitis, are in danger of developing dissemination of herpes simplex, also known as Kaposi’s varicelliform eruption (see FIG. 6.29). DIAGNOSIS • Most often, the diagnosis is based on the clinical appearance. • The Tzanck preparation (see Chapter 6, “Superficial Viral Infections”) may be helpful, but it lacks sensitivity. • Viral culture is the current standard of diagnosis, but the sensitivity declines rapidly as the lesions begin to heal. • Diagnosis in tissue culture using monoclonal antibodies or polymerase chain reaction is sensitive; however, it is very expensive and has not been approved by the U.S. Food and Drug Administration for the diagnosis of genital lesions. • Serologic testing may be useful, according to CDC guidelines, for those with (a) recurrent genital signs and symptoms and negative cultures, (b) a clinical diagnosis of genital herpes without laboratory confirmation, and (c) a partner with genital herpes. It is not recommended for screening of the general population.

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DIFFERENTIAL DIAGNOSIS

He rp e s Zo st e r See Chapter 6, “Superficial Viral Infections.” • Herpes simplex may be dermatomal and may appear clinically identical to herpes zoster. • A history of recurrences suggests HSV.

Prim ary Syp h ilis (Ch an cre ) See FIGS. 19.15 and 19.16. • Classically, the lesion has been described as being “painless”; however, secondarily infected lesions may be painful. • The border is indurated.

Ch an cro id • There are multiple painful ulcers (see FIGS. 19.22 and 19.23).

19.15 Chancre of primary syphilis. This ulcer has a rolled, indurated border (chancre) and a “clean” base.

MANAGEMENT

19.16 Chancre of primary syphilis. Note the lesion on the anus.

Syst e m ic An t iviral Th e rap y Prim a r y H erp es Sim p lex

Pat ie n t Ed ucat io n • The patient should be given written educational materials and clear instructions regarding safe sexual practices. • The use of condoms should be encouraged. • The patient should be advised about asymptomatic viral shedding. • The risk of neonatal infection should be emphasized to both female and male patients. To p ical Th e rap y • Topical antivirals are of limited effectiveness and are not recommended. • Symptomatic relief may be achieved with cold compresses, viscous lidocaine (Xylocaine), EMLA (eutectic mixture of lidocaine and prilocaine), or oral analgesics.

• Acyclovir (200 mg five times daily or 400 mg three times daily for 10 days) or • Famciclovir (Famvir) (250 mg three times daily for 10 days) or • Valacyclovir (Valtrex) (1 g twice daily for 7 to 10 days) Recu r ren t H erp es Sim p lex : Ep iso d ic Th era p y

Treat at the first sign of the prodrome. • Acyclovir (400 mg three times daily for 5 days, 800 mg twice daily for 5 days, or 800 mg three times daily for 3 days) or • Famciclovir (125 mg twice daily for 5 days or 1,000 mg twice daily for 1 day or • Valacyclovir (500 mg twice daily for 3 days or 1,000 mg daily for 5 days continued on page 331

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MANAGEMENT Continued Recu r ren t H erp es Sim p lex w it h Mo re t h a n Six Recu r ren ces p er Yea r o r Ch ro n ic Recu r ren t Er yt h em a Mu lt ifo r m e (Da ily Su p p ressive Th era p y)

• Treat as for recurrent HSV for 5 days, then continue therapy with acyclovir (400 mg twice daily) or • Famciclovir (250 mg twice daily) or • Valacyclovir (500 mg once daily or 1,000 mg once daily) • After 1 year of treatment with these agents, the medication should be discontinued to determine the recurrence, and the dosage can be adjusted as needed. • The safety of daily acyclovir has been established for a period of 6 years and for famciclovir and valacyclovir for 1 year. Acyclo vir-Resist a n t H erp es Sim p lex

• This is seen in patients with AIDS. • Coresistance to famciclovir and valacyclovir has been reported. • Foscarnet can be given (40 mg/kg IV two to three times daily for 14 to 21 days).

POINTS TO REMEMBER • Oral antiviral treatment should be initiated, if possible, during the prodromal phase. • Asymptomatic infections are common and contribute significantly to HSV transmission because of subclinical viral shedding. • Condoms are clearly not foolproof, because the virus spreads by contact with herpes sores and condoms may not cover all sores.

• Recurrent HSV after foscarnet treatment is often acyclovir sensitive.

He rp e s Sim p le x in Pre g n an t Wo m e n • The safety and efficacy of oral antiviral therapy during pregnancy have not been established. • Although acyclovir readily crosses the placenta, several studies did not reveal any increased risk to the developing fetus. • Antiviral therapy is recommended for pregnant women who are experiencing a primary HSV infection. • If vaginal delivery occurs through an infected birth canal, the neonate should be observed, and any suspicious lesions should be cultured. • If no symptoms or signs are present during labor, vaginal delivery is recommended. • Although the risk of neonatal infection is lower in women with recurrent HSV than it is in women with primary infection, the presence of active herpetic lesions or symptoms of vulvar pain or burning may call for cesarean delivery, regardless of the type of maternal herpetic infection.

HELPFUL HINTS • A recent study found that 500 mg Valtrex, taken once daily by people with HSV-2, decreased by 50% the risk of transmitting the infection to uninfected partners. This suggests that Valtrex can be prescribed in so-called discordant couples—those in which one partner is infected and the other is not. • Maternal acquisition of HSV-1 or HSV-2 during pregnancy accounts for most neonatal HSV infections, which often result in infant deaths.

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Syp h ilis BASICS • Syphilis is a systemic STD caused by the spirochetal bacterium Treponema pallidum. It is divided into primary, secondary, early latent, late latent, and tertiary stages. • Tertiary syphilis is exceedingly rare in the modern era, presumably because most infected patients have had exposure to multiple courses of antibiotics during the course of their lives, and this treatment prevents the infection from progressing.

• The chancre may occur at the base of the penis in condom wearers. • A visible chancre is less common in women. • In women, lesions may occur on the labia majora or minora, the clitoris, or the posterior commissure. • Anal lesions may occur after receptive anal intercourse (see FIG. 19.16). • Less frequently, extragenital chancres can occur. CLINICAL MANIFESTATIONS

Prim ary Syp h ilis DESCRIPTION OF LESIONS • A painless ulceration is seen, with a rolled, indurated border (chancre) (see FIG. 19.15). • Lesions are usually single, but they may be multiple. • The base of the ulcer is “clean” unless it is superinfected. • There are no vesicles. DISTRIBUTION OF LESIONS • The primary chancre most often presents on or near the glans penis in men; it appears less commonly on the shaft of the penis.

• The primary chancre is usually asymptomatic. • Regional adenopathy may be present. • An untreated chancre heals within 3 months. DIAGNOSIS The following diagnostic methods are used: • Darkfield examination of the ulceration • Skin biopsy • Nontreponemal serologic tests such as Venereal Disease Research Laboratory, rapid plasma reagin, and the automated reagin test; these become positive at a rate of 25% of patients per week of infection

DIFFERENTIAL DIAGNOSIS

He rp e s Sim p le x • Lesions are generally painful. • Vesicles precede the ulceration. Ch an cro id • Chancroid is unusual in the United States. • In Africa, chancroid is often present as a coinfection. • Lesions are painful.

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MANAGEMENT • Test for HIV infection and retest 3 months later if negative.

No n –Pe n icillin -Alle rg ic Pat ie n t s • Benzathine penicillin G (2.4 million units IM in a single dose)

Pe n icillin -Alle rg ic Pre g n an t Pat ie n t s • Desensitization to penicillin • Subsequent treatment with benzathine penicillin G (2.4 million units IM, with a second dose 1 week later) HIV-In fe ct e d Pat ie n t s • Benzathine penicillin G (2.4 million units IM in one dose) • Some experts recommend repeated treatment

Pe n icillin -Alle rg ic No n p re g n an t Pat ie n t s • Doxycycline (100 mg PO twice daily for 2 weeks) or • Tetracycline (500 mg four times daily for 2 weeks)

POINTS TO REMEMBER • Patients should be evaluated at 3 and 6 months after treatment. Nontreponemal tests should be negative or have decreased fourfold in titer. • If the antibody titer does not drop fourfold, suspect treatment failure, reinfection, or HIV infection.

Secon d ary Syp h ilis DESCRIPTION OF LESIONS • Scaly, erythematous, oval, papulosquamous papules appear (FIG. 19.17) and are usually asymptomatic. 19.17 Secondary syphilis. Scaly, erythematous oval patches and papules are noted. (Image courtesy of Ed Zabawski, D.O.)

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333

• Mucous patches may be noted (FIG. 19.18). • “Moth-eaten” alopecia (FIG. 19.19) and condyloma latum (FIG. 19.20) are also seen in secondary syphilis. DISTRIBUTION OF LESIONS • Lesions are widespread and include the palms (FIG. 19.21), soles, scalp, and mucous membranes. CLINICAL MANIFESTATIONS • Generalized adenopathy and mild systemic symptoms are often present. 19.18 Secondary syphilis. Mucous patches are present, and characteristic copper-colored palmar lesions are seen.

DIAGNOSIS • The diagnosis is often suggested by the clinical presentation. • If available, a darkfield examination of serum expressed from lesions can confirm the diagnosis, or • Positive treponemal (fluorescein treponemal antibody) and nontreponemal serologic tests (100% of non-HIV-infected patients, usually at a titer greater than 1:16 for the nontreponemal test) confirm the diagnosis, or • A skin biopsy with silver or immunoperoxidase stain may confirm the diagnosis. • Serologic titers may be negative in HIV-infected persons.

19.19 Secondary syphilis. Note the “moth-eaten” appearance of alopecia in this patient.

19.20 Secondary syphilis. Condyloma latum is noted. These moist, wartlike papules are highly infectious.

19.20 Secondary syphilis. Condyloma latum is noted. These moist, wartlike papules are highly infectious.

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19.21 Secondary syphilis. Characteristic copper- or “ham”-colored, papulosquamous lesions are seen on this patient’s palms. (Image courtesy of Ashit Marwah, M.D.)

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Laten t Syp h ilis DIFFERENTIAL DIAGNOSIS • Latent syphilis is manifested by positive serologic tests for nontreponemal and treponemal antibodies in the absence of clinical manifestations. It is divided into early latent syphilis and late latent syphilis. • Early latent syphilis is syphilis documented to be of less than 1 year in duration and is treated with the same regimen as primary and secondary infections. • The duration of late latent syphilis is more than 1 year or is unknown. The recommended treatment is benzathine penicillin 2.4 million units intramuscularly weekly for 3 weeks. HIV-infected patients with latent syphilis of any duration should have a cerebrospinal fluid examination to rule out neurosyphilis before treatment.

Pit yriasis Ro se a See FIGURES 4.1 to 4.4. • Usually, pityriasis rosea is confined to the skin above the knees, and it spares the face, palms, and soles. It is prudent to check syphilis serologic tests in patients with pityriasis rosea.

Ot h e r Diag n o se s • Other papulosquamous eruptions such as psoriasis, lichen planus, and drug eruptions should be considered.

Tertiary Syp h ilis • Tertiary syphilis occurs about 20 years after the onset of untreated syphilis, and it is rare in the antibiotic era. • Treatment is the same as for late latent syphilis.

Con gen ital Syp h ilis • Congenital syphilis can affect infants born to mothers with untreated syphilis, with syphilis treated during pregnancy with erythromycin, with syphilis treated less than 1 month before delivery, and with syphilis treated with penicillin without a fourfold decrease in serologic titer. • The CDC recommends that all pregnant women be tested for syphilis at least once during pregnancy and at the time of delivery in at-risk populations.

MANAGEMENT • This is the same as for primary syphilis. • The serologic titer should fall fourfold in 6 months. If it does not, the patient should have a cerebrospinal fluid examination. If it is negative, some experts advise retreatment with benzathine penicillin (2.4 million units weekly for 3 weeks).

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Ch a n cro id BASICS • Chancroid is an ulcerative STD that is most common in developing countries and is rare in the United States and Western Europe. In the United States, it is associated with the use of crack cocaine. • The causative organism, Haemophilus ducreyi, a gramnegative rod, is fastidious and requires specific conditions for culture. • Chancroid occurs as a mixed infection with syphilis or herpes simplex in 10% of cases. • Clinical infection is more common in men than in women. DESCRIPTION OF LESIONS • The earliest manifestation is a papule, which becomes a pustule and ulcerates. • Fully developed lesions are painful, with undermined borders and peripheral erythema (FIGS. 19.22 and 19.23). • Borders are not indurated. • There may be satellite ulcers. 19.22 Chancroid. This patient has multiple painful ulcers on the glans penis.

DISTRIBUTION OF LESIONS • The location of lesions depends on the site(s) of inoculation. • In men, the prepuce, balanopreputial fold, and the shaft of the penis are the typical sites. • In women, lesions are noted on the labia majora, posterior commissure, or perianal area. • Extragenital lesions have been described. CLINICAL MANIFESTATIONS • The incubation period is 25 days. • Tenderness and pain are common. • Unilateral or bilateral inguinal adenopathy (buboes) may be present. DIAGNOSIS

19.23 Chancroid. Multiple painful ulcers and a bubo are present.

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• The diagnosis is often made based on the clinical appearance. • A negative darkfield examination, syphilis serologic testing, and HSV cultures help to exclude other diagnoses. • Obtaining a culture is difficult. • A Gram stain shows characteristic “schools of fish” or “Chinese characters.” • Polymerase chain reaction may help in making a diagnosis.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

MANAGEMENT • Drug Therapy • Azithromycin (1 g PO in a single dose) or • Ceftriaxone (250 mg IM in a single dose) or • Erythromycin (500 mg PO four times daily for 7 days) or • Ciprofloxacin (500 mg PO twice daily for 3 days) • Pregnant women and HIV-infected patients should be treated with erythromycin. • Symptomatic improvement usually occurs in 3 days; objective improvement is seen in 7 days. • Complete healing may take more than 2 weeks. • HIV testing should be performed on all patients and repeated 3 months later if negative.

DIFFERENTIAL DIAGNOSIS

He rp e s Sim p le x • Herpes simplex is preceded by blisters, and the borders are not undermined. Chronic HSV • Chronic HSV in patients with AIDS may resemble chancroid. Primary Syphilis • In primary syphilis, the borders are indurated, not undermined, and the lesion is generally painless.

POINTS TO REMEMBER • Chancroid is rare in the United States, but epidemics have been described in crack cocaine users. • Chancroid predisposes to HIV infection because of recruitment of CD4 cells into the ulcer. • Always test for coinfection with HIV, syphilis, and HSV.

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Lym p h o gra n u lo m a Ven ereu m BASICS • Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis types L1, L2, and L3. It is most often sexually transmitted. • LGV is most common in Southeast Asia, Africa, Central America, and the Caribbean. LGV accounts for 2% to 10% of genital ulcer disease in India and Africa. • An inconspicuous cutaneous ulceration occurs at the site of inoculation, and it often heals without being noticed. DESCRIPTION OF LESIONS • Evanescent papulopustule or ulceration occurs. • Regional lymphadenitis is characteristic. The groin fold divides lymph nodes into upper and lower groups (“the groove sign”) (FIG. 19.24). Sometimes, the adenopathy is bilateral. • Fluctuance and sinus tracts may develop. DISTRIBUTION OF LESIONS • The primary lesion, if present, is found on the penis, vaginal wall, cervix, or perirectally. It is rarely seen in women.

19.24 Lymphogranuloma venereum. Regional lymphadenitis (“the groove sign”) is present.

CLINICAL MANIFESTATIONS • • • •

LGV may be associated with malaise and joint stiffness. Scarring may result in genital lymphedema. Erythema nodosum occurs in 10% of women with LGV. Rectal exposure can lead to proctocolitis, which if not treated promptly leads to chronic colorectal strictures and fistulas.

DIAGNOSIS • The diagnosis of LGV depends mainly on the exclusion of other causes of suppurative adenopathy and serologic testing: a complement fixation test, and two immunofluorescent tests. • Culture of the organism is also available. MANAGEMENT • Doxycycline (100 mg PO twice daily for 3 weeks minimum) or • Alternative regimen (and in pregnant women): erythromycin (500 mg PO four times daily for 3 weeks minimum) • Buboes may need to be aspirated or incised and drained.

POINTS TO REMEMBER • Infection is rare in the United States. • Cutaneous manifestations are usually inapparent. 338

DIFFERENTIAL DIAGNOSIS

Cat scrat ch Dise ase • Usually, there is a history of traumatic contact with cats at a site proximal to involved lymph nodes. Pyo g e n ic Ad e n it is • A positive Gram stain and bacterial cultures may be found. Tub e rculo us Ad e n it is • A positive acid-fast bacillus stain and cultures and a positive purified protein derivative test are obtained.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Gra n u lo m a In gu in a le

(Do n o va n o sis)

BASICS

DISTRIBUTION OF LESIONS

• Granuloma inguinale is a chronic granulomatous ulcerative disease of the genitalia caused by the gram-negative bacillus Calymmatobacterium granulomatis. It is thought to be sexually transmitted, with low infectivity. • It is rare in the United States and is widespread in the tropics and subtropics. The frequency of the disease in homosexuals suggests that the causative organism may reside in the gastrointestinal tract.

• Granuloma inguinale appears in the genital, pubic, perineal, groin, or perianal areas. • Extragenital lesions occur in 3% to 6% of cases. CLINICAL MANIFESTATIONS • The presence of pain or adenitis suggests superinfection. DIAGNOSIS

DESCRIPTION OF LESIONS • The initial lesion is a papule or a nodule that ulcerates. • The ulcer is painless and has an undermined border. • There is no regional adenitis.

• Smears from the edge of the lesion may show characteristic Donovan bodies (organisms within macrophages). • The biopsy specimen should be taken from the edge of the lesion.

DIFFERENTIAL DIAGNOSIS

Syp h ilis • Syphilis must be excluded by darkfield and serologic examinations. • The borders of the ulcers are indurated, not undermined.

MANAGEMENT • The treatment of choice is doxycycline (100 mg twice daily for 3 weeks minimum or until the ulcers have healed). • Alternative regimens: • Azithromycin (1,000 mg once weekly for at least 3 weeks or until the ulcers have healed) or

• Ciprofloxacin (750 mg twice daily for at least 3 weeks or until the ulcers have healed) or • Erythromycin (500 mg four times daily for at least 3 weeks or until the ulcers have healed) or • Trimethoprim-sulfamethoxazole (one double-strength tablet twice daily for at least 3 weeks or until the ulcers have healed)

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C H AP T ER

Bites, Stings, and Infestations

20 OVERVIEW INSECTS, TICKS, MITES • Insect bite reactions • Lym e disease (lym e borreliosis) • Scabies: m ite infestation LICE INFESTATIONS (PEDICULOSIS) • Head lice (pediculosis capitis) • Body lice (pediculosis corporis) • Pubic lice WATERBORNE STINGS AND SEASHORE INFESTATIONS • Jellyfish stings • Seabather’s eruption (“sea lice”) • Cutaneous larva m igrans (“creeping eruption”)

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In much of the world, insect bites commonly serve as vectors that transport diseases such as malaria, leishmaniasis, filariasis, and rickettsial diseases. In modern industrial societies, insect bites are more of a nuisance than a potential carrier of a life-threatening illness. On the East Coast and in the Midwest of the United States, mosquitoes and biting flies as well as ticks account for most bites. In arid areas, including much of the Southwest and parts of California, flying insects are less common, and crawling arthropods are the primary cause of bites and stings. West Nile virus, of much concern in the United States, is a mosquito-borne infection that can cause encephalitis. It was originally seen in New York State in 1999 and is now being reported throughout the country.

In sect Bit e Rea ct io n s BASICS • Insects that bite include mosquitoes, fleas, flies, ticks, chiggers, and lice. Mosquito and fly bites occur most often from outdoor exposures, particularly in the summer. Flea bites are most often acquired indoors from pets. • Insects that sting include bees, wasps, hornets, and fire ants. • There is individual variability in the attraction of insects, possibly related to pheromones. Furthermore, reactions to bites and stings are probably related to individual hypersensitivity. • The physical insult of an insect bite or sting causes little injury; instead, lesions occur as a result of the body’s immune response to injected foreign chemicals and proteins introduced by the bite or sting. The time it takes for reactions to develop reflects the immune mechanism involved.

Pat h o g e n e sis • Immediate hivelike skin lesions reflect hypersensitivity to the bite or sting. They are mediated by immunoglobulin E (FIG. 20.1). • Delayed pruritic papules, nodules, and vesicles usually become symptomatic within 48 hours after the insult. They are manifestations of delayed hypersensitivity (type IV cellmediated immunity).

20.1 Angioedema caused by a bee sting. This patient developed an immediate hypersensitivity reaction after being bitten on the lip.

DESCRIPTION OF LESIONS • Bite reactions typically present as intensely pruritic erythematous papules that commonly are excoriated. • Bite reactions may be indistinguishable from ordinary hives. • Grouping of lesions often occurs, particularly after flea bites (“breakfast, lunch, and dinner”; FIG. 20.2).

20.2 F lea bites. Note the arrangement of lesions in groups of three (“breakfast, lunch, and dinner”); the fourth lesion probably represents a “midnight snack.”

Chap ter 20 • Bites, Stings, and Infestations

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• Lesions may have a central punctum and crust and also may become vesicobullous (FIG. 20.3). • Insect bite reactions are also known as papular urticaria when lesions persist for longer than 48 hours. DISTRIBUTION OF LESIONS

20.3 Bullous arthropod bite reaction. Note the tense bulla that resulted from a chigger bite.

• Lesions are found on exposed areas, more often on nonclothed body parts such as distal lower extremities, forearms, and hands. • The papules of flea bites are typically asymmetric in distribution. • Lesions are also commonly seen on the lower legs, forearms, lower trunk, and waist; the axillary and anogenital areas are usually spared. Flying insects tend to bite on the upper trunk or extremities, whereas crawling insects tend to bite or sting on the lower trunk or extremities. Although this is not always true, it often helps narrow down the cause. CLINICAL MANIFESTATIONS • Insect bites may be a chronic, recurrent problem or simply a nuisance. • The purpose of bites is usually to obtain a blood meal, which means that they often occur in multiples. The purpose of stings is usually self-defense, which means that they occur singly; the glaring exception is fire ants, which sting as much as they can. • Itching may be intense and may persist for weeks. • Secondary bacterial infection may occur. • Stings generally cause immediate pain and are therefore usually remembered. • Bites often go unnoticed, and the lesions that arise from them may not appear for days after the bite because of what is often a delayed immune-mediated hypersensitivity reaction. Consequently, a patient may seek medical advice for unexplained itchy bumps or blisters. Presumably, bites go unnoticed because it is to the arthropod’s advantage to obtain its blood meal without being detected, which serves to increase its survival value. DIAGNOSIS • The diagnosis is usually made on clinical appearance and history. • Inquiry about household pets currently and formerly residing in the house may be a clue to the diagnosis. If the residence was formerly host to a dog or cat infested with fleas, the fleas left behind may have found new human hosts. • A skin biopsy is not diagnostic, but it may show suggestive findings consisting of a dense lymphocytic infiltrate (resembling lymphoma) with many eosinophils. The responsible agent is rarely found in a biopsy specimen.

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Urt icaria Un re lat e d t o In se ct Bit e s See also Chapter 17, “Drug Eruptions.”

Fib e rg lass De rm at it is • Nonspecific itching is noted. • The patient has a history of exposure (e.g., works with roofing materials).

• This type of urticaria lacks a central punctum. • It is often indistinguishable from insect bites.

Scab ie s • See the discussion later in this chapter.

DIFFERENTIAL DIAGNOSIS

POINTS TO REMEMBER MANAGEMENT • A careful history and knowledge of the patient’s environment and possible exposures should be sought. • Symptoms may persist for weeks after the original bites. • Other causes should be diligently sought if symptoms persist for more than 4 to 6 weeks.

HELPFUL HINTS • Patients who seek medical help generally do not consider “mundane” insect bites to be the cause of their dermatosis or itching; rather, they seek attention because they assume that other factors cause their problem. • Poisons normally used by exterminators do not kill fleas.

• Insect repellents that contain N,N-diethyl-mtoluamide (DEET) help prevent bites and stings. • Acute reactions to stings are treated symptomatically with topical or intralesional steroids and oral antihistamines; people with severe reactions from stings may profit from desensitization therapy. • Anaphylactic reactions require epinephrine, systemic steroids, and antihistamines. • If flea infestation is suspected, pets should be evaluated by a veterinarian. If fleas are present in the home, thorough vacuuming and shampooing of flea-infested areas and sometimes even fumigation may be necessary.

Chap ter 20 • Bites, Stings, and Infestations

343

Lym e Disea se

(Lym e Bo r relio sis) BASICS

20.4 Lyme disease, erythema migrans. A solitary, annular, targetlike, erythematous plaque of erythema migrans is seen.

• Lyme disease, or Lyme borreliosis (LB), is a systemic infection caused by the spirochete Borrelia burgdorferi. Bacteria are introduced into the skin via a bite from an infected Ixodes tick. • The tick has to be attached for 24 hours for the organism to be transmitted. • Once in the skin, the spirochete may stay localized at the site of inoculation, or it may disseminate via the blood and lymphatics. Hematogenous dissemination can occur within days or weeks of the initial infection. The organism can travel to other parts of the skin, the heart, the joints, the central nervous system, and other parts of the body. • The tick vector of LB, I. dammini, is found in the northeastern and midwestern United States, where most cases are reported. I. scapularis in the southeastern United States, I. pacificus on the Pacific coast, and I. ricinus, the sheep tick, in Europe are also vectors. Because the disease depends on deer, mice, ticks, and bacteria, it is limited geographically to the areas where all these organisms are present. • LB can occur in any season, although it is most prevalent during the warmer months from May through September during the nymphal stage of the tick. The ticks cling to vegetation (not trees) in grassland, marshland, and woodland habitats. They transfer to animals and humans brushing against the vegetation. DESCRIPTION OF LESIONS

20.5 Lyme disease. In this patient, erythema migrans is manifested by concentric rings with resolving central vesicles.

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• Initially, the LB lesion is a red macule or papule at the site of a tick bite. The bite itself usually goes unnoticed (only 15% of patients report a tick bite). Approximately 2 to 30 days after infection, the rash appears. • The lesion expands to form an annular erythematous lesion, erythema migrans (EM), which is the classic lesion of LB (FIG. 20.4). The lesion measures from 4 to 70 cm in diameter, generally with central clearing. • The center of the lesion, which corresponds to the putative site of the tick bite, may become darker, vesicular, hemorrhagic, or necrotic (FIG. 20.5).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

• Lesions may be confluent (not annular), and concentric rings may form. • Multiple lesions occur in approximately 20% of patients, likely a result of bacteremia (FIGS. 20.6 and 20.7). These secondary lesions tend to be more uniform in morphology than the primary lesion. DISTRIBUTION OF LESIONS • Common sites are the thigh, groin, trunk, and axillae. • Because secondary lesions spread hematogenously, they are less restricted than primary lesions in terms of location. CLINICAL MANIFESTATIONS

Early Lym e Dise ase • At the early stage of disease, flulike symptoms, such as malaise, arthralgias, headaches, and a low-grade fever and chills, may occur. Other symptoms include stiffness of the neck and difficulty in concentrating. • The EM rash itself is usually asymptomatic. In t e rm e d iat e , Ch ro n ic, an d Lat e Lym e Dise ase • Some of the signs and symptoms of LB may not appear for weeks, months, or even years after the initial tick bite and are believed to be caused by immunopathogenic mechanisms. The signs and symptoms of intermediate, chronic, and late Lyme disease include: • Arthritis in one or more large joints; nervous system problems that may include pain, paresthesias, Bell’s palsy, headaches, and memory loss; and cardiac dysrhythmias. • Rarely, a lesion of lymphocytoma cutis may develop, usually occurring on the earlobe or nipple. These lesions are bluish red nodules. • Acrodermatitis chronica atrophicans (ACA) is a manifestation of chronic LB that begins as an inflammatory phase marked by edema and erythema, usually on the distal extremities. Later, atrophy occurs, and thin “cigarettepaper” skin is seen. Because of the loss of subcutaneous fat, underlying venous structures are more visible, and the skin becomes thin, atrophic, and dry. • Both lymphocytoma cutis and ACA are very rare findings in the United States and are seen primarily in Europe. The clinical differences probably result from the different antigenic strains of Borrelia. • Late Lyme disease refers to symptoms, primarily rheumatologic and neurologic, that occur months to years after initial infection. It is not unusual for patients to first present with late extracutaneous symptoms without ever having had an initial EM lesion or other overt symptoms of early Lyme disease. This may occur because the patient was asymptomatic or because early disease was not recognized by the patient or correctly diagnosed by the health care provider.

20.6 Lyme disease. Multiple confluent lesions of erythema migrans are noted.

20.7 Lyme disease. Multiple annular lesions of erythema migrans are seen here.

Chap ter 20 • Bites, Stings, and Infestations

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DIAGNOSIS • The diagnosis of LB is often difficult because the disease mimics many other conditions. • Viral infections, such as influenza and mononucleosis, also may manifest with rash, aches, fever, and fatigue. • Drug eruptions and insect bite reactions other than those caused by the Ixodes tick closely match the rash of early LB.

Early Diag n o sis To diagnose early LB, the following are important: • There is a history of tick exposure or bite in an area endemic for LB. • The specific tick is identified as a potential vector of LB. • The various presentations of EM are recognized.

Lab o rat o ry Te st in g • Serologic testing, using enzyme-linked immunosorbent assay (ELISA) and Western blot analyses for B. burgdorferi, is notoriously unreliable. • At the early presenting stage of LB, serologic testing has been reported to be positive in only 25% of infected

patients. After 4 to 6 weeks, approximately 75% of these patients test positive, even after antibiotic therapy. • Patients with past LB and those who have been vaccinated may be persistently seropositive. • The poor reputation of serologic testing is derived somewhat from the many false-negative test results of patients treated very early in the course of the disease and from the many misdiagnosed cases of supposed LB. • The U.S. Centers for Disease Control and Prevention currently recommends a two-step testing procedure consisting of a screening ELISA or immunofluorescent assay followed by a confirmatory Western immunoblot test on any samples with positive or equivocal results on ELISA. • Infrequently, spirochetes may be identified using silver or antibody-labeled stains. • Other diagnostic measures, such as polymerase chain reaction and cultures for B. burgdorferi have met with some success; however, these techniques are time-consuming and expensive. The Borrelia organism is fastidious, and culture of skin biopsy specimens is not readily available.

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DIFFERENTIAL DIAGNOSIS

Tin e a Co rp o ris • See Chapter 7, “Superficial Fungal Infections.” • There may be a history of exposure to fungus. • Lesions are also annular (ringlike) and clear in the center; however, tinea corporis has an “active” scaly border (epidermal involvement). • Lesions are potassium hydroxide positive (FIG. 20.8), or the fungal culture grows dermatophytes. • Tinea corporis generally itches.

Gran ulo m a An n ulare • For a full discussion of this condition, see Chapter 4, “Inflammatory Eruptions of Unknown Cause.” Eryt h e m a Mult ifo rm e • For a full discussion of this condition, see Chapter 25, “Cutaneous Manifestations of Systemic Disease.”

Acut e Urt icaria • See Chapter 18, “Diseases of Vasculature.” • At times, this may be indistinguishable from LB. • Lesions may have eccentric shapes (FIG. 20.9). • Individual lesions disappear within 24 hours. • It generally itches.

20.8 Tinea corporis. The scaly border is potassium hydroxide–positive.

20.9 Acute urticaria. Lesions have bizarre, eccentric shapes in this patient.

Chap ter 20 • Bites, Stings, and Infestations

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MANAGEMENT

Tick Re co g n it io n • Ixodes ticks are much smaller than dog ticks. In their larval and nymphal stages, they are no bigger than a pinhead; unengaged adult ticks are the size of the head of a match (FIG. 20.10). Tick Re m o val • An attached tick should be removed carefully by using a pair of tweezers. The tick should be grasped by the head (not the body), as close as possible to the skin, to avoid force that may crush it. It is then gently pulled straight out of the patient’s skin (FIG. 20.11). Tre at m e n t o f Eryt h e m a Mig ran s (Early Lym e Bo rre lio sis) • Doxycycline (100 mg twice per day for 21 days [do not use in children younger than 10 years or in pregnant women]) or • Amoxicillin (500 mg three times per day for 21 days) or • Ceftriaxone or cefuroxime (500 mg twice per day for 21 days [expensive; use only if patient is unable to tolerate the other antibiotics]) • Azithromycin (Zithromax) and erythromycin: secondline drugs that should be considered in pregnant patients who are allergic to beta-lactam antibiotics Pre ve n t io n • People who are outdoors in endemic areas in the summer should wear long pants and socks, use insect repellents, and frequently look for ticks on themselves and their clothing.

20.10 Ixodes tick. An adult tick is the size of the head of a match.

20.11 Dog tick. An intact engorged adult dog tick being removed by the head.

Lym e Dise ase Vaccin e (LYMErix) • A vaccine directed against the outer surface protein A of B. burgdorferi was removed from the United States market in 2002.

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HELPFUL HINTS • Patients can be reinfected. There is no lasting immunity to LB. • Most patients at the EM stage are seronegative. • An additional tick-borne coinfection by Ehrlichia species and Babesia microti has been reported with increasing frequency. Such coinfection is suggested by a very high fever or toxicity. • Antibiotic prophylaxis after tick bites is controversial. Clearly, prevention of bites is a better means of avoiding disease. • Health care providers must understand the limitations of serologic tests. • Wearing clothing with white colors improves the odds of seeing ticks on clothing before they attach. • Regular tick inspections and removal of ticks before they have been attached for 24 hours is another important way to reduce the risk of contracting Lyme disease.

POINTS TO REMEMBER • Serologic testing is usually negative early in the course of infection. • Serologic testing should not be used to make a diagnosis, only to help confirm it.

SEE PATIENT HANDOUT “Lym e Dise ase ” AND “Lym e Dise ase : Pre ve n t io n ” ON THE SOLUTION SITE

Chap ter 20 • Bites, Stings, and Infestations

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Sca b ies: Mit e In fest a t io n BASICS

20.12

Scabies. A fertilized female mite is visible.

• Scabies is a skin infestation caused by the mite Sarcoptes scabiei var. hominis. It is usually spread by skin-to-skin contact, most frequently among family members and by sexual contact in young adults. Occasionally, epidemics occur in nursing homes and similar extended-care institutions, where scabies is spread by person-to-person contact and possibly by mite-infested clothing and bed linen. The diagnosis can be easily overlooked, and treatment is often delayed for long periods. • The diagnosis of scabies should be considered when an individual complains of intractable, persistent pruritus, especially when other family members, consorts, or fellow inhabitants of an institution, such as a nursing home or school, have similar symptoms. • Although scabies is found more commonly in poor, crowded living conditions, it occurs worldwide and is not limited to the impoverished or those who practice poor personal hygiene. African-American and Afro-Caribbean individuals infrequently acquire scabies; the reason is unknown.

Pat h o g e n e sis • A fertilized female mite (FIG. 20.12) excavates a burrow in the stratum corneum, lays her eggs, and deposits fecal pellets (scybala) behind her as she advances. • The egg laying, scybala, or other secretions act as irritants or allergens, which may account for the itching and the subsequent delayed type IV hypersensitivity reaction that occurs approximately 30 days after infestation. A DESCRIPTION OF LESIONS • The initial lesions of scabies include tiny pinpoint vesicles and erythematous papules, some of which evolve into burrows, the classic telltale lesions of scabies (FIGS. 20.13 and 20.14).

B 20.13 A an d B Scabies. Lesions are present on the flexor wrists. Note linear burrows.

20.14 Scabies. This close-up view shows a burrow (arrow) on the palm.

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• The burrow is a linear or S-shaped excavation that is pinkish-white and slightly scaly and ends in the pinpoint vesicle or papule. This is where the mites may be found. • Burrows are easiest to find on the hands, particularly in the finger webs and wrists in adults and on the palms and soles in infants. • Sometimes burrows can be highlighted by applying black ink with a felt-tipped pen to the suspected areas. DISTRIBUTION OF LESIONS • Lesions are most often located on the interdigital finger webs (FIG. 20.15), sides of the hands and feet, flexor wrists, umbilicus, waistband area, axillae, ankles, buttocks, and groin. • Children and adults rarely have lesions above the neck; this is an important diagnostic sign. • Infants tend to have more widespread involvement, including the face and scalp and especially the palms and soles. • Immunocompromised patients also tend to have a widespread distribution of lesions. CLINICAL MANIFESTATIONS • Because the incubation period from initial infestation to the onset of pruritus is approximately 1 month, it is not uncommon for contacts to be asymptomatic, especially if they have been recently infested. • Itching (nocturnal pruritus) has traditionally been considered a symptom that is characteristic of scabies; however, it should be kept in mind that pruritus that occurs in many other skin conditions also tends to be more severe during the nighttime hours, when people are inclined to be less distracted by their daytime routines.

Co urse an d Se co n d ary Le sio n s • Initially, itching is rather mild and focal, but when lesions begin spreading rapidly, usually after 4 to 6 weeks, it can sometimes become intolerable. • A generalized distribution of lesions is probably the result of a hypersensitivity reaction. In this case, a more pleomorphic array of lesions, such as “juicy” papules and nodules, may be seen. • Hemorrhagic crusts and ulcerations may replace the primary lesions. • In men, itchy papules and nodules, particularly on the penis and scrotum, are virtually pathognomonic for scabies (FIG. 20.16).

20.15

Scabies. Finger web and groin lesions are noted.

20.16 Scabies. Characteristic pruritic papules are present on this patient’s penis.

Chap ter 20 • Bites, Stings, and Infestations

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Clin ical Varian ts Scab ie s in In fan t s • Frequently, intact vesicles are seen on the palms and soles. A typical clinical picture of an infant with scabies is one who doggedly pinches his or her skin. Scab ie s in t h e Eld e rly • Patients, particularly in an institutional setting, can have intense pruritus and few papular lesions, excoriations, or simply have dry, scaly skin.

20.17 Norwegian scabies. This child with Down’s syndrome has verrucous plaques on his hands and thickened dystrophic nails. The lesions are teeming with scabies mites.

No rwe g ian o r Crust e d Scab ie s • Norwegian, or crusted, scabies (FIG. 20.17) occurs in people with varying degrees of immune deficiency such as that seen in Down’s syndrome, leukemia, nutritional disorders, and acquired immunodeficiency syndrome (AIDS) (see also Chapter 24, “Cutaneous Manifestations of HIV Infection,” and FIG. 24.14). • The lesions tend to involve large areas of the body. • The hands and feet may be scaly and crusted with a thick keratotic material that can also be seen under the nails. • There may be wartlike vegetations on the skin; these are hosts to thousands of mites and their eggs. DIAGNOSIS A conclusive diagnosis is made by finding scabies mites, eggs, or feces.

20.18

Scabies. Scraping for scabies is performed.

DIFFERENTIAL DIAGNOSIS • Insect bites, such as fleas, generally spare areas that are covered (e.g., the groin and axillae). • Pruritus associated with systemic diseases, such as renal disease, hepatic disease, lymphomas, AIDS, leukemias, and Hodgkin’s disease, should be excluded.

• A drop of mineral oil is applied to the most likely lesion (usually a vesicle on the finger web or wrist is chosen). The site is then scraped with a surgical blade (FIG. 20.18), the scrapings are placed on a slide, and a cover slip is then applied (see also FIGS. 24.15 and 24.16). • Adults, who are more efficient scratchers than children, tend to remove the definitive evidence of scabies (i.e., mite) with their fingernails. Because mites are few and are particularly difficult to find in adults, the time and effort spent searching for the mite may be better used by taking a thorough history and counseling the patient and his or her contacts. Thus, if scabies is strongly suspected on clinical grounds, scabicidal treatment should be initiated.

Ot h e r Diag n o se s • Atopic dermatitis or dyshidrotic eczema should be considered. • Drug eruptions and other itchy rashes, including urticaria, tinea, xerosis, and contact dermatitis, should also be kept in mind. 352

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MANAGEMENT • Treatment is directed at killing the mites with a scabicide. It is also aimed at affording rapid symptomatic relief using appropriate oral antihistamines and topical corticosteroids, if necessary. • Management of institutional scabies: • Treatment must be conducted in an organized, cooperative fashion. • A scabicide and/or oral ivermectin (see below) is administered to all patients, staff, family members, and frequent visitors. • Laundering of all bed linen and clothes is necessary shortly after treatment.

Pe rm e t h rin (Elim it e an d Act icin ) • The prescription drugs Elimite and Acticin both contain permethrin cream 5%. They are safe and effective scabicides that are currently considered the treatment of choice for scabies. • They have not been proven to be safe in infants younger than 2 months or in pregnant and nursing women. • These instructions for use should be followed: • After a warm bath, the cream is applied to all skin surfaces “from head to toe” (including the palms, soles, and scalp in small children) and is left on for 8 to 12 hours, usually overnight. It is washed off the next morning. • If indicated, other family members and contacts should be treated simultaneously. All bed linen and intimate undergarments should be washed in hot water after treatment is completed. • Generally, only one treatment is necessary; however, a second treatment is often recommended in 4 to 5 days, especially in long-standing cases and for infants with scabies of the palms and soles. • Patients should be advised that it is normal to continue itching for days or weeks after treatment, albeit less intensely. The medication should not be applied repeatedly. Systemic antihistamines and a potent class 3 or 4 topical corticosteroid can be used for these symptoms. Lin d an e (Kwe ll Lo t io n , Scab e n e ) • This is the generic name for gamma benzene hexachloride. This agent is available as a 1% lotion or cream. Lindane stimulates the nervous system of the parasite, causing seizures and death. Until recently, it was the mainstay of scabies treatment; now it is recommended as an alternative agent, to be used only if other agents fail or are not tolerated. • It also requires a prescription. • It is also safe and effective, but controversy has arisen about its safety after several reports of neurotoxicity in infants. Ultimately, it was concluded that the drug was overused in these cases and led to systemic absorption. California has banned the use of lindane for treatment of lice and scabies.

• Lindane is to be avoided in infants, in pregnant or nursing women, or in people with a history of seizure disorders. • There have been reports of resistance to this agent. • These instructions for use should be followed: • Used as an overnight treatment, it is applied from the neck to toes, and the patient is instructed to wash it off in 8 to 12 hours. • Treatment may be repeated in 4 to 5 days if there is little symptomatic improvement.

Pre cip it at e d Sulfur Oin t m e n t (6% ) • This is used in pregnant or lactating women and in infants younger than 2 months. It is applied nightly for 3 nights. • Although it is messy and malodorous, it is effective and safe. Ive rm e ct in • Ivermectin (Stromectol) is an antihelmintic that can be administered (off-label) in a single oral dose. This agent is not currently approved by the U.S. Food and Drug Administration for the treatment of scabies in humans, and no studies have been done to establish its safety for use in pregnancy or in children. • It may be used when topical therapy is difficult or impractical (e.g., widespread infestations in nursing homes). • It has been used safely and effectively in patients who are seropositive for human immunodeficiency virus and in some patients with Norwegian scabies. • This agent may be administered adjunctively with a topical scabicide. • It is available in 3- and 6-mg tablets. • Dosage: 0.2 mg/kg in a single oral dose that is repeated in 10 days. For 6-mg tablets, the dosages are given in TABLE 20.1. Cro t am it o n (Eurax Lo t io n an d Cre am ) • This preparation, a 10% cream or lotion, has an unknown mechanism of action. • It is not very effective against scabies.

Tab le 20.1 IVERMECTIN DOSAGE FOR TREATMENT OF SCABIES WITH 6-MG TABLETS WEIGHT (KG)

NO. OF TABLETS

15–24 25–35 36–50 51–65 66–79 80

0.5 1 1.5 2 2.5 3–4

Chap ter 20 • Bites, Stings, and Infestations

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HELPFUL HINTS Think scabies when you see: • An infant with palmar or plantar vesicles or pustules • More than one family member, roommate, or sexual partner who is itching • Pruritic scrotal or penile nodules • Vesicles in the finger webs

SEE PATIENT HANDOUT “Scab ie s” ON THE SOLUTION SITE

354

POINTS TO REMEMBER • Scabies mimics other skin diseases. • Scabies rarely occurs above the neck in immunocompetent adults. • Contacts should be treated simultaneously to avoid “ping-ponging” (reinfection). • Treatment failure may result from noncompliance (i.e., treating lesions only) or reinfection. • Symptoms may persist after appropriate treatment. • Lesions that resemble insect bites, an eczematous dermatitis, and so-called neurotic excoriations may confuse an unsuspecting diagnostician. • Because the scabies mite can survive away from the skin for 2 to 5 days on inanimate objects such as clothing of an affected person, it is believed that indirect contact with such personal items can transmit the organism. This is most applicable in immunocompromised and institutionalized elderly patients.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Lice In fest a t io n s

(Ped icu lo sis)

BASICS • There are two species of sucking lice: Pediculosis humanus and Phthirus pubis (pubic lice, sometimes called “crabs”). • P. humanus is further divided into two subspecies: P. humanus capitis (the head louse) and P. humanus corporis (the body louse).

He ad Lice (Pe d iculo sis Cap it is) • Head lice spread from human to human; epidemics of head lice are most commonly seen in schoolchildren. • Head lice occur more often in girls and women than in boys and men; they are unusual in African-Americans, but not in African blacks. Bo d y Lice (Pe d iculo sis Co rp o ris) • Body lice are most often found in situations of poor personal hygiene, such as in homeless people. • They are historically prevalent in war conditions.

20.19

Head lice. The nits are attached to the hair shaft.

Pub ic Lice • Pubic lice are generally transmitted by sexual contact. DESCRIPTION OF LESIONS

He ad Lice • There are no primary lesions; however, secondary crusts and eczematous dermatitis resulting from scratching may be present. • Nits (louse eggs) are cemented to the hairs (FIG. 20.19). • It is difficult to find living lice. Bo d y Lice • Lesions begin as small papules. • Later, secondary lesions develop from scratching and may produce crusted papules, infected papules, and ulcerations.

20.20 Pubic lice. A small brown living crab louse is seen at the base of hairs (arrow).

Pub ic Lice • Small living brown lice may be seen at the base of hairs (FIG. 20.20). • Blue macules (maculae ceruleae) may occur on nearby skin. DISTRIBUTION OF LESIONS

He ad Lice • Only the scalp is involved. Bo d y Lice • Covered areas (under infested clothing) of the body may be affected. Pub ic Lice • Pubic hair, eyebrows, eyelashes, and axillary hair may be infested.

Chap ter 20 • Bites, Stings, and Infestations

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CLINICAL MANIFESTATIONS

He ad , Pub ic, an d Bo d y Lice • Itching is the predominant symptom. • Affected children with head lice may be asymptomatic. • There is a possibility of secondary infection from scratching. • With the exception of body lice, which have historically been known to carry epidemic typhus, trench fever, and relapsing fever, lice are not known to transmit any disease. DIAGNOSIS

He ad Lice • Knowledge of an epidemic at school generally alerts parents or school nurses to look for evidence of lice. • White nits may be very obvious on a background of darker hair.

• A hair may be plucked and examined for nits using the low power of a microscope. • A nit is attached to the base of a hair shaft when the egg is first laid and remains cemented to the growing hair.

Bo d y Lice • The diagnosis is made not from examining the patient but closely inspecting the seams of his or her clothing, where the lice are found. Pub ic Lice • Lice may be present. • Pruritus is noted. • Blue macules may be seen. • Often, a sexual partner has “crabs.”

DIFFERENTIAL DIAGNOSIS

He ad Lice • Atopic dermatitis of the scalp should be considered. Bo d y Lice an d Pub ic Lice • Atopic dermatitis or another type of eczematous dermatitis should be considered. • Scabies should be excluded.

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MANAGEMENT

He ad Lice • Remove nits with a fine-tooth comb after soaking the hair in a vinegar solution; this helps soften the cementing substance that attaches the nit to the hair. First -Lin e Trea t m en t Nix Cre m e Ri n se, RID , an d Act i c i n (over-the-counter)

• These products all contain low concentrations of permethrin; they are very effective in killing adult lice and nymphs but not as effective in killing nits (eggs). • There has been a growing resistance of head lice to these agents. • How to use these products: • The hair is washed with a nonmedicated shampoo and is towel dried; the agent is applied as a cream rinse, allowed to remain in place for 10 minutes, and then rinsed off thoroughly. • Because these agents do not destroy nits effectively, a second application (using the same technique) often is recommended 7 to 10 days after the initial therapy. • The latest treatment resembles a powerful blow-dryer, which delivers a blast of heated air to dry out lice and their eggs in one half-hour treatment. The practicality and efficacy of this device remain to be proven. St ra t egies fo r Resist a n t Ca ses Ov i d e (Malathion Lotion 0.5%)

• This agent is considered the most effective treatment for head lice. • It is both a pediculicide and an ovicide. • Caution: Ovide Lotion is flammable. Treated areas that are wet with this product should be kept away from open flames and electric heat sources such as hair dryers. • How to use Ovide: • The lotion is applied to dry hair in a quantity sufficient to wet hair and scalp.

• It is then massaged into the scalp and is left on for 8 to 12 hours. Heat (e.g., hairdryers, hot curlers) should not be used to dry the lotion. • The hair is then rinsed, and the nits are removed with a fine-tooth (nit) comb. • Treatment should be repeated in 7 to 10 days if lice are still present (using the same technique). El i m i t e Cre a m (5% Permethrin Cream)

• This is available by prescription. • It is left on overnight under an occlusive shower cap. • The application is repeated in 1 week to destroy any remaining eggs. Ot h er Trea t m en t Op t io n s

• Oral ivermectin has not yet been approved for the treatment of head lice. The dosage is 0.2 mg/kg in a single dose. A second treatment may be required. • Petrolatum such as Vaseline Petroleum Jelly is quite messy and difficult to remove, but it is an inexpensive and sometimes effective method that asphyxiates the lice and nits. It is applied to the entire scalp and is left on under a shower cap overnight.

Pub ic Lice • Kwell (Lindane) shampoo USP 1% is an ectoparasiticide and ovicide effective against Sarcoptes scabiei. It is lathered and is left on for 10 minutes. • RID and Nix lotions are also effective. • Treatment should include contacts of infested patients, especially sexual partners. Bo d y Lice • A shower and clean clothing generally cure body lice. • Clothing should be washed at hot temperatures to kill the lice.

HELPFUL HINTS • Shaving of pubic, scalp, or body hair is not necessary to treat lice. • In resistant cases, particularly after repeated treatment failures, delusions of parasitosis should be considered in the differential diagnosis in adult patients.

SEE PATIENT HANDOUT “He ad Lice ” ON THE SOLUTION SITE Chap ter 20 • Bites, Stings, and Infestations

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Wa t erb o r n e St in gs a n d Sea sh o re In fest a t io n s Visiting the beach and swimming in saltwater or freshwater expose people to a variety of creatures. Encounters with jellyfish (e.g., sea nettle, Portuguese man-of-war, thimble jellyfish) can cause skin reactions.

Jellyfish Stin gs BASICS • Two types of stinging jellyfish are seen floating in the coastal waters off North America: the smaller sea nettle and the rarer, more dangerous Portuguese man-of-war, whose poison can be fatal. • The tentacles of jellyfish have many stinging nematocysts, which contain a hollow poisonous tip and hooks. The hooks hold the jellyfish onto the victim while the nematocysts discharge the toxic venom. DESCRIPTION OF LESIONS

20.21 Jellyfish sting. Note the curvilinear, whiplike shape of the lesions.

• The shape of the lesions, which resemble linear welts that develop at the site of contact, often give the victim the appearance of having been whipped (FIG. 20.21). • Lesions may fade or may blister and become necrotic, depending on the amount of injected venom and the victim’s sensitivity. DISTRIBUTION OF LESIONS • The distribution is asymmetric and unilateral. CLINICAL MANIFESTATIONS • Victims usually describe a stinging or burning sensation. • The sting of the Portuguese man-of-war is more painful than a common jellyfish sting. It has been described as feeling like being struck by a lightning bolt, and some victims dread it more than a shark bite (FIG. 20.22). • There have been reported cases of anaphylactic reactions and fatalities from both sea nettle and Portuguese man-ofwar stings. DIAGNOSIS

20.22 Portuguese man-of-war sting. Note the linear shape of the lesions. The sting of the Portuguese man-of-war is more painful than a common jellyfish sting.

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• The diagnosis is based on the reported sting occurring in an endemic area and its characteristic eruption.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

POINT TO REMEMBER • Severe stings that result in systemic reactions may require life-support measures such as on-site resuscitation.

DIFFERENTIAL DIAGNOSIS • Other bites or stings should be considered.

Seabath er’s Eru p tion (“Sea Lice”) BASICS • This intensely pruritic eruption develops under swimwear, presumably because the responsible larvae become trapped under the garments. • It occurs several minutes to 12 hours after exposure to the larvae of the thimble jellyfish (Linuche unguiculata) in the saltwater off the coast of Florida and in the Caribbean. • This condition has also been contracted off the coast of Long Island, New York, where it has been reputedly caused by the larvae of a sea anemone.

MANAGEMENT • Mild stings may be treated symptomatically with cool soaks and topical steroids. • For more severe reactions, the affected area should be washed with seawater, alcohol, or vinegar to remove nematocysts and to inactivate any toxins that remain.

DISTRIBUTION AND DESCRIPTION OF LESIONS • Erythematous macules and papules occur under swimwear (FIGS. 20.23 A and B). CLINICAL MANIFESTATIONS • The pruritus is worse at night and tends to prevent the patient from sleeping. • Fever and malaise, the next most common symptoms, are experienced more often by children than by adults. • Lesions last for 2 to 14 days and resolve spontaneously.

A

B 20.23 A an d B Seabather’s eruption. This patient has just returned from bathing off the coast of Florida. The lesions are confined to the area covered by her bathing suit.

Chap ter 20 • Bites, Stings, and Infestations

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DIAGNOSIS MANAGEMENT • Treatment for both seabather’s eruption and swimmer’s itch is symptomatic. • After bathing, immediate removal of the swimwear for washing, or rinsing of the swimwear while it is still being worn, may help prevent seabather’s eruption. • Immediate towel drying after swimming in freshwater may prevent swimmer’s itch.

360

• The diagnosis can be made when the patient has bathed in an endemic area and displays inflammatory papules on the area covered by the bathing suit.

DIFFERENTIAL DIAGNOSIS • Swimmer’s itch (cercarial dermatitis) occurs on exposed sites after freshwater swimming. • It is caused by Schistosoma organisms that invade the skin. These organisms are the microscopic larvae of the parasitic flatworm. • After being released from host snails, the larvae swim in water until they penetrate the skin of a warm-blooded host, such as a duck or a human.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Cu t a n eo u s La r va Migra n s

(“Creep in g Er u p t io n ”)

BASICS • As the name suggests, cutaneous larva migrans is a cutaneous eruption that creeps or migrates in the skin. It results from the invasion and movement of various hookworm larvae that have penetrated the skin through the feet, lower legs, or buttocks. • Ancylostoma braziliense, A. caninum, A. ceylanicum, Uncinaria stenocephala (dog hookworm), Bunostomum phlebotomum (cattle hookworm), A. duodenale, and Necator americanus are the primary hookworms that cause cutaneous larvae migrans in the United States. • The adult hookworm (nematode) resides in the intestines of dogs, cats, cattle, and monkeys. The feces of these animals contain hookworm eggs that are deposited on sand or soil, hatch into larvae if conditions are favorable, and then penetrate human skin, which serves as a “dead-end” host. • At greatest risk are gardeners, farm workers, and people who sunbathe or walk on sandy beaches by the seashore. • Larva currens, a distinct variant of cutaneous larva migrans, is caused by Strongyloides stercoralis and may produce visceral disease. Visceral larva migrans is caused by another species of hookworm. DESCRIPTION OF LESIONS • Lesions have a characteristic curvilinear, serpentine shape (FIG. 20.24).

20.24 Cutaneous larva migrans. Note the serpiginous, erythematous, raised, tunnellike lesions in typical locations.

DISTRIBUTION OF LESIONS • Areas that come into contact with sand or contaminated soil, most commonly the feet (farmers) or buttocks (sunbathers on nude beaches), are affected. CLINICAL MANIFESTATIONS • This benign eruption is usually pruritic and self-limited because the larvae usually die within 4 to 6 weeks. DIAGNOSIS • The diagnosis is based on the characteristic clinical appearance. • If the patient has been vacationing on the beach in an area endemic for cutaneous larva migrans, consider the condition when diagnosing a local itchy eruption on one foot.

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DIFFERENTIAL DIAGNOSIS

MANAGEMENT • Class 1 superpotent topical steroids (e.g., clobetasol cream) for itching • Topical thiabendazole suspension (500 mg/5 mL under occlusion three times per day for 1 week) • Oral thiabendazole (Mintezol; 50 mg/kg/day in two daily doses for 2 to 5 days) or • Albendazole (400 mg daily for 3 days [this drug has fewer side effects than thiabendazole]) • Liquid nitrogen, applied to the active, advancing end of the lesion

Gran ulo m a An n ulare • Lesions are annular. • It lacks scale and vesicles and does not itch. Tin e a Pe d is • Potassium hydroxide examination is positive. Ot h e r Diag n o se s • Other bites or stings (e.g., jellyfish) should be considered.

HELPFUL HINT • If the patient has been vacationing on the beach in an endemic area, consider cutaneous larva migrans as a cause of a local itchy eruption on one foot.

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C H AP T ER

Benign Skin Neoplasm s

21 OVERVIEW • Benign lesions such as melanocytic nevi, skin tags, seborrheic keratoses, cherry angiomas, and epidermoid cysts are expected consequences of the skin’s normal, age-appropriate, often hereditary, maturation process. • As with most skin lesions, familiarity breeds recognition. This chapter, along with Chapter 22, presents the various common benign and malignant neoplasms in their diverse clinical guises. • Skin lesions—particularly pigmented skin lesions—often present a difficult and puzzling conundrum for the nondermatologist health care provider. Questions such as “Am I missing a melanoma?” “Is this mole suspicious?” and “Is this a skin cancer?” may arise. In reality, the answer is not always apparent. In fact, the decision of whether a lesion is benign or malignant is often a challenge for many dermatologists as well. Distinguishing between a benign pigmented lesion such as melanocytic nevus or a seborrheic keratosis and a potentially fatal skin cancer such as melanoma creates the most concern among health care providers.

MELANOCYTIC NEVI • • • • • • • •

Junctional m elanocytic nevus Com pound m elanocytic nevus Derm al m elanocytic nevus Blue nevus Halo nevus Spitz nevus Congenital m elanocytic nevus Atypical nevus (dysplastic nevus, Clark’s nevus) SEBORRHEIC KERATOSIS

• Stucco keratosis • Derm atosis papulosa nigra • Sign of Leser-Trélat SKIN TAGS SEBACEOUS HYPERPLASIA CYSTS • Epiderm oid • Pilar • Milium LIPOMA CHONDRODERMATITIS NODULARIS CHRONICA HELICIS DERMATOFIBROMA FIBROUS PAPULE HYPERTROPHIC SCAR KELOID COMMON ANGIOMAS • • • • •

Cherry angiom a Venous lake Angiokeratom as Spider angiom a Pyogenic granulom a

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Mela n o cyt ic Nevi BASICS

21.1 Junctional melanocytic nevi. These small, flat, lesions are uniform in color.

• Melanocytic nevi (MN), commonly called moles or “beauty marks,” are, most often, benign proliferations of normal skin components. They are composed of nevus cells that are derived from melanocytes, the pigment-producing cells that colonize the epidermis. • The acquisition of MN is greatest in childhood and adolescence. In addition to an hereditary predisposition, it has been suggested that their onset is a response to sun exposure. • During adulthood, the development of new lesions tapers off, and many existing lesions gradually lose their capacity to form melanin and become skin-colored or disappear completely. • MN may be congenital or acquired, and they are much more often seen in patients with light or fair skin than in blacks or Asians. • Acquired MN are sometimes associated with melanoma; however, the frequency of transformation into a melanoma is not known. Congenital nevi, on the other hand, especially when very large, hold the greater risk of malignant transformation (see later discussion).

Ju n ction al Melan ocytic Nevi • These small, macular (flat), frecklelike lesions are uniform in color. Individual lesions may be brown to dark brown to black (FIG. 21.1). • Histologic examination reveals melanocytic nevus cells located at the dermoepidermal junction. • Whether acquired or congenital, junctional MN are most prevalent on the face, arms, legs, trunk, genitalia, palms, and soles (FIG. 21.2). 21.2 Junctional melanocytic nevus (congenital). This small lesion is extremely unlikely to become malignant.

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DIFFERENTIAL DIAGNOSIS The most important lesions in the differential diagnosis of junctional MN include: • Dysplastic nevus (atypical mole; see later discussion) • Lentigo maligna (see FIG. 22.47) • Melanoma (see Chapter 22)

Fre ckle s (Ep h e lid e s) • These small, tan macules appear on the sun-exposed skin of fair-skinned people (FIG. 21.3). • They darken after sun exposure and lighten when they are no longer exposed to the sun. Le n t ig o (Plural: Le n t ig in e s) o r “Live r Sp o t ” These small, acquired tan macules occur on sun-exposed areas during middle and elderly age. They are uniform in color (FIG. 21.4). Most often, they appear on the face, dorsal hands (FIG. 21.5), extensor forearms, and anterior legs.

21.3 Freckles (ephelides). Freckles come and go with sun exposure. They are most often seen in people who have fair skin.

21.4 Solar lentigines. Note the uniformity in color (compare with FIGS. 22.47 and 22.48).

21.5 Solar lentigines. These extremely common tan macules arise on sun-exposed areas during middle age.

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Com p ou n d Melan ocytic Nevi • Compound MN are elevated, dome-shaped papules or papillomatous nodules. • Uniformly brown to dark brown, they may contain hairs and are seen most often on the face, arms, legs, and trunk (FIGS. 21.6 and 21.7). • Their histologic structure combines features of junctional and dermal nevi (see next section).

Derm al Melan ocytic Nevi

21.6 Compound melanocytic nevi. Elevated, domeshaped papules that are most often seen on the face, arms, legs, and trunk. These lesions tend to lose pigmentation as the patient ages.

• Dermal MN may be elevated and dome-shaped, wartlike, or pedunculated. • Most often skin-colored, they may be tan or brown, or they may be dappled with pigmentation. Lesions tend to lose pigmentation with age and become skin-colored (FIG. 21.8). • They are most often seen on the face and neck. • Microscopy reveals that dermal MN cells are located in the dermis. CLINICAL MANIFESTATIONS OF DERMAL NEVI AND COMPOUND NEVI • Dermal nevi and compound nevi are asymptomatic unless they are irritated or inflamed. • Very rarely do they transform to malignant melanoma. DIAGNOSIS • The diagnosis is based on clinical appearance or, if necessary, a histopathologic evaluation after removal.

21.7 Compound melanocytic nevi. In individuals with dark skin, such lesions tend to be more intensely pigmented.

DIFFERENTIAL DIAGNOSIS OF DERMAL NEVI AND COMPOUND NEVI Dermal nevi and compound nevi often resemble one another as well as the following: • • • • • • •

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Atypical nevus Neurofibromas Skin tags (acrochordons) Basal cell carcinomas Seborrheic keratoses Angiofibroma (fibrous papules) Nodular melanoma

21.8 Dermal melanocytic nevus. This lesion was pigmented when the patient was in her teens and twenties.

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Clin ical Varian ts Blue Ne vi • These lesions are a benign variant of dermal MN that are heavily pigmented. They occur as blue-gray or blue-black macules, papules, or nodules (FIG. 21.9) and are rarely malignant. The dark brown pigment that creates a bluish color to these lesions is caused by the Tyndall phenomenon. • Like the more common dermal and compound MN, blue nevi usually begin to appear in adolescence or early adulthood. Halo Ne vi • Halo nevi are MN that are encircled by a white halo of depigmentation. The halo represents a regression of a preexisting nevus caused by a lymphocytic infiltrate. Frequently, the entire nevus disappears, and the area regains normal pigmentation. • Most often, halo nevi are initially seen on preadolescents; they usually appear on the trunk (FIG. 21.10). • If a halo nevus is seen on an adult, two very rare possibilities should be considered: the lesion may be malignant, or a melanoma may be present elsewhere on the body. Biopsy and removal are indicated in this situation. Also bear in mind that in a patient of any age, a biopsy should be performed if the nevus has an atypical clinical appearance. Sp it z Ne vi • These nevi are a distinctive variant of MN. In the past, they were referred to as “juvenile melanomas,” but now they are recognized as benign. In children, the lesions may appear as pink papules; sometimes they are heavily pigmented and are jet black in color. • A heavily pigmented, small, spindle-cell variant of Spitz nevus may be seen on the legs of women. • It is prudent to completely excise these lesions to minimize the risk of recurrence and possible confusion with a malignant lesion.

21.9 Blue nevus. This is a variant of melanocytic nevus. Note the blue-gray color caused by the Tyndall effect. Compare to the tan-colored nevus on this boy’s face.

21.10 Halo nevus. An inflamed compound nevus has lost some of its original tan pigmentation. It is encircled by a white halo of depigmentation. Ultimately, the nevus may disappear, and the area will regain normal pigmentation.

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Con gen ital Melan ocytic Nevi

21.11 Small to medium-sized congenital hairy nevus. This lesion is evenly pigmented and symmetric and probably has little, if any, malignant potential.

• Often generating great concern in both patents and pediatricians, congenital melanocytic nevi (CMN) are MN that are present at birth or arise during the first year of life. • By definition, CMN are present at birth or soon thereafter, although some small CMN are clearly so-called “tardive” and may appear as late as up to 2 years of age. • CMN occur in about 1% of children. • On histopathology, in contrast to acquired MN described above, the nevus cells of CMN tend to be deeper in the dermis and subcutaneous fat and are often present in the skin appendages such as nerves and hair follicles. • CMN vary considerably in size and are commonly classified as small (under 1.5 cm), intermediate (1.5 to 19.9 cm) (FIG. 21.11), or large/giant (20 cm). (These figures are based on the predicted final adult size of lesions.) • Physical findings include the following: • CMN are generally relatively evenly pigmented and tan or brown, especially those that are thin. • Some lesions can have an array of colors. • The malignant potential of small or medium-sized CMN is controversial. However, many experts believe that a small nevus does not significantly increase the lifetime risk of developing melanoma. • CMN are of the greatest concern when they are 20 cm or larger in diameter. These nevi, which are often called giant pigmented hairy nevi, “garment nevi,” or “bathing trunk nevi,” may develop into melanoma—the lifetime risk is estimated to be between 3.3 and 6.0% (FIG. 21.12).

21.12 Giant pigmented hairy nevus. A patient with this lesion may have a greater than 6% lifetime risk of melanoma.

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MANAGEMENT OF MELANOCYTIC NEVI • All MN should be carefully examined and biopsy should be considered, particularly if there is any suggestion of clinical atypia. • However, for most MN, biopsy is not indicated. Persons with numerous MN, particularly atypical nevi (see later discussion), are at greater risk for developing malignant melanoma.

In d icat io n s fo r Re m o val • Atypical appearance • Cosmetic reasons • Repeated irritation by clothing, such as a bra strap • Persistent discomfort (a lesion that itches, hurts, or bleeds)

Me t h o d s o f Re m o val Lesions can be removed by shave excision (which is often followed by electrodesiccation) or by elliptic excision (see Chapter 26, “Diagnostic and Therapeutic Procedures”). • Shave (tangential) excision: This method is fast and economical, and it generally provides satisfactory cosmetic results. Its disadvantage is that it often results in only partial removal of the lesions, which infrequently necessitates a second excisional procedure. • Elliptic excision: This technique is performed with the intent of removing lesions completely. Surgical margins can be identified. However, elliptic excision is slower than shave excision. It also requires suturing and suture removal, and it results in linear scars that may not be as cosmetically pleasing as scars that result from shave excisions.

POINTS TO REMEMBER • Any pigmented lesion that changes rapidly in size or color or that has an atypical appearance should be removed for biopsy. • A primary care physician should have a low threshold for referral to a dermatologist if there is any concern regarding the diagnosis and management of a pigmented lesion. • All MN that are removed should be submitted for microscopic evaluation. • Large CMN have a low but real risk of malignant transformation and the development of melanoma.

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At yp ica l Nevu s

(Dysp la st ic Nevu s, Cla rk ’s Nevu s) BASICS • The atypical nevus, which is also called dysplastic nevus, an atypical mole, or Clark’s nevus, is a controversial and confusing lesion. Even among dermatopathologists, there is no consensus regarding the histopathologic criteria for its diagnosis. • Some individuals have only a few atypical nevi, and their risk of melanoma may not be much higher than those individuals without such nevi. • This much is agreed: When a patient has numerous atypical nevi and there is a positive family history of melanoma, the potential for melanoma in that patient and in his or her family is extremely high. Such dysplastic nevi may be inherited as an autosomal dominant trait (see discussion of familial atypical mole syndrome). • Atypical nevi are rarely seen in black, Asian, or Middle Eastern populations. DESCRIPTION OF LESIONS Atypical nevi have some or all of the following features:

21.13 Atypical nevus (dysplastic nevus). Note the raised center and indistinct border; such a nevus is sometimes called a “sunny-side-up egg lesion.” It is generally larger than a common mole.

• They are usually larger than common moles and frequently measure 5 to 15 mm in diameter. • Their borders are usually irregular, notched, and ill-defined. • They have a macular appearance, but the centers may be raised (for this reason, they are sometimes called “sunnyside-up egg lesions”) (FIG. 21.13). • Their coloration (tan, brown, black, pink, or red) is irregular. DISTRIBUTION OF LESIONS • Atypical nevi are most often found on the trunk, legs, and arms; generally, the face is spared. CLINICAL MANIFESTATIONS • The exact risk of an individual atypical nevus developing into a melanoma is uncertain. • Unlike dermal and compound nevi, these lesions often continue to appear into adulthood. • Differentiating them clinically from melanoma is often difficult.

Clin ical Varian ts Sp o rad ic At yp ical Ne vi • A patient with an isolated atypical nevus and no family history of multiple atypical nevi or melanoma probably carries little risk of developing melanoma and should not necessarily be identified as prone to melanoma. 21.14 Multiple dysplastic nevi. Note the characteristic distribution on the trunk. 370

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Mult ip le At yp ical Ne vi • The exact risk of an individual nevus developing into a melanoma is uncertain (FIG. 21.14). • In certain situations, atypical nevi are considered possible precursors to, as well as potential markers for, the development of melanoma that may occur de novo without evolving from a precursor dysplastic nevus.

2. Many nevi—often more than 50—are present, and some of them are atypical moles. 3. Moles show certain dysplastic features when examined under the microscope.

DIFFERENTIAL DIAGNOSIS

Fam ilial At yp ical Mo le Syn d ro m e • Those persons who meet the following criteria are considered to have an extremely high potential for developing malignant melanoma: 1. Patients with a first-degree (e.g., parent, sibling, or child) or second-degree (e.g., grandparent, grandchild, aunt, uncle) relative who has a history of malignant melanoma have heightened risk.

MANAGEMENT • The method chosen for removing suspected atypical nevi depends on the purpose of treatment. • If melanoma is suspected, complete excision should be performed. • If melanoma is not suspected, the lesion can be removed and prepared for biopsy with a shave or punch biopsy technique.

• Other MN (see earlier discussion) • Malignant melanoma • Pigmented basal cell carcinoma

• Patients who meet the criteria for familial atypical mole syndrome should examine their own skin every 2 to 3 months, in addition to having a full body examination and regular screening visits performed by a dermatologist. • High-risk patients and their families should be taught self-examination to detect changes in existing moles and should be given printed material with photographs to help them recognize the features of malignant melanoma.

Pre ve n t io n • Patients with many atypical nevi should avoid excessive sun exposure and should routinely use a sunscreen with a sun protective factor of 15 or greater.

POINTS TO REMEMBER • The risk of melanoma is greatly increased in patients with multiple atypical nevi and a personal or family history of melanoma. • Once a diagnosis of multiple atypical nevi is established, other family members should be examined. • A person with an isolated atypical nevus probably carries little risk of developing melanoma and should not be identified as melanoma prone. • Melanoma risk is greater in those persons who have one relative with melanoma than in those with no affected relative. The lifetime risk of melanoma may approach 100% in persons with atypical nevi who are from melanoma-prone families (i.e., individuals having two or more first-degree relatives with melanoma). • Patients with the familial atypical multiple mole and melanoma syndrome (also known as the dysplastic nevus syndrome) should be monitored vigilantly.

HELPFUL HINT • Despite the fact that patients with many dysplastic nevi are at a very high risk of developing a melanoma, the notion of removing all of their dysplastic nevi to reduce their risk of melanoma is generally believed to be ill advised. To consider these nevi to be precursors of melanomas creates undo anxiety for patients but does not appear to decrease their potential for developing melanomas.

SEE PATIENT HANDOUT “At yp ical Ne vus (Mo le )” ON THE SOLUTION SITE

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Seb o r rh eic Kera t o sis BASICS • A seborrheic keratosis (SK) is an extremely common benign skin growth that becomes apparent in people older than 40 years of age. These lesions are the most common neoplasms in the elderly, and they have virtually no malignant potential. • Patients often report a positive family history of SKs, and men and women are equally frequently affected. • SKs have been whimsically described as “barnacles in the sea of life” and “maturity spots”; these metaphors are intended to allay patients’ anxieties. DESCRIPTION OF LESIONS 21.15 Seborrheic keratoses. The largest, darkest, lesion has a warty, rough-surfaced, tortoise shell-like, “stuck-on” appearance. The lesions in the background are also SKs; these lesions are unusual before 30 years of age. (Compare with images of melanoma in Chapter 22: FIGS. 22.35–22.43.)

• The typical SK has a warty, “stuck-on” appearance that ranges from tan to dark brown to black. The “dry,” crumbly, keratotic surface of some lesions is sometimes rubbed or picked off, only to recur later. • The use of the word “seborrheic,” a misnomer, stems from the occasional “greasy” or shiny appearance of the lesions; SKs are actually epidermal in origin, with no sebaceous derivation. • The appearance of individual lesions tends to vary considerably, even on the same patient. Lesions may be warty and tortoiseshell-like (FIG. 21.15); scaly, flat, or almost flat (FIG. 21.16); or small pigmented papules similar to skin tags (discussed later) (FIG. 21.17). • The color, shape, and surface characteristics of SKs can change with the age and location of individual lesions. Lesions are often smooth and symmetric, uniformly pigmented, and small. To the untrained eye, however, these lesions may resemble melanomas (i.e., they may be asymmetric, have irregular or notched borders, and vary in color).

21.16 Seborrheic keratoses. This lesion is almost flat. Lesions are found on the arms and legs.

21.17 Seborrheic keratoses. Multiple pigmented papules, some of which are clinically indistinguishable from skin tags, are evident. (See FIG. 21.22.) 372

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DISTRIBUTION OF LESIONS • SKs most often are located on the back, chest, and face, particularly along the frontal hairline (FIG. 21.18) and scalp. They are also frequently found on the arms, legs, and abdomen (FIG. 21.19). • Smaller lesions similar to skin tags can be seen around the neck, under the breast, or in the axillae. • In women, lesions are often seen under and between the breasts. • When many lesions are present, the distribution is usually bilateral and symmetric. DIAGNOSIS • With experience, SKs are easily recognized. • If necessary, a shave biopsy (using a no. 15 scalpel blade) or curettage (see Chapter 26, “Diagnostic and Therapeutic Procedures”) may be performed for histologic confirmation.

21.18 Seborrheic keratoses. The frontal hairline and temples are common locations.

DIFFERENTIAL DIAGNOSIS • • • • • • •

Malignant melanoma Pigmented basal cell carcinoma Verruca vulgaris Solar lentigo (especially early flat SKs) Pigmented solar keratosis (actinic keratosis) MN Dysplastic nevus

Clin ical Varian ts

21.19 Seborrheic keratoses. These lesions are in a typical location. Note the different colors, sizes, and shapes of the various lesions in this patient.

St ucco Ke rat o se s • These are a nonpigmented variant of SK; they are seen most often in the elderly. Descrip t io n o f Lesio n s

• Stucco keratoses are skin-colored or whitish papules that become whiter and scalier when they are scratched. They typify the “dry, stuck-on” type of seborrheic keratosis. Dist rib u t io n o f Lesio n s

• They are commonly found on the distal lower leg, particularly around the ankles (FIG. 21.20), and they may also be seen on the dorsal forearms.

De rm at o sis Pap ulo sa Nig ra • This common manifestation is diagnosed primarily in African-American, Afro-Caribbean, and sub-Saharan African blacks; however, it is also seen in darker-skinned persons of other races. Lesions start appearing in adolescence and increase in number as persons age.

21.20 Stucco keratoses. These lesions have a whitish, “stuck-on” appearance. They occur especially on the dorsum of the foot and around the Achilles tendon area.

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• Dermatosis papulosa nigra (DPN) lesions are histopathologically identical to SKs and are considered to be of autosomal dominant inheritance. Descrip t io n o f Lesio n s

• Lesions are darkly pigmented and, in contrast to typical SKs, they have minimal, if any, scale. Dist rib u t io n o f Lesio n s

• DPNs are generally seen on the face, especially the upper cheeks and lateral orbital areas (FIG. 21.21).

21.21 Dermatosis papulosa nigra. The lesions of this common inherited condition appear as small, pigmented papules on the face that resemble SKs and are histologically indistinguishable from them.

MANAGEMENT • Patients with SKs are often referred to dermatologists with a presumptive diagnosis of warts or moles or to have these lesions evaluated for cancer, particularly melanoma. • Learning to recognize SKs should obviate the need for many of these referrals. When a patient is referred, a biopsy (generally a shave biopsy) is performed if necessary to confirm the diagnosis or to distinguish SK from a pigmented basal cell carcinoma, MN, wart, or melanoma. • Because some patients have numerous lesions, it is an impractical expenditure of time and money to perform

Sig n o f Le se r-Tré lat • This condition refers to the sudden appearance of multiple SKs in a short period or a rapid increase in their size. • It is a rare phenomenon and is presumed by some observers to be a cutaneous sign of leukemia or internal malignant disease, especially of the gastrointestinal tract, prostate, breast, ovary, uterus, liver, or lung. However, in light of the frequency of malignant disease in the elderly, and the ubiquitous presence of SKs in this age group, the relationship is believed by some observers to be fortuitous.

multiple biopsies of lesions, as long as the clinical appearance is typical. • An excisional biopsy should always be performed whenever malignant melanoma is suspected.

Tre at m e n t • Cryosurgery is performed with liquid nitrogen spray, cotton swab application, or light electrocautery and curettage (treating the base of the lesion helps to prevent recurrence) (see Chapter 26, “Diagnostic and Therapeutic Procedures”); or • Excisional surgery, which results in scar formation, is unnecessary, unless a biopsy of a completely removed lesion is required to rule out malignant disease.

HELPFUL HINT • SKs present in many shapes, colors, and sizes. It is a good idea to become familiar with these lesions by consistently examining the skin of all adult patients.

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POINTS TO REMEMBER • SKs are mainly a cosmetic concern, except when they are inflamed or irritated and can be an annoyance. The challenge for primary care clinicians is to distinguish these lesions from skin cancer, particularly malignant melanoma. • Lesions may be quite numerous on some persons. Because SKs may, at times, be confused with melanoma, careful visual examination of all lesions should be performed.

Sk in Ta gs BASICS • These benign skin lesions are extremely common. They are sometimes referred to as acrochordons, fibroepithelial polyps, or, if large, soft fibromas or pedunculated lipofibromas. They are often seen in the body folds of obese persons. • Skins tags were formerly suspected by several investigators to be markers for intestinal polyps or, possibly, internal malignant diseases, but current evidence suggests that this association is not justifiable. DESCRIPTION OF LESIONS • Skin tags are generally 1- to 10-mm fleshy papules. • They may be skin-toned, tan, or darker than the patient’s skin. They are sessile or pedunculated in shape. • They are most often found on the neck (FIG. 21.22), the axillae, the inframammary area, the groin (especially the inguinal creases), the upper thighs, and the eyelids (FIG. 21.23).

21.22 Skin tags (acrochordons). Pigmented papules are present around this patient’s neck.

CLINICAL MANIFESTATIONS • Skin tags are primarily of cosmetic concern; however, they may become a nuisance from the irritation of necklaces and underarm shaving, for example. • In women, they tend to grow larger and more numerous over the course of a pregnancy. • They are often seen in association with acanthosis nigricans (See Chapter 14, “Disorders of Pigmentation”). DIAGNOSIS • Skin tags are easy to recognize; a skin biopsy is rarely necessary.

DIFFERENTIAL DIAGNOSIS • Pedunculated SKs • Compound or dermal nevi • Neurofibromas

21.23 Skin tag (acrochordon). A solitary, skin-colored skin tag is present on the eyelid.

MANAGEMENT • Small skin tags are easily removed by snipping them off at their base using iris scissors, with or without prior local anesthesia (see Chapter 26, “Diagnostic and Therapeutic Procedures”). The crushing action of the scissors results in little bleeding or pain. • Skin tags, if disregarded, occasionally may spontaneously self-destruct. After torsion, they become necrotic and autoamputate. Chapter 21 • Benign Skin Neop lasm s

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HELPFUL HINT • A rapid and painless treatment for small skin tags is to dip a needle holder or nontoothed forceps into liquid nitrogen for 15 seconds and then gently grasp each skin tag for about 10 seconds. There is little or no collateral

damage, just a narrow rim of erythema. Multiple lesions can be treated using this method. The frozen skin tag will be shed in approximately 10 days. This is a good approach for skin tags hanging on the eyelids (FIGS. 21.24 and 21.25).

A

21.25 Skin tags (acrochordons). Axillary lesions treated with liquid nitrogen.

B 21.24 A an d B Pedunculated fibroepithelioma (skin tag). A: Skin tag on eyelid. B: Treatment is performed with liquid nitrogen. Frost appears at the tip of the needle holder and on the skin tag. The frozen skin tag will be shed in 7 to 10 days.

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Seb a ceo u s H yp erp la sia BASICS • Sebaceous hyperplasia refers to small, benign papules on the face of adults representing hypertrophy of the sebaceous glands. • These fairly common lesions are often confused with basal cell carcinomas. DESCRIPTION OF LESIONS • The yellow or cream-colored papules are often doughnutshaped with a dell (umbilication) in the center (FIGS. 21.26 A and B). • They are small in diameter (1 to 3 mm). • Telangiectasias are present on the raised borders.

A

DISTRIBUTION OF LESIONS • Lesions occur on the forehead and cheeks. CLINICAL MANIFESTATIONS • Lesions are asymptomatic. • They may be of cosmetic concern. DIAGNOSIS • The diagnosis is made by the lesion’s typical clinical appearance (“little bagels”). • Biopsy is indicated if basal cell carcinoma is suspected.

B 21.26 A an d B Sebaceous hyperplasia. A: Multiple yellowish papules are present. Note the central dell and telangiectasias. B: Close-up view.

DIFFERENTIAL DIAGNOSIS • Basal cell carcinoma (see Chapter 22, “Premalignant and Malignant Skin Neoplasms”)

MANAGEMENT • The patient should be reassured about the benign nature of this condition. • Light electrocautery, shave biopsy, or laser ablation may be performed to remove lesions, if desired, although these lesions tend to recur.

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Cyst s BASICS • A cyst is a sac containing semisolid or liquid material. The sac contains keratin and lipid-rich debris. A cyst has an epithelial lining that produces keratin. • Cysts tend to be hereditary, arise in adulthood, and may occur as multiple lesions. • Epidermoid cysts, the most common type, are derived from the epithelium of the hair follicle and connect to the surface of the skin with a keratin-filled central pore that looks like a blackhead (FIGS. 21.27 A and B). • Pilar cysts, the second most common type, have a thicker wall that develops from a stratified epithelium. Pilar cysts lack a central pore (FIG. 21.28).

A

DESCRIPTION OF LESIONS • Lesions appear as smooth, discrete, freely movable, domeshaped nodules. • Cysts that have previously been infected, ruptured, drained, or scarred may be firmer and less freely movable. • Lesions range from 0.5 to 5.0 cm in diameter. • Often, there is a central pore (seen in epidermoid cysts), from which cheesy-white, malodorous keratin material can be expressed. DISTRIBUTION OF LESIONS

B 21.27 A an d B Epidermoid cyst. These lesions often occur on the back. They appear as smooth, discrete, freely movable, dome-shaped ballotable masses. A: Cyst. B: Compression of the lesion, which has the same consistency as an eyeball or a fully inflated balloon.

• Epidermoid cysts occur most often on the face, behind the ears, and on the neck, trunk, scrotum, and labia. • Pilar cysts are most often located on the scalp. CLINICAL MANIFESTATIONS • Cysts are usually asymptomatic, unless they are inflamed or infected. • Scrotal and pilar cysts may calcify. • Pilar cysts are generally devoid of overlying scalp hair.

Clin ical Varian ts Milia Ba sics

• Milia (singular, milium) are extremely common epidermal cysts that contain keratin. • They can occur in people of any age. They may arise in traumatic scars or in association with certain scarring skin conditions, such as porphyria cutanea tarda.

21.28 Pilar cyst. Note the absence of hair. The pressure from the enlarging cyst has destroyed the hair follicles. These lesions are freely movable.

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Descrip t io n o f Lesio n s

• They are 1.0 to 2.0 mm in diameter and are white to yellow (FIG. 21.29). • They are often mistaken for the closed comedones of acne (“whiteheads”) (FIG. 21.30; see FIG. 1.4). Dist rib u t io n o f Lesio n s

• Milia are most often noted on the face, especially around the eyes and on the cheeks and forehead. DIAGNOSIS • On palpation, an intact epidermoid or pilar cyst feels smooth; when compressed, it feels like an eyeball or a fully expanded balloon (see FIGS. 21.27 A and B). • If necessary, a biopsy or an incision and drainage can be performed to confirm the diagnosis.

21.29 Milia. These epidermal cysts contain keratin. They are 1.0 to 2.0 mm in diameter and are white to yellow.

DIFFERENTIAL DIAGNOSIS • Lipoma should be considered when cystlike lesions are found on the trunk, the back of the neck, and extremities. However, the consistency of a lipoma is rubbery and somewhat softer than that of a cyst (see FIGS. 21.27 A and B). Lipomas are also irregular in shape.

MANAGEMENT

Ep id e rm o id an d Pilar Cyst s • The entire cyst wall does not have to be completely removed to prevent recurrence. However, a large epidermoid or pilar cyst can be removed through a small hole created by a punch biopsy tool (see Chapter 26, “Diagnostic and Therapeutic Procedures”). • For incision and drainage, a fluctuant, infected cyst may be incised with a no. 11 blade, drained, and then packed with iodoform gauze. • The contents of inflamed or so-called “infected” cysts are most often sterile or contain normal skin flora; thus pre- or postoperative antibiotics are probably unnecessary.

21.30 Milia. These lesions are often mistaken for the closed comedones of acne (“whiteheads”).

HELPFUL HINT • Erythematous, tender, or draining epidermal and pilar cysts are often misdiagnosed as being infected rather than inflamed, and patients are accordingly treated unnecessarily with oral antibiotics.

Milia • In contrast to closed comedones (which they resemble), milia must first be incised (usually with a no. 11 blade) before their contents can be expressed. • Alternatively, they can be destroyed with light electrodesiccation. Chapter 21 • Benign Skin Neop lasm s

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Lip o m a BASICS • A lipoma is a benign, subcutaneous tumor composed of fat cells. • Dercum’s disease is a syndrome of multiple tender lipomas that develop in middle-aged women. • Angiolipomas may be tender or painful. DESCRIPTION OF LESIONS

21.31 Lipomas. Multiple, rubbery, flesh-colored nodules are palpable on this patient.

• Lipomas are rubbery, generally asymptomatic masses; they range in size from small nodules (FIG. 21.31) to large tumors (FIG. 21.32). • They are usually irregular in shape and may be greater than 7 cm in length. DISTRIBUTION OF LESIONS • Lipomas occur most commonly on the trunk, the back of the neck, the upper arms, and the forearms. DIAGNOSIS • The diagnosis is made on clinical grounds. • A biopsy should be performed if the diagnosis is uncertain.

DIFFERENTIAL DIAGNOSIS • As noted earlier, a lipoma may be confused with an epidermoid cyst. However, the latter “feels like an eyeball” and has a regular dome shape. 21.32 Angiolipomas. This patient has tender, tumorsized, fatty subcutaneous lesions. MANAGEMENT • Lesions may be excised or removed using liposuction.

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Ch on d rod erm atitis Nod u laris Ch ron ica Helicis BASICS • Chondrodermatitis nodularis chronica helicis (CNH) is a relatively common, benign, painful condition of the apex of the helix or on the antihelix of the ear. • CNH is characterized by one or more spontaneously appearing tender papules. • CNH occurs most commonly in fair-skinned individuals with severely sun-damaged skin. • CNH can occur in patients at any age but mostly affects middle-aged to older individuals. It more often occurs in men; 10% to 35% of cases involve women. Age at onset is similar in men and women. • The onset of CNH may be precipitated by pressure, trauma, or cold. Sleeping on the affected side or holding a telephone instrument to the involved ear can be quite painful. • Spontaneous resolution is unusual; the condition often continues unless treated. • The cause of CNH is unknown. • Neural hyperplasia and a secondary perichondritis probably account for the tenderness associated with this condition.

21.33 Chondrodermatitis nodularis chronica helicis. This tender papule has a central keratotic punctum. (Note the similarity to FIG. 22.4.)

CLINICAL MANIFESTATIONS • The nodule—actually papular in size—usually enlarges rapidly to a maximum size, approximately 4 to 8 mm, and remains stable. • The lesions are firm, tender, well demarcated, and round to oval with a raised, rolled edge and central ulcer or crust (FIG. 21.33). • The most common location is the apex of the helix. Distribution on the antihelix is more common in women.

DIFFERENTIAL DIAGNOSIS See also Chapter 22. • Actinic keratosis • Keratoacanthoma • Squamous cell carcinoma

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MANAGEMENT • Intralesional injections of steroids such as triamcinolone (Kenalog; 20 to 40 mg/mL) (FIG. 21.34) may relieve discomfort and result in resolution. Several visits for these injections may be necessary. • If the patient sleeps on the affected side, then changing sides or using pressure-relieving pillows or pads may be helpful. A CNH pressure-relieving pillow is available from CNH Pillow, P.O. Box 1247, Abilene, TX 79604; phone (800) 255-7487. • Biopsy is indicated if the diagnosis is in doubt. The biopsy is necessary to differentiate CNH from actinic keratoses, squamous cell carcinoma, and, less commonly, basal cell carcinoma, because many patients with CNH have chronic solar damage and a history of skin cancer. • If conservative methods to relieve symptoms are unsuccessful, surgical approaches are almost always needed. • Wedge excision, curettage, electrocauterization, carbon dioxide laser ablation, and excision of the involved skin and cartilage are often curative.

21.34 Chondrodermatitis nodularis chronica helicis. Treatment with intralesional triamcinolone is sometimes effective in relieving tenderness and may result in resolution of this lesion.

HELPFUL HINT • Most often the patient with CNH seeks medical attention because of the pain associated with the skin lesion(s). In contrast, the cutaneous tumors listed in the differential diagnosis of CNH are usually painless.

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Ben ign Fib ro u s a n d Va scu la r Lesio n s Derm atofibrom as BASICS • Also known as fibrous histiocytomas and sclerosing hemangiomas, dermatofibromas are common dermal fibrous tumors of unknown cause. • Dermatofibromas occur most commonly on the legs, trunk, and arms, especially in women older than 20 years of age. The lesions are benign growths that are usually brought to medical attention either to rule out skin cancer or because of cosmetic concerns. DESCRIPTION OF LESIONS • A lesion may be a papule or a nodule. It may be elevated with a dome shape, flat, or depressed below the plane of the surrounding skin (FIG. 21.35). • The color can vary, even in a single lesion, and can be skincolored, chocolate brown, red, or even purple. • The surface may be smooth or scaly, depending on whether the lesion has been traumatized (e.g., by shaving).

21.35 Dermatofibroma. This pigmented, firm papule is a very common finding on the extremities in many patients.

DIAGNOSIS • Typically, a dermatofibroma feels like a firm, pea-sized, buttonlike papule that is fixed to the surrounding dermis (accounting for the “dimple” or “collar button” sign) (FIGS. 21.36 A and B). • It is freely movable over deeper adipose tissue.

A DIFFERENTIAL DIAGNOSIS • Cysts and lipomas are either compressible or rubbery. • MN (moles) are also not as firm as dermatofibromas. • A malignant melanoma is more variable in shape and size than a dermatofibroma. • Dermatofibrosarcoma protuberans (DFSP) is a locally aggressive tumor with a high recurrence rate. DFSP is an uncommon soft tissue neoplasm with intermediate to low-grade malignancy, and metastases rarely occur.

B 21.36 A an d B Dermatofibroma. A: This papule is in a typical location. B: Note the “dimple” or “collar button” (retraction) sign that is elicited on compression of the lesion.

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POINTS TO REMEMBER MANAGEMENT • If there is any doubt about the diagnosis, a biopsy should be performed. • The patient should be informed that if the lesion is removed, the scar may be more cosmetically objectionable than the original lesion.

• No treatment is necessary; however, local excision can be performed for biopsy confirmation or cosmetic concerns, or if the lesion is symptomatic. • Deep shave excision is another alternative; however, the lesion may recur.

Fibrou s Pap u les BASICS • Fibrous papules (angiofibromas, fibrous papules of the nose or face; FIG. 21.37) are relatively common benign lesions that may be difficult to distinguish from compound or dermal nevi; furthermore, they often may resemble a basal cell carcinoma (see also FIG. 22.27). • Histopathology reveals a combined vascular and fibrous proliferation. DESCRIPTION OF LESIONS

21.37 Fibrous papules (angiofibromas, fibrous papules of the nose). These are dome-shaped, pale or pink, firm papules with a shiny appearance and may be difficult to distinguish from compound or dermal nevi. They often may resemble a basal cell carcinoma.

• Generally they are dome-shaped, pale or pink firm papules with a shiny appearance. They usually range from 1 to 5 mm in diameter. • Lesions appear in adults and usually as a single lesion, but, occasionally, several lesions may be present. • Most are noted on the nose; less commonly, they are found on the cheeks and chin.

MANAGEMENT • No treatment is necessary. • If necessary, they are biopsied if the diagnosis is in doubt or to rule out a basal cell carcinoma. • They may also be removed for cosmetic reasons.

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H yp ert ro p h ic Sca rs a n d Kelo id s BASICS • A hypertrophic scar is defined as a widened or unsightly scar that does not extend beyond the original boundaries of the original injury. Hypertrophic scars appear within weeks of skin injury. • A keloid is an overgrowth of dense fibrous tissue, a scar whose size far exceeds that which would be expected from the extent and margins of an injury to the skin. Keloid, derived from the Greek chele (crab’s claw), describes the lateral growth of tissue into unaffected skin. • Hypertrophic scars and keloids represent an exaggerated formation of scar tissue in response to skin injuries such as lacerations, insect bites, ear piercing, and surgical wounds. • They may also result from healed inflammatory lesions (e.g., acne, chickenpox) (FIGS. 21.38 and 21.39). • In recent years, the popularity of skin piercing procedures and tattooing has increased the frequency of these undesirable scars and has expanded the sites on the body where they may occur. • Exaggerated scars occur less frequently at the extremes of age—the very young and elderly—however, increasing numbers of presternal keloids, as well as hypertrophic scars may be seen in older age groups and result from coronary artery bypass surgery or intravenous Port-A-Caths (peripherally inserted central venous catheters) used to deliver fluids and medications. • Keloids are more likely to occur in Hispanics, Asians, and particularly individuals of African descent than in Caucasians. There is no racial preponderance noted with hypertrophic scarring.

Pat h o g e n e sis • In susceptible individuals, when there is an overproduction of collagen, the excess collagen becomes piled up in fibrous masses and an exaggerated formation of scar tissue. • Hypertrophic scars: Scanning electron microscopy reveals flattened collagen bundles that are parallel in orientation. • Keloid: Unlike hypertrophic scar formation, the electron microscope reveals a number of distinguishing features, including randomly organized collagen fibers in a dense connective tissue matrix.

21.38 Hypertrophic scars. The scars on this boy’s shoulders resulted from healed chickenpox lesions.

21.39 Keloid. These scars appeared in sites of former inflammatory acne lesions.

DESCRIPTION OF LESIONS • Hypertrophic scars and keloids are firm, shiny, hairless papules, nodules, or tumors; they may be flesh-colored, tan, or brown. • If lesions are inflamed or are of recent onset, they may be red (erythematous) or purple (violaceous).

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DISTRIBUTION OF LESIONS • Both hypertrophic scars and keloids most commonly arise in the same anatomic locations: the sternum, the shoulders, the deltoid region of the upper arm, and the upper back. • The most common sites on the head and neck are the earlobes, mandibular border, and posterior neck. The earlobe is typically affected secondary to earring posts (FIGS. 21.40 and 21.41). CLINICAL MANIFESTATIONS

21.40 Keloid. The earlobes are a common location. This violaceous lesion is inflamed.

• Both hypertrophic scars and keloids may be tender, painful, or pruritic; however, keloids, by virtue of their excessive size, are generally more problematic and are of much greater cosmetic concern to patients. • Unlike keloids, the hypertrophic scar reaches a certain size and subsequently stabilizes or regresses, whereas keloids do not regress without treatment and tend to recur after excision. DIAGNOSIS • The diagnosis of hypertrophic scars and keloids is made on the basis of clinical appearance.

21.41 Keloid. This lesion was also caused by earlobe piercing. Large lesions such as this are more likely to occur in African-Americans.

MANAGEMENT

Pre ve n t io n • Prevention is essential. Patients who tend to develop hypertrophic scars or keloids should be advised to discontinue or avoid repetitive skin trauma such as tattooing and skin piercing, particularly in areas that are prone to abnormal scarring such as the presternal areas and earlobes.

• Conditions such as inflammatory acne and cutaneous infections should be treated promptly to prevent scarring. Despite preventive measures, keloids may form in simple clean wounds or may occur in the absence of trauma.

Tre at m e n t H yp ert ro p h ic Sca rs

• Intralesional corticosteroids with triamcinolone acetate (TAC) in varying concentrations (5 to 40 mg/mL) are continued on page 387

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MANAGEMENT Continued

•

•

• •

injected directly into the scar (FIG. 21.42); this has been the mainstay of treatment for hypertrophic scars and keloids. Use of a 25- to 27-gauge needle at 4- to 6-week intervals often helps flatten the lesions. Additionally, these injections are also useful for diminishing itching and tenderness. Side effects from these injections include hypopigmentation, atrophy, and telangiectasias (FIG. 21.43). Corticosteroids reduce excessive scarring by reducing fibroblast growth and promoting collagen degradation. Such injections must be administered cautiously to avoid overtreatment, which may result in skin atrophy, telangiectasias, and an overdepressed scar. Topical corticosteroids: A clear surgical tape that is uniformly impregnated with flurandrenolide, a corticosteroid, has been shown to soften and flatten keloids over time. Pulsed-dye lasers have been used successfully and safely on some persistent hypertrophic scars. If they are in amenable locations, hypertrophic scars can sometimes be removed by simple excision, provided that wound closure can occur without undue tension on the surgical site.

21.42 Treatment of keloids with intralesional cortisone. Triamcinolone (Kenalog, Aristocort) is being injected into this patient’s presternal lesions.

Kelo id s

• Intralesional corticosteroid injections • As with hypertrophic scars, intralesional TAC, often in concentrations as high as 40 mg/mL, can help flatten keloids and diminish itching and erythema. • Such high concentrations are generally necessary for denser, more recalcitrant lesions. Similarly, complications of repeated corticosteroid injections include atrophy, telangiectasias, and pigmentary alteration. • Excision, in combination with other postoperative modalities, such as TAC injections, compression dressings, radiotherapy, or injected interferon, are sometimes effective. • Careful operative technique that closes surgical wounds with minimal tension is important. This is followed by postoperative injection of TAC 2 to 3 weeks postoperatively, followed by repeat injection in 3 to 4 weeks. • After excisional treatment alone, keloids frequently recur (more than 50% of the time); however, when excision is combined with injected steroids or other modalities, the recurrence rate is diminished. • However, it should be noted that preoperative or intraoperative steroid injection can delay wound healing and increase the possibility of wound dehiscence. A lower steroid dose is preferred because of the potential complications of intralesional steroids, including depigmentation and dermal atrophy.

21.43 Keloid after intralesional cortisone injection. This shiny scar shows the possible untoward aftereffects of intralesional steroid injections: atrophy, telangiectasias, and perilesional hypopigmentation.

• Laser therapy. Lasers have been used as alternatives to cold excision for keloids; however, the use of this equipment is expensive. As with excisional therapy, results are best when laser therapy is combined with postoperative injected steroids.

continued on page 388

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MANAGEMENT Continued • Combined modality treatment of keloids. Effective treatment may involve excision followed by: • Pressure dressings (compression therapy) during the postoperative period to wounds of patients in whom hypertrophic scars and keloid formation occur. This includes earlobe button compression, pressure earrings, Ace bandages, elastic adhesive bandages, compression wraps, and Lycra bandages. Compression therapy is based on the finding that pressure has long been known to have thinning effects on skin. • Occlusive dressings: The application of silicone gel sheeting has not proven to be very effective. Any antikeloidal effects appear to result from a combination

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of occlusion and hydration, rather than from an effect of the silicone. • Topical imiquimod (Aldara) cream: Postoperative application of imiquimod 5% cream induces local production of interferon alpha, which, in turn, is known to enhance keloidal collagenase activity and reduce the synthesis of collagen. A recent study has demonstrated a lower recurrence rate of keloids when imiquimod is applied postoperatively. • Other medications: In addition to topical imiquimod, other methods that are sometimes used to treat keloids and hypertrophic scars include intralesional interferon, oral verapamil, intralesional bleomycin, 5-fluorouracil, and botulinum toxin.

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Ben ign Va scu la r Lesio n s Com m on An giom as BASICS • There are many different types of angiomas, benign growths that consist of small blood vessels. These tumors can be located anywhere on the body. Some of the different types include spider angiomas, cherry angiomas, and angiokeratomas.

Ch e rry An g io m as • These lesions, which are also known as Campbell De Morgan spots, ruby spots, and senile angiomas, are extremely common benign vascular neoplasms. • They are asymptomatic, easily diagnosed, cherry- to plumcolored papules that develop primarily on the trunk (FIG. 21.44). • The angiomas are found in fair-skinned adults older than 40 years of age.

21.44 Multiple cherry angiomas. These cherry- and plum-colored papules are common in fair-skinned persons older than 40 years of age.

Ve n o us Lake s • Venous lakes (venous varices) are another common benign vascular neoplasm. They are generally macules or papules that are dark blue to purple and may be seen on the lower lip (FIG. 21.45), face, ears, and eyelids (see also FIG. 12.18). • The lesions usually occur in patients older than 60 years of age.

21.45 Venous lake. This is a common lesion among seniors. If a patient is concerned about its appearance, the lesion can be removed with electrocautery or laser destruction. They appear on the lower lip and on the external ears.

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An g io ke rat o m as (Fo rd yce An g io ke rat o m as) • Angiokeratomas (Fordyce angiokeratomas) are most often found on the scrotum (FIG. 21.46) or vulva (FIG. 21.47), and they consist of multiple red-purple asymptomatic papules (“caviar spots”). • They are usually first noticed in young adulthood.

DIFFERENTIAL DIAGNOSIS • The diagnosis of all these lesions is usually made on clinical grounds.

21.46 Angiokeratomas. These red-purple papules are most often found on the scrotum; they are usually first noticed when the patient is a young adult.

MANAGEMENT • Reassure the patient that the lesions are benign. • If the lesions are a cosmetic concern, they may be treated with electrocautery, cryosurgery with liquid nitrogen, or laser therapy.

Sp id er Telan giectasias (Sp id er An giom as)

21.47 vulva.

Angiokeratomas. Lesions are seen here on the

• A spider angioma (nevus araneus) is a cluster of telangiectasias, or dilated capillaries, that radiate from a central arteriole (FIG. 21.48). • It is more commonly seen in women and may be associated with pregnancy or oral contraceptive use. Spider angiomas are also seen in patients with hyperestrogenic conditions, such as chronic liver disease. They may also be seen in healthy children. • Lesions appear as spokelike capillaries radiating from a slightly raised central arteriole. Compression of the central arteriole completely blanches the lesions. • Spider angiomas most often occur on the face and trunk. Lesions are asymptomatic and are primarily of cosmetic concern.

MANAGEMENT

21.48 Spider angioma. This lesion is actually a cluster of telangiectasias radiating from a central arteriole. Compression of the central arteriole completely blanches the lesion. 390

• Light electrocautery or laser destruction of the spider angioma may be performed if the lesion presents a cosmetic problem. Occasionally, lesions regress spontaneously. • Other types of telangiectasias may serve as a clue to an underlying collagen vascular disease, such as the periungual telangiectasias of systemic lupus erythematosus and dermatomyositis or the telangiectasias seen in scleroderma and the CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal motility disorders, sclerodactyly, and telangiectasia) (see Chapter 25, “Cutaneous Manifestations of Systemic Disease”).

Part One • Com m on Skin Conditions: Diag nosis and Managem ent

Pyogen ic Gran u lom a BASICS • Pyogenic granuloma (PG) is a common vascular hyperplasia of the skin and mucous membranes that occurs most often in children and young adults. • Lesions can also arise during pregnancy (such a lesion is known as a granuloma gravidarum). They are also associated with oral contraceptive use. • The cause of PGs is unknown, but minor trauma and hormonal factors appear to be factors in their development. DESCRIPTION OF LESIONS • PG lesions are benign, rapidly developing, red, purple, or red-brown, dome-shaped papules or nodules. They resemble hemangiomas or granulation tissue (“proud flesh”). • PGs are generally solitary and range in size from a few millimeters to 3 to 4 cm in diameter (FIG. 21.49). The bases of lesions are often surrounded by a collarette of skin. PG papules or nodules may be crusted. • Lesions are asymptomatic but tend to bleed after minor trauma.

21.49 Pyogenic granuloma. This patient has a typical dusky red nodule with a collarette of skin. These lesions tend to bleed when traumatized.

DISTRIBUTION OF LESIONS • Lesions most frequently occur at sites of minor trauma, such as the fingers and toes, but they also may be seen on the trunk. • During pregnancy, lesions tend to occur on the lips (FIG. 21.50), gums, and buccal mucosa. Spontaneous resolution often occurs after childbirth. DIAGNOSIS • The diagnosis is usually based on the typical clinical appearance and biopsy.

21.50 Pyogenic granuloma. This patient is pregnant (see also FIG. 23.5).

MANAGEMENT DIFFERENTIAL DIAGNOSIS In children: • Hemangioma In adults: • Nodular (amelanotic) melanoma • Skin cancer (e.g., basal cell carcinoma, squamous cell carcinoma) • Kaposi’s sarcoma

• If there is any doubt about the diagnosis, a biopsy should be performed. • The lesion is generally destroyed by electrocautery, laser therapy, cryosurgery, or excisional surgery. Recurrences are not uncommon if the lesion is not completely removed.

POINT TO REMEMBER • The clinical presentation of a rapidly developing, friable, vascular lesion in a child or pregnant woman suggests a PG. Chapter 21 • Benign Skin Neop lasm s

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C H AP T ER

22

Prem alignant and Malignant Skin Neoplasm s OVERVIEW

SOLAR KERATOSIS SQUAMOUS CELL CARCINOMA • Bowen’s disease (squam ous cell carcinom a in situ) • Squam ous cell carcinom a of m ucous m em branes KERATOACANTHOMA BASAL CELL CARCINOMA • Superficial basal cell carcinom a • Morpheaform basal cell carcinom a MELANOMA • • • •

Superficial spreading m elanom a Nodular m elanom a Lentigo m aligna and lentigo m aligna m elanom a Acral lentiginous m elanom a PAGET’S DISEASE OF THE BREAST AND EXTRAMAMMARY PAGET’S DISEASE

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• This chapter is intended to help health care providers distinguish skin cancers from precancers and benign growths. The ability to make clinical diagnoses, to identify benign versus malignant lesions, especially in their less classic presentations, is an important skill that comes with focused, repetitive visual scrutiny. • By far, the most important skin lesion for the health care provider to recognize is melanoma. • The therapy of malignant lesions should be undertaken only by persons experienced in skin cancer therapy.

So la r Kera t o sis BASICS • An aging population that is living longer, in an atmosphere with a declining ozone layer and with more outdoor and leisure time to bask in this ultraviolet environment, has led to a dramatic increase in sun-related skin damage (dermatoheliosis) and precursors to skin cancer such as solar keratoses. It is estimated that 60% of predisposed people older than 40 years have at least one solar keratosis, and many of them have new solar keratoses each year. • Solar keratosis, also commonly known as actinic keratosis, is the most common sun-related skin growth. Whether this lesion is benign (premalignant) or malignant (squamous cell carcinoma in situ) from its onset is controversial. What is accepted, however, is that solar keratoses have the potential to develop into invasive squamous cell carcinomas. • Solar keratoses are more common in men, particularly those who work, or have worked, in outdoor occupations, such as farmers, sailors, and gardeners, and those who participate in outdoor sports. The incidence of solar keratosis, as with all of the skin cancers described in this chapter, is highest in Australia and in the Sun Belt of the United States. • It is estimated that 1 in 20 lesions eventually becomes squamous cell carcinoma. It is also accepted that the invasive carcinomas that develop from these actinic keratoses are of a very slow-growing, indolent, unaggressive type, and the prognosis usually is excellent. Distant metastases are extremely rare. Consequently, among dermatologists, there is an ongoing debate regarding the need to be aggressive or laissez-faire in the approach to these lesions. PATHOGENESIS • The development of solar keratoses, which is directly proportional to sun exposure, is seen in people who are fairskinned, burn easily, and tan poorly. • These lesions are rare in dark-skinned persons.

22.1 Solar keratoses. Rough, scaly papules are present on the scalp. This is a typical finding in bald, elderly men with fair complexions who have spent much of their lives working outdoors. The lesions in this patient are more easily palpated than visualized.

Hist o p at h o lo g y • Cellular atypia is present, and the keratinocytes vary in size and shape. Mitotic figures are common. • The histologic changes of individual cells are indistinguishable from those seen in squamous cell carcinomas. DESCRIPTION OF LESIONS • Lesions usually appear as multiple discrete, flat or elevated, verrucous, scaly lesions. Their texture typically feels rough to the touch (FIG. 22.1). • They typically have an erythematous base covered by a white, yellowish, or brown scale (hyperkeratosis) (FIG. 22.2). • Lesions are usually 3 to 10 mm in size and can gradually enlarge, thicken, and become more elevated and thus develop into a hypertrophic solar keratosis (FIGS. 22.3 and 22.4) or a cutaneous horn (FIGS. 22.5 and 22.6).

22.2 Solar keratoses. Thicker, tan-colored, hyperkeratinized lesions are more obvious in this patient. Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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22.5 Solar keratosis. This large cutaneous horn was produced by an underlying hypertrophic solar keratosis. 22.3 Solar keratoses, hypertrophic. The solar keratoses occur primarily in areas of sun-exposed skin in this elderly woman.

22.6 Solar keratosis. This cutaneous horn was also produced by an underlying solar keratosis. A biopsy was performed to rule out squamous cell carcinoma. 22.4 Solar keratosis. The pinna of the ear is a very common site for these lesions in men. (Note the similarity to FIG. 21.33, an illustration of chondrodermatitis nodularis chronica helicis.)

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• A cutaneous horn is a hornlike projection of keratin. In addition to solar keratoses, warts and squamous cell carcinomas in situ (Bowen’s disease) may also produce a cutaneous horn on their surface. • Sometimes, solar keratoses are tan or dark brown (pigmented solar keratosis) (FIG. 22.7) and are often clinically indistinguishable from a solar lentigo (see FIG. 21.4 ) • In time, a solar keratosis may develop into a squamous cell carcinoma. DISTRIBUTION OF LESIONS • Solar keratoses are most often seen on a background of sundamaged skin. • They are found chiefly on sun-exposed areas: the face, especially on the nose, temples, and forehead. • They are also commonly noted on the bald areas of the scalp and the tops of the ears in men, the dorsa of the forearms (FIG. 22.8) and the dorsa of the hands, the “V” of the neck, and the neck below the occipital hairline and below the ears. • The vermilion border of the upper lip is another very common site for solar keratoses (FIG. 22.9).

22.8 Solar keratoses, hypertrophic. The forearms are a common site of these lesions.

22.9 Solar keratosis. The vermilion border of the upper lip is a common site of sun damage.

22.7 Solar keratosis, pigmented. This lesion is slightly rough to the touch.

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• They may also occur on any area that is chronically or repeatedly exposed to the sun, such as the legs in women. • Extensive involvement of the mucous membranes of the lower lips (generally the lower lip) is known as actinic cheilitis (FIG. 22.10). CLINICAL MANIFESTATIONS • Solar keratoses are usually asymptomatic, but they may itch and become tender or irritated. Patients often report one or several “dry” scaly bumps on sun-exposed areas that do not respond to moisturizers. • They are of cosmetic concern to many patients. • They may regress spontaneously. 22.10 Actinic cheilitis. This patient is undergoing treatment with topical 5-fluorouracil for multiple solar keratoses of his lower lip.

DIFFERENTIAL DIAGNOSIS

Sq uam o us Ce ll Carcin o m a See later discussion. • Solar keratosis may be indistinguishable from a squamous cell carcinoma. • Untreated, squamous cell carcinoma becomes indurated, with a tendency to ooze, ulcerate, or bleed.

Basal Ce ll Carcin o m a See later discussion. • Classically, this lesion is a pearly, shiny papule with telangiectasias. • It may be indistinguishable from solar keratosis, particularly when it is small, ulcerated, manipulated, or pigmented.

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DIAGNOSIS • Clinically, very small lesions are often better felt than seen. Palpation of these scaly growths reveals a gritty, sandpaperlike texture. • A shave biopsy is performed if the diagnosis is in doubt.

Ve rruca Vulg aris (Wart ) • Warts may also be indistinguishable from solar keratoses. Se b o rrh e ic Ke rat o sis See also Chapter 21, “Benign Skin Neoplasms.” • A seborrheic keratosis may, at times, be indistinguishable from a solar keratosis. • Seborrheic keratosis has a “stuck-on” appearance and may occur in areas not exposed to the sun.

Ch o n d ro d e rm at it is No d ularis He licis See also Chapter 21, “Benign Skin Neoplasms.” • These lesions, when present on the helices or antihelices of the ears, may be easily confused with solar keratoses.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

MANAGEMENT • Prevention begins with educating the patient to limit sun exposure by using sunscreens and wearing protective clothing. • Treatment is achieved by destruction of solar keratoses (see Chapter 26, “Diagnostic and Therapeutic Procedures”).

De st ruct ive Me t h o d s • Liquid nitrogen (LN2) is the mainstay of treatment for solar keratoses. LN2 is most useful when lesions are few in number. It is applied to individual lesions for 3 to 5 seconds. • For thick, hyperkeratotic lesions, biopsy followed by electrocautery or electrocautery alone is performed.

acid accumulates preferentially in the dysplastic cells. On exposure to irradiation with light of the appropriate wavelength, oxygen-derived free radicals are generated, and cell death results. • Chemical peels and dermabrasion are also used in patients with numerous facial solar keratoses. • Diclofenac sodium 3% (Solarase) gel is a nonsteroidal anti-inflammatory preparation that has been introduced as a topical treatment for solar keratoses. This agent appears to be less irritating than the standard 5-FU products and Aldara; however, its efficacy does not match theirs.

Ch e m o t h e rap y • Topical application of Efudex, a 5-fluorouracil (5-FU) cream, is a method that may be used when lesions are too numerous to treat individually. 5-FU interferes with the synthesis of DNA; it destroys dysplastic cells and spares normal cells. Enough medication is applied to cover the entire area with a thin film. This is done twice daily for 2 to 4 weeks for facial lesions. Other body sites require longer treatment (e.g., 6 to 8 weeks for the arms). • Alternatively, a 0.5% 5-FU cream (Carac) may be applied only once daily. This preparation is reportedly less irritating than the stronger 5% 5-FU agents. • During this treatment, the lesions become increasingly red and crusted, and subclinical lesions become visible. This situation can result in a very red, disfiguring complexion; however, if the patient completes the treatment, the lesions usually heal within 2 weeks of stopping treatment, the skin becomes smooth, and the majority of the solar keratoses are gone (FIGS. 22.11 A and B). Im m un o t h e rap y • Imiquimod (Aldara) 10% cream is a local inducer of interferon. It is applied twice weekly to involved skin for 16 weeks until a response similar to that described with 5-FU agents is elicited. Ot h e r Tre at m e n t s • Topical tretinoin (Retin-A) has been shown to reverse mild actinic damage to the skin. • Photodynamic therapy can also be used to treat multiple actinic keratoses. In this treatment, topical 5-aminolevulinic

B

22.11 A an d B Solar keratoses. A: Before treatment, few lesions are clinically visible. B: Two weeks after treatment with topical 5-FU, crusting and erythema are evident in areas that had lesions that were not initially apparent.

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HELPFUL HINTS • Because solar keratoses are more often easily felt than seen, the clinician should run ungloved fingers over the patient’s skin to detect all lesions. • The number of solar keratoses is directly related to cumulative sun exposure. Childhood exposure or sun damage is “accumulated like interest on money in the bank”; some of this damage seems to be reversed and prevented by sun avoidance and sun protective measures. • Sunscreens should also be applied to the lower lip to prevent actinic cheilitis. • Topical 5-FU treatment can be likened to using a “smart bomb” in which the “bomb” (in this case 5-FU) targets only the “enemy” (the rapidly growing dysplastic cells). • Imiquimod (Aldara) cream may “immunize” patients against their own dysplastic keratinocytes; in fact, some dermatologic surgeons use it prophylactically to prevent recurrence. Aldara is applied two times per week for a full 16 weeks.

POINTS TO REMEMBER • If a lesion persists or recurs, despite treatment, it should be examined by biopsy. • The decision to treat solar keratoses can be based on cosmetic reasons, symptom relief, or, most important, the prevention of malignancy.

SEE PATIENT HANDOUTS “So lar Ke rat o sis (Act in ic Ke rat o sis)” an d “Sun Pro t e ct io n Ad vice ” ON THE SOLUTION SITE

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Sq u a m o u s Cell Ca rcin o m a BASICS • Squamous cell carcinoma (SCC) is a malignant epithelial tumor arising from keratinocytes of the epidermis. • It is the second most common type of skin cancer. SCC is diagnosed much less frequently than basal cell carcinoma (BCC), but it carries a risk of metastasis. It occurs in an older age group than does BCC. • Although it is very rare in dark-skinned persons, SCC can be more aggressive in these individuals. • The majority of SCCs arise in solar keratoses (see earlier discussion). Such SCCs that develop from solar keratoses are slow growing, minimally invasive, and unaggressive, and the prognosis is usually excellent because distant metastases are extremely rare. • An SCC may appear de novo without a preceding solar keratosis. • When a metastasis from a cutaneous SCC (non–mucous membrane) does occur, it is more likely to result from lesions that appear on the ears or on the vermilion border of the lips, from lesions that are poorly differentiated, from recurrent lesions, or from tumors larger than 2 cm in diameter. • Also apt to be more aggressive are SCCs that may occur from causes other than sun exposure. For example, a SCC may arise in long-standing scars or from sites previously exposed to ionizing radiation and long-term exposure to psoralen and ultraviolet A light (PUVA) (see Chapter 3, “Psoriasis”). A SCC may also emerge from pre-existing human papilloma virus infection (verrucous carcinoma), in the skin of organ transplant recipients, or chronic inflammatory lesions (e.g., cutaneous lupus erythematosus), as

well as cutaneous ulcers (e.g., venous stasis ulcers) or other nonhealing wounds. • As with solar keratosis and BCCs (see later discussion), SCC is related to sun exposure and is noted more frequently in those with a greater degree of outdoor activity.

Hist o p at h o lo g y • In the in situ type of SCC (Bowen’s disease), only the full thickness of the epidermis is involved. The basement membrane remains intact. Atypical keratinocytes (squamous cells) show a loss of polarity and an increased mitotic rate. • An invasive SCC penetrates into the dermis. It has various levels of anaplasia and may manifest relatively few to multiple mitoses and may display varying degrees of differentiation such as keratinization. Risk o f Me t ast asis • The risk of metastasis of SCC depends on its degree of differentiation, depth of penetration, and location. • SCC occurs in several clinical variants that vary in their aggressiveness. • In situ SCC (Bowen’s disease) has a low incidence of metastasis. • An SCC arising in a solar keratosis also has a low incidence of metastasis. • Lesions on mucous membranes have the highest risk of metastasis. • Tumors that are induced by ionizing radiation or those that arise in old burn scars or in inflammatory lesions also are also more likely to metastasize.

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DESCRIPTION OF LESIONS • Lesions appear as papules, plaques, or nodules (FIG. 22.12) that grow slowly. • Lesions are scaly or ulcerated. • Lesions may have a smooth or thick hyperkeratotic surface (FIG. 22.13). • As with solar keratoses, an SCC may also produce a cutaneous horn on its surface. • An SCC may appear as a reddish brown nodule. It may, at times, be indistinguishable from a hypertrophic solar keratosis or a BCC. • Tumors may ulcerate when they are neglected (FIG. 22.14).

22.12 Squamous cell carcinoma. This nodular lesion arose from a solar keratosis.

DISTRIBUTION OF LESIONS • Lesions occur in the same locations as do solar keratoses: sun-exposed areas such as the face, the dorsa of the forearms and hands, and the “V” of the neck. • In men, SCCs tend to arise on the bald areas of the scalp and on the tops of the ears as well as the posterior neck below the occipital hairline. • In women, lesions tend to occur on the legs as well as other relatively sun-exposed locations. • In individuals of African origin there is an equal frequency in sun-exposed and unexposed areas. CLINICAL MANIFESTATIONS • Most SCCs are asymptomatic, although bleeding, pain, and tenderness may be noted.

22.13 Squamous cell carcinoma. This hyperkeratotic nodule arose in an immunocompromised patient in a site previously exposed to ionizing radiation.

22.14 Squamous cell carcinoma. This neglected tumor has ulcerated. 400

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

• Slow-growing, firm papules with the ability to produce scale (keratinization) tend to be more clearly differentiated and less likely to metastasize. • Softer, nonkeratinizing lesions are less well differentiated and are more likely to spread (FIG. 22.15).

Clin ical Varian ts In t rae p it h e lial Sq uam o us Ce ll Carcin o m a • Bowen’s disease (SCC in situ) and erythroplasia of Queyrat are intraepithelial SCCs that often arise in sites that are not exposed to the sun such as the trunk or extremities. When an SCC in situ lesion occurs on the penis, it is referred to as erythroplasia of Queyrat (FIG. 22.16). • Bowen’s disease (FIG. 22.17) is one of the few skin cancers that should be considered as a diagnosis in AfricanAmerican, Afro-Caribbean, and African blacks. This non–sun-related skin cancer tends to arise on the extremities de novo (FIG. 22.18).

22.15 Squamous cell carcinoma. This poorly differentiated nodule has the potential to metastasize.

22.16 Erythroplasia of Queyrat. This subtle, nonhealing, shiny erosion on the perimeatal area of the glans penis proved to be an SCC in situ. (Courtesy of Joseph S. Eastern, M.D.)

22.17 Bowen’s disease (squamous cell carcinoma in situ). These lesions closely resemble scaly psoriatic or eczematous plaques.

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• If a frank SCC occurs in an old scar (FIG. 22.19) or in a lesion of discoid lupus erythematosus, the lesion should be treated aggressively.

Sq uam o us Ce ll Carcin o m a o f Muco us Me m b ran e s • This condition (FIG. 22.20) may present as leukoplakia, nonhealing fissures, or ulcerations. Such lesions have significant metastatic potential. • Treatment is beyond the scope of this publication. (text continued on page 405)

22.18 Bowen’s disease in an African-American woman. This plaque arose de novo in a non–sun-exposed location.

22.19 Squamous cell carcinoma arising in a burn scar. The likelihood of metastasis of this lesion is significant.

22.20 Squamous cell carcinoma of the lip. This lesion also has a significant metastatic potential.

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

DIFFERENTIAL DIAGNOSIS

Me lan o m a See later discussion.

So lar Ke rat o sis (Act in ic Ke rat o sis) • This lesion is often indistinguishable from SCC (see earlier discussion).

• An amelanotic melanoma (lacking typical pigmentation) or an ulcerated melanoma may also be impossible to distinguish from a SCC.

Basal Ce ll Carcin o m a See later discussion of BCC.

Pso riasis/ Ecze m a • Bowen’s disease resembles a scaly solitary psoriatic or eczematous plaque (see Chapter 2, “Eczema,” and Chapter 3, “Psoriasis” ).

• BCCs are generally pearly and telangiectatic. • They appear at a younger age than do SCCs. • BCC may be indistinguishable from SCC, particularly if the lesion is ulcerated.

Ke rat o acan t h o m a See later discussion. • This lesion also may be clinically and, at times, histopathologically, indistinguishable from a SCC. • It is fast growing. • Usually, it has a typical central crater.

MANAGEMENT

Tre at m e n t • Electrocautery and curettage for small lesions (generally smaller than 1 cm). This is done in a fashion similar to that performed for BCC treatment (see subsequent discussion). It is particularly useful on flat surfaces (e.g., forehead, cheek) and SCC in situ (Bowen’s disease). • As with superficial BCCs, selected SCCs may be treated rapidly using cryosurgery with LN2. • Total excision, the preferred method of therapy for SCC, permits histologic diagnosis of the tumor margins. • Immunotherapy • Imiquimod (Aldara) 5% cream is approved for the treatment of solar keratoses (see previous discussion), for superficial BCCs (see later discussion), and “offlabel” for SCC in situ (Bowen’s disease). • It is applied twice weekly to involved skin for 16 weeks until a significant inflammatory response occurs. • Aldara may also have some utility in treating selected patients who have highly differentiated SCCs and in some renal transplant patients, who tend to develop numerous SCCs.

Se b o rrh e ic Ke rat o sis • This extremely common benign skin growth becomes apparent after 40 years of age (see Chapter 21, “Benign Skin Neoplasms”). Ve rruca Vulg aris • A wart may also resemble a SCC (see Chapter 6, “Superficial Viral Infections”).

• Micrographic (Mohs’) surgery (see Chapter 26, “Diagnostic and Therapeutic Procedures”; FIGS. 26.26 A–D) is useful for excessively large or invasive carcinomas, for recurrent lesions, for lesions with poorly delineated clinical borders, for SCCs within an orifice (e.g., ear canals or nostrils), and for carcinomas in locations where preservation of normal tissue is extremely important (e.g., tip of the nose, eyelids, nasal alae, ears, lips, and glans penis) (see later discussion). It is also a treatment of choice for a lesion in an area of late radiation change. • Radiation therapy is used for those patients who are physically debilitated or who are unable to, or refuse to undergo, excisional surgery. It is also suitable for larger, advanced lesions.

Pre ve n t io n • Sun avoidance measures • Sunscreens and hats • Sunglasses with ultraviolet protection • Tinted windshields and side windows in cars • Sun-protective garments • Avoidance of contact with known carcinogenic compounds

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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HELPFUL HINTS • A subungual SCC can easily be mistaken for a verruca. • High-risk SCCs may require imaging studies • Lymph node biopsy is indicated for suspected nodal involvement.

SEE PATIENT HANDOUT “Sun Pro t e ct io n Ad vice ” ON THE SOLUTION SITE SEE PATIENT HANDOUT “Sq uam o us Ce ll Carcin o m a” ON THE SOLUTION SITE

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POINTS TO REMEMBER • An early lesion of SCC is difficult to distinguish from a precursor solar keratosis. • SCCs that develop from solar keratoses are generally unaggressive. • An SCC that is histopathologically described as being “poorly differentiated” should be treated more aggressively. • SCCs arising on a mucous membrane such as the glans penis, lip, or from a chronic ulcer or an SCC arising in an immunocompromised patient should be regarded as potentially metastatic.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Kera t o a ca n t h o m a BASICS • A keratoacanthoma (KA) is a unique lesion with a characteristic clinical appearance. There is controversy about the benign versus malignant nature of this lesion. A KA resembles an SCC histologically; some dermatologists and dermatopathologists consider it to be a low-grade variant of an SCC and believe that it should be treated as such. Lesions may be clinically impossible to differentiate from SCCs. • KAs generally occur in persons older than 65 years of age. • If ignored, KAs often regress spontaneously. This fact lends support to the theory that this lesion is benign in nature. DESCRIPTION OF LESIONS • A KA usually occurs as a single, dome-shaped, erythematous or skin-colored nodule with a central keratin core (central crater) with an overlying crust (FIGS. 22.21 and 22.22). It resembles the appearance of a volcano. • It generally attains a diameter of 1.0 to 2.5 cm.

22.21 Keratoacanthoma. This “volcanolike” nodule arose over a period of 2 weeks. Note the characteristic crusting in the center.

DISTRIBUTION OF LESIONS • As with the nonmelanoma skin cancers such as BCC and SCC, lesions tend to appear on the sun-exposed areas of the face, ears, neck, dorsa of hands, and forearms. CLINICAL MANIFESTATIONS • Lesions arise quickly, usually developing in 3 to 4 weeks. • Spontaneous regression may result in a small depressed scar. DIAGNOSIS • An excisional or incisional biopsy is often recommended so that the complete architecture of the lesion can be evaluated histologically. (An insufficient biopsy, such as a shave biopsy, may result in a histology that is indistinguishable from a SCC.) • When KAs appear in areas in which it is difficult to perform an excisional biopsy, such as the nose and external ears, a deep shave biopsy is often adequate to obtain sufficient tissue.

22.22 Keratoacanthoma. This nodule arose over a period of 4 weeks in a characteristic location.

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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POINT TO REMEMBER

DIFFERENTIAL DIAGNOSIS

• A KA is a lesion that resembles an SCC (FIG. 22.23). • SCC • Verruca vulgaris

MANAGEMENT

22.23 Keratoacanthoma. Clinically this lesion is difficult to distinguish from a hypertrophic solar keratosis or a SCC. (See FIG. 22.8.)

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• Excisional removal is the treatment of choice; however, a small minority of dermatologists prefer to simply observe these lesions and await spontaneous resolution. • A deep shave biopsy with or without electrodesiccation in selected cases often results in a permanent cure. • Intralesional 5-FU may be used. • Micrographic (Mohs’) surgery may be necessary for recurrences.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Ba sa l Cell Ca rcin o m a BASICS • BCC is the most common skin cancer and the most common cancer overall. • Although this lesion qualifies as a cancer, its morbidity, if recognized and treated early, is usually inconsequential. A BCC is usually slow growing and very rarely metastasizes, but it can cause significant local invasion and considerable destruction if it is neglected or treated inadequately.

Hist o p at h o lo g y • Cells of nodular BCC typically have large, hyperchromatic, oval nuclei and little cytoplasm. They appear rather uniform, and, if present, mitotic figures are usually scant. • Nodular tumor aggregates may be of varying sizes, but tumor cells tend to align more densely in a palisade pattern at the periphery of these nests. Cleft formation, known as “retraction artifact,” commonly occurs between BCC nests and stroma because of shrinkage of mucin during tissue fixation and staining.

22.24 Basal cell carcinoma. A pearly papule with ulceration (“rodent ulcer”) and telangiectasias is the “classic” presentation of a nodular BCC.

Risk Fact o rs • Many of the same risk factors that predispose to solar keratoses and SCCs are responsible for the development of BCCs, although BCC tends to occur at a younger age than solar keratosis, SCC, and KA. • Risk factors for BCC include the following: • Age older than 40 years • Male sex • Positive family history of BCC • Light complexion (as in SCCs and solar keratoses, BCCs are rare in blacks and Asians) with poor tanning ability • Long-term sun exposure DESCRIPTION OF LESIONS • The classic lesion, the nodular BCC, is also the most common type (FIG. 22.24). Nodular BCCs occur most commonly on the head, neck, and upper back and may have some of the following features: • A pearly, shiny, semitranslucent, papule or nodule (FIG. 22.25) • A rolled (raised) border (FIG. 22.26) • Telangiectases over the surface, thus accounting for a history of bleeding with minor trauma • Erosion or ulceration (“rodent ulcer”) caused by a gnawed appearance (see FIG. 22.24)

22.25 Basal cell carcinoma. Here the lesion is a shiny, pearly, translucent papule.

22.26 Basal cell carcinoma. This is a close-up view of the lesion shown in FIGURE 22.23, showing rolled borders with telangiectasia. Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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• A lesion can sometimes present as a small, nonhealing erosion (FIG. 22.31). • Brownish to blue-black pigmentation (pigmented BCC) is seen in more darkly pigmented persons (FIGS. 22.27 and 27.28).

22.27 Basal cell carcinoma, pigmented. This lesion could easily be mistaken for a melanoma. Note the pearly surface.

22.28 Basal cell carcinoma, pigmented. Note the pearly, waxy surface.

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DISTRIBUTION OF LESIONS • Lesions occur on the head and neck in 85% of all affected persons. • Lesions occur on sun-exposed areas (e.g., the face, especially on the nose, cheeks, forehead, periorbital area, lower face, and the back of the neck) (FIGS. 22.29–22.32). CLINICAL MANIFESTATIONS • Lesions are often ignored, asymptomatic, and slow growing. • Very mild trauma, such as face washing or drying with a towel, may cause bleeding. • In time, lesions may ulcerate (e.g., “the sore that will not heal”). 22.30 Basal cell carcinoma. The nose is a common site for BCC. Note the central crust, rolled borders, and telangiectasia.

22.31 Basal cell carcinoma. This small erosion proved to be a BCC.

22.29 Basal cell carcinoma. This is another lesion with typical features.

22.32 Basal cell carcinoma. The ear, particularly in men, is a frequent site. Note the tortuous telangiectasias.

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Clin ical Varian ts Sup e rficial Basal Ce ll Carcin o m a • A superficial BCC occurs as a scaly pink to red-brown patch with a threadlike border (FIG. 22.33). • The lesions tend to be indolent, asymptomatic, and the least aggressive of BCCs. • Lesions are sometimes multiple, occurring primarily on the trunk and proximal extremities. • When solitary, a lesion of superficial BCC may resemble psoriasis, eczema, a seborrheic keratosis, or Bowen’s disease (SCC in situ). • There is no clear association between superficial BCC and sun exposure. 22.33 Superficial basal cell carcinoma. The back is a common place to find a superficial BCC. Note the distinct border. Often patients are not aware of these lesions, which resemble psoriatic plaques as well as Bowen’s disease.

Mo rp h e afo rm Basal Ce ll Carcin o m a This is the least common and most aggressive form of BCC. • Lesions appear as whitish, scarred atrophic plaques with surrounding telangiectasia (FIG. 22.34). • The margins of these lesions are often difficult to evaluate clinically; as with icebergs, what is seen on the surface is not always what lies under the surface. • Consequently, morpheaform BCCs are generally more difficult to treat than other BCCs. • A morpheaform BCC may be mistaken for scar tissue. DIAGNOSIS • The diagnosis is generally made by shave or excisional biopsy. • A shave biopsy suffices for the diagnosis of most BCCs (see Chapter 26, “Diagnostic and Therapeutic Procedures”).

22.34 Morpheaform basal cell carcinoma. A whitish, atrophic, scarlike plaque is present, with surrounding telangiectasias and pearly papules surrounding it.

DIFFERENTIAL DIAGNOSIS • SCC (see earlier discussion) • Solar keratosis (see earlier discussion) • Sebaceous hyperplasia (see Chapter 21, “Benign Skin Neoplasms”) • Angiofibroma (fibrous papule of the nose) (see FIG. 21.37) and lesions of sebaceous hyperplasia (see FIG. 21.26), benign neoplasms that are often easily confused with BCC • Seborrheic keratosis, which may be indistinguishable from a pigmented BCC • Intradermal nevus (see Chapter 21, “Benign Skin Neoplasms”)

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Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

MANAGEMENT

Pre ve n t io n • Techniques involve sun avoidance, use of sunscreens with a sun protection factor (SPF) of at least 15, and wearing protective clothing. • People with a history of skin cancer should learn skin self-examination and should have annual skin examinations performed by a physician. Tre at m e n t See Chapter 26, “Diagnostic and Therapeutic Procedures.” • Electrodesiccation and curettage. The overall cure rate exceeds 90% for low-risk BCCs. This method is quick, simple, and less expensive than most other procedures. • Cryosurgery with LN2. Superficial BCCs may be treated rapidly using this method. However, nodular lesions, particularly selected lesions on the eyelid and ear, are ideally treated with a temperature probe before cryosurgery is performed. Successful treatment is highly dependent on the experience of the operator. • Excision, permitting histologic diagnosis of margins. Cosmetic results compare favorably with those of curettage; however, surgical excision is more time-consuming and costly than curettage. • Immunotherapy with 5% imiquimod cream (Aldara), a topical immunomodulator, is approved for the treatment

HELPFUL HINTS • Patients should always be undressed for adequate examination of the skin. • Avoidance of exposure to ultraviolet radiation is encouraged. Preventive measures include carefully planning outdoor activities before 10 a.m. and after 4 p.m., wearing a broad-brimmed hat during outdoor activities, and using sunscreens with an SPF of 15 or greater.

of superficial BCCs. It is applied five times per week for a full 6 weeks. • Micrographic (Mohs’) surgery (see Chapter 26, “Diagnostic and Therapeutic Methods”; FIGS. 26.26A–D) for morpheaform, recurrent, or large lesions, as well as for lesions in “danger zones” (e.g., the nasolabial area, around the eyes, behind the ears, in the ear canal, and on the scalp). • Mohs’ micrographic surgery is a microscopically controlled method of removing skin cancers that allows for controlled excision and maximum preservation of normal tissue. Excisions are repeated in the areas proven to be cancerous until a completely cancer-free plane is reached. • Mohs’ surgery is time-consuming and expensive, and it may require extensive reconstruction of surgical wounds. However, it provides the most reliable method of determining adequate margins, it has a very high cure rate of 98% to 99% for BCCs, and it preserves the maximum amount of normal tissue around the cancer. • Radiation therapy for elderly debilitated patients or for those who are physically unable to undergo excisional surgery. The disadvantages include the potential for late radiation changes in the skin, as well as the inability to examine skin margins because tissue is not obtained. It is rarely used today.

POINTS TO REMEMBER • A BCC is, by far, the most common type of skin cancer. • As with SCC and solar keratoses, BCCs are induced by ultraviolet radiation in susceptible persons. • Almost 50% of patients with BCC will have another one within 5 years. • Recurrent BCCs are generally more aggressive than primary lesions. • Patients with BCC have an increased risk of melanoma.

SEE PATIENT HANDOUT “Sun Pro t e ct io n Ad vice ” ON THE SOLUTION SITE

SEE PATIENT HANDOUT “Basal Ce ll Carcin o m a” ON THE SOLUTION SITE

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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Mela n o m a BASICS • Malignant melanoma, more appropriately referred to (nonredundantly) as melanoma, is a cancer of melanocytes, the cells that produce pigment. Melanoma generally occurs in the skin and, much less commonly, in the eyes, ears, gastrointestinal tract, leptomeninges of the central nervous system, and oral and genital mucous membranes. • It is the most common cancer in women aged 25 to 29 years and is second only to breast cancer in women aged 30 to 34 years. • It is also commonly seen in patients with defects of DNA repair such as xeroderma pigmentosum and in patients with familial atypical mole syndrome. • It is also more often seen in patients who have an abundance of melanocytic nevi. • Although BCC and SCC (nonmelanoma skin cancers) are associated with long-term exposure to sunlight, melanoma is more likely to occur with infrequent but strong exposures that result in sunburns. Nonmelanoma skin cancers are more likely to be found on chronically sun-exposed areas such as the face; in contrast, melanomas are more likely to occur on areas that are less often exposed and more frequently burned, specifically the backs of men and the legs of women. • By far, the most important skin lesion for the health care provider to recognize is melanoma. Melanoma is one of the

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only skin diseases that can be fatal if neglected; consequently, early recognition and prompt removal of a melanoma can save a life.

Risk Fact o rs Persons at greatest risk for melanoma have the following characteristics: • Age generally older than 20 years, particularly older than 60 years • A light complexion, an inability to tan, and a history of sunburns • Moles that are numerous, changing, or atypical (dysplastic nevi) • A personal or family history of melanoma (first-degree relatives) • A personal or family history of BCCs or SCCs

Hist o p at h o lo g y • Superficial spreading melanoma (SSM), lentigo maligna melanoma (LMM), and acral lentiginous melanoma (ALM) have an early in situ (radial growth) phase characterized by increased numbers of intraepithelial melanocytes, which are large and atypical as well as being arranged haphazardly at the dermal-epidermal junction. They show upward (pagetoid) migration and lack the biologic potential to metastasize.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

• Invasion into the dermis may confer metastatic potential and is characterized by a distinct population of melanoma cells with mitoses and nuclear pleomorphism within the dermis (papillary, reticular) and, possibly, the subcutaneous fat. DISTRIBUTION OF LESIONS • In white women, the most common lesion sites for SSM are the upper back, the lower leg between the knees and ankle, and the arms. Lesions are relatively fewer on covered areas such as under bras and swimsuits. • In white men, the most common lesion sites for SSM are the upper back, anterior torso, and the upper extremities. • In both white women and white men, other types of melanoma (e.g., LMM) may occur on the head, neck, and sun-exposed arms. Nodular melanomas are seen on the legs and trunk. • Malignant melanoma is very rare in dark-skinned persons and Asians. However, when it does occur, it tends to be present on acral, non–sun-exposed areas such as the palms of the hands, soles of the feet, or in the nail bed. It is referred to as acral lentiginous melanoma. CLINICAL MANIFESTATIONS

Warn in g Sig n s • New, changing (evolving), or unusual moles. A changing mole is the most common sign of melanoma.

• Symptomatic moles (e.g., moles that itch, burn, or are painful). Nevi are generally asymptomatic, unless inflammation or invasion occurs. • An initial slow horizontal growth phase, if left untreated, is followed in months or years by a vertical growth phase (lesions that extend vertically in the skin), which indicates invasive disease and potential metastasis. • White coloration may indicate regression or scarring.

Pro g n osis • Five-year survival is based on the thickness of the tumor. Once a diagnosis of melanoma is established, further treatment is determined by the scale known as Breslow’s measurement (TABLE 22.1). The thickness of the lesion is measured from the top of the granular layer of the skin to the deepest tumor cell. Melanomas that are thicker than 4 mm are associated with a high rate of distant and nodal metastasis.

Tab le 22.1 BRESLOW’S MEASUREMENT TUMOR THICKNESS (MM)

5-YEAR SURVIVAL (%)

0.75 0.76–1.50 1.51–2.25 2.26–3.00 3.00

98–99 94 83 72–77 50

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Tab le 22.2 CLARK’S LEVELS GRADE I II III IV V

LOCATION IN DERMIS In situ disease confined to the epidermis Melanoma cells in papillary dermis Melanoma cells filling papillary dermis Melanoma cells in reticular dermis Melanoma cells in subcutaneous fat

• Prognosis may also be determined by the grade of the melanoma, as determined by its location in the dermis using Clark’s levels (TABLE 22.2). • Sentinel lymph node status is also used for prognostication (see later in this chapter). • Other important prognostic factors include the sex of the patient (women have a better prognosis than men), age (the prognosis worsens with increasing age), and the presence of ulceration or regional or distant spread. 22.35 Superficial spreading melanoma. Note the “ABCDE” features: asymmetry, notched border, varied colors, and diameter of more than 6 mm, plus evolution (change in lesion).

Sup e rficial Sp re ad in g Me lan o m a • Of the four major clinicopathologic types of melanoma, SSM is by far the most common (FIGS. 22.35 and 22.36). • It may arise de novo or in a preexisting nevus. • The lesions of SSM may conform to some (or all) of the “ABCDE” criteria for melanoma, in which the primary lesion is a macular lesion or an elevated plaque that displays the following: A: Asymmetry. If you draw an X and a Y axis through the middle of a lesion and “fold” the lesion on itself, the halves will not match. B: Border that is irregular or notched (like a jigsaw puzzle).

22.36 Superficial spreading melanoma. Note the central area (whitish gray) that represents regression.

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C: Color that is varied or has different shades (may have brown, black, pink, blue gray, white, or admixtures of these colors). The blue color results from the Tyndall effect, an optical illusion that occurs when light reflects off brown or black pigment in the deeper layers of the skin. The red color results from an inflammatory response that the immune system is mounting against the tumor. When this response is successful, the tumor regresses, and an ivory-white color results (FIG. 22.36). D: Diameter greater than 6 mm (the size of a pencil eraser), but a lesion may be smaller when first detected (FIGS. 22.37 and 22.38).

22.37 Superficial spreading melanoma. This lesion, which is more brown in color than in the preceding figure, also has color variegation, evidence of regression, and an irregular border. (Note the resemblance to seborrheic keratoses in Chapter 21.)

22.38 Superficial spreading melanoma. An early melanoma was present on this patient’s back. This lesion illustrates two colors. The presence of dark pigmentation and irregular shape prompted biopsy of the lesion.

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E: Evolution, or change in a preexisting lesion, has recently been added to the criteria. Any change—in size, color, elevation—or any new symptom such as bleeding, itching, or crusting (FIGS. 22.39 and 22.41) should prompt suspicion. DIAGNOSIS • Clinical diagnosis is based on ABCDE criteria (FIG. 22.40). • Elliptic excisional biopsy should include all of the visible lesion.

22.39 Superficial spreading melanoma. Melanoma of the ear. Note the superficial spreading component (brown color) at the base and the nodule arising from it.

22.40 Superficial spreading melanoma. The radial growth phase is represented by the large area; the black, nodular component of this lesion represents the invasive vertical growth phase. The “ABCDE” features are present in this lesion.

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DIFFERENTIAL DIAGNOSIS See also Chapter 21, “Benign Skin Neoplasms.”

Se b o rrh e ic Ke rat o sis • Seborrheic keratosis, particularly if the lesion is variegated in color or jet black (see Chapter 21, “Benign Skin Neoplasms”), should be considered. The “stuck-on” appearing lesions of this condition are most often confused with malignant melanoma by clinicians who are not dermatologists (FIG. 22.42).

22.41 Superficial spreading melanoma. The scaling in the center of this lesion represents ulceration and is a poor prognostic sign.

Basal Ce ll Carcin o m a • Pigmented BCC may be clinically indistinguishable from SSM or other types of malignant melanoma (see FIGS. 22.27 and 22.28). Dysp last ic o r At yp ical Ne vus • A dysplastic nevus or a melanocytic nevus with an atypical appearance may also be clinically indistinguishable from melanoma (see FIG. 21.13).

22.42 In situ melanoma. Note jet-black coloration of the lesion on this man’s forehead in comparison to the surrounding brown seborrheic keratoses. This patient’s wife noticed the “ugly duckling” lesion, which was out of character with his usual seborrheic keratoses.

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Clin ical Varian ts

22.43 Nodular amelanotic melanoma. This lesion arose de novo; it has a great probability of metastasizing.

22.44 Nodular melanoma. This is a nodule with surrounding satellite lesions that represent local “in transit” metastases.

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No d ular Me lan o m a • The lesion of a nodular melanoma arises de novo as a nodule or plaque (FIGS. 22.43–22.45). It occurs in 10% to 15% of patients. Because of a rapid vertical growth phase, lesions invade early. • Nodular melanoma lesions have the following characteristics: • They are blue, blue black, or nonpigmented (as in amelanotic melanoma); their color is more uniform than that of SSM. • They may ulcerate and bleed with minor trauma. • They occur most commonly on the legs and trunk. • They may be indistinguishable from a pyogenic granuloma (see FIG. 21.49).

22.45 Nodular melanoma. This crusted nodule was initially mistaken for an inflamed seborrheic keratosis. On biopsy the lesion had a Breslow’s measurement greater than 4 mm in depth.

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

Le n t ig o Malig n a an d Le n t ig o Malig n a Me lan o m a • Lentigo maligna (LM) is a type of lentigo that is found on the face of elderly patients with chronically sun-damaged skin. LM is considered to be a potential precursor to melanoma (FIG. 22.46). • LM lesions are characterized by: • A gradually enlarging tan to brown macule with irregular borders • Slow growth over 5 to 20 years • An irregular color and border • When an LM invades the dermis, it is then referred to as an LMM. The prognosis of LMM is similar to that of other subtypes of melanoma and is dependent on the thickness of the tumor (FIGS. 22.47 A and B). 22.46 Lentigo maligna. Note in the darker parts of this lesion the irregular border of this malignant melanoma in situ. Note similarity to solar lentigo (see FIG. 21.4).

A

B 22.47 A an d B Lentigo maligna melanoma. A: Biopsy of this pigmented lesion demonstrated invasion into the dermis. B: The same patient; note involvement of the nasal mucosa.

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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Acral Le n t ig in o us Me lan o m a • ALM is the least common subtype of melanoma. • These malignancies most often appear in blacks and Asians. • The lesions of ALM tend to occur on areas that do not bear hair, such as the palms, soles, and periungual skin (FIG. 22.49). • ALM has a tendency toward early metastasis (FIG. 22.49).

22.48 Acral lentiginous melanoma. Note the size and variegated pigmentation of this lesion. (Courtesy of Charles Miller, M.D., San Diego Naval Hospital.)

22.49 Acral lentiginous melanoma. A podiatrist who was treating the lesion as a wart referred this patient; the lesion did not resolve with destructive therapy. It was, in fact, a level V melanoma (melanoma cells were located in the subcutaneous tissue). (Courtesy of Art Huntley, M.D., University of California at Davis.)

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• A subungual ALM presenting as diffuse nail discoloration or a longitudinal pigmented band within the nail plate is potentially confused with subungual hematoma or junctional nevus. Pigment spread to the proximal or lateral nail folds (Hutchinson’s sign) is a hallmark of ALM (FIGS. 22.50 and 22.51).

22.50 Junctional nevus. This fairly common lesion may present a worrisome quandary (to biopsy or not to biopsy). Note the even, linear bands of pigmentation in this patient’s nail bed.

22.51 Acral lentiginous melanoma. Hutchinson’s sign shows uneven pigmentation spreading beyond the nail into surrounding skin.

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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MANAGEMENT

Wo rkup fo r Pat ie n t s wit h Me lan o m a • The most important aspects of the initial workup for patients with cutaneous melanoma are a careful history, review of systems, and physical examination. • Recently published data have shown that baseline and surveillance laboratory studies (e.g., lactate dehydrogenase level, liver function tests); chest radiography; and other imaging studies (e.g., computed tomography, positron emission tomography, bone scanning, magnetic resonance imaging) are not typically beneficial for patients without signs or symptoms of metastasis. Such routine tests have not proven to have efficacy in the detection of occult disease in asymptomatic patients with localized melanoma. • A metastatic workup should be initiated if physical findings or symptoms suggest disease recurrence or if the patient has documented nodal metastasis based on results from a SLNB. Sen t in el Lym p h No d e Bio p sy

• SLNB is a method used to detect the first lymph node draining from the site of a melanoma. • It is generally indicated for pathologic staging of the regional nodal basin(s) for primary tumors of at least 1 mm depth and when certain high-risk histologic features (e.g., ulceration, extensive regression) are present in thinner melanomas. • SLNB and lymphatic mapping indicate whether to perform regional lymphadenectomy (in the absence of clinically palpable nodes) in patients with thicker melanomas (1 mm or more in depth). • The probability of sentinel node positivity increases with increasing tumor thickness, from less than 1% for melanomas measuring 1 mm or smaller to as high as 36% for melanomas measuring 4 mm or larger. The ideal candidate for SLNB is the patient with a melanoma thicker than 1.0 mm without clinical or radiographic evidence of regional lymph node or distant metastases. • This minimally invasive procedure allows the pathologist to detect micrometastases. • A negative sentinel node obviates the need for further lymph node dissection.

• Technique • A technetium 99–labeled colloid (for the preoperative scanning) and a vital blue dye (for the intraoperative visualization) are injected around the area of the primary melanoma or biopsy scar (at the time of wide local excision/reexcision). • The sentinel node is thus identified and excised and examined for the presence of micrometastasis using both routine histology and immunohistochemistry. • Sentinel node status (positive or negative) is the most important prognostic factor for recurrence and is the most powerful predictor of survival in melanoma patients. • There is conflicting data and controversy about the value of SLNB for melanoma patients. While SLNB enhances metastatic staging for patients with deeper primaries and provides a more accurate determination of the patient’s prognosis, its positive therapeutic role has yet to be established. • If results are positive (i.e., metastatic), an elective lymph node dissection (ELND) is usually performed as a separate procedure at a later date. ELND is not recommended for lesions that are less than 1 mm thick unless lymph nodes are palpable. The decision about whether to perform ELND on thicker lesions (1 to 4 mm) is controversial. • Prophylactic lymph node dissection for primary cutaneous melanoma of intermediate thickness initially was believed to confer a survival advantage on patients with tumors of 1 to 4 mm in depth. Subsequent prospective randomized clinical trials have shown no survival benefit for elective lymphadenectomy for melanomas of varying thicknesses on the extremities and only marginal, if any, benefit for nonextremity melanomas. Su rgica l Trea t m en t

• Elliptic excision should include the entire visible lesion down to the subcutaneous fat. • Surgical margins of 5 mm are currently recommended for melanoma in situ. • For lesions with a thickness of less than 1 mm, a 1-cm margin of normal skin is usually adequate.

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MANAGEMENT Continued • Amputation, regional lymph node dissection, and regional chemotherapy perfusion are sometimes necessary for ALMs (FIGS. 22.52 and 22.53). • In more advanced stages of melanoma, chemotherapy and radiation therapy have not been very effective for achieving remission of metastatic disease.

22.52 Metastatic melanoma. Note the lymphedema and multiple metastatic nodules on this patient’s leg. The skin is the most common organ to which melanoma metastasizes.

• Vaccines, interleukin-2, and arterial limb perfusion are adjuncts to surgery. In fact, an injectable recombinant interferon-alpha 2B (Intron A) has been shown to improve the 5-year survival rate significantly in patients with thick lesions, lymph node involvement, or both.

Lo n g -Te rm Man ag e m e n t • Patients who have had melanoma should be followed every 3 months for the first 2 years and annually thereafter. • At each visit, the patient’s entire cutaneous surface and lymph nodes should be examined. • Patients with invasive disease require an annual chest radiograph, complete blood count, and liver function studies.

22.53 Metastatic melanoma. The unusual brown-blue coloration in this patient is the result of widespread melanin pigmentation in the tissues.

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POINTS TO REMEMBER • Sun protection should be stressed in those with a personal or family history of melanoma. The need to protect children (beginning at an early age) from excessive sun exposure should also be emphasized. • Anyone who has a history of melanoma needs lifelong skin surveillance, because 3% of these patients will develop a second melanoma within 3 years. • Patients should be taught self-examination. • Patients should be advised to have all first-degree relatives undergo a dermatologic examination to check for dysplastic nevi or melanoma. • Any lesion that looks suspicious must be examined by biopsy.

• An amelanotic melanoma is easily overlooked because of its lack of pigmentation. • Removal of thin lesions (less than 0.76 mm) is curative in almost all patients. • Early detection is the key to saving lives, because the treatments for metastatic melanoma are limited. Once a melanoma is metastatic, there is no uniformly effective adjuvant chemotherapy. • No definite proof of survival benefit has been found for performing SLNB versus a group of people who had similar melanomas but no SLNB. • Furthermore, there is no evidence to support the necessity of a complete lymph node dissection following a positive sentinel node section.

HELPFUL HINTS • Trauma from rubbing or irritation does not cause malignant degeneration of moles. • Total skin examination that includes the legs should be performed when evaluating a female patient for possible skin cancer. • To identify growing lesions, total body photographs allow for the assessment of existing and new lesions anywhere on the body. • The use of the “ugly duckling” sign, wherein skin examination is focused on recognition of a lesion that simply looks different from the rest, may assist with detection of lesions that lack the classic ABCDE criteria for melanoma.

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SEE PATIENT HANDOUT “Sun Pro t e ct io n Ad vice ” ON THE SOLUTION SITE

Pa get ’s Disea se o f t h e Brea st a n d Ex t ra m a m m a r y Pa get ’s Disea se BASICS Paget’s disease of the breast (PDB) and extramammary Paget’s disease (EMPD) are intraepidermal skin cancers that are often indicative of more severe underlying malignancies. Both diseases—particularly EMPD—can have a subtle, insidious course and tend to be ignored, misdiagnosed, or unrecognized by patients and clinicians alike. A high index of suspicion and prompt identification and treatment of these conditions can be lifesaving.

Paget’s Disease of th e Breast • PDB is a relatively uncommon clinical presentation of intraductal carcinoma of the breast. It occurs almost exclusively in postmenopausal women; men are rarely affected. PDB accounts for 1% to 4% of breast cancers. Invariably, the PDB lesion is associated with an intraductal carcinoma of the underlying mammary gland. • In more than half of the cases, there is no associated palpable breast mass, and mammography results are often normal. Patients with PDB are, on average, 5 to 10 years older than patients with the more common types of breast carcinoma. It is not unusual for PDB patients to remain undiagnosed and untreated for a prolonged period because the PDB lesion is usually insidious and slow growing, and it is often asymptomatic. Furthermore, PDB is often mistakenly diagnosed as a chronic eczematous condition. • Not infrequently, an elderly patient may be too embarrassed to mention the lesion to her family or clinician, thereby further delaying diagnosis and treatment.

22.54 Paget’s disease of the breast. This patient had had an eczemalike lesion of the nipple, areola, and surrounding skin for several years. On biopsy, the patient was found to have an infiltrating ductal carcinoma of the underlying breast tissue. (Courtesy of Michael Fisher, M.D., of the Albert Einstein College of Medicine, Bronx, New York.)

Pat h o p h ysio lo g y • PDB is an underlying intraductal carcinoma of the breast, with retrograde extension into the overlying epidermis through mammary duct epithelium. • The epidermis becomes infiltrated with characteristic Paget’s cells that cause thickening of the nipple and the areolar skin. CLINICAL MANIFESTATIONS BASICS • Patients with PDB often present with a chronic unilateral rash on the nipple, areola, or surrounding skin; less commonly, the lesion originates and remains on the nipple. • Typically, the lesion appears as a sharply marginated red plaque with an irregular border and eczemalike appearance (FIG. 22.54). • When the nipple is involved, it may become scaly, crusted, have a bloody nipple discharge, become deformed, or retracted (FIG. 22.55).

22.55 Paget’s disease of the breast. Here the nipple and areola are involved. The process began insidiously in one nipple. Note the bloody nipple discharge, which stained the clothing and bras of this patient before she sought treatment. (Courtesy of Michael Fisher, M.D., of the Albert Einstein College of Medicine, Bronx, New York).

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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DIAGNOSIS • Punch, wedge, or excisional biopsy of the lesional skin of the nipple-areola complex, including the dermal and subcutaneous tissue for microscopic examination, is performed for the accurate diagnosis of PDB.

DIFFERENTIAL DIAGNOSIS

At o p ic De rm at it is • In addition to various unusual neoplasms, atopic dermatitis of the nipples and areolae should be included in the differential diagnosis. • Atopic dermatitis often presents bilaterally (FIG. 22.56), but it may present unilaterally. • Atopic dermatitis occurs in association with a personal or family history of atopy (see Chapter 2, “Eczema”). It should respond rapidly to topical corticosteroid therapy.

22.56 Atopic dermatitis on the nipples and areolae (bilateral). Note the obliteration of the margins of the nipples and areolae, as well as the oozing and fissuring of the left breast. These lesions responded readily to topical corticosteroids.

Extram am m ary Paget’s Disease • EMPD is a rare condition that is similar to PDB; the primary difference is the anatomic location. EMPD targets the genital skin, perianal skin, and other cutaneous sites rich in apocrine glands. • Histologic features of PDB and EMPD disease are similar. • EMPD is four to five times more likely to occur in women than in men. The condition most commonly appears in patients ages 50 to 60.

Pat h o p h ysio lo g y • EMPD arises as a primary cutaneous adenocarcinoma in most cases. The epidermis becomes infiltrated with characteristic Paget’s cells—neoplastic cells that show glandular differentiation. 22.57 Extramammary Paget’s disease. This pruritic eczematous plaque had been present for many years. Biopsy confirmed EMPD. Initially, treatment consisted of both antifungals and topical steroids, with no resolution. Not only is this condition rare, it is especially rare in men.

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CLINICAL MANIFESTATIONS • The initial lesion may present as a unilateral, erythematous, sharply marginated, eczema-simulating, slow-growing plaque that may be indistinguishable from PDB (FIG. 22.57).

Part One • Com m on Skin Conditions: Diagnosis and Manag em ent

• Not infrequently, lesions may be ill-defined and resemble eczema, intertrigo, tinea cruris, candidiasis, and other conditions (see “Differential Diagnosis” section). • EMPD has usually been present for a long time before biopsy is performed to confirm the diagnosis (see FIG. 22.58). • Some, but not all, cases of EMPD are associated with an underlying adenocarcinoma.

DIFFERENTIAL DIAGNOSIS • The differential diagnosis of EMPD is more extensive than that of PDB, and EMPD may simulate many neoplastic and inflammatory conditions before the diagnosis is made.

DIAGNOSIS • The diagnosis of EMPD requires a high degree of clinical suspicion, followed by skin biopsy with pathologic correlation.

MANAGEMENT • It is beyond the scope of this discussion to describe the therapies for breast cancer. • However, as in other types of confirmed breast carcinoma, treatment of PDB can include surgery, radiation therapy, chemotherapy, and hormonal treatment as indicated.

• Mastectomy (radical or modified) and lymph node clearance are appropriate for patients with PDB who have a palpable mass and underlying invasive breast carcinoma. • Because EMPD often extends beyond the visibly involved clinical margins, a wide, controlled surgical excision of all the involved epidermis is the most effective treatment.

POINTS TO REMEMBER • PDB is uncommon and unilateral, whereas eczematous dermatitis of the nipples is common and tends to present bilaterally. • Any unilateral, chronic eczematous lesion of the breast or nipple (“nipple eczema”) that is unresponsive to topical corticosteroid therapy should be biopsied. • EMPD is a rare disorder that is easily overlooked, but it must be considered in the differential diagnosis of patients with chronic genital or perianal dermatitis. • PDB and EMPD closely resemble eczema. It is important to consider PDB or EMPD among patients in whom supposed eczema of the breast or perineum does not clear with appropriate therapy.

Chap ter 22 • Prem alignant and Malig nant Skin Neoplasm s

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P ART T W O

System ic Con dition s an d th e Skin

C H AP T ER

23

Skin and Hair During Pregnancy

OVERVIEW During pregnancy, various skin changes occur. Many of these changes are seen so frequently that they are considered normal. Pregnancy can also alter the course of certain preexisting skin conditions or systemic diseases that have cutaneous involvement, for example: • Systemic lupus erythematosus and scleroderma may flare. • Acne may improve, or it may worsen. • Dyshidrotic eczema may appear de novo, or a flare-up of preexisting lesions may occur. • Condylomata acuminatum may enlarge considerably and may proliferate. However, it should always be kept in mind that many common skin diseases unrelated to pregnancy should be considered when evaluating a pregnant patient with a skin disorder.

HYPERPIGMENTATION • Linea nigra CONNECTIVE TISSUE CHANGES • Striae gravidarum • Keloids VASCULAR PHENOMENA • Spider telangiectasias • Palm ar erythem a HAIR CHANGES • Telogen effluvium • Hirsutism OTHER FINDINGS • Pregnancy gingivitis • Pyogenic granulom as • Erythem a nodosum SPECIFIC DERMATOSES OF PREGNANCY • • • •

Pruritic urticarial papules and plaques of pregnancy Pruritus gravidarum Recurrent cholestasis of pregnancy Pem phigoid gestationis OTHER CONDITIONS

• Pruritic folliculitis of pregnancy • Im petigo herpetiform is

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Freq u en t ly Seen Sk in Ch a n ges Th a t Are Co n sid ered No r m a l • Melasma (for a more complete discussion, see Chapter 14, “Pigmentary Disorders”). The “mask of pregnancy” (formerly known as chloasma) occurs in more than 50% of women. It is worsened by exposure to the sun. Melasma is also seen in women taking oral contraceptives and, on occasion, de novo in women in whom no explanation is obvious. • Darkening of preexisting freckles and nevi.

HELPFUL HINT • Pregnancy does not appear to affect survival adversely in women who have preexisting malignant melanoma. 23.1 Linea nigra and striae gravidarum. The linea alba darkens during pregnancy, but the normal color usually returns after delivery. In contrast, although the purplish color of striae gravidarum fades over time, the striae themselves are permanent.

MANAGEMENT • For patients with melasma caused by pregnancy, it is usually best to keep sun exposure to a minimum and to wait for fading, which often takes place spontaneously. Treatment of persistent nongestational melasma consists of diligent sun avoidance and, frequently, the use of skin bleaching creams (see Chapter 14, “Pigmentary Disorders”). • Darkened freckles, nevi, and linea nigra usually regress postpartum.

Con n ective Tissu e Ch an ges • Striae gravidarum (striae cutis distensae related to pregnancy) or “stretch marks.” It is thought that these are caused by the combination of increased adrenocortical activity and rapid tissue growth and distension, which result in tearing of the collagen matrix of the dermis and a weakness of elastic fibers. Typically, striae are reddish pink to violaceous, linear, atrophic bands that are located on the abdomen, hips, buttocks, and breasts. The striae are permanent, but the purplish color fades with time. • Proliferation and enlargement of skin tags, with some persisting after pregnancy. • Occasional growth of preexisting keloids. For example, this may occur in the scars of an abdominal hysterectomy or a cesarean section (FIG. 23.2). Growth of preexisting keloids is a not-uncommon problem in women of African descent.

Hyp erp igm en tation MANAGEMENT Hyperpigmentation is presumed to be secondary to increased levels of estrogens and melanocyte-stimulating hormone. It frequently manifests as follows: • Darkening of the linea alba (which becomes the linea nigra). There may also be darkening of the nipples and surrounding areolae, as well as darkening of the axillae, thighs, umbilicus, perineum, and external genitalia (FIG. 23.1).

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• There is no proven effective treatment for striae. • If desired, skin tags may be easily removed (see Chapter 21, “Benign Skin Neoplasms”). • Keloids may diminish in size postpartum; if they do not, treatment with intralesional steroids may be helpful (see Chapter 21, “Benign Skin Neoplasms”).

23.2 Keloids. These lesions are growing well beyond the border of the cesarean section scar.

Vascu lar Ph en om en a • Spider telangiectasias. These can result from the high levels of estrogen in pregnancy (FIG. 23.3). • Scattered petechiae in the lower extremities. These are the result of increased capillary fragility and increased hydrostatic pressure in this region. • Palmar erythema, flushing, and increased sweating (FIG. 23.4) • Venous varicosities of the legs and feet • Hemorrhoids • Edema of the leg, face, or eyelids

MANAGEMENT

23.3 Spider telangiectasias. These can result from the high levels of estrogens in pregnancy.

• Most vascular phenomena resolve postpartum. However, varicosities may persist and may worsen with additional pregnancies.

Hair Ch an ges • Telogen effluvium. Hair loss may occur from 1 to 5 months postpartum and is generally followed by total regrowth. Rarely, the regrowth may not be as thick as prepregnancy hair growth. (See Chapter 10, “Hair and Scalp Disorders Resulting in Hair Loss.”) • Hirsutism. Mild degrees of hirsutism are common. The face is frequently affected, although hair growth may be pronounced on the extremities as well. Hirsutism normally regresses after delivery, but it may recur in subsequent pregnancies. (See Chapter 11, “Hirsutism.”)

23.4 Palmar erythema. Flushing and increased sweating may also occur during pregnancy.

Chap ter 23 • Skin and Hair During Pregnancy

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MANAGEMENT • Because both telogen effluvium and hirsutism usually resolve spontaneously, no specific management is needed. However, excessive hirsutism warrants investigation for an endocrinologic abnormality.

Oth er Fin d in gs Skin conditions during pregnancy can also include the following: 23.5 Pyogenic granuloma. Lesions tend to occur on the lips and gums.

• Increased nail fragility and brittleness and distal separation of the nail plate (onycholysis) may occur. • Edema and hyperemia of the gums (“pregnancy gingivitis”) have been noted. • Pyogenic granulomas often develop on the lips and gums and usually regress shortly postpartum (FIG. 23.5). • Erythema nodosum, an apparently autoimmune skin condition, is usually associated with infections, sarcoidosis, malignant diseases, and drugs, but it can also be precipitated by pregnancy alone (FIG. 23.6). • Erythema multiforme has a variety of causes, including pregnancy.

MANAGEMENT

Pre g n an cy Gin g ivit is • Good dental hygiene (adequate brushing and flossing) is essential, because the problem is exacerbated by plaque and calculus.

23.6 Erythema nodosum. These tender nodules occurred during pregnancy and resolved postpartum.

Pyo g e n ic Gran ulo m as • Treatment may be deferred until after delivery or performed during pregnancy, if necessary. Options include cryodestruction, electrodesiccation, and excisional surgery (see Chapter 21, “Benign Skin Neoplasms”). Eryt h e m a No d o sum • Erythema nodosum tends to clear postpartum and to recur in subsequent pregnancies. Treatment is with bed rest and mild analgesics. Eryt h e m a Mult ifo rm e • Like erythema nodosum, erythema multiforme resulting from pregnancy tends to clear spontaneously and is managed symptomatically. Underlying causes other than pregnancy (e.g., infection) should be sought and treated.

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Sp ecifi c Der m a t o ses o f Pregn a n cy BASICS The specific dermatoses of pregnancy are a group of cutaneous eruptions that are unique to pregnancy. Historically, these eruptions have been variously classified, resulting in overlapping and confusing terminology. The following discussion should help to simplify the approach to these entities.

Pru ritic Urticarial Pap u les an d Plaq u es of Pregn an cy • A common dermatosis of late pregnancy, pruritic urticarial papules and plaques of pregnancy (PUPPP), is, as its name suggests, a pruritic eruption consisting of urticarial papules that coalesce into plaques (FIG. 23.7). Initially, the papules are found in the striae cutis distensae (i.e., stretch marks) of the abdomen, and they generally spare the area surrounding the umbilicus. Later, they can be found on the thighs and buttocks, where they coalesce to form plaques. PUPPP tends to spare the face, palms, soles, and mucous membranes. • The itching, which can become quite intense, generally begins in the last few weeks of the third trimester of pregnancy. It can be sufficiently discomforting to require potent topical—and sometimes oral—corticosteroids. • The natural history of PUPPP is, in most cases, spontaneous resolution within a few days of delivery. It does not appear to increase infant morbidity. Recurrences in subsequent pregnancies are unlikely, and if they do take place, they tend to be less severe. • Some dermatologists broaden the clinical description of PUPPP to include the following: • A rash resembling that of a drug eruption • A targetlike rash that resembles erythema multiforme • A vesicular eruption

23.7 Pruritic urticarial papules and plaques of pregnancy. Lesions are located in the stretch marks. Note the periumbilical sparing.

These dermatologists thus suggest that PUPPP be renamed “polymorphic eruption of pregnancy.”

Pru ritu s Gravid aru m • This condition, characterized by common, benign, generalized itching, begins in the later stages of pregnancy. • The patient’s complaints often seem to be out of proportion to the visible changes on the skin. There are no primary skin lesions, and the condition clears after delivery. • Pruritus gravidarum is considered by some investigators to be possibly a variation of PUPPP without lesions. • Management of pruritus gravidarum is aimed at symptomatic control of pruritus with the use of bland emollients and topical antipruritic agents. Oral antihistamines are sometimes effective.

Chap ter 23 • Skin and Hair During Pregnancy

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Recu rren t Ch olestasis of Pregn an cy

Pem p h igoid Gestation is

• Also known as intrahepatic cholestasis of pregnancy, recurrent cholestasis of pregnancy is a rare form of reversible cholestasis that appears in the second half of pregnancy. It generally occurs during the second or third trimester of pregnancy, although onset in the first trimester has also been reported. • This condition is caused by hyperbilirubinemia and bile acid accumulation in the skin. • It initially manifests as severe, generalized pruritus followed by the clinical appearance of jaundice. The degree of itching correlates with levels of serum and skin bile acid. There are no primary skin lesions; however, excoriations may result from the patient’s scratching. • The condition clears after delivery but may recur in future pregnancies. The incidence of premature birth, intrapartal fetal distress, stillbirth, and low birth weight appears to be increased in the children of affected women. • Ideally, treatment should be directed to decrease maternal bile acid levels; however, traditionally, symptomatic therapy including bland emollients, cholestyramine resins, topical antipruritic agents and, sometimes, oral antihistamines, has been used. • Recently, oral ursodeoxycholic acid, directed to decrease serum bile acid levels and dosed at 15 mg/kg/day, has been reported to be effective in improving fetal prognosis.

• Pemphigoid gestationis, previously known as herpes gestationis, is a rare, intensely pruritic vesicobullous autoimmune dermatitis that may be clinically confused with PUPPP. The term “herpes” derives from the grouped herpetiform clustering of blisters that sometimes occurs; there is no relation to herpesvirus infection. • The skin lesions of pemphigoid gestationis are polymorphic, ranging from urticarial papules or plaques to bullae that are small and vesicular or large and tense (FIG. 23.8). • Lesions tend to appear in the second or third trimester. • The diagnosis can be confirmed by direct immunofluorescent testing of the skin. • Treatment generally requires systemic corticosteroids in gradually tapered doses. In mild cases, topical cortico steroids and oral antihistamines may be sufficient. • Some reports have suggested that women with pemphigoid gestationis may have an increased risk of fetal morbidity and mortality, as well as an increased chance of giving birth prematurely and of having an infant with a lower birth weight; however, the extent, if any, of this increased risk remains controversial. Rarely, a neonate may develop transient blisters. • Postpartum flares are common. Symptoms may recur with menses or with administration of oral contraceptives; these findings suggest that hormonal factors play a strong role. • Pemphigoid gestationis often recurs in subsequent pregnancies, with earlier and more florid consequences; however, it has been known to skip an ensuing pregnancy.

Oth er Con d ition s • Pruritic folliculitis of pregnancy manifests as a papular, acnelike eruption. Some dermatologists consider this condition a variant of acne. • Impetigo herpetiformis, an extremely rare dermatosis, is considered a form of generalized pustular psoriasis.

23.8 Pemphigoid gestationis. This pregnant woman has multiple pus-filled sterile vesicles and bullae.

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C H AP T ER

24

Cutaneous Manifestations of HIV Infection Mary Ruth Buchness

OVERVIEW • The first organ that may be affected in human immunodeficiency virus (HIV) infection is the skin. Before the advent of highly active antiretroviral therapy (HAART), the inevitable decrease in CD4 cells with disease progression was accompanied by a variety of HIV-associated skin diseases. HIV infection was often suspected initially based on the occurrence of cutaneous diseases, such as Kaposi’s sarcoma (KS) or severe molluscum contagiosum, or in a patient with particularly severe or recalcitrant manifestations of a common skin disease, such as psoriasis. • With the use of HAART, the number and frequency of cutaneous manifestations have plummeted in the United States and other countries. Furthermore, in patients with advanced HIV infection, the cutaneous manifestations often remit spontaneously when HAART is started. Nonetheless, some patients have viral resistance to these drugs or personal or economic reasons for not taking HIV medications, and in this group, the severe cutaneous manifestations of advanced HIV infection may still be seen. • Acute HIV infection is characterized by a morbilliform rash resembling measles, and fever, lymphadenopathy, sore throat, and malaise may accompany the eruption. • As the number of CD4 cells decreases to fewer than 200/mm3 during the course of infection, signaling the onset of acquired immunodeficiency syndrome (AIDS), skin manifestations become more severe and increase in number.

HIV-ASSOCIATED HERPES SIMPLEX HIV-ASSOCIATED HERPES ZOSTER HIV-ASSOCIATED MOLLUSCUM CONTAGIOSUM HIV-ASSOCIATED CONDYLOMA ACUMINATUM HIV-ASSOCIATED (EPIDEMIC) KAPOSI’S SARCOMA HIV-ASSOCIATED BACILLARY ANGIOMATOSIS HIV-ASSOCIATED SYPHILIS HIV-ASSOCIATED NORWEGIAN SCABIES HIV-ASSOCIATED EOSINOPHILIC FOLLICULITIS HIV-ASSOCIATED ORAL HAIRY LEUKOPLAKIA HIV-ASSOCIATED ORAL CANDIDIASIS HIV-ASSOCIATED APHTHOUS ULCERS HIV-ASSOCIATED DRUG ERUPTIONS HIV-ASSOCIATED PRURITUS HIV-ASSOCIATED SEBORRHEIC DERMATITIS HIV-ASSOCIATED PSORIASIS HIV-ASSOCIATED LIPOATROPHY

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H IV-Asso cia t ed H erp es Sim p lex BASICS • In the immunocompromised host, the clinical manifestations and course of herpes simplex virus (HSV) infection differ in patients with defective cell-mediated immunity, as seen in HIV infection. (See Chapter 6, “Superficial Viral Infections,” and Chapter 19, “Sexually Transmitted Diseases,” for a full discussion of HSV infections in immunocompetent hosts.) • Recurrent lesions may affect mucous membranes and possibly become chronic, centrifugally expanding ulcerations. These ulcerations last 1 month or more in an HIV-positive patient and are an AIDS-defining diagnosis. • Lesions may become resistant to acyclovir, or they may develop into chronic keratotic papules. Because acyclovir resistance is associated with prior treatment of suboptimal doses, it is important not to undertreat HIV-positive patients who also have HSV infections. DESCRIPTION OF LESIONS

24.1 Herpes simplex. Shown here is HIV-associated chronic ulcerated herpes simplex that is resistant to acyclovir. This patient is receiving intravenous foscarnet.

24.2 Herpes simplex. Mucosal papules are present in this patient with AIDS.

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• Initially, there are the typical grouped vesicles on an erythematous base, which evolve into pustules, erosions, and crusts. • Ultimately, the following lesions may occur: • Chronic digital ulcerations (FIG. 24.1) • Mucosal erosions or papules (FIG. 24.2) • Centrifugally expanding ulcerations with scalloped borders • Keratotic or wartlike papules or plaques (FIG. 24.3)

24.3

Herpes simplex. Crusted, wartlike papules are noted.

DISTRIBUTION OF LESIONS • Intraoral areas, including the tongue, buccal mucosa, palate, and gingivae may be involved. • Chronic ulcerative lesions may appear in perianal areas. These lesions can extend into the intergluteal cleft (FIG. 24.4). • Keratotic lesions may occur in any location. CLINICAL MANIFESTATIONS • Lesions may be more severe and more extensive than in immunocompetent hosts. • Severe or chronic erosions, ulcerations, or keratotic lesions should alert the clinician to the presence of advanced immunosuppression.

24.4 Herpes simplex. Chronic ulcerated lesions and scattered intact vesicles are present in a patient with AIDS.

DIAGNOSIS • See Chapter 6, “Superficial Viral Infections,” and Chapter 19, “Sexually Transmitted Diseases,” for more detailed discussions.

DIFFERENTIAL DIAGNOSIS

He rp e s Zo st e r • Lesions of herpes zoster may involve only part of a dermatome and may be clinically indistinguishable from HSV lesions. • When in doubt, sufficient doses of antiviral medications are recommended for herpes zoster infection. Underdosing must be avoided. De cub it us Ulce r • These lesions affect bony prominences in debilitated patients and do not extend to the intergluteal cleft.

• In the keratotic type of cytomegalovirus infection, disseminated infection is associated with retinal findings, so an ophthalmologic examination is essential.

Disse m in at e d Mycoba cterium a vium-intra cellula re Co m p le x • Patients may have oral ulcerations. • This infection is associated with severe systemic disease and fever in HIV-infected patients. Disse m in at e d Hist o p lasm o sis • Patients may have oral and cutaneous ulcerations. • Disseminated histoplasmosis is associated with systemic disease.

Cut an e o us Cyt o m e g alo virus In fe ct io n • In cytomegalovirus infection, perianal ulcers develop as an extension of gastrointestinal involvement. Skin biopsy shows characteristic viral inclusion bodies.

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POINTS TO REMEMBER MANAGEMENT • If the patient has malabsorption or if lesions do not respond to other treatment, acyclovir (5 to 10 mg/kg every 8 hours) is infused over 1 hour. The dosage interval should be increased in patients with renal failure. • Failure to respond to intravenous acyclovir indicates acyclovir resistance. • Acyclovir resistance can be prevented by avoiding undertreatment and intermittent treatment. • Foscarnet (40 mg/kg intravenously every 8 hours) is used in acyclovir-resistant patients. • Strains that recur after treatment with foscarnet are usually acyclovir sensitive.

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• Long-term suppressive therapy with acyclovir has been associated with acyclovir resistance. • Treatment should continue until clinical lesions resolve completely. • Clinicians should be careful not to underdose with antiviral agents.

H IV-Asso cia t ed H erp es Zo st er BASICS • Herpes zoster is most common in elderly patients and in immunocompromised persons, although it may occur in anyone who has a history of chickenpox. • See Chapter 6, “Superficial Viral Infections,” for a more detailed discussion. DESCRIPTION OF LESIONS • Grouped vesicles or bullae on an erythematous base affect all or part of a dermatome. • Lesions evolve into pustules and crusts and may erode. Chronic ulcerations and crusted or verrucous lesions may occur. • Severe scarring may result (FIG. 24.5).

24.5 Herpes zoster. This patient developed severe scarring from his infection.

DISTRIBUTION OF LESIONS • Any dermatome can be affected. • Disseminated herpes zoster virus may occur. • Occasional dissemination may lead to 25 or more lesions outside of the primary and two contiguous dermatomes (FIG. 24.6). • The disease usually begins with typical dermatomal herpes zoster virus that becomes widespread and chronic. • The eruption may be indistinguishable from varicella. CLINICAL MANIFESTATIONS • Prodromal symptoms of pain and itching may be severe enough to lead to a suspicion of serious illness. For example, the prodromal pain of thoracic zoster has led to critical care unit admission to rule out myocardial infarction. • Regional adenopathy may occur. • Varicella pneumonia may develop. • Cutaneous lesions may become chronic in patients with AIDS.

24.6 Disseminated herpes zoster. Note the initial dermatomal involvement on the buttock. (Courtesy of Herbert A. Hochman, M.D.)

POINTS TO REMEMBER MANAGEMENT • Intravenous acyclovir (10 mg/kg every 8 hours) is given for 10 to 14 days. • Dosage intervals are increased in patients with renal failure. • If lesions improve but persist beyond 10 to 14 days, treatment is continued until all lesions resolve. • If lesions fail to resolve, the virus may be resistant to acyclovir. • Acyclovir-resistant varicella-zoster virus infection responds to foscarnet (40 mg/kg every 8 hours until lesions resolve).

• Undertreatment may lead to viral resistance. • Patients with herpes zoster can transmit the virus as chickenpox to nonimmune persons.

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H IV-Asso cia t ed Mo llu scu m Co n t a gio su m BASICS • Molluscum contagiosum is caused by a poxvirus; the condition is most commonly seen in immunocompetent children and less commonly in healthy adults. • Multiple and extensive facial lesions, as well as lesions with atypical morphology, should alert the practitioner to the possibility of HIV infection. • See Chapter 6, “Superficial Viral Infections,” for further discussion. DESCRIPTION OF LESIONS

24.7 Molluscum contagiosum. This patient has “giant” molluscum lesions on his arm.

• Papules may be dome-shaped or, more commonly, are atypical in appearance. • Size may be up to, or greater than, 1 cm (giant molluscum contagiosum). • Lesions may lack central umbilication or may have several umbilications. • Lesions on hairy areas tend to penetrate hair follicles. • Lesions may be extensive (hundreds to thousands in number) in patients with advanced AIDS. • Patients receiving HAART tend to have rare molluscum, with the more typical morphology seen in immunocompetent hosts. • The appearance of new lesions may follow a downward fluctuation in immunity caused by a concurrent infection, such as influenza. DISTRIBUTION OF LESIONS

24.8 Molluscum contagiosum. This HIV-positive patient has a large molluscum contagiosum lesion on the shaft of his penis as well as other scattered smaller lesions. Also note onychomycosis of his thumbnail, which is another sign of immunodeficiency.

• All areas of the body may be affected (FIG. 24.7), but lesions are most common on the face and genitals (FIG. 24.8). • In men, possible extensive involvement of the beard area may result from shaving (see FIG. 6.18). CLINICAL MANIFESTATIONS • There is occasional tenderness or inflammation. • Lesions are often a great cosmetic concern to patients.

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DIFFERENTIAL DIAGNOSIS

Disse m in at e d Cryp t o co cco sis • Cutaneous lesions may be clinically identical to those of molluscum contagiosum (FIG. 24.9). • Affected patients are usually systemically ill, although cutaneous involvement may be the first sign of illness. • Crush preparation with India ink shows encapsulated yeast. • When in doubt, biopsy can be used to identify the lesions. • Patients with cutaneous dissemination have neurologic involvement, and a faster diagnosis can be made by cerebrospinal fluid examination. Disse m in at e d Hist o p lasm o sis • This is a less common cause of molluscum contagiosum–like lesions than cryptococcosis. • Cutaneous histoplasmosis is always indicative of systemic infection.

24.9 Disseminated cryptococcosis. Note the resemblance of these papules to those of molluscum contagiosum.

POINT TO REMEMBER MANAGEMENT • Treatment is individualized for each patient. No specific treatment is universally more effective than any other. • Topical tretinoin is a useful adjunctive treatment in cases of molluscum contagiosum of the beard. • Surgical treatment is with curettage or liquid nitrogen cryosurgery. • Trichloroacetic acid 25% to 75% may be applied to individual lesions. • Podofilox (Condylox) 5% may be applied to lesions twice per day, 3 days per week. • Imiquimod 5% (Aldara) cream may be effective and should be used daily if possible. • Treatment is long term and is unlikely to eradicate all lesions unless the patient’s immunity improves. Lesions may remit spontaneously after the patient is started on HAART, and knowledge of this fact will sometimes persuade a reluctant patient to begin treatment for HIV infection.

• Cutaneous lesions of disseminated cryptococcosis and histoplasmosis may look identical to lesions of molluscum contagiosum.

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H IV-Asso cia t ed Co n d ylo m a Acu m in a t u m See also Chapter 19, “Sexually Transmitted Diseases.” DIFFERENTIAL DIAGNOSIS BASICS • Ninety percent of HIV-infected men have anal human papillomavirus (HPV) infection. • Of the many subtypes of HPV, the most common subtype is the oncogenic subtype HPV 16. • Seventy-three percent of HIV-infected men with HPV have multiple subtypes. • The increasing rate of anal cancer that has been seen in the United States over the past three decades is a result of the increasing rate of infection with HIV and HPV. • More than half of HIV-infected men with anal condyloma develop anal intraepithelial neoplasia (AIN). HIV-infected patients with AIN are more likely to develop invasive cancer than nonimmunocompromised patients. Estimated time to progression from AIN to invasive cancer is 10 to 20 years. • There have been fewer studies of HIV-infected women, but it is known that 49% of HIV-infected women have latent cervical HPV infection, with high oncogenic risk types, persistent infection, and an increased risk of cervical dysplasia and cancer. DESCRIPTION OF LESIONS • Four morphologic types of anogenital condyloma acuminata have been described. • The verrucous type is associated with coinfection with at least four subtypes, including HPV 16. These patients are at high risk for the development of high-grade AIN. • In the leukoplakic type, a majority of patients have HPV 16, but with fewer numbers of coinfecting subtypes and a lower risk of high-grade AIN. • The other types are erythroplakic (erythematous, possibly erosive) and bowenoid (flat, tan plaques).

Carcin o m a (Sq uam o us Ce ll Carcin o m a) • This is the most important diagnosis to exclude. This can only be done by skin biopsy of atypical lesions or of an atypical area within a lesion. In flam m at o ry Co n d it io n s • Atypical, nonverrucous lesions may be confused with an inflammatory dermatosis such as perianal psoriasis, lichen planus, or lichen simplex chronicus. • For a detailed discussion of the differential diagnosis of condyloma acuminatum, refer to Chapter 19, “Sexually Transmitted Diseases.”

MANAGEMENT • The treatment of condyloma acuminata in HIVpositive patients is the same as that in HIV-negative patients. However, condyloma acuminata are difficult to eradicate because intact cellular immunity is necessary to clear the skin of viral lesions. See Chapter 19, “Sexually Transmitted Diseases,” for treatment information. • Some experts advocate anal cytology smears in HIVinfected patients with anogenital HPV. This is not currently recommended by the U.S. Centers for Disease Control because the rate of progression of AIN to invasive cancer, the reliability of the screening method, and the safety and effectiveness of treatment for AIN are all unknown.

DISTRIBUTION OF LESIONS • Lesions may occur anywhere on the anogenital skin. • Lesions may also occur on the vaginal or rectal mucous membranes. Rectal condylomata may be a cause of recurrent anal condyloma, and affected patients should be referred for evaluation by a rectal surgeon. • In addition, lesions may appear on the skin at the angles of the mouth or on the intraoral membranes. DIAGNOSIS • Diagnosis is made on clinical grounds. • Lesions that appear to be atypical (e.g., with ulcerations), that fail to respond to several treatments, or that grow in spite of treatment should be biopsied to evaluate for malignant degeneration.

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POINTS TO REMEMBER • Condyloma acuminata in HIV-infected patients are often caused by oncogenic subtypes of HPV, and lesions may undergo malignant degeneration. • Condylomata that appear to be clinically atypical, do not respond to treatment, or enlarge in spite of treatment should be biopsied to evaluate for malignant degeneration.

H IV-Asso cia t ed (Ep id em ic) Ka p o si’s Sa rco m a BASICS • Epidemic KS is an AIDS-defining diagnosis. • Because it is found almost exclusively in men who have had homosexual contact, KS is thought to be sexually transmitted. • KS is exceedingly rare in women, and women with KS are presumed to have had sexual contact with bisexual men. • KS is associated with infection with human herpesvirus 8 (HHV-8), which has been detected in saliva and in semen of affected patients. • Lesions may resolve spontaneously as immunity improves. A similar phenomenon has been observed in immunocompromised renal transplant recipients. DESCRIPTION OF LESIONS • Violaceous macules, papules, or nodules occur (FIGS. 24.10 and 24.11). • Limb edema with subtle violaceous discoloration of the skin may be present.

24.10 Epidemic Kaposi’s sarcoma. Note the resemblance to the lesions of bacillary angiomatosis in FIGURE 24.12.

DISTRIBUTION OF LESIONS • Lesions are most common acrally, on the nose, penis, and extremities. • Mucous membranes may be affected. • Lesions may be disseminated in advanced HIV infection. CLINICAL MANIFESTATIONS • Most commonly, lesions are asymptomatic. • Edema occurs with lymphatic involvement, usually in the extremities, but sometimes it affects the face. • Oral lesions can cause pain, difficulty with eating, and loss of teeth.

DIFFERENTIAL DIAGNOSIS • Pyogenic granuloma • Bacillary angiomatosis • Disseminated M. avium-intracellulare complex (see earlier discussion)

24.11 Epidemic Kaposi’s sarcoma. Multiple papules and nodules are present on this patient’s leg.

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POINTS TO REMEMBER MANAGEMENT • All forms of KS regress spontaneously with successful treatment of immunodeficiency with HAART.

Disse m in at e d Cut an e o us Kap o si’s Sarco m a • Disseminated involvement that does not regress with HAART requires systemic chemotherapy. Lym p h an g it ic Kap o si’s Sarco m a • Lymphatic involvement that does not respond to HAART requires systemic chemotherapy. • Intermittent sequential compression boots can be used to decrease edema and to increase the comfort level of the patient. Lo calize d Cut an e o us o r Muco sal Kap o si’s Sarco m a • Radiation therapy is used, particularly for facial lesions. • Intralesional vinblastine is given in doses of 0.1 to 0.6 mg/mL. • Liquid nitrogen cryosurgery is used for macular lesions. • A retinoid gel, alitretinoin (Panretin), applied three to four times daily as tolerated, is useful for macular lesions.

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• KS in an HIV-infected patient is an AIDS-defining diagnosis. • Treatment of individual lesions does not prevent the occurrence of new lesions. • Lesions may resolve spontaneously in patients receiving effective antiretroviral therapy, so it is beneficial to delay surgical treatment until the patient has been receiving HAART for several months.

H IV-Asso cia t ed Ba cilla r y An gio m a t o sis BASICS • Bacillary angiomatosis, which was first reported in 1983, is seen almost exclusively in HIV-positive patients with advanced disease. Cases have been extremely rare in recent years. • Bacillary angiomatosis is caused by the bacilli Bartonella henselae and B. quintana. • Bacillary angiomatosis is a systemic infection, and lesions have been described in nearly every organ of the body. • Untreated bacillary angiomatosis can be fatal. DESCRIPTION OF LESIONS • Lesions may occur as erythematous, dome-shaped papules and nodules (FIG. 24.12); they can also be flatter, violaceous lesions; subcutaneous nodules; or rarely, necrotic tumors.

24.12 Bacillary angiomatosis. Dome-shaped papules and nodules are present.

DISTRIBUTION OF LESIONS • Bacillary angiomatosis can occur on any location of the skin or internally. CLINICAL MANIFESTATIONS • There may be associated fever. • Untreated lesions can lead to respiratory obstruction, gastrointestinal bleeding, and local or systemic infection. • Deaths have been reported from laryngeal obstruction and disseminated intravascular coagulopathy. DIAGNOSIS • Skin biopsy shows a lesion resembling pyogenic granuloma, with characteristic clusters of bacilli. • Culture is available only in research centers.

DIFFERENTIAL DIAGNOSIS • Pyogenic granuloma (see FIG. 21.49) may be clinically identical to lesions of bacillary angiomatosis. • Epidemic KS (HIV-associated) should be considered.

MANAGEMENT • Doxycycline (100 mg twice per day) or • Erythromycin (250 to 500 mg four times per day) • Treat until lesions have resolved (usually 3 to 4 weeks) Chapter 24 • Cutaneous Manifestations of HIV Infection

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H IV-Asso cia t ed Syp h ilis BASICS • An intact cell-mediated immune system is necessary to “cure” the infection. • Unusual manifestations of syphilis have been reported in patients with coinfection with HIV. These include negative serologic examination for syphilis in the presence of active secondary syphilis, relapse after treatment that should have been adequate, fulminant cutaneous lesions with induration and necrosis (FIG. 24.13), and fulminant neurosyphilis resulting in permanent neurologic deficits. • See Chapter 19, “Sexually Transmitted Diseases,” for a more detailed discussion.

POINTS TO REMEMBER • If syphilis is suspected in an HIV-infected patient and the serologic test is negative, then a skin biopsy should be performed. • The only medication for the treatment of syphilis that adequately penetrates the blood-brain barrier is intravenous aqueous penicillin, which should be given at a dosage of 2 to 4 million units every 4 hours for 10 to 14 days in cases of suspected or proven neurosyphilis. Patients who are allergic to penicillin should undergo desensitization.

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24.13 Syphilis in a patient with acquired immunodeficiency syndrome. Note the necrotic lesions.

H IV-Asso cia t ed No r w egia n Sca b ies BASICS • “Norwegian” scabies is an infestation with Sarcoptes scabiei var. hominis in an immunocompromised host. • Immunocompetent hosts are able to limit the number of mites (10 to 12) that remain in the epidermis. • The rash and itching are the result of a delayed hypersensitivity response to the mite, its eggs, and its fecal products. • Immunocompromised hosts are not able to contain the population of mites and may be infested with millions of mites. These patients may not itch because of their defective cellmediated immunity. • HIV-infected patients with Norwegian scabies infestation pose a significant risk for transmission of scabies to household contacts and medical personnel. • See Chapter 20, “Bites, Stings, and Infestations,” for a more complete description of this condition.

24.14 Norwegian scabies in a patient with acquired immunodeficiency syndrome. Note the crusted papules and the white linear burrows.

DESCRIPTION OF LESIONS • Fine, white, linear lesions from female mites may be visualized burrowing into the skin (FIG. 24.14). • Crusted, keratotic plaques are characteristic in Norwegian scabies. • Atypical acral lesions may be seen in HIV-infected patients. DIAGNOSIS • Mineral oil preparation is done by scraping the epidermal surface of a burrow with a scalpel that has been dipped in mineral oil. • The scraping is examined with a low-power microscope. Mites, ova, or fecal pellets are seen (FIGS. 24.15 and 24.16). 24.15

Scabies. Mites, ova, and fecal pellets are shown.

24.16

Scabies. Fecal pellets are shown here.

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DIFFERENTIAL DIAGNOSIS

Pso riasis • Psoriatic lesions tend to be located on extensor aspects of the extremities. • Predominance of scale in the finger webs should lead to suspicion of Norwegian scabies. So lar Ke rat o se s • Norwegian scabies on sun-exposed areas in elderly patients can mimic solar keratoses (FIG. 24.17).

24.17 Norwegian scabies in a patient with acquired immunodeficiency syndrome. The lesions resemble solar keratoses.

MANAGEMENT

Scab icid e s • Permethrin 5% (Elimite) cream is applied, after a warm bath, to all skin surfaces from head to toe, including the palms, soles, and scalp in small children; it is left on for 8 to 12 hours, usually overnight, and is washed off the next morning; or • Lindane 1% (Kwell) lotion is applied from head to toe after bathing. Treatment should be continued once weekly until there is no evidence of residual lesions.

POINTS TO REMEMBER • Norwegian scabies is an infestation with millions of scabies mites and is highly contagious. Failure to treat patients promptly has led to epidemics affecting dozens of people. • Because of the immunodeficiency in patients with Norwegian scabies, prolonged treatment may be necessary. • Household contacts and medical staff who come into contact with the patient or the patient’s bedclothes should undergo treatment as for scabies in an immunocompetent host, regardless of symptoms.

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Lindane is not as effective as permethrin and may cause neurologic toxicity, particularly in children and in elderly patients. • Ivermectin, 0.2 mg/kg by mouth, has been shown to be effective in eradicating infection. However, it is not approved by the U.S. Food and Drug Administration for this use.

Ke rat o lyt ic Ag e n t s • Keratolytic agents, such as 10% to 40% salicylic acid, remove crusts and allow penetration of the scabicides.

Ot h er H IV-Asso cia t ed Diso rd ers HIV-Associated Eosin op h ilic Follicu litis DIFFERENTIAL DIAGNOSIS BASICS • HIV-associated eosinophilic folliculitis, also known as eosinophilic pustular folliculitis, is an extremely pruritic rash that is seen in the later stages of HIV infection. • Eosinophilic folliculitis appears to be a hypersensitivity reaction because of the large numbers of eosinophils that are seen in the skin, but no consistent association with specific allergens has been reported. • Very few patients with eosinophilic folliculitis respond to antihistamines. • HIV-infected patients have high circulating levels of interleukins 4 and 5, the cytokines that are chemotactic for eosinophils, so a seemingly allergic manifestation such as eosinophilic folliculitis may be a result of the general immunologic derangement in these patients. • Eosinophilic folliculitis has become rare now that the use of HAART has decreased the number of cases of advanced HIV infection. DESCRIPTION OF LESIONS • Primary lesions are urticarial papules measuring 3 to 5 mm that look like insect bites. • Pustules may be present, but they are not the predominant lesions. • In many cases, only excoriations are present because of the intense pruritus. • Patients with long-standing eosinophilic folliculitis may develop lichenification secondary to repeated scratching. DISTRIBUTION OF LESIONS • Lesions may occur anywhere, but they are prominent on the “seborrheic areas” of the skin (e.g., scalp, face, chest, and upper back). CLINICAL MANIFESTATIONS • Severe pruritus may interfere with the patient’s ability to function. DIAGNOSIS • Skin biopsy shows perifollicular and follicular infiltration by eosinophils. • Occasionally, peripheral eosinophilia may be present.

Bact e rial Fo lliculit is • See also Chapter 5, “Superficial Bacterial Infections,” for a more complete discussion. • Bacterial folliculitis may be clinically indistinguishable from eosinophilic folliculitis. • Gram’s stain and bacterial culture should be performed. Pityrosporum Fo lliculit is • Pityrosporum folliculitis may be clinically indistinguishable from eosinophilic folliculitis. • Potassium hydroxide preparation of pus shows yeast and hyphae. • Periodic acid–Schiff stain of skin biopsy specimen shows yeast and hyphae. Art h ro p o d Bit e Re act io n • Arthropod bite reaction may be clinically and histologically indistinguishable from eosinophilic folliculitis. • Lesions are less likely to be folliculocentric. • The patient’s history should include possible exposure to arthropods (e.g., fleas, lice, scabies, bedbugs, and mosquitoes).

MANAGEMENT • Topical steroids, antihistamines, and antibiotics are usually ineffective. • Ultraviolet B phototherapy is effective. Patients should be referred to a qualified phototherapy center. In the summer, sunlight is effective. • Isotretinoin (40 mg/day) is usually effective. Treatment must be continued for at least 3 months and may need to be continued on a long-term basis. Once the lesions have resolved, an attempt to taper the dosage to the lowest effective dose should be made. Cholesterol and triglyceride levels require monitoring on a monthly basis because of the side effect of hyperlipidemia. Because the protease inhibitors also cause hyperlipidemia, patients may need to be started on a cholesterol-lowering medication concomitantly. • Itraconazole (200 mg twice daily) may be effective.

POINT TO REMEMBER • Eosinophilic folliculitis, as described herein, is almost always associated with HIV infection. Chapter 24 • Cutaneous Manifestations of HIV Infection

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HIV-Associated Oral Hairy Leu kop lakia BASICS • Oral hairy leukoplakia is a marker of HIV infection that is thought to be caused by Epstein-Barr virus infection of the oral mucosa. It is rarely seen in patients receiving HAART. • See Chapter 12, “Disorders of the Mouth, Lips, and Tongue,” for a detailed discussion. DESCRIPTION OF LESIONS

24.18 Oral hairy leukoplakia. White plaques resembling corrugated cardboard are fixed to the mucosa.

• White plaques resembling “corrugated cardboard” (FIG. 24.18 [see also FIG. 12.12]) are fixed to the mucosa; they are not friable, as in candidiasis (see subsequent discussion). DISTRIBUTION OF LESIONS • Lesions most often appear on the lateral aspects of the tongue. CLINICAL MANIFESTATIONS • Lesions are usually asymptomatic. • Patients occasionally complain of a burning sensation of the tongue.

MANAGEMENT • Treatment is necessary only in symptomatic cases. • Surgical excision can be performed, but lesions recur at the margins. • Acyclovir (3.2 g/day) is given if lesions recur on cessation of treatment. However, the use of acyclovir for oral hairy leukoplakia may result in the development of acyclovir resistance for concurrent HSV infection. • Topical tretinoin 0.05% solution may be applied for 15 minutes once daily using a gauze sponge. • Podophyllin 25% solution is applied sparingly to one side of the tongue at a time and is allowed to air dry. This is repeated once weekly.

HIV-Associated Oral Can d id iasis

24.19 Oral candidiasis. These curdlike lesions can be easily removed with gauze. 452

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• Candidiasis (“thrush”) is also seen in immunocompromised patients and in neonates. • Curdlike or erosive lesions can easily be removed with gauze or a tongue blade (FIG. 24.19). • Lesions are more common on the dorsal aspect of the tongue, oropharynx, angles of mouth, and buccal mucosa. • The potassium hydroxide preparation shows yeast.

MANAGEMENT • In patients with severe immunosuppression, intermittent or prolonged topical or oral antifungal treatment is usually necessary. • Meticulous dental hygiene and an oral rinse containing 0.12% chlorhexidine gluconate may be effective. • Oral therapy with fluconazole (Diflucan) produces remission within approximately 1 week. Fluconazole 100 mg daily is more effective than nystatin 500,000 IU four times daily or clotrimazole troche 10 mg five times per day. • Maintenance therapy or intermittent therapy with fluconazole is essential to prevent relapse.

HIV-Associated Ap h th ou s Ulcers BASICS

24.20 Aphthous ulcer in a patient with acquired immunodeficiency syndrome. These lesions can be quite painful.

• Aphthous ulcers may be severe in HIV-infected patients (FIG. 24.20). • The pain may interfere with the patient’s ability to eat. • Mucosal pain leads to difficulties with eating and drinking, with resultant weight loss and dehydration. • See the discussion of mucous membranes in Chapter 12, “Disorders of the Mouth, Lips, and Tongue” (see FIGS. 12.1 and 12.2).

MANAGEMENT • Topical steroids may be applied directly to the ulcerations. • Stomatitis elixir, consisting of equal parts of magnesium carbonate or magnesium hydroxide suspension, viscous lidocaine, diphenhydramine elixir 12.5 mg/ 5 mL, and 1 g tetracycline powder, to be swished and spat out of the mouth as needed, is useful for pain. • Thalidomide (100 mg by mouth twice per day) is effective, with notable toxic effects of sedation, neutropenia, peripheral neuropathy, and teratogenicity.

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patients with AIDS develop an allergy, followed by the aminopenicillins. • When the drug allergy causes a typical morbilliform eruption, it is possible to continue the offending medication and treat the patient’s symptoms with antihistamines and topical steroids. More serious drug eruptions are characterized by urticaria, mucosal involvement, target lesions, erythroderma, and tenderness of the skin. Any of these signs or symptoms requires prompt discontinuation of the offending medication. • Mucosal involvement and target lesions are indicative of erythema multiforme or Stevens-Johnson syndrome, whereas erythroderma and skin tenderness are seen in toxic epidermal necrolysis (FIG. 24.21). The nonnucleoside reverse transcriptase inhibitor nevirapine has been associated with severe cases of Stevens-Johnson syndrome. For a complete discussion of drug eruptions, see Chapter 17, “Drug Eruptions.”

HIV-Associated Pru ritu s 24.21 Drug eruption. Toxic epidermal necrolysis has resulted from treatment with nevirapine. (Courtesy of Ashit Marwah, M.D.)

HIV-Associated Dru g Eru p tion s BASICS • Drug eruptions are common in the HIV-infected population because of the large number of medications taken by these patients. The most commonly implicated medication is sulfamethoxazole/trimethoprim, to which at least 60% of

MANAGEMENT • Careful history taking and a physical examination rule out dermatologic disease as the cause. • Patients should discontinue use of deodorant and antibacterial soaps; superfatted soaps are the least drying. • Patients should be instructed to limit bathing to once per day. • Emollients should be applied after the patient has bathed and patted dry; ointments are more emollient than creams, which are more emollient than lotions. • Patients need to try different preparations to find which is most cosmetically acceptable and effective.

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BASICS • Pruritus is a common and troubling symptom in HIVinfected patients. It often has a multifactorial origin. • Many patients use antibacterial or deodorant soaps with the mistaken belief that these will decrease the risk of infection. In fact, these soaps dry the skin and make the patients itchy and more susceptible to cutaneous infection because of the excoriations that result. • Patients may become itchy because of subclinical drug eruptions or as a medication-related side effect. • Patients may be colonized with Staphylococcus aureus, which is known to be a cause of pruritus in HIV-infected patients.

• Patients who do not obtain relief with over-the-counter moisturizers often do well with ammonium lactate 12% lotion or cream (Lac-Hydrin). • Anti-itch preparations containing calamine, pramoxine, menthol, camphor, and oatmeal may be soothing. • Sedating antihistamines are useful, especially before bedtime. • Topical steroids should be prescribed for dermatitis, which may result from dry skin. • Ultraviolet B phototherapy is palliative. For further discussion of pruritus, see Chapter 15, “Pruritus: The ‘Itchy’ Patient.”

HIV-Associated Seborrh eic Derm atitis

HIV-Associated Psoriasis

BASICS

BASICS

• Seborrheic dermatitis is a scaly skin condition that affects up to 5% of the human population. • In immunocompetent patients, it may be associated with an overgrowth of saprophytic Pityrosporum yeast on the scalp and face; it is not known whether the same is true in HIVinfected patients. • The frequency and severity of seborrheic dermatitis are increased in HIV-infected patients, for unknown reasons. • Seborrheic dermatitis appears commonly in hospitalized patients, probably because of the changes in hygiene (e.g., inability to shampoo the hair) experienced during illness. • For description and distribution of lesions, as well as management, see Chapter 4, “Inflammatory Eruptions of Unknown Cause.”

• Psoriasis is a scaly skin disease that affects 1% to 2% of the general population. • Psoriasis is not more common in HIV-infected patients, but it may present in a more severe or unusual form and may be recalcitrant to the usual treatments. • The most severe manifestation is Reiter’s disease (see Chapter 25, “Cutaneous Manifestations of Systemic Disease”), which includes psoriatic lesions, arthritis, urethritis, and conjunctivitis. A new onset of severe psoriasis in a patient at risk for HIV should lead to HIV testing. • Combined treatment with methotrexate and sulfonamides can lead to fatal bone marrow suppression. • The use of systemic steroids for treatment of psoriasis may result in life-threatening pustular psoriasis. • See Chapter 3, “Psoriasis,” for a more complete discussion.

POINT TO REMEMBER • Seborrheic dermatitis is common in HIV-infected patients, and the sudden onset of severe, recalcitrant seborrheic dermatitis should lead to an inquiry regarding risk factors for HIV and HIV testing.

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24.22 Lipodystrophy. Note the atrophic “nasolabial bands” between the nasolabial lines and the cheeks.

(NRTIs), notably stavudine (Zerit), and with protease inhibitors. In addition, host factors play a role, in that white patients with CD4 counts under 100 cells/mm3 and body mass indices less than 24 kg/m2 have a significant risk of developing lipoatrophy independently of HIV medications. • Facial lipoatrophy is a marker of a person who is infected with HIV. It causes severe psychologic problems and depression in many patients, even after the treatment has lowered the viral load to undetectable levels. DESCRIPTION OF LESIONS

HIV-Associated Lip oatrop h y BASICS • The complete syndrome of HIV-associated lipodystrophy consists of lipoatrophy of the face and extremities, truncal obesity with the development of a buffalo hump, triglyceridemia, and insulin resistance. • The cause of the condition is multifactorial. It is associated with treatment with nucleoside reverse transcriptase inhibitors

MANAGEMENT • Avoidance of NRTIs, especially stavudine. • Careful selection of protease inhibitors. Atazanavir (Reyataz) does not cause the same lipid abnormalities or body fat changes associated with some of the other protease inhibitors. • Switching therapy may stop the progression of lipoatrophy. • Filler substances have been used successfully to treat facial lipoatrophy and to reduce the stigma that is felt by patients with HIV infection. In the United States, poly-L-lactic acid (Sculptra) and calcium hydroxyapatite microspheres (Radiesse) are currently approved for the treatment of HIV-associated lipoatrophy. Many more filler substances are being used in other countries for this indication.

POINTS TO REMEMBER • NRTIs and protease inhibitors are the main causes of facial lipoatrophy. • Patients with HIV are extremely stressed by facial lipoatrophy. • Facial lipoatrophy can be treated with injections of poly-L-lactic acid or calcium hydroxyapatite microspheres. 456

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• There is loss of facial fat to varying degrees. • In severe cases, there is hollowing of the cheeks and development of a “nasolabial band” between the nasolabial lines and the cheeks (FIG 24.22). Loss of the fat in the temporal, periorbital, and cheek areas gives prominence to the underlying bony structure, producing a skeletal look. DISTRIBUTION OF LESIONS • Initially the cheeks are affected. • Later, the temporal and periorbital fat disappears.

• Treatment of patients with severe lipoatrophy using poly-L-lactic acid requires an average of six treatments over 6 months by a skilled injector to achieve good results; these last an average of 2 years. Results are not immediate but develop 4 to 6 weeks after injection as the skin begins to form new collagen on the poly-L-lactic acid matrix. • Treatment with calcium hydroxyapatite microspheres results in immediate correction and may require only a single treatment. The microspheres provide a matrix on which new collagen is formed by the skin. Because the reabsorption of the microspheres may occur more rapidly than new collagen formation, a touch-up treatment may be required approximately 3 months after the initial treatment. Results last for a year or more. • When lipoatrophy is treated by a skilled injector, side effects are rare.

C H AP T ER

25

Cutaneous Manifestations of Systemic Disease Herbert P. Goodheart and Peter G. Burk

OVERVIEW • The cutaneous surface, nails, hair, and oral cavity often afford clues to many underlying disorders. The skin is sometimes referred to as a “window” to disease. For example, the presence of jaundice, palmar erythema, pruritus, and spider telangiectasias points to liver disease. The appearance of pyoderma gangrenosum, erythema nodosum, or severe aphthous stomatitis may indicate inflammatory bowel disease. • By appreciating skin signs of systemic diseases, the health care provider can often lead his or her patient to an early diagnosis and expedient and appropriate treatment. • This chapter reviews some of the cutaneous manifestations of systemic diseases and it highlights recent developments in their management. CONNECTIVE TISSUE DISEASES

ENDOCRINE DISEASES Diabetes-associated lesions • Necrobiosis lipoidica diabeticorum • Diabetic bullous disease • Diabetic neuropathic ulcers • Acanthosis nigricans • Eruptive xanthom as • Diabetic derm opathy • Perforating folliculitis (Kyrle’s disease) • Dissem inated granulom a annulare • Scleredem a of Buschke-Löwenstein Thyroid Disease • Pretibial m yxedem a • Warm , m oist, and velvety skin • Alopecia with diffuse hair loss • Nails • Hair LIPID ABNORMALITIES • • • • •

Eruptive xanthom as Planar xanthom as Xanthelasm a Tuberous xanthom as Tendinous xanthom as

• • • • • • • •

System ic lupus erythem atosus Drug-induced lupus erythem atosus Subacute cutaneous lupus erythem atosus Chronic cutaneous lupus erythem atosus Neonatal lupus erythem atosus Derm atom yositis Scleroderm a and m orphea Crest syndrom e and progressive system ic sclerosis ERYTHEMA NODOSUM CUTANEOUS SARCOIDOSIS INFLAMMATORY SKIN DISORDERS

• Reiter’s syndrom e • Pyoderm a gangrenosum • Exfoliative derm atitis NEUROCUTANEOUS SYNDROMES • Neurofibrom atosis • Tuberous sclerosis

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En d o crin e Disea ses BASICS • Many different skin lesions are seen in conjunction with endocrine diseases. Some cutaneous lesions are directly related to the degree of endocrine dysfunction and may be caused by an excess or lack of a hormone acting on a specific tissue, such as warm and moist skin associated with hyperthyroidism or dry and cool skin associated with hypothyroidism. • In a disease such as diabetes, it may be difficult to link these skin findings to a specific degree of endocrine dysfunction (e.g., necrobiosis lipoidica diabeticorum with the level of hyperglycemia).

Diab e t e s Me llit us • Diabetes mellitus is a disease characterized by a disturbance in the production of insulin or resistance to insulin activity, which results in abnormal glucose metabolism. • Diabetes causes cellular changes, such as microangiopathy of small blood vessels. This causes organ damage, including retinal disease, renal dysfunction, and possibly cutaneous lesions. • Diabetes can also affect immune function and can lead to an increase of bacterial, fungal, and yeast infections. 25.1 Necrobiosis lipoidica diabeticorum. This diabetic patient has early lesions that consist of yellow-red plaques. Epidermal atrophy and telangiectasias tend to occur later.

25.2 Necrobiosis lipoidica diabeticorum. This diabetic patient has more advanced lesions than those seen in FIGURE 25.1. Epidermal atrophy and telangiectasias are seen here.

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Diabetes-Associated Lesion s: Necrobiosis Lip oid ica Diabeticoru m • Necrobiosis lipoidica diabeticorum (NLD) is characterized by yellow-red to brown, translucent plaques with epidermal atrophy and telangiectasia (FIG. 25.1). As lesions progress, the center becomes depressed and yellow (FIG. 25.2). Ulceration is not uncommon. • NLD appears most commonly on the pretibial areas, but it may arise on other sites. • NLD is more common in women than in men. • Treatment for NLD is not very satisfactory. The condition is typically chronic with variable progression and scarring. • NLD is seen more frequently in type 1 than in type 2 diabetes and may occur before the onset of clinical diabetes. Lesions may ulcerate. A minority of patients have no clinical evidence or family history of diabetes; in these patients, the term necrobiosis lipoidica is used. Currently, the term necrobiosis lipoidica is used to encompass all patients with the same clinical lesions regardless of whether diabetes is present or not.

DIFFERENTIAL DIAGNOSIS • The lesions of NLD can be similar to those of morphea (see later discussion) and other localized sclerosing lesions.

MANAGEMENT • High-potency topical steroids or intralesional steroid injections are used and can lessen the inflammation of early active lesions and the active borders of enlarging lesions, but these have little beneficial effect on atrophic lesions that are burned out. In fact, with atrophic lesions, steroid use may cause further atrophy. • Because localized trauma can cause NLD to ulcerate, protection of the legs with support stockings may be helpful. • Antiplatelet aggregation therapy with aspirin and dipyridamole has produced varied results but overall has shown some beneficial effects.

• Pentoxifylline (Trental) is a drug used for the treatment of intermittent claudication. Pentoxifylline is believed to decrease blood viscosity by increasing fibrinolysis and red blood cell deformity. It also inhibits platelet aggregation. • Topical application of bovine collagen is believed to improve granulation tissue by supporting fibroblast activity and promote wound debridement by increasing the number of macrophages and neutrophils at the wound site. • Ticlopidine, nicotinamide, clofazimine, and perilesional heparin injections have been used in uncontrolled studies and appeared to benefit some patients with NLD.

Diabetes-Associated Lesion s: Diabetic Bu llou s Disease • Diabetic bullous disease (bullosis diabeticorum) manifests as large, tense, subepidermal, noninflammatory blisters (FIG. 25.3). • Lesions most often arise spontaneously on the lower extremities, especially the ankles and feet. The development of multiple lesions at several locations may occur. • Lesions tend to arise in patients with long-standing diabetes mellitus who have multiple complications of the disease.

DIFFERENTIAL DIAGNOSIS • Bullous diabetic lesions can be differentiated from bullous pemphigoid by the characteristic location of lesions and negative direct immunofluorescence of skin biopsies.

25.3 Diabetic bullous disease. This large, tense blister arose spontaneously in a characteristic location.

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MANAGEMENT • Blisters generally heal spontaneously within 2 to 6 weeks of onset. • Topical antibiotics are recommended until the lesions heal.

Diabetes-Associated Lesion s: Diabetic Neu rop ath ic Ulcers 25.4 Diabetic ulcer of the heel (mal perforans). These lesions are noted at sites of pressure, such as the heel in this patient.

• Diabetic neuropathic ulcers (mal perforans) (FIG. 25.4) most often occur at sites of pressure (e.g., the heel), particularly in areas of poor sensory function and poor circulation. They are usually painless as a result of peripheral neuropathy. • Diabetic foot ulcers occur as a result of the loss of protective sensation. • Other factors, such as mechanical changes in conformation of the bony architecture of the foot and atherosclerotic peripheral arterial disease, may be contributing causes. DIAGNOSIS • Diabetic neuropathic ulcers should be distinguished from infections and other ulcerations and cutaneous neoplasms that may present as ulcerations.

MANAGEMENT 25.5 Acanthosis nigricans. Note the characteristic hyperpigmentation in a typical location. This patient has insulinresistant diabetes. (Image courtesy of Bernard Cohen, M.D.)

• It is beyond the scope of this discussion to describe all therapies for diabetic foot ulcers. However, management can include glycemic control, special footwear, topical wound management, daily saline soaks, surgical debridement, and skin grafting when necessary. • Becaplermin (Regranex*), a recombinant human platelet-derived growth factor, is available in gel form for topical therapy (in conjunction with good ulcer care) and is reported to promote healing of diabetic neuropathic foot ulcers. • Hyperbaric oxygen therapy may be useful.

Oth er Fin d in gs in Diabetic Patien ts • Acanthosis nigricans (FIG. 25.5) sometimes occurs in insulin-resistant diabetes (also see FIGS. 14.19 and 14.20). • Cutaneous candidiasis (FIG. 25.6) may also occur (see also FIGS. 7.31–7.33) (see Chapter 7, “Superficial Fungal Infections”). 25.6 Cutaneous candidiasis. These satellite pustules were positive for Candida albicans. 460

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*There is currently a “black box” warning about an increased risk of cancer from the use of this agent.

• Eruptive xanthomas are seen as skin markers for various primary genetic disorders such as certain types of hyperlipidemias or secondary to diabetes (see later discussion). • Diabetic dermopathy is characterized by small brownish, atrophic, scarred, hyperpigmented plaques (FIG. 25.7) • Lesions occur primarily on the anterior lower legs in patients with type 1 and type 2 diabetes. • It is typically a late manifestation of diabetes and is usually asymptomatic. • Diabetic dermopathy must be differentiated from lesions caused by trauma. • Perforating folliculitis (Kyrle’s disease) consists of firm, rough, hyperkeratotic papules, which are often hyperpigmented in dark-skinned people. • There is a high incidence of perforating folliculitis in patients with long-standing diabetes who are undergoing long-term hemodialysis. • Lesions are found most commonly on the extensor surfaces of the extremities. Itching can be intense. • Disseminated granuloma annulare consists of annular dermal papules (see Chapter 4, “Inflammatory Eruptions of Unknown Cause”). It occurs both in patients with clinical diabetes and sometimes in individuals with only abnormal glucose levels. • Scleredema of Buschke-Löwenstein is a rare manifestation of diabetes mellitus. The lesion is a sclerotic, thickened plaque characteristically seen on the upper back.

25.7 Diabetic dermopathy. Small, asymptomatic, brownish, atrophic, scarred, hyperpigmented plaques are seen on the shins of this diabetic patient.

DIAGNOSIS • The diagnoses of many of these entities are generally made on clinical grounds. • A skin biopsy may be necessary to confirm the diagnosis.

Lab o rat o ry Evaluat io n • Serum glucose levels and glycosylated hemoglobin A1 are determined to confirm the diagnosis of diabetes mellitus. • Skin biopsies of lesions of necrobiosis lipoidica and granuloma annulare demonstrate palisading granulomas with degeneration of collagen. • Skin biopsy of perforating folliculitis demonstrates basophilic material in the dermis, with transepidermal elimination. • Skin biopsies of diabetic dermopathy show thickening of blood vessels and mild perivascular infiltrate. • Diabetic bullous lesions have subepidermal blistering on hematoxylin and eosin staining of skin biopsy tissue; direct immunofluorescence of skin biopsies in these lesions is negative for immunoglobulins. • Diabetic neuropathic ulcers are rarely examined by biopsy. • Perforating folliculitis can be differentiated from other keratotic papules by the size and distribution of lesions and by a skin biopsy.

HELPFUL HINT • Careful consideration should be given before performing a skin biopsy on a patient with diabetes, particularly on areas such as the lower extremities.

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Th yroid Disease BASICS

25.8 Pretibial myxedema, Graves’ disease. Erythematous plaques with early involvement. (Image courtesy of Ashit Marah, M.D.)

• Thyroid hormones profoundly influence the growth and differentiation of epidermal and dermal tissues. • Abnormal levels of thyroid hormone produce striking changes in the texture of the skin, hair, and nails. • Some of the associated skin alterations in thyroid disease are the result of a deficiency or a high toxic level of tissue thyroid hormone. Other skin disorders seen with thyroid disease, such as vitiligo and alopecia areata, are associated clinical findings that are not directly related to thyroid hormone function but are seen on occasion in patients with thyroid disease. • Findings such as pretibial myxedema are caused by circulating autoimmune -globulin, which acts as a thyroid-stimulating hormone. • Hyperthyroidism may be caused by Graves’ disease, subacute thyroiditis, toxic goiter, and thyroid carcinoma. • Hypothyroidism may be caused by iodine deficiency (cretinism), Hashimoto’s thyroiditis, pituitary dysfunction with thyroid-stimulating hormone deficiency, and surgical or radiation ablation of the thyroid. • Patients with thyroid disease may be hyperthyroid at one point in their clinical course and hypothyroid at another time. DESCRIPTION OF LESIONS • Hyperthyroid skin lesions may include the following: • Warm, moist, and velvety skin • Alopecia with diffuse hair loss • Nail changes with onycholysis (Plummer’s nails) • Hyperpigmentation • Pretibial myxedema lesions—flesh-colored, waxy infiltrated translucent plaques (FIGS. 25.8 and 25.9) • Hyperthyroid findings may include the following: • Nervousness and tremor • Weight loss • Tachycardia with atrial fibrillation • Proximal muscle weakness

25.9 Pretibial myxedema, Graves’ disease. Note the progressive exuberant hypertrophy with folding of the skin on the shins and tops of the feet.

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• Graves’ disease • Exophthalmos (FIG. 25.10) • Hypothyroid skin lesions may include the following: • Myxedema of the skin with generalized thickening and a dry, coarse feel; yellow skin secondary to carotenemia • Hair changes—coarse, sparse hair; lateral third of eyebrows lost • The following conditions may be associated with thyroid disease: • Alopecia areata • Vitiligo • Connective tissue diseases • Multiple endocrinopathy syndrome • Urticaria DISTRIBUTION OF LESIONS

25.10 Exophthalmos. This patient has Graves’ disease. Note the lid retraction and proptosis.

• Pretibial myxedema lesions are found most frequently on the lower legs. CLINICAL MANIFESTATIONS • Hyperthyroid skin changes that result from the hypermetabolic state (e.g., warm, moist, flushed skin) occur during the active thyrotoxic stage of thyroiditis, during active Graves’ disease, and in patients with toxic goiters. These skin changes may gradually resolve when the patient returns to a euthyroid state. • Graves’ disease lesions (pretibial myxedema) occur in up to 4% of patients with this disease. The skin lesions and eye lesions usually do not resolve, even after treatment of the thyroid disease brings a return to a euthyroid state. • Hypothyroid skin changes (e.g., cool, dry skin) are related to the length and severity of the clinical hypothyroid state. These skin lesions gradually improve some months after the patient returns to a euthyroid state. DIFFERENTIAL DIAGNOSIS DIAGNOSIS • Diagnosis of both hyperthyroid and hypothyroid disease is made by specific thyroid function tests. • Graves’ disease is diagnosed clinically and with confirmatory thyroid function tests.

Lab o rat o ry Evaluat io n • Elevated thyroid-stimulating hormone levels are the most sensitive screening test for hypothyroidism. • Serum thyroid hormone levels can be most accurately measured by obtaining free thyroxine and free triiodothyronine levels. • Antithyroglobulin antibodies and antithyroid microsomal antibodies are often positive in Graves’ disease and Hashimoto’s thyroiditis. • Long-acting thyroid stimulator is elevated in 50% of patients with Graves’ disease. • Skin biopsies in Graves’ disease show increased staining of hyaluronic acid with mucin stains in the reticular and papillary dermis.

• Pretibial myxedema must be differentiated from other skin diseases with increased mucin production, such as papillary mucinosis and scleredema.

MANAGEMENT • Functional symptoms (e.g., increase or decrease of sweating, dry skin, hair and nail changes) of hyperthyroidism and hypothyroidism may improve after appropriate treatment of thyroid disease and return to a euthyroid state. • Treatment of pretibial myxedema lesions can be attempted with high-potency topical steroids and intralesional steroids, although the response is generally poor. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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Cu t a n eo u s Ma n ifest a t io n s o f Lip id Ab n o r m a lit ies: Xa n t h o m a s BASICS • Abnormalities of lipid metabolism, with high circulating levels of various lipoproteins, can result in deposition of cholesterol and other lipids in the skin, tendons, and other organs. • Xanthomas result from the deposition of cholesterol and other lipids found in tissue macrophages in the skin and tendons. There is also a high correlation between abnormal lipoproteinemia and the development of atherosclerosis. • Lipoprotein abnormalities have been classified into primary (genetic) lipoproteinemia and secondary lipoproteinemia resulting from underlying diseases. • Primary lipoproteinemias are phenotypic expressions of various genetic disorders of lipid metabolism with the following characteristics: • Type I, familial lipoprotein lipase deficiency: elevated chylomicrons • Type IIA, familial hypercholesterolemia: elevated lowdensity lipoproteins • Type IIB, familial hyperlipidemia: elevated low-density lipoproteins and very-low-density lipoproteins • Type III, familial dysbetalipoproteinemia: elevated intermediate-density lipoproteins • Type IV, endogenous familial hypertriglyceridemia: elevated triglycerides • Type V, familial combined hyperlipidemia: elevated chylomicrons and elevated very-low-density lipoproteins • Secondary hyperlipoproteinemias result from disturbances in cholesterol and triglyceride metabolism caused by cholestatic liver disease, diabetes mellitus, pancreatitis, multiple myeloma, and nephrotic syndrome. These disorders may mimic any of the genetic lipoprotein abnormalities and may produce similar xanthomatous deposits in tissues.

A

B 25.11 A an d B Eruptive xanthomas. A: This 28-year-old male patient has a triglyceride level of 31,000 and a cholesterol level of 580 mg/dL. B: This is the same patient after 2 months of a low-fat diet and a cholesterol-lowering drug.

DESCRIPTION OF LESIONS • Eruptive xanthomas are smooth, yellow, papular lesions (2 to 5 mm) (FIGS. 25.11 A and B). There is sometimes a red halo around the lesions. • Planar xanthomas are flat to slightly palpable yellow lesions. • Xanthelasma (xanthoma palpebrarum) is a form of planar xanthoma (FIG. 25.12).

25.12 Xanthelasma. Periorbital yellow-orange plaques are present on the upper inner eyelids. This patient was normolipemic when this photograph was taken. 464

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• Tuberous xanthomas are small (0.5 cm) to large (3 to 5 cm), firm, yellow papules and nodules (FIG. 25.13). • Tendinous xanthomas are subcutaneous thickenings around tendons and ligaments. DISTRIBUTION OF LESIONS • Eruptive xanthomas appear most frequently over the knees, elbows, and buttocks. • Planar xanthomas are found in the palmar creases but may also be generalized. • Xanthelasma lesions are usually found on the eyelids and medial canthus. • Tuberous xanthomas are found on the elbows, knees, and buttocks. • Tendinous xanthomas affect the Achilles tendon, extensor tendons of the wrists, elbows, and knees.

25.13 Tuberous xanthomas. These are firm papules and nodules in a patient with hyperlipidemia type II.

CLINICAL MANIFESTATIONS • Eruptive xanthomas tend to appear suddenly over the extensor surfaces and pressure points. These lesions are usually seen in association with very high levels of triglycerides (2,000 to 4,000 mg/dL). Uncontrolled diabetes mellitus and acute pancreatitis are both common underlying causes of their surfacing on the skin. • Planar xanthomas are usually asymptomatic. Palmar xanthomas are seen with type III lipoproteinemia. Diffuse planar xanthomas are found in patients with multiple myeloma. • Xanthelasma lesions grow slowly over years. More than 50% of patients with xanthelasma have normal lipoprotein levels. • Tuberous xanthomas also are slow growing. They are associated with familial hypercholesterolemia but can also occur in patients with high triglyceride levels. • Tendinous xanthomas occur in patients with hypercholesterolemias.

DIFFERENTIAL DIAGNOSIS • Eruptive xanthomas must be differentiated from cutaneous sarcoid papules and cutaneous histiocytosis. • Tuberous xanthomas can be confused with rheumatoid nodules and subcutaneous granuloma annulare.

DIAGNOSIS • The diagnosis is made by clinical evaluation of skin and subcutaneous lesions. • Skin biopsy is confirmatory for xanthomas.

Lab o rat o ry Evaluat io n • Fasting blood levels of triglycerides and cholesterol should be determined. • Lipoprotein electrophoresis demonstrates specific lipoprotein abnormalities. • Skin biopsy of xanthomas demonstrates collections of lipids in foamy macrophages in the dermis. • Serum glucose levels and glycosylated hemoglobin A1 are determined to rule out diabetes mellitus. • Serum amylase levels should be examined to rule out pancreatitis. • Serum protein electrophoresis should be performed to rule out multiple myeloma.

MANAGEMENT • Patients with lipid disorders and xanthomas must be appropriately evaluated for primary and secondary lipoprotein abnormalities. Treatment of the underlying cause may reverse both eruptive and tuberous xanthomas over time. • Dietary restrictions and cholesterol-lowering drugs may reverse some changes associated with hypercholesterolemia. • Xanthelasmas of the eyelids can be removed by application of 25% to 50% trichloroacetic acid, by local electrodesiccation, laser therapy, and excision; however, lesions can recur. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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Co n n ect ive Tissu e Disea ses System ic Lu p u s Eryth em atosu s BASICS

25.14 Systemic lupus erythematosus. A “butterfly rash” is evident. Note the sparing of the nasolabial areas that are often involved with seborrheic dermatitis.

25.15 Systemic lupus erythematosus. A photodistribution on the face and the “V” of the neck are evident in this patient. Note the violaceous color suggestive of connective tissue disease. Similar findings are noted in dermatomyositis. 466

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• Systemic lupus erythematosus (SLE) is a chronic, idiopathic, multisystemic, autoimmune disease associated with polyclonal B-cell activation. Fibrinoid degeneration of connective tissue and the walls of blood vessels associated with an inflammatory infiltrate involving various organs may result in arthralgia or arthritis, kidney disease, liver disease, central nervous system disease, gastrointestinal disease, pericarditis, pneumonitis, myopathy, and splenomegaly, as well as skin disease. • The cutaneous manifestations of SLE result from the production of multiple autoantibodies that deposit immune complexes at the dermal–epidermal junction. • Current investigators have reclassified lupus skin lesions into three distinct groups: • Acute cutaneous lupus erythematosus (ACLE) lesions are strongly associated with active SLE; however, ACLE lesions may occasionally be seen in subacute cutaneous lupus erythematosus (SCLE). • SCLE comprises the second category. • Chronic cutaneous lupus erythematosus (CCLE) traditionally had been referred to as discoid lupus erythematosus (DLE). DLE lesions may be seen in both SLE and CCLE. • SLE is seen in a 9:1 female-to-male ratio; it is more common in blacks and Hispanics. • Approximately 10% of patients with SLE have a firstdegree relative with the disease. An association of lupus and human leukocyte antigens (HLA) -DR2 and -DR4 has been seen. • The following 4 of the 11 American Rheumatologic Association criteria for lupus are related to the skin and are considered lupus-specific lesions: • The classic malar or “butterfly” rash (FIG. 25.14) is a persistent erythema over the cheeks that tends to spare the nasolabial creases. Sometimes, this is the initial symptom of lupus, and it often occurs after sun exposure. • Photosensitivity (FIG. 25.15) occurs as an exaggerated or unusual reaction to sunlight. The reaction may resemble a drug eruption.

• Discoid lesions (discoid lupus erythematosus) are erythematous lesions that evolve into scaly, atrophic scarring plaques (FIG. 25.16). Such discoid lesions affect 10% to 15% of patients with SLE. • Oral ulcerations may develop, often on the hard palate or nasopharynx. • Nonspecific lesions of lupus that may be seen in SLE and other connective tissue diseases include the following: • The “spider” type of telangiectasia is usually seen in SLE, scleroderma, and dermatomyositis. Macular (matlike) telangiectasias usually occur in scleroderma. • Periungual telangiectasias are seen in SLE, as well as in dermatomyositis and scleroderma. • Palmar telangiectasias are usually seen in SLE. • Vasculitis, palpable purpura, and vasculitic ulcers usually occur in SLE and scleroderma. • Raynaud’s phenomenon is associated with SLE and scleroderma. • Livedo reticulitis, panniculitis, thrombophlebitis, urticaria, urticarial vasculitis, frontal alopecia (“lupus hair”) and diffuse nonscarring alopecia, palmar erythema, and bullae are associated primarily with SLE.

25.17 Systemic lupus erythematosus. Livedo reticularis is present.

DISTRIBUTION OF LESIONS • The lesions of ACLE tend to occur in sun-exposed areas such as the face, dorsa of the forearms, the hands, and the “V” of the neck. • The lesions of DLE may occur on the face, scalp, ears, neck, or oral mucosa, or they may be widespread (see later discussion). • On the lower extremities, livedo reticularis (FIG. 25.17) and vasculitic ulcers (FIG. 25.18) may be seen.

25.18 Systemic lupus erythematosus. Vasculitic ulcers are seen on this patient’s legs.

25.16 Systemic lupus erythematosus (discoid lupus erythematosus). Lesions of DLE, consisting of erythematous, scaly, disc-shaped scarring plaques, are present in this patient, who has SLE. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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• On the dorsal hands, violaceous plaques that spare the skin overlying the joints are characteristic of SLE. Conversely, in dermatomyositis, the joints are affected (Gottron’s papules). Ulcerated vasculitic lesions on the fingertips may also develop (FIG. 25.19). CLINICAL MANIFESTATIONS • Fatigue, fever, and malaise may be the presenting nonspecific symptoms. • Signs or symptoms are related to the specific organ or area involved (e.g., arthralgia). • Flare of lupus is common during pregnancy. • The following hematologic abnormalities may be associated with SLE: idiopathic thrombocytopenic purpura, hemolytic anemia, leukopenia, and clotting abnormalities, which may be related to the anticardiolipin syndrome. Other associated conditions and symptoms include rheumatoid arthritis, Sjögren’s syndrome, seizures, and the occurrence of multiple spontaneous abortions. DIAGNOSIS According to the American Rheumatologic Association, a person has SLE if four or more of the following criteria are present: 1. “Butterfly” rash 2. Lesions of CCLE or DLE 3. Photosensitivity 4. Oral ulcers 5. Arthritis in two or more joints 6. Serositis 7. Renal disorder 8. Neurologic disorder 9. Hematologic disorder 10. Immunologic disorder: anti-DNA, anti-Smith (anti-Sm) antibody, or a false–biologic-positive syphilis serologic result 11. Antinuclear antibodies (ANAs)

Lab o rat o ry Evaluat io n • Antinuclear antibody (ANA) titers are positive in 95% of patients with SLE. The peripheral rim pattern is associated most strongly with lupus erythematosus, although other patterns commonly are present. • Anti-dsDNA (antibody to native double-stranded DNA) is present in 60% to 80% of patients and is more specific for SLE. • Anti-Sm antibody has a strong specificity for SLE. This is particularly relevant in patients in whom anti-dsDNA results are negative and may help exclude underlying systemic involvement. • Antiphospholipid antibodies are present in 25% of patients. • The erythrocyte sedimentation rate is usually elevated.

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25.19 Systemic lupus erythematosus. Necrotic, painful, vasculitic ulcers are present on the fingertips.

• Hypocomplementemia occurs in 70% of patients and is noted especially when there is renal involvement in active SLE. • The lupus band test involves the direct immunofluorescence of uninvolved, non–sun-exposed skin. When positive, it is

DIFFERENTIAL DIAGNOSIS

Facial Le sio n s Ro sa cea

See Chapter 1, “Acne and Related Disorders.” • Presence of acnelike papules and pustules in addition to malar erythema • Absence of systemic complaints • Negative ANA titers

suggestive of the presence of renal disease. This test has been largely supplanted by the aforementioned serologic tests.

Ot h e r Co n d it io n s • Other connective tissue diseases, such as scleroderma and dermatomyositis (see later discussion) • Other photosensitivity conditions, such as polymorphous light eruption • Other causes of renal, hematologic, and central nervous system (CNS) disease

Seb o r rh eic Der m a t it is

See Chapter 2, “Eczema.” • Patients respond readily to topical steroids • Lack of systemic complaints • Negative ANA titers

Dru g-In d u ced Lu p u s Eryth em atosu s BASICS • The clinical and serologic picture of drug-induced lupus erythematosus is often indistinguishable from that of SLE. • A syndrome resembling SLE can be induced by certain drugs: hydralazine, procainamide, phenytoin, isoniazid, quinidine, beta-blockers, sulfasalazine, and lithium; however, patients with drug-induced lupus syndromes develop cutaneous lesions much less commonly than is typically seen in SLE.

• Arthralgia or arthritis, generally affecting the small joints, is often the only clinical symptom. Myalgia, pleuritis, pericarditis, fever, and hepatosplenomegaly may occur. • The classic SLE-type lesions of butterfly rash and mucosal ulcerations, for example, are usually absent in drug-induced lupus erythematosus. CNS manifestations and renal involvement are also rare. • In 90% of patients, ANAs are present in a homogenous or speckled pattern. • Withdrawal of the offending drug, followed by a regression of symptoms, helps confirm the diagnosis.

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MANAGEMENT

Sun -Re lat e d Sym p t o m s • Excessive sun exposure should be avoided; the patient should be counseled in the use of broad-spectrum sunscreens. Cut an e o us DLE • See the later discussion of the management of CCLE. Se ve re ly Ill Pat ie n t s • The mainstays of therapy for systemic disease are systemic steroids (prednisone), given in a dosage of 0.5 to 1 mg/kg/day. • Administration of oral antimalarials such as hydroxychloroquine (Plaquenil) and chloroquine (Aralen) are

sometimes used as first-line therapy. They both may be very effective in the treatment of skin lesions. • Other therapeutic agents include: • Dapsone, gold, oral retinoids such as isotretinoin (Accutane), and immunosuppressive drugs such as azathioprine (Imuran) and cyclophosphamide (Cytoxan) and methotrexate may be helpful. • Mycophenolate (CellCept) as well as interferon alpha-2a and alpha-2b (Roferon and Intron A) may also be used. • Immunosuppressive and antimalarial agents are used as adjuvant therapy to treat systemic disease because of their steroid-sparing effects. • Thalidomide and intravenous -globulin are used to control recalcitrant cases.

Su bacu te Cu tan eou s Lu p u s Eryth em atosu s BASICS • SCLE tends to be less severe than SLE and rarely progresses to renal or CNS involvement. • SCLE is characterized by photodistributed erythematous lesions that are nonscarring. • SCLE occurs most commonly in young and middle-aged white women. • Patients may have some of the American Rheumatologic Association criteria for SLE, but serious disease with renal involvement is uncommon. DESCRIPTION OF LESIONS • Lesions are papulosquamous and closely resemble psoriasis or pityriasis rosea (FIG. 25.20).

25.20 Subacute cutaneous lupus erythematosus. This patient has scaly, papulosquamous lesions. (Image courtesy of Herbert A. Hochman, M.D.)

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• Lesions are often annular and heal without scarring (FIG. 25.21). DISTRIBUTION OF LESIONS • Lesions occur on the upper trunk, the “V” of the neck, and the extensor surfaces of the arms and hands. • The face is often spared. DIAGNOSIS • Sjögrens anti-SS-A (anti-Ro) and anti-SS-B (anti-La) antibodies are often found, although the absence of these antibodies does not exclude the diagnosis. • Low titers of ANA may be present.

25.21 Subacute cutaneous lupus erythematosus. Note the annular plaques.

CLINICAL MANIFESTATIONS • Fatigue, malaise, and arthralgias may be noted. • Sjögren’s syndrome, idiopathic thrombocytopenic purpura, urticarial vasculitis, and morphea also have been reported in association with SCLE.

DIFFERENTIAL DIAGNOSIS • Psoriasis • Pityriasis rosea

MANAGEMENT • Treatment of SCLE is much like that of CCLE and SLE. • It focuses mainly on the avoidance of excessive sun exposure and the use of broad-spectrum sunscreens and topical steroids, oral antimalarials, dapsone, gold,

oral retinoids, thalidomide, and immunosuppressive drugs. • Because patients with SCLE have a better prognosis than patients with SLE, the clinician must weigh the potential toxicities of these agents against their benefits before initiating therapy.

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Ch ron ic Cu tan eou s Lu p u s Eryth em atosu s BASICS

25.22 Chronic cutaneous lupus erythematosus. Lesions of DLE have caused scarring alopecia in this patient who has no evidence of SLE.

• CCLE consists of scarring plaques. • DLE is, by far, the most common form of CCLE. • Other CCLE variants include hypertrophic lupus erythematosus, lupus erythematosus panniculitis, and lupus profundus. • DLE is a chronic, scarring, photosensitive dermatosis. DLE may occur in patients (approximately 25%) with SLE. • If the initial workup of patients who present solely with localized lesions of DLE shows no evidence of SLE, then those patients are considered to be at low risk (less than 5%) for SLE to develop. DESCRIPTION OF LESIONS • Lesions begin as well-defined, erythematous plaques that evolve into atrophic, disc-shaped plaques, characterized by scale, accentuated hair follicles, follicular plugging, and a combination of hypopigmentation and hyperpigmentation. • DLE often involves the scalp and produces scarring alopecia (FIG. 25.22), which can be quite extensive (FIG. 25.23).

25.23 Chronic cutaneous lupus erythematosus. Extensive, progressive scarring alopecia and external ear involvement are evident in this patient, who has neither serologic nor clinical evidence of systemic disease. 25.24 Chronic cutaneous lupus erythematosus. Widespread lesions of DLE are noted. Note the postinflammatory hyperpigmentation.

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DISTRIBUTION OF LESIONS • Patients with DLE often are divided into two groups: those with localized disease and those with widespread disease. Localized DLE occurs when only the head, neck, and external ears (see FIG. 25.23) are affected, whereas widespread DLE occurs when other areas are involved (FIG. 25.24). • SLE is more likely to develop in patients with widespread involvement of DLE. CLINICAL MANIFESTATIONS • Lesions of DLE are relatively asymptomatic, but they may itch or be tender. • Rarely, squamous cell carcinoma develops in hypertrophic chronic lesions.

DIFFERENTIAL DIAGNOSIS • Sarcoidosis should be considered. • Lichen planus is another possible diagnosis. • CCLE variants include the following: • Hypertrophic lupus erythematosus is a wartyappearing form of CCLE. • Lupus erythematosus panniculitis is an inflammation of subcutaneous tissue. • When lupus panniculitis occurs with a lesion of CCLE overlying it, it is referred to as lupus profundus.

DIAGNOSIS • The clinical appearance is confirmed by a punch biopsy of the skin.

MANAGEMENT • Excessive sun exposure should be avoided. • Broad-spectrum sunscreens that block both ultraviolet A (UVA) and ultraviolet B (UVB) are used. • Potent topical steroids are generally effective for treating isolated lesions. Facial lesions should be treated with lowto medium-potency agents. If necessary, high-potency or superpotent agents may be used for short periods. • Intralesional steroid injections are helpful in CCLE lesions that are refractory to topical therapy.

• Systemic agents may be indicated when lesions are widespread or unresponsive to topical or intralesional therapy. Agents such as the antimalarials hydroxychloroquine (Plaquenil) and chloroquine (Aralen) comprise the first line of systemic therapy. • Systemic steroids, dapsone, oral retinoids, gold, clofazimine, methotrexate, thalidomide, tetracycline or erythromycin combined with niacinamide, and mycophenolate mofetil (CellCept) have proved to be helpful in selective cases.

POINTS TO REMEMBER • Patients with widespread involvement are more likely to develop SLE. • Most patients with CCLE do not have and will not develop SLE. Even so, many patients who are given the diagnosis of CCLE describe themselves as having “lupus” and are convinced that they have the more serious disease.

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Neon atal Lu p u s Eryth em atosu s BASICS

25.25 Neonatal lupus erythematosus. These annular erythematous plaques that look like “ringworm” appeared shortly after birth in this 3-month-old infant of an Ro-positive mother.

MANAGEMENT

Cut an e o us Man ife st at io n s • Low-potency, nonfluorinated topical steroids are given. • Sun exposure should be avoided. He art Blo ck • Experimental therapy using dexamethasone, which crosses the placental barrier, has been used to treat heart block in utero with minimal success. • Pacemaker implantation is frequently required.

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• Neonatal lupus erythematosus (NLE) is a rare autoimmune syndrome that affects 1% to 2% of infants born of mothers who are anti-Ro (SS-A) antibody positive. • Mothers may or may not show any of the signs or symptoms of connective tissue disease at the time of birth of the affected infant; however, some features of Sjögren’s syndrome or lupus erythematosus (e.g., dry mouth, dry eyes, or arthralgias) do ultimately develop in most of these women. This situation may occur many years after the birth of the child; however, in most of these women, SLE does not develop. DESCRIPTION OF LESIONS • The rash of NLE is a benign, self-limited eruption that appears at birth and tends to disappear by approximately 6 months of age. • The rash is characterized by annular (ringlike) erythematous plaques or smaller erythematous patches that generally are apparent at birth or several days thereafter (FIG. 25.25). CLINICAL MANIFESTATIONS • NLE is characterized by either benign skin disease or congenital heart block, or both, in about 10% of cases. • Involvement of joints, kidneys, and CNS is rare. • Congenital heart block presents a 20% mortality risk and often requires the insertion of a pacemaker. The onset of heart block generally occurs a few weeks before term and is seen at birth. • Unlike the skin lesions, the cardiac problems associated with NLE are permanent.

Derm atom yositis BASICS • Dermatomyositis is an inflammatory skin and muscle disease that is related to polymyositis; in fact, both conditions are considered to be the same disease except for the presence or absence of the rash. Cutaneous manifestations without detectable muscle disease are known as amyopathic dermatomyositis. • The female-to-male ratio is 2:1. • An autoimmune origin, which may be initiated by a virus in genetically susceptible people, has been proposed as a possible cause of dermatomyositis. As a result, antibodies that attack the skin and muscle are produced. • An overlap syndrome with scleroderma or lupus (mixed connective tissue disease) is characterized by the presence of antiribonucleoprotein (anti-RNP) antibodies. • Adults with dermatomyositis appear to have an increased risk of malignant diseases. The skin disease often follows the clinical course of exacerbations and remissions of the cancer. Most malignant diseases are the common cancers (e.g., colon and breast cancer) that occur in a general aging population.

25.26 Dermatomyositis. This child has the characteristic heliotrope (pink-purple) erythema of the upper eyelids, as well as lesions on the cheeks, nose, and “butterfly” area, that are suggestive of SLE.

DESCRIPTION AND DISTRIBUTION OF LESIONS • The heliotrope rash consists of red or violaceous coloration around the eyes and is associated with periorbital edema (FIG. 25.26). (The change in color may be a subtle clinical finding, particularly in dark-skinned patients.) • Gottron’s papules consist of erythematous or violaceous, flat-topped papules on the dorsa of the hands (FIG. 25.27). Lesions are located on the joints of the fingers; they begin as papules and later become atrophic and hypopigmented. • Poikiloderma is a characteristic rash of dermatomyositis, consisting of telangiectasia, atrophy, hyperpigmentation, and hypopigmentation. Poikiloderma occurs on the extensor aspects of the body, upper back (shawl sign), forearms, and “V” of the neck (see also FIG. 25.15). Atrophic lesions occur particularly on the knees and elbows. • Periungual telangiectasias and nail dystrophy occur. Nail fold changes consist of periungual telangiectases and/or a characteristic hypertrophy of the cuticle (FIG. 25.28).

25.27 Dermatomyositis. Gottron’s papules are violaceous, flat-topped papules located on the knuckles of the fingers in this child with juvenile dermatomyositis.

CLINICAL MANIFESTATIONS • Progressive, bilateral, symmetric, proximal muscle weakness develops, as suggested by difficulty with brushing or combing hair and standing from a seated position. • Muscle tenderness or pain is usually not a complaint. • Photosensitivity is evidenced in areas of poikiloderma. • Arthralgias occur in one third of patients. • There may be features of an overlap syndrome.

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• Pulmonary fibrosis affects 10% of patients, particularly in the presence of anti-Jo 1 (histidine) or anti-PL 12 (alanine) antibodies. • Evidence of vasculitis (e.g., palpable purpura or ulcers) may be present. • Calcinosis cutis is seen in the juvenile form of dermatomyositis. • Myocardial disease may be an associated finding. • Dysphagia may occur. DIAGNOSIS • The findings on skin biopsy are often nonspecific but are generally suggestive of a connective tissue disease. • Elevation of creatine phosphokinase levels is often a reliable indicator of muscle involvement. • Aldolase levels may be increased. • Electromyography may aid in the diagnosis. • Muscle biopsy may aid in the diagnosis as well. • The presence of autoantibodies, such as anti-DNA, antiRNP, and anti-Ro, may be found. Anti-M-1 antibody is highly specific for dermatomyositis, but it is present in only 25% of patients.

MANAGEMENT

Skin • Avoidance of excessive sun exposure • Use of broad-spectrum sunscreens • Antimalarial drugs: hydroxychloroquine (Plaquenil), 5 mg/kg/day for 4 to 6 weeks; then titrate according to clinical response • Low-dose oral methotrexate Syst e m ic Sym p t o m s • Physical therapy • Systemic steroids (when used for systemic symptoms, may also improve skin conditions)

POINT TO REMEMBER • The adult form of dermatomyositis may be associated with internal malignant diseases; patients older than age 50 years should be evaluated with this possibility in mind. 476

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25.28 Dermatomyositis. Periungual telangiectasias are present. Note the thickening of the cuticles and the nail dystrophy in this patient.

DIFFERENTIAL DIAGNOSIS • SLE should be considered. • Mixed connective tissue disease or overlap syndrome is another possibility. • When only the muscle is involved, other myopathies should be considered.

• Immunosuppressive therapy, including low-dose oral methotrexate • Cyclosporine • Cyclophosphamide • Azathioprine • Plasmapheresis • Interferons • Intravenous high-dose -globulin

Sclerod erm a an d Morp h ea BASICS • Scleroderma is an autoimmune connective tissue disease in which excess collagen results from an increase in number and activity of fibroblasts. Induration and thickening of the skin and subcutaneous tissues result. This process is triggered by vascular inflammation and infiltration of activated T4 cells. • The origin of scleroderma is unknown. As in lupus, scleroderma may be seen either in a systemic or localized cutaneous form.

Classificat io n • Morphea, or localized scleroderma, is limited to the skin and has rarely been reported to progress to systemic scleroderma. The female-to-male ratio is 3:1. • Systemic scleroderma may be divided as follows: • CREST syndrome (defined subsequently), which accounts for 90% of the cases of systemic sclerosis, is a relatively benign variant with a delayed appearance of visceral involvement. • Progressive systemic sclerosis is a chronic multisystem disease that affects the skin and internal organs and has a very poor prognosis. • In systemic sclerosis, the female-to-male ratio is 4:1. DESCRIPTION OF LESIONS

Mo rp h e a • A localized, indurated, hairless plaque has a characteristic “lilac” border (FIG. 25.29). • Patients may have a single plaque or multiple plaques. • White, ivory, or hyperpigmented permanent scars result when lesions heal.

25.29 Morphea. This ivory-colored plaque has the characteristic “lilac” border. This boy has multiple plaques.

CREST Syn d ro m e an d Pro g re ssive Syst e m ic Scle ro sis • Acrosclerosis refers to ill-defined, indurated fibrotic skin, which occurs peripherally and gradually involves the forearms. • Sclerodactyly consists of thickened, sausage-shaped digits in which the skin becomes tight and bound down. Gradually, the skin becomes shiny, stiff, waxy, and atrophic (FIG. 25.30).

25.30 Scleroderma with acrosclerosis and sclerodactyly. The patient has tapered, shiny, stiff, waxy fingers. Note the painful vasculitic lesions on the fingertips. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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DISTRIBUTION OF LESIONS • In morphea, lesions are commonly found on the trunk; they may become widespread (generalized morphea) or linear (linear morphea), which may have the characteristic frontoparietal distribution (coup de sabre) (FIG. 25.31). • In CREST syndrome, the cutaneous involvement is usually limited to acral areas (hands, feet, face, and forearms). • Patients with progressive systemic sclerosis often have widespread, progressive disease. CLINICAL MANIFESTATIONS

25.31

Linear morphea. Coup de sabre lesions are present.

25.32 Scleroderma. Note the shortened finger resulting from distal bone resorption.

• Morphea (localized scleroderma) is generally asymptomatic, usually “burns out” spontaneously, and leaves a scar. • CREST syndrome consists of the following: • Calcinosis cutis, most commonly occurring on the palms, fingertips, and bony prominences • Raynaud’s phenomenon • Esophageal dysfunction • Sclerodactyly (“claw deformity”) • Telangiectasia (macular lesions) on the face, lips, palms, back of hands, and trunk • Manifestations of progressive systemic sclerosis include the following: • Raynaud’s phenomenon, often an early symptom, which consists of pain and a characteristic sequence of color changes of the distal fingers from white to purple to red in response to cold exposure • Diffuse involvement and symptoms secondary to the tightening of the skin, with difficulty in opening the mouth and loss of manual dexterity; later, contractures of the hands, painful fingertip ulcers resulting from vasculitis, and shortening of fingers resulting from distal bone resorption (FIG. 25.32) • Esophageal dysfunction, dysphagia, bloating, and diarrhea • Systemic symptoms including shortness of breath, difficulty in swallowing, and arthralgia • Masklike facies • Possibly, rapid progression of kidney disease, reduced breathing capacity, cardiac disease, and renal failure DIAGNOSIS

Mo rp h e a • The diagnosis is generally made on clinical grounds and skin biopsy. • The serologic examination is generally negative. CREST Syn d ro m e • The diagnosis is generally made on clinical grounds. • Positive anticentromere antibody is seen in 70% of patients. Pro g re ssive Syst e m ic Scle ro sis • The diagnosis is generally made on clinical grounds. • The Scl-70 antibody is present in approximately 30% of patients. 478

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DIFFERENTIAL DIAGNOSIS • • • •

Other connective tissue diseases Mixed connective tissue disease Overlap syndromes Lichen sclerosis

POINT TO REMEMBER • CREST syndrome has a more favorable prognosis than progressive systemic sclerosis, although visceral involvement may occur late in the course of the disease.

HELPFUL HINTS MANAGEMENT

Lo calize d Scle ro d e rm a • Topical, intralesional, and systemic steroids may be helpful in the early inflammatory stage. • Vitamin D analogues (calcitriol, calcipotriene), UVB, UVA, and methotrexate may also be of some benefit.

• Therapy of systemic scleroderma should include full range-of-motion exercises. • Some evidence suggests that some European cases of morphea may result from Borrelia burgdorferi infection. This connection has not been demonstrated in the United States.

CREST Syn d ro m e an d Pro g re ssive Syst e m ic Scle ro sis These conditions are difficult to treat and remain a great challenge. The following agents and approaches have been used with minimal success: • The following drugs are currently under investigation for this indication: nifedipine, angiotensin-converting enzyme inhibitors, prostaglandins, immunosuppressive agents, D-penicillamine, colchicine, -interferon, and relaxin. • Systemic steroids, minocycline, psoralen and UVA light, lung transplantation, autologous stem cell transplantation, etanercept, and thalidomide have also been used.

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Er yt h em a No d o su m BASICS

25.33 Erythema nodosum. Acute red, tender nodules appeared in this patient after she began taking oral contraceptives.

• Erythema nodosum (EN) is an acute inflammatory reaction of the subcutaneous fat. It is considered a delayed hypersensitivity reaction to various antigenic stimuli. • EN is three times more common in females than in males and has a peak incidence between 20 and 30 years of age. • Sarcoidosis, streptococcal infections, pregnancy, and the use of oral contraceptives are the most common causes of EN in the United States. • In children, streptococcal pharyngitis is the most likely underlying cause. • Approximately 40% of cases are idiopathic. • In addition to sarcoidosis and pregnancy, EN is associated with a variety of conditions: deep fungal infections (in endemic areas), including coccidioidomycosis, histoplasmosis, and blastomycosis; tuberculosis; Yersinia enterocolitica infection; inflammatory bowel disease, including ulcerative colitis and Crohn’s disease; malignant disease, including lymphoma and leukemia; radiation therapy; and Behçet’s syndrome. Drugs such as sulfonamides, penicillin, gold, amiodarone, and opiates also have been implicated as causes of EN. DESCRIPTION OF LESIONS • Lesions begin as bright red, deep, extremely tender nodules (FIG. 25.33). • During resolution, lesions become dark brown, violaceous, or bruiselike macules (“contusiform”) (FIG. 25.34). DISTRIBUTION OF LESIONS • EN tends to occur in a bilateral distribution on the anterior shins, thighs, knees, and arms. CLINICAL MANIFESTATIONS

25.34 Erythema nodosum. These are healing “contusiform” lesions.

• Malaise, fever, arthralgias, and periarticular swelling of the knees and ankles may accompany the panniculitis. • Other symptoms may also be present, depending on the cause of EN. • Spontaneous resolution of lesions occurs in 3 to 6 weeks, regardless of the underlying cause. • Generally, EN indicates a better prognosis in patients who have sarcoidosis. DIAGNOSIS

MANAGEMENT • Treatment is symptomatic, consisting of bed rest, leg elevation, nonsteroidal anti-inflammatory drugs (NSAIDs), or iodides. • Systemic corticosteroids, which often bring dramatic improvement, can be used if an infectious cause is excluded. • Treatment or avoidance of the underlying cause, if discovered, should be attempted. 480

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• The diagnosis of EN is usually made on clinical grounds, but a biopsy may be helpful for confirmation.

Lab o rat o ry Evaluat io n • Usually, a complete blood count, erythrocyte sedimentation rate, throat culture, antistreptolysin titer, purified protein derivative skin test, and chest film are all that are necessary. • A excisional skin biopsy will show panniculitis with infiltration of lymphocytes in the septa of the fat. • Additional tests, such as gastrointestinal tract evaluation and serum angiotensin-converting enzyme determination, can be performed if suggested by the review of systems and physical examination.

Cu t a n eo u s Sa rco id o sis BASICS • Sarcoidosis is an example of a systemic disease in which cellular granulomatous infiltrates produce dermal skin lesions. • Sarcoidosis is a chronic multisystemic disease of unknown origin. Most often, it presents with bilateral hilar adenopathy, pulmonary infiltration, eye lesions, and arthralgias; less commonly, there is involvement of the spleen and salivary and lacrimal glands, as well as gastrointestinal and cardiac manifestations. • Sarcoidosis is seen most commonly in young adults, particularly in blacks in the United States and South Africa. It is also more common in Scandinavians. • Of patients with sarcoidosis, 20% to 35% have cutaneous involvement. It usually accompanies systemic involvement but may be the only site of involvement. • African-Americans have a greater risk of developing more serious problems such as cystic bone lesions, chronic uveitis, and chronic progressive disease. DESCRIPTION OF LESIONS • Specific lesions of cutaneous sarcoid include the following: • Dermal papules, nodules, or plaques that are brown or violaceous (FIG. 25.35). • Lesions that may be annular, serpiginous, or atrophic. • Lesions that can also appear on dorsa of hands, fingers, toes, and forehead. • Lupus pernio, a distinct variant, which consists of reddish purple plaques around the nose, ears, lips, and face (FIG. 25.36). Lupus pernio also occurs with a higher frequency in African-Americans and Puerto Ricans than in whites. • Subcutaneous nodules (Darier-Roussy nodules). These usually nontender, firm, oval, flesh-colored or violaceous 0.5- to 2-cm nodules are found on the extremities or trunk. • Nonspecific cutaneous lesions associated with sarcoid include the following: • EN may occur in acute sarcoidosis (see the earlier discussion of EN). It more commonly affects Scandinavian populations. • Ichthyosis may be noted.

25.35 Cutaneous sarcoidosis. Dermal nodules are seen in a periorificial distribution (i.e., around the mouth, eyes, and nares). Note the sarcoidal lesions arising in the scars of this patient’s neck.

DISTRIBUTION OF LESIONS • Lesions tend to be located periorificially (e.g., around the eyelids, nasal ala, tip of nose, earlobes, and lips). • Lesions may occur in old scars anywhere on the body. Scars from previous traumas, surgery, venipuncture, or tattoos may become infiltrated and may be red or purple. • Scalp lesions may produce scarring alopecia. • Ichthyosiform and lesions of EN tend to occur on the pretibial area.

25.36 Cutaneous sarcoidosis (lupus pernio). These reddish purple and “apple jelly” beaded papules are located periorificially.

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CLINICAL MANIFESTATIONS • Skin lesions are generally asymptomatic; however, they are often of great cosmetic concern because they occur commonly on the face. • EN associated with sarcoidosis generally resolves spontaneously and suggests a better prognosis. • Löfgren’s syndrome (EN and arthritis) is a clinical variant of sarcoidosis.

DIFFERENTIAL DIAGNOSIS

Gran ulo m a An n ulare • This condition is discussed in Chapter 4, “Inflammatory Eruptions of Unknown Cause.” Cut an e o us Tub e rculo sis • This is also known as lupus vulgaris.

DIAGNOSIS • “Apple jelly” nodules are seen on blanching lesions with a glass slide (diascopy). These nodules represent the gross appearance of granulomas. • Skin biopsy demonstrates noncaseating granulomas (sarcoidal granulomas). • A chest radiograph may demonstrate bilateral hilar adenopathy and other characteristic changes. • Abnormal laboratory evaluations may include the following: • Elevated angiotensin-converting enzyme levels • Hypergammaglobulinemia • Hypercalcemia

HELPFUL HINTS • Systemic steroids should not be used routinely to treat cutaneous lesions; rather, potent topical steroids, intralesional steroids, or oral antimalarials should be tried first. If possible, systemic steroids are best reserved for more serious systemic involvement. • Oral antimalarials can lead to irreversible retinopathy and blindness. Eye examination is necessary before and during antimalarial therapy. • Granulomatous acne rosacea may mimic sarcoidosis clinically and histopathologically. It is referred to as lupus miliaris disseminatus faciei.

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MANAGEMENT • Potent topical steroids are applied under occlusion, if necessary. • Intralesional steroid injections can help flatten lesions. • Oral antimalarial agents such as hydroxychloroquine (Plaquenil) and chloroquine are administered for therapeutically unresponsive or widespread disease. • Oral corticosteroids should be used only on a shortterm basis. • If corticosteroids are not effective, immunosuppressants such as methotrexate and azathioprine may be effective. Other agents that have been used to treat cutaneous sarcoidosis include cyclosporine, oral isotretinoin, allopurinol, and thalidomide. Chlorambucil also has been reported to be effective, but the risk of malignant disease is great with this medication.

In fl a m m a t o r y Sk in Diso rd ers Reiter’s Syn d rom e BASICS • Reiter’s syndrome (RS), also referred to as reactive arthritis, is an idiopathic inflammatory process affecting the skin, joints, and mucous membranes. The classic triad of urethritis, conjunctivitis, and arthritis is found in only 40% of cases at the time of the initial clinical presentation. • RS is seen most commonly in young white men of European origin. • Initial symptoms often occur after nongonococcal urethritis (e.g., chlamydial infection) or infection with an enteric pathogen (e.g., Shigella and Yersinia). • HLA-B27 is frequently positive in patients with RS and portends a poorer prognosis. DESCRIPTION OF LESIONS Skin lesions are often indistinguishable from psoriasis; however, RS often manifests certain characteristic findings such as the following: • Keratoderma blennorrhagicum (FIG. 25.37) consists of scaly, red, inflammatory, psoriasislike lesions on the palms and soles. The lesions may have a thick scale and may be pustular. • Scaling red plaques or erosions may be found on the glans penis (circinate balanitis) (FIG. 25.38). • Nail changes may include findings such as those seen in psoriasis (e.g., onycholysis and subungual hyperkeratosis); furthermore, subungual pustules with resultant shedding of nails may occur. • Oral lesions are usually painless, irregularly shaped, white plaques on the tongue that resemble geographic tongue.

25.37 Reiter’s syndrome. Keratoderma blennorrhagicum. Scaly, red-brown, inflammatory, pustular, psoriasislike lesions are present on the soles.

DISTRIBUTION OF LESIONS • Keratoderma blennorrhagicum is most often noted on the palms and soles. • Psoriasislike plaques may be seen on the scalp, elbows, knees, buttocks, shaft of the penis, and scrotum. CLINICAL MANIFESTATIONS • RS is a multisystemic disease that may present with fever, malaise, dysuria, arthralgias, and red irritated eyes with accompanying cutaneous lesions. • Frequently, RS has a self-limited course, but it may become a chronic, relapsing condition. • RS is common in patients with human immunodeficiency virus (HIV) disease. (See Chapter 24, “Cutaneous Manifestations of HIV Infection.”) • The arthritis of RS is an asymmetric oligoarthritis that commonly involves large joints (elbows, knees); it may also

25.38 Reiter’s syndrome. In circinate balanitis, psoriasiform lesions occur on the glans penis and the scrotum.

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involve smaller joints. Sacroiliitis and ankylosing spondylitis may occur. • Ocular disease may include conjunctivitis with intense red conjunctival injection and, less commonly, iritis and keratitis. • Urethritis is a nonspecific urethral inflammation with a purulent exudate and dysuria. DIAGNOSIS • The diagnosis is generally made on clinical grounds.

Lab o rat o ry Evaluat io n • HLA-B27 is positive in 75% of patients. • ANA and rheumatoid factor are usually negative. • The histopathologic features of skin lesions in RS are indistinguishable from those of psoriasis. • HIV testing should be performed.

MANAGEMENT

Mild Case s • RS may be treated with topical steroids for the skin lesions. • NSAIDs are prescribed for pain. Se ve re Case s • Oral methotrexate is sometimes used on a weekly basis for severe cases.

POINT TO REMEMBER • During initial or recurrent episodes, most patients with RS do not manifest the complete triad of urethritis, conjunctivitis, and arthritis.

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DIFFERENTIAL DIAGNOSIS

Pso riasis wit h Art h rit is See Chapter 3, “Psoriasis.” • Psoriasiform skin lesions • Arthritis similar to that seen in RS • No ocular symptoms • No urethritis Be h çe t ’s Syn d ro m e • Painful oral ulcers • Arthritis • Iritis • Vasculitic skin lesions Can d id al Balan it is • Positive potassium hydroxide examination or fungal culture

• Oral steroids may be necessary; however, tapering of steroids can produce an extreme flare of the pustular lesions. • Oral retinoids such as 13-cis-retinoic acid (Accutane) and acitretin (Soriatane) have also been used to treat skin lesions. • Methotrexate, cyclosporine, UVB/UVA, and infliximab (Remicade) have also been used to treat the cutaneous manifestations.

Pyod erm a Gan gren osu m BASICS • Pyoderma gangrenosum (PG) is an uncommon condition of uncertain origin. • It is a unique, painful, inflammatory, ulcerative process of the skin. • It is often seen in association with certain systemic diseases including ulcerative colitis, regional enteritis, rheumatoid arthritis, and leukemia; however, some investigators believe it to be a distinct disease. DESCRIPTION OF LESIONS • Skin ulcers are 2 to 10 cm in diameter. • They are deep ulcerations with an erythematous to violaceous border. The border is often undermined (a probe can be placed under the overhanging edge of the lesion). • Lesions may be multiple. • Lesions heal with scarring (FIG. 25.39).

25.39 Pyoderma gangrenosum. This large ulceration is beginning to heal with a craterlike (cribriform) scar.

DISTRIBUTION OF LESIONS • Skin ulcers are most commonly found on the lower extremities (shins and ankles). CLINICAL MANIFESTATIONS • Lesions can appear as a rapidly expanding, painful, skin ulcer (FIG. 25.40). • It is usually self-limited, and spontaneous healing may occur. • Patients often have associated oligoarticular arthritis. • Ulcerations of PG occur after trauma or injury to the skin in some patients; this process is termed pathergy. • Diseases associated with PG include the following: • Ulcerative colitis • Regional enteritis (Crohn’s disease) • Rheumatoid arthritis • Myelogenous leukemia • In 50% of patients, no underlying systemic disease is present.

25.40 Pyoderma gangrenosum. This acute ulceration was initially considered to be a necrotic reaction to a spider bite. The patient was found to have regional enteritis (Crohn’s disease).

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DIAGNOSIS • The diagnosis of PG is generally made on a clinical basis. This is often done by excluding other causes of similarappearing cutaneous ulcerations including infection, stasis ulcers, malignant disease, vasculitis, collagen vascular diseases, diabetes, and trauma, as described subsequently.

Lab o rat o ry Evaluat io n • Skin biopsy of the edge of the ulcer may be performed to rule out other causes of skin ulcers, such as infections or malignant disease; however, the pathologic findings for PG are nonspecific. • Bacterial, fungal, and viral cultures of the ulcer are performed if clinically indicated. • Workup for systemic disease should include complete blood count with differential, erythrocyte sedimentation rate, sequential multichannel autoanalyzer 20, ANA, Venereal Disease Research Laboratory test, rheumatoid factor, and a chest radiograph. • Serum or urine protein electrophoresis, peripheral smear, and bone marrow aspirate are performed, if indicated, to evaluate for hematologic malignant diseases. • A gastrointestinal series for inflammatory bowel disease should be done if clinically indicated.

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DIFFERENTIAL DIAGNOSIS

Cut an e o us Malig n an t Dise ase s • Basal cell carcinoma • Squamous cell carcinoma In fe ct io us Pro ce sse s • Bacterial infections • Deep fungal infections • Herpes simplex virus infections In flam m at o ry Pro ce sse s • Collagen vascular diseases • Polyarteritis nodosa • Behçet’s disease • Wegener’s granulomatosis • Antiphospholipid antibody syndrome

MANAGEMENT • The treatment of underlying associated diseases does not necessarily promote the healing of PG.

To p ical an d In t rale sio n al Th e rap y • Local compresses, antiseptic washes, and topical antibiotics may be useful. • Superpotent topical corticosteroids, cromolyn sodium 2% solution, nitrogen mustard, and 5-aminosalicyclic acid may be tried. • Intralesional steroid injections (triamcinolone acetonide, 10 mg/mL) are administered into the edge of the ulcer. Syst e m ic Th e rap y • Oral steroids for several weeks to months (starting at 60 to 80 mg prednisone daily and tapering the steroid slowly). Systemic steroids may be given alone or in combination with dapsone, azathioprine, or chlorambucil.

In patients with steroid-resistant PG, oral cyclosporine has been shown to be effective. • The following drugs have also met with some success: mycophenolate mofetil (CellCept), tacrolimus, cyclophosphamide, thalidomide, and nicotine chewing gum. • Intravenous therapy can be administered using pulsed methylprednisolone, pulsed cyclophosphamide, or human immunoglobulin. • Surgical grafting and microvascular free flaps are best reserved for after the disease has become inactive.

Ot h e r Th e rap ie s • Hyperbaric oxygen has been used. • Biologics such as etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade) may prove useful. See Chapter 3, “Psoriasis,” for a discussion of the biologics.

Exfoliative Derm atitis

POINT TO REMEMBER • Surgical débridement of the lesions of PG should be avoided, if possible, because of the pathergy that may occur with surgical manipulation or grafting. This can result in further wound enlargement.

BASICS • Exfoliative dermatitis (ED), known as erythroderma in the United Kingdom and l’homme rouge in France, refers to a total, or almost total, redness or scaling of the skin. • It is an uncommon disorder seen more often in male patients; 50 years is the average age of occurrence. • In children, ED most often is secondary to severe atopic dermatitis. • In adults, psoriasis is the most frequently associated skin disease (see Chapter 3, “Psoriasis”). • ED may appear suddenly or gradually, occasionally accompanied by fever, chills, and lymphadenopathy. • ED may be a stage in the natural history of severe eczematous dermatitis or psoriasis. • Less commonly, ED has been reported as a finding in the following skin disorders: • Allergic contact dermatitis • Stasis dermatitis with secondary autoeczematization

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• Papulosquamous dermatitis of acquired immunodeficiency syndrome • Graft-versus-host disease • Seborrheic dermatitis (Leiner’s disease) in infants • Pemphigus foliaceus • Pityriasis rubra pilaris (a rare disorder of keratinization) • ED may occur as a reaction to the following drugs: sulfonamides; penicillins; antimalarials; lithium; phenothiazines; barbiturates; gold; allopurinol; NSAIDs, including aspirin; captopril; codeine; and phenytoin. • It may be a complication or presenting symptom of the following malignant diseases: • Mycosis fungoides (cutaneous T-cell lymphoma) • Sézary syndrome (leukemic variant of mycosis fungoides) • Hodgkin’s disease • Non-Hodgkin’s lymphoma and leukemia • It is an idiopathic phenomenon in 20% to 30% of cases without any preceding dermatosis or systemic disease. DESCRIPTION OF LESIONS • Marked generalized erythema is followed by scaling (FIGS. 25.41 and 25.42). • Pruritus may be severe. • There is edema and increased warmth of the skin. • Lymphadenopathy, usually a reactive type (dermatopathic lymphadenopathy), is often present. • Unlike toxic epidermal necrolysis, ED spares the mucous membranes. DISTRIBUTION OF LESIONS 25.41 Exfoliative erythroderma (exfoliative dermatitis). This patient has generalized erythema (l’homme rouge, “red man syndrome”). The etiology of his erythroderma was never determined.

25.42 Exfoliative erythroderma. This patient has severe, widespread psoriasis. Note the marked scaling. 488

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• ED usually begins in a limited area; however, it may rapidly become generalized. CLINICAL MANIFESTATIONS • Unless patients have a known preexisting skin condition or concurrent physical evidence of a skin disease such as psoriasis, the clinical appearance and symptoms of most cases of ED tend to be similar, consisting of the following: • Erythema is followed by scaling. • Pruritus may develop. • Edema and increased warmth of skin are usually present. • Lymphadenopathy, usually a reactive type (dermatopathic lymphadenopathy) and secondary to the marked inflammatory changes in the skin, may be seen; however, lymphoma should be considered, particularly if the lymph nodes are large or unilateral. • Thermoregulatory disturbances are manifested by fever or, more frequently, by hypothermia. If widespread inflammation occurs, the barrier efficiency of the skin may be impaired secondary to extensive vasodilatation. • Protein loss secondary to a massive shedding of scale may occur, with resultant hypoalbuminemia.

• Rarely, high-output cardiac failure may develop, particularly in patients with a history of cardiac disease. • The following chronic changes may also be seen: • Scaling of palms and soles (keratoderma) • Thickening and lichenification of the skin • Scalp involvement, occasionally producing nonscarring alopecia • Nail dystrophy, onycholysis (separation of the nail plate from the nail bed), or nail shedding • Pigmentary changes (postinflammatory hypopigmentation or hyperpigmentation) • Persistent generalized erythema • Conjunctivitis, keratitis, or ectropion DIAGNOSIS • The diagnosis of ED is made on a clinical basis. The diagnosis of the underlying cause is often elusive. Clinical findings, such as the characteristic lichenification and crusting of atopic dermatitis or nail pitting that suggests psoriasis, may be found. • Eliciting a history of drug ingestion or a preexisting dermatosis may be valuable. • Laboratory testing can provide serologic evidence of Sézary’s syndrome or leukemia.

• Patch testing during a period of remission may uncover a contact allergen.

Hist o p at h o lo g y • Histologic findings of the various causes are similar and are generally nondiagnostic; however, a diligent search for lymphoma, particularly mycosis fungoides, must be pursued with repeated skin biopsies. Lab o rat o ry Evaluat io n The following are possible positive laboratory findings: • • • • • •

Anemia (usually the anemia of chronic disease) Decreased serum levels of protein and albumin Leukocytosis Eosinophilia Elevated sedimentation rate Elevated immunoglobulin E level (possibly supporting the diagnosis of atopic dermatitis) • Leukemia (found by peripheral blood smear) • Imaging studies with computed tomography or magnetic resonance imaging if lymphoma or Hodgkin’s disease is suspected

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DIFFERENTIAL DIAGNOSIS • Toxic epidermal necrolysis is a potentially fatal condition that involves the skin and mucous membranes. Marked erythema is quickly followed by sloughing of the skin. This condition is often the result of a severe drug reaction.

MANAGEMENT • Treatment is directed toward the underlying cause, if it is known. For example, suspected etiologic drugs or contactants should be eliminated. • Bed rest, cool compresses, lubrication with emollients, antipruritic therapy with oral antihistamines, and low- to intermediate-strength topical steroids are used. • Systemic antibiotics can be administered if signs of secondary infection are observed • In severe cases, patients frequently require hospitalization, where measures such as fluid replacement, temperature control, expert topical skin care, and systemic corticosteroids may be used. • Isotretinoin (Accutane) has been used when pityriasis rubra pilaris is the underlying cause

Exfo liat ive De rm at it is Se co n d ary t o Pso riasis • Possible precipitating factors (e.g., ultraviolet exposure) or drugs that are suspected to provoke ED (e.g., antimalarials) should be avoided. • Systemic and topical steroids are helpful, except that they may worsen psoriasis and have been known to precipitate ED or an acute fulminant form of pustular psoriasis, known as pustular psoriasis of Von Zumbusch. This worsening of psoriasis tends to occur after steroid withdrawal.

POINTS TO REMEMBER • In its more severe manifestations, ED is a medical and dermatologic emergency. Consultation and ongoing management, using the expertise of both disciplines, are often necessary. • In many cases, the underlying cause is never established.

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• If conservative therapy fails, methotrexate, cyclosporine, and retinoids (e.g., acitretin) are additional therapeutic options. • Phototherapy, photopheresis, and photochemotherapy, as well as monoclonal antibodies such as infliximab (Remicade) and Adalimumab (Humira), may be effective. • For a further discussion of psoriasis, see Chapter 3, “Psoriasis.”

Pro g n o sis • The course of ED depends on its underlying origin. ED resulting from a drug eruption may clear in days to weeks, whereas in some cases, the disease may persist for many years, with exacerbations and remissions and no diagnosis. • The prognosis of ED depends largely on the underlying etiology. • In patients with an identified underlying cause, the course and prognosis generally parallel the primary disease. • ED caused by a drug eruption usually clears when the drug is stopped. • Acute, severe episodes, particularly in elderly persons or in persons with preexisting heart disease, have a more guarded prognosis. • In patients with idiopathic ED, the prognosis is poor, and recurrences are not uncommon.

Neu ro cu t a n eo u s Syn d ro m es Neurocutaneous diseases are genetically determined disorders that show both cutaneous and neurologic involvement.

Neu rofibrom atosis BASICS • Neurofibromatosis (NF), or von Recklinghausen’s disease, is an autosomally inherited disease in which macular pigmented skin lesions (café au lait spots) and skin tumors (neurofibromas) occur in patients in whom a wide range of CNS or spinal cord lesions may ultimately develop. • The incidence of NF is 4 per 10,000 births. Fifty percent of cases are thought to be inherited in an autosomal dominant fashion; the remaining cases are the result of spontaneous new mutations. • There are two genetic types of NF: • NF1 is caused by a mutation in a gene on chromosome 17q11.2. This gene has been isolated and encodes neurofibromin. This protein may act as a tumor-suppressor gene by binding to Ras protein. • NF2, which is localized to chromosome 22q11, is characterized by bilateral acoustic neuromas and fewer skin manifestations. The protein for this gene has not been isolated, but it may also act as a tumor-suppressor gene.

25.44 Neurofibromatosis 1. Soft, rubbery, flesh-colored papules and nodules are seen on this patient’s face.

DESCRIPTION OF LESIONS • Café au lait spots are multiple, light brown macules that are greater than 1 cm in diameter (FIG. 25.43). • Cutaneous neurofibromas are soft, rubbery, skin-colored or tan papules and nodules (FIG. 25.44). • Plexiform neuromas manifest as large, drooping tumors, which on palpation feel like a “bag of worms” (FIG. 25.45). • Axillary or inguinal freckling (Crowe’s sign) consists of small pigmented macules in some patients and is considered to be pathognomonic for NF1 (FIG. 25.46).

25.43 Neurofibromatosis 1. The multiple light brown macules are café au lait spots.

25.45 Neurofibromatosis 1. This plexiform neuroma feels like a “bag of worms.”

25.46 Neurofibromatosis 1. Crowe’s sign (axillary “freckles”) is considered pathognomonic for the disease. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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DISTRIBUTION OF LESIONS • Café au lait spots most often appear on the trunk and extremities. • Neurofibromas may appear on the face, trunk, and extremities. CLINICAL MANIFESTATIONS • Café au lait spots are usually present at birth or shortly thereafter. • Cutaneous neurofibromas may first develop in adolescence, and new lesions may continue to emerge during the patient’s lifetime. Up to 5% of skin tumors may develop into neurofibrosarcomas. • Ocular lesions (Lisch nodules) are asymptomatic, pigmented iris hamartomas seen in 80% of patients with NF. • CNS tumors, optic gliomas, and spinal cord tumors may develop at any age. • CNS involvement usually consists of benign lesions such as optic gliomas, acoustic neuromas, and meningiomas. CNS lesions may become astrocytomas. • CNS involvement may occur in up to 10% of patients with NF. • Spinal cord tumors may produce spinal cord damage and paraplegia. • Many patients with NF have seizure disorders and mental retardation. • Macrocephaly may be present in up to 16% of patients. • Musculoskeletal disorders are uncommon, but pseudoarthrosis of the tibiae and kyphoscoliosis may be diagnostic in some patients with NF. • Gastrointestinal symptoms may occur in some patients in whom intussusception and obstruction of the small intestine develop from intraabdominal neurofibromas. • Endocrine disorders occur; 3% to 5% of affected children have sexual precocity associated with short stature. • Pheochromocytomas characterized by life-threatening severe hypertension occur in less than 1% of patients with NF. DIAGNOSIS

Ne uro fib ro m at o sis 1 • Café au lait spots are seen in 10% to 20% of the general population; however, six or more café au lait spots that are greater than 0.5 cm in diameter in infants or greater than 1 cm in diameter in adults are supportive of the diagnosis of NF1. • A first-degree relative with NF1 supports the diagnosis. • Other findings supportive of the diagnosis include the following: • Crowe’s sign • Lisch nodules • Distinctive osseous lesions such as sphenoid dysplasia or thinning of long bone cortex

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Ne uro fib ro m at o sis 2 • Bilateral masses of the eighth cranial nerve (acoustic neuromas) are suggestive. • A first-degree relative with NF2 supports the diagnosis. Lab o rat o ry Evaluat io n • Skin biopsies of café au lait macules may show macromelanosomes on electron microscopy, but these findings are not diagnostic. • Biopsies of neurofibromas show characteristic Schwann cells and neuronal cells. • Magnetic resonance imaging studies of the brain and cervical spine may be helpful in NF1 patients with symptoms of CNS disease and in patients with suspected NF2 disease.

DIFFERENTIAL DIAGNOSIS

Se g m e n t al Ne uro fib ro m at o sis • Café au lait macules localized to one area of the body • Cutaneous localized neurofibromas • Absence of CNS tumors • Lack of inheritance (somatic mutation) McCun e -Alb rig h t Syn d ro m e • Pigmented macular lesions • Polyostotic fibrous dysplasia • Precocious puberty

MANAGEMENT • Surgical removal of symptomatic or disfiguring neurofibromas • Follow-up for the development of neurofibrosarcomas, optic gliomas, acoustic neuromas, and pheochromocytomas • Genetic counseling for patients and their families

Tu berou s Sclerosis BASICS • Tuberous sclerosis (TS; Bourneville’s disease) is a disease in which cutaneous lesions may be seen in association with hamartomatous tumors of the CNS and other organs. The classic triad of TS includes the following: • Adenoma sebaceum • Epilepsy • Mental retardation, although at least 50% of affected persons show no evidence of mental retardation • TS, which is inherited in an autosomal dominant fashion, is found in fewer than 1 per 10,000 births. • Two genetic loci have been identified. The first gene (TSC1) is on chromosome q34 and produces tuberin. The second gene (TSC2) is on chromosome 16p13 and produces a second protein, hamartin. • Tuberin and hamartin are thought to act together to regulate cell differentiation and proliferation. Defects in these gene products may result in the growth of multiple hamartomas in TS. DESCRIPTION OF LESIONS • Ash-leaf macules are hypopigmented, characteristically oval, and sometimes linear or “confetti-shaped” macular lesions. • So-called adenoma sebaceum (actually angiofibromas) are pink to reddish-brown, dome-shaped papules (FIG. 25.47). • Periungual fibromas (Koenen’s tumors) are smooth, firm, skin-colored papules. • A pebbly, skin-colored “peau d’orange” or “pigskinlike” dermal plaque (“shagreen patch”) has fine hypopigmentation resembling confetti. DISTRIBUTION OF LESIONS

25.47 Tuberous sclerosis. This patient has adenoma sebaceum (angiofibromas). Note the similarity to acne lesions.

• Ash-leaf spots are more common on the trunk and proximal extremities. • Adenoma sebaceum papules are symmetric in distribution and are most commonly located on the nose, nasolabial folds, and cheeks. More widespread distribution involves the forehead, ears, and scalp. • Periungual fibromas occur around and under the nails on the periungual areas of the fingers and toes (FIG. 25.48). • “Shagreen patches” appear on the trunk, most often in the lumbosacral region. CLINICAL MANIFESTATIONS • Ash-leaf macules and “shagreen patches” are usually present at birth. • Adenoma sebaceum may begin to develop in late childhood and adolescence.

25.48 Tuberous sclerosis. Periungual fibromas (Koenen’s tumors) are noted. Chap ter 25 • Cutaneous Manifestations of System ic Disease

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Ce n t ral Ne rvo us Syst e m Le sio n s • Gliomatous brain tumors (tubers), which may calcify in 50% of patients • Seizure disorders in 60% to 70% of patients, with fewer than 50% showing evidence of mental retardation • Retinal and optic nerve gliomas Ot h e r Fin d in g s • In 50% to 60% of patients, cardiac rhabdomyomas of the atrium, which rarely cause cardiac obstructive disease • Renal hamartomas • In about 15% of patients, renal tumors (angiomyolipomas) and polycystic kidneys, which must be differentiated from renal carcinoma • Gastrointestinal tumors with microhamartomatous polyps of the rectum • Possible bone cyst formation and periosteal new bone growth and sclerosis DIAGNOSIS Two major or one major and two minor criteria are necessary for a definite diagnosis of TS.

Majo r Diag n o st ic Crit e ria 1. Adenoma sebaceum 2. Hypopigmented ash-leaf macules (three or more) 3. Shagreen patch 4. Periungual fibroma 5. Cortical tuber 6. Cardiac rhabdomyosarcoma 7. Subependymal nodule 8. Subependymal giant cell astrocytoma 9. Lymphangiomatosis 10. Renal angiolipoma Min o r Diag n o st ic Crit e ria 1. Multiple dental enamel pits 2. Hamartomatous rectal polyp 3. Bone cyst 4. Gingival fibroma 5. Nonrenal hamartoma 6. Retinal achromic patch 7. Confetti skin lesions: fine, hypopigmented macules (2 to 4 mm) that look as though they are “sprinkled” on the lower legs 8. Multiple renal cysts Lab o rat o ry Evaluat io n • Cranial magnetic resonance imaging • Posteroanterior and lateral skull films (for adults) to demonstrate calcifications of gliomas of the brain • Echocardiography for rhabdomyomas • Renal ultrasonograms to search for tumors • Skin biopsy of cutaneous lesions 494

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DIFFERENTIAL DIAGNOSIS OF ADENOMA SEBACEUM

Acn e ifo rm Pap ule s • They often resemble adenoma sebaceum. • Acne has a waxing and waning course. • A skin biopsy is necessary only if the diagnosis is in doubt.

MANAGEMENT • Follow-up of infants with ash-leaf spots to monitor the development of seizure disorder or mental retardation • Follow-up of patients with TS to monitor the development of cardiac or renal lesions • Removal of cosmetically objectionable or disfiguring adenoma sebaceum by excision, electrocautery, dermabrasion, or laser resurfacing • Surgical removal of painful periungual fibromas • Genetic counseling of patients with TS and their families after computed tomographic scanning is performed on the parents and siblings of the affected patient (these studies have demonstrated CNS lesions in asymptomatic parents of TS patients)

P ART T H REE

Derm atologic Procedures

C H AP T ER

26

Diagnostic and Therapeutic Procedures

OVERVIEW • Because of the ready availability of the skin to examination, a number of diagnostic measures—many of which are noninvasive—can lead to a specific diagnosis. • Examples include potassium hydroxide (KOH) examination and fungal culture (see later discussions), Tzanck preparation (see FIG. 6.26), scabies preparation (see FIG. 20.18), Wood’s light examination (see FIG. 14.4), and patch testing (see FIG. 2.33). • Skin biopsies using punch, shave, snip, or excisional methods are relatively free of complications. • Therapeutic modalities such as cryosurgery (see later discussion), phototherapy (discussed in Chapter 3, “Psoriasis”) and advanced surgical procedures such as Mohs’ micrographic surgery (see later discussion) are but a few of the many available treatments for skin disorders.

FUNGAL TESTS • Potassium hydroxide test • Fungal culture SKIN BIOPSY • • • •

Local anesthesia Shave biopsy and shave rem oval Scissor (snip) biopsy and snip excision Punch biopsy SIMPLE ELLIPTICAL EXCISION

• • • •

Underm ining technique Wound closure Suture m aterial Suturing COMEDO EXTRACTION SIMPLE PUNCH BIOPSY METHOD TO REMOVE CYSTS ELECTRODESICCATION AND CURETTAGE

• Curettage • Electrodesiccation CRYOSURGERY • Cotton tip applicator technique • Cryospray technique • Postoperative course and wound care MOHS’ MICROGRAPHIC SURGERY DRESSINGS AND WOUND MANAGEMENT

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Po t a ssiu m H yd ro x id e Test BASICS • The KOH examination has the advantage of providing an immediate diagnosis of a superficial fungal infection, rather than having to wait weeks for the results of a fungal culture. • It is a simple, rapid method to detect fungal elements in skin, nails, and hair. TECHNIQUE

Co lle ct io n o f Sp e cim e n • Collection is optimal when no surface artifacts (e.g., topical medications) are present. Sk in

26.1 Potassium hydroxide examination. Collection of scale from the “active” border of a lesion.

• Gently scrape scale from the “active border” with a no. 15 scalpel blade (FIG. 26.1). Na ils

• Trim the nail. • Use a no. 15 scalpel blade or a 1- to 2-mm curette (FIG. 26.2) under the nail surface to obtain scale. H a ir

• Pluck broken hairs with forceps or use a toothbrush to obtain scale and hairs (FIG. 26.3).

Pre p arat io n • Use a KOH solution such as Swartz-Lamkins fungal stain or a KOH solution with dimethyl sulfoxide. • Gather a thin layer of scale or scale plus hair on a slide and cover it with a coverslip. • With an eyedropper, place a single drop of a KOH solution at the edge of the coverslip and allow it to spread under the coverslip by capillary action (FIG. 26.4). 26.2 Potassium hydroxide examination. Collection of scale from under the nail after trimming.

26.3 Potassium hydroxide examination. Collection of scale from the scalp of a child using a toothbrush. 498

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26.4 Potassium hydroxide examination. A single drop of a KOH solution is placed at the edge of the coverslip.

• Heat the undersurface of the slide gently with a lighter or a match until bubbling begins. • Blot excess KOH solution with tissue paper held at the edge of the coverslip.

Ob se rvat io n • Examine under low light intensity (condenser down). • Begin with a low-power scan to identify scale and possibly hyphae. • Become aware of artifacts that are easily confused with hyphae and spores, such as hairs, clothing fibers, keratinocyte cell borders, and air bubbles (FIG. 26.5). • Use high power to confirm the presence of hyphae or spores (FIGS. 26.6–26.11). 26.6 Potassium hydroxide examination. Dermatophyte. Note the wavy, branched hyphae with uniform widths coursing over cell borders.

26.5 Potassium hydroxide examination. Artifacts. Note the clothing fibers on the left and the single hair shaft on the right.

26.7 Potassium hydroxide examination. Tinea versicolor. Note the short, stubby hyphae (“spaghetti”) and the clusters of spores (“meatballs”).

26.8 Potassium hydroxide examination. Candida. Spores and pseudohyphae (spores lack septae).

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499

Cult ure • Place fungal cultures on Sabouraud’s agar or on Dermatophyte test medium and incubate for 1 to 4 weeks (FIG. 26.12). • Clinical Laboratory Improvement Act guidelines may require the practitioner to use outside laboratory facilities for performing fungal cultures.

26.9 Potassium hydroxide examination. Candida. Pseudohyphae with budding spores (higher magnification).

26.12 F ungal culture using the Dermatophyte test medium. Note the positive result on the left indicated by the color change from yellow to red and the monomorphic colony growth. On the right are discrete mucoid growths of a yeast contaminant that confirm that the color change to red is a false-positive result.

26.10 Potassium hydroxide examination. Ectothrix. Note the spores outside the hair shaft.

26.11 Potassium hydroxide examination. Endothrix. Note spores inside the hair shaft (“sack of marbles”). 500

Part Three • Derm atologic Procedures

Sk in Bio p sy • Various skin biopsy techniques are available to the practitioner: shave biopsy, scissor or snip biopsy, punch biopsy, and excisional biopsy. The surgical tools and approaches vary according to size, shape, depth, and location of a lesion. • Obtaining the appropriate amount of tissue to provide adequate information about the disease is the most important factor to keep in mind when deciding on the proper biopsy technique. • Do not choose the biopsy specimen site indiscriminately. • Evaluate the site according to the clinical impression, the lesion’s location, the estimated depth of the pathologic process, the planned tissue studies, and the ensuing cosmetic result. • The choice of biopsy technique requires some knowledge of where the pathologic process is likely to be located.

Lo cal An e st h e sia Methods to decrease pain caused by injections include the following. • • • • •

Use a small, 30-gauge needle. Add a buffer (sodium bicarbonate) to the lidocaine. Inject very slowly. Distract the patient by talking continuously. Minimize the number of injection sites by reinjecting into areas that are already numb.

Sh ave Biop sy an d Sh ave Rem oval BASICS • This is used for the diagnosis and therapeutic removal of superficial (epidermal and upper dermal) skin lesions, such as melanocytic nevi, warts, seborrheic and solar keratoses, pyogenic granulomas, and skin tags, as well as other benign and malignant skin tumors. • It is used to obtain biopsy specimens to confirm skin disease before a more definitive surgical procedure (e.g., basal or squamous cell carcinoma). • It is very useful for flattening and diagnosing nevi, particularly in the facial area.

Ad van t ag e s • It is fast and economical. • The technique is easy to learn. • Wound care is simple. • Cosmetic results are generally excellent. • It does not use sutures. • It is useful for difficult-to-reach sites (e.g., ear canal, orbit of the eye). • It is useful in areas of poor healing (e.g., the lower leg in elderly or diabetic patients).

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Disad van t ag e s • It is not indicated for lesions that extend into the subcutaneous layer. • It is not indicated when a full-thickness biopsy is necessary (e.g., inflammatory dermatoses). • It should not be performed on lesions suspected of being melanoma because of the difficulty in clinically determining the maximum thickness or extent of a lesion. TECHNIQUE

A

B 26.13 A an d B Shave biopsy. A: Local anesthesia creates a wheal that elevates the lesion above the surrounding skin. B: The lesion is stabilized with the free hand; the blade, which is parallel to the skin surface, is drawn through the lesion.

• Anesthetize the area adjacent to the lesion with an injection into the superficial dermis with 1% plain lidocaine using a 30-gauge needle. If necessary, use epinephrine in a 1:100,000 or 1:200,000 dilution. Use lidocaine without epinephrine in finger and toe areas to avoid vascular compromise. • Administer local anesthesia with lidocaine to create a wheal and elevate the lesion above the surrounding skin (FIG. 26.13A). • Apply traction with the thumb and index finger of the free hand on either side of the lesion to stabilize it. • Place a no. 15 scalpel blade flat on the skin; use in a slight sawing motion with smooth strokes parallel to the skin surface and draw the middle of the blade through the lesion (FIG. 26.13B). • Release traction when the lesion becomes sufficiently free; use small forceps with teeth to hold and elevate the lesion to complete the “shave” and then to deliver it to a bottle of formalin. • Use electrocautery or further shaving to “feather” jagged edges. • Apply Monsel’s solution (ferric subsulfate) or aluminum chloride 35% with a cotton pledget (Q-Tip) to rapidly achieve hemostasis. Hemostasis is possible only if the field is wiped dry of blood. • Send all pigmented lesions to a pathologist; nonpigmented skin tags do not need to be sent for pathologic evaluation.

Scissor (Sn ip ) Biop sy an d Sn ip Excision BASICS • Various lesions can be removed from the skin in a short period of time. • Certain elevated or pedunculated lesions, such as warts, nevi, seborrheic keratoses, and skin tags, are ideally suited for removal with scissors. Many can be precisely removed level to the skin.

Ad van t ag e s • It is fast; many lesions can be removed in one visit. • It is economical. • Frequently, it can be performed without anesthesia.

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Disad van t ag e s • None exist, except for the possibility of obtaining an inadequate amount of tissue if a specimen is to be sent for histopathologic examination. TECHNIQUE • It may be possible to snip off thin, small lesions without any anesthesia; larger lesions require the administration of local anesthesia. Anesthetize the area of larger lesions in the same manner as for scalpel shave excisions. • Gently hold the lesion with small forceps without teeth and pull it to cause slight tenting of the epidermis and upper dermis (FIG. 26.14). • Use straight or curved sharp iris scissors with fine points to snip off the lesion. • Use light electrodesiccation at the base of the lesion, or apply a styptic (e.g., Monsel’s solution) or aluminum chloride 35% to cause hemostasis (stinging or burning may result if the lesion has not been anesthetized). Local pressure also is effective in preventing blood flow. • Trim away any slight elevation or irregularity of the margin with scissors.

26.14 Snip excision. This filiform wart is snipped off after having been anesthetized with lidocaine.

Pu n ch Biop sy BASICS • Performance of a punch biopsy involves the use of a 3- to 5-mm cylindric cutting instrument (“punch”) to remove all or part of a lesion. • This method is most useful for biopsy of relatively flat, inflammatory lesions such as seen in psoriasis, lichen planus, and vasculitis.

Ad van t ag e s • The specimen obtained is uniform. • This is an effective method to evaluate inflammatory skin diseases. • It is an efficient biopsy method for full-thickness skin. • The operative site heals rapidly. • Skin closure establishes a barrier to infection almost immediately after the procedure. Disad van t ag e s • The sample may not adequately show the entire lesion; a second technique (i.e., an elliptic biopsy) may be necessary for adequate demonstration of tumor architecture. • It is not suited for lesions primarily located in the subcutaneous tissue. • Areas to be avoided are the digits, around the facial nerve, or in any region where the operator is unfamiliar with the underlying anatomy.

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TECHNIQUE

26.15 Punch biopsy. Traction of surrounding skin is provided by the fingers while the punch is rotated.

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Part Three • Derm atologic Procedures

• In contrast to shave biopsy, a more thorough approach to sterile technique is necessary. • Cleanse the lesion and surrounding skin with 70% isopropyl alcohol, povidone-iodine (Betadine), or chlorhexidine (Hibiclens). • Anesthetize the area with an injection into the deep dermis of 1% plain lidocaine using a 30-gauge needle. If necessary, use epinephrine in a 1:100,000 or 1:200,000 dilution (FIG. 26.15). • With the fingers of the nondominant hand, stretch the skin at a 90-degree angle to the natural wrinkle lines. • Hold the punch between the thumb and forefinger. • Gently push the punch downward into the dermis while advancing it slowly and twirling it back and forth until it “gives.” Caution should be used over thin tissue or over vital structures. • It is important to push the punch deep enough to obtain underlying fat tissue for an adequate sample. • Withdraw the punch along with the tissue sample. If the sample does not come out with the punch, cut it at the base while depressing the surrounding skin. • Remove the tissue specimen with forceps with teeth and then cut the specimen, if necessary, with iris scissors. Take care to avoid crushing the specimen and distorting the tissue sample. • Place firm pressure on the circular skin wound to curtail bleeding. • A single suture for closure is all that is usually necessary.

Sim p le Ellip t ic Ex cisio n BASICS • Excisions are useful for obtaining tissue samples for biopsy specimens and for the removal of many benign and cancerous lesions. • Excisional biopsies may be performed on discrete lesions, such as cysts, basal or squamous cell carcinomas, malignant melanomas, or other solitary tumors and nevi. • An incisional biopsy is the incomplete or partial removal of a lesion that may be too big or poorly located to perform a complete excision (e.g., a suspected melanoma that is too large to remove).

Ad van t ag e s • It provides a more extensive tissue sample of a lesion that is too large for a shave or a punch biopsy. • The margins of submitted tissue can be examined for possible involvement (e.g., basal cell carcinoma, squamous cell carcinoma and melanoma). • It often affords a definitive cure for many benign and malignant lesions. Disad van t ag e s • It is time-consuming. • It is less economical than shaves or snips. • It usually requires a return visit for suture removal. TECHNIQUE • The operator should be familiar with the underlying and surrounding anatomy. • A thorough approach to sterile technique is necessary: sterile gloves and sterile drapes should be used. • To achieve the best cosmetic results, place the lines of incision in or parallel to the relaxed skin tension lines. This placement is demonstrated by observing wrinkle lines and the effect of pinching the skin. • Once a direction for the long axis of the ellipse has been chosen, draw an ellipse around the lesion before administering a local anesthetic. This approach minimizes tissue distortion, which may cause difficulty in subsequent planning of the ellipse. Use gentian violet or a surgical skin marker to mark the skin. • Make sure that the excision has a length-to-width ratio of at least 3:1 and that the apices are at a 30-degree angle. • Anesthetize the area by local infiltration with lidocaine and epinephrine 1:100,000. • Use a No. 15 scalpel blade to make the incision. Use the dominant hand with the index finger and thumb of the other hand placed on either side of the incision. This pushes the skin under tension downward and away from the scalpel (FIG. 26.16 A). • Start the incision using the point of the scalpel held in a vertical position at the apex of the ellipse (FIG. 26.16 B). Use the belly of the scalpel along the side of the ellipse to elongate the incision.

A

B 26.16 A an d B Excision. A: The incision is started using the point of the scalpel, held in a vertical position, at the apex of the lesion. Traction is accomplished with the nondominant hand. B: The tissue is dissected free of the underlying fat. Forceps are used to hold the apex of the skin being removed. Chap ter 26 • Diagnostic and Therapeutic Procedures

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• Obtain an optimal tissue sample for histologic examination. The scalpel should cut through the full thickness of the skin, including the upper subcutaneous fat. • Dissect the tissue free of the underlying fat after making incisions on both sides of the ellipse. Use forceps with teeth to hold the apex of the skin being removed. • If the defect is large, dissect (undermine) the ellipse using curved, blunt-tipped scissors (e.g., Steven’s tenectomy or Gradle scissors), making certain that the plane of the dissection is at the same level throughout. Undermining allows for the mobilization of tissue so that it can be advanced to close the defect; it also allows skin edges to come together with less tension and allows eversion of the wound edges with suturing.

C

Un d erm in in g Tech n iq u e • To perform undermining, use blunt-tipped scissors while elevating the skin edge by forceps with teeth or a skin hook (FIG. 26.16 C). • Advance scissors to the desired degree and open them to stretch the underlying skin. If necessary, repeat this procedure several times to achieve the desired skin mobility for wound closure. • Remove any remaining tissue septa using the open blades of the scissors. • Undermining is most effective when performed at the level of superficial fat tissue. This reduces the possibility of injury to nerves and blood vessels in the facial and neck areas. • Wound repair is facilitated if an adequate ellipse has formed, the edges are perpendicular to the skin, and skin lines are followed. • Meticulous hemostasis must occur after undermining. Apply direct pressure or perform electrocoagulation (FIG. 26.16 D). • Place subcutaneous sutures after undermining; this will allow approximation of the edges of the wound to close the wound (FIG. 26.16 E).

D

E 26.16 C, D an d E Excision. C: Undermining is performed using blunt-tipped scissors while the skin edge is elevated by forceps. D: Hemostasis is achieved with an electrocautery device. E: Deeper, nonabsorbable sutures are used to approximate the wound edges.

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Wou n d Closu re • Wounds should be closed in layers. • The closure of dead space is necessary when large, subcutaneous vacuities have been created, such as after removal of subcutaneous cysts. • Dermal, buried sutures are important on areas of the body that overlie large muscle groups, such as the upper trunk.

Sut ure Mat e rial • Obtain hemostasis (a “dry field”) before initiating wound closure. • Choice of suture material depends on the size and degree of tension on the wound and the area of placement. • For facial or limb areas, Vicryl or Dexon sutures are suitable for the deeper layers as they are absorbable. 5-0 or 6-0 synthetic (Prolene or Ethilon) sutures are recommended for epidermal closure on the face. • On the upper trunk, greater skin support is required for proper wound closure. Therefore, Maxon or polydioxanone sutures are recommended; 3-0 or 4-0 are preferred. • An absorbable suture, Monocryl, is very easy to handle, causes little tissue reaction, excellent tensile strength, and lasts up to 3 months in tissue. Sut urin g • Simple, interrupted skin sutures are most commonly used in this procedure. • The method of “halving” is the most effective technique for wound closure. “Halving” allows for equal distribution of wound tension (FIG. 26.16 F). • Place the first suture in the center of the ellipse. • Place the second and third sutures in the centers of the remaining wound lengths. • Repeat this procedure until the wound is completely closed. • Apply an occlusive dressing (a perforated plastic film or sheet with an absorbable pad) or pressure dressing, if necessary, to prevent postoperative bleeding (FIG. 26.16 G). • Suture removal depends on wound tension, area of location, and depth of placement. • Generally, removal of facial sutures may be necessary in 5 days; removal of sutures in the trunk and extremities may be required in 1 to 2 weeks.

F

G 26.16 F an d G Excision. F: Closure. Interrupted skin sutures are placed using the method of “halving.” The first suture was placed in the center of the ellipse. G: Dressing. A transparent dressing overlying Steri-Strips allows for visualization of the wound as it heals.

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Co m ed o Ex t ra ct io n • Removal of comedones involves a comedo extractor, an instrument that minimizes skin injury. Use a round loop extractor to apply uniform, smooth pressure to dislodge comedonal contents (FIGS. 26.17 A and B). • To loosen lesions that offer resistance, insert a pointed instrument, needle, or a no. 11 blade to carefully incise and expose the contents. • Extraction can be a useful adjunct to topical therapy when blackheads and whiteheads are somewhat resistant to topical retinoids. • Pretreatment with a topical retinoid for 4 to 6 weeks often facilitates the procedure. Performance of comedo extraction is now less common since the use of topical retinoids. A

B 26.17 Comedo extraction. A: Gentle pressure is exerted along the rim of this closed comedo. B: The contents are extruded.

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Sim p le Pu n ch Biop sy Meth od to Rem ove Cysts • A large lesion such as an epidermoid or pilar cyst can be removed through a small hole and heals with excellent aesthetic results. • If the results of this procedure are not completely satisfactory, a standard excision can be performed at a future date. TECHNIQUE • Superficially administer local anesthesia over the cyst (FIG. 26.18 A). • Punch the center of the cyst (the “pore”) with a 4-, 6-, or 8-mm disposable punch (FIG. 26.18 B). • Dissect the cyst wall using forceps, iris scissors, and manual pressure around the cyst (FIGS. 26.18 C and D). • Close the defect with a 4-0 nylon stitch.

B

C

A 26.18 A Punch biopsy removal of a cyst. A: This epidermoid cyst has a central “pore.”

D 26.18 B, C an d D Punch biopsy removal of a cyst. B: A 6-mm disposable punch creates an opening. C: After dissection with iris scissors, pressure is exerted with the operator’s thumbs. D: The cyst wall is extracted.

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Elect ro d esicca t io n a n d Cu ret t a ge BASICS • The technique of electrodesiccation and curettage is a means to remove or destroy many types of benign superficial skin lesions such as warts, seborrheic keratoses, solar keratoses, pyogenic granulomas, and skin tags. • In experienced hands, it is often used as a method to treat skin cancers such as small basal cell and squamous cell carcinomas. • Electrodesiccation uses monopolar high-frequency electric currents to destroy lesions; curettage is a scraping or scooping technique performed with a dermal curette, which has a round or oval sharp ring. • Electrodesiccation without curettage (as an alternative to shave procedures) is often used to eliminate warts, skin tags, and spider angiomas and to flatten lesions (e.g., melanocytic nevi). Conversely, curettage without electrodesiccation may also be used to remove many of these epidermal lesions. • Curettage is a “blind technique” in which the specimen cannot be examined for margin control.

Ad van t ag e s • It is fast and economical. • It is useful for difficult-to-reach sites, e.g., ear canal, orbit of the eye. • It is useful in areas of poor healing, e.g., the lower leg in elderly or diabetic patients. • Secondary infection is uncommon. Disad van t ag e s • The procedure is “blind”; margins of lesions can only be guessed. • Cosmetic results are unpredictable; hypopigmentation and scarring may result. • Healing is by secondary intention and takes 2 to 3 weeks, which is longer than healing after an excisional procedure. • Obtaining biopsy specimens from curettage is discouraged.

Cu rettage TECHNIQUE • Anesthetize the area to be biopsied in a similar manner to that described in the sections “Skin Biopsy” and “Shave Biopsy and Shave Removal.” The local anesthetic creates a wheal and elevates the lesion above the surrounding skin. • Apply traction with the thumb and index finger of the free hand on either side of the lesion; this stabilizes it and keeps it taut. • Hold a sharp curette like a pencil and draw it through the tissue with strokes pushed away with the thumb until an adequate amount of tissue is removed (usually when the dermis is reached) (FIG. 26.19). • Obtain hemostasis with Monsel’s solution (ferric subsulfate) or aluminum chloride 35% after wiping the field dry of blood.

Electrod esiccation • Electrodesiccation may be used before or after curettage or used alone. • It causes superficial destruction with a charring of the skin. TECHNIQUE 26.19 Curettage. Note the traction exerted by the operator’s fingers.

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• Perform this procedure after administering local anesthesia. • Use the lowest possible setting to prevent unnecessary tissue destruction.

Cr yo su rger y BASICS • Cryosurgery entails the destruction of tissue by freezing in a controlled manner to produce sharply circumscribed necrosis. Tissue destruction results from intercellular and extracellular ice formation, denaturing of liquid protein complexes, and cell dehydration. Second or subsequent freeze–thaw cycles result in more cellular damage than a single cycle. • Liquid nitrogen (LN2) at –195.8 C is the standard agent that is used. It is applied with a cotton swab, a cryospray gun, or a cryoprobe, and it is stored in a special vacuum container. • Cryosurgery should be used only when a confident clinical diagnosis has been made. • It is most commonly used on warts and solar keratoses.

produce, with either the swab or spray technique, a solid ice ball that extends 2 mm onto normal skin.

Co t t o n Tip Ap p licat o r Te ch n iq ue • Place LN2 in a Styrofoam cup. • Dip a cotton swab into the cup. • Touch the lesion with the saturated cotton-tipped applicator, with a minimal amount of pressure, and create a 2- to 3-mm zone of freeze around the lesion for a total of 4 to 5 seconds (FIG. 26.20). • The skin turns white. Care must be taken to avoid dripping onto surrounding normal skin.

Ad van t ag e s • Cryosurgery is an inexpensive, rapid, and simple technique that does not require complicated apparatus. • Anesthesia is usually not necessary. • Postoperative pain is minimal. • Bleeding is not a problem during or after treatment. • Sutures are not necessary, and scarring is generally minimal or absent. • It is a relatively risk-free treatment for the cryosurgeon who treats some skin conditions in patients who are infected with human immunodeficiency virus. These include patients with molluscum contagiosum, condylomata acuminatum, Kaposi’s sarcoma, and warts. Disad van t ag e s • Young children do not tolerate cryosurgery well. • Scarring may occur, particularly if lesions are overzealously frozen or if the patient tends to heal with hypertrophic scars or keloids. • Postinflammatory pigmentary alterations may occur; more often, hypopigmentation results because of the destruction of melanocytes. TECHNIQUE Standardization of freeze times is difficult to categorize for the treatment of benign and premalignant lesions. The goal is to

26.20 Cryosurgery. Liquid nitrogen is applied with a cotton pledget.

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Cryo sp ray Te ch n iq ue • A handheld Cryogun, which operates under a working pressure of approximately 6 psi, is the standard instrument. Nozzle attachments with apertures of varying diameter for spray application are available (the “A” nozzle applies the greatest amount of spray; the “D” applies the least amount for delicate work) (FIGS. 26.21 and 26.22). • Generally, no local anesthesia is necessary. • For smaller lesions, this procedure involves treating the center of the lesion and allowing the freeze to spread laterally. • The time of application varies, depending on the thickness of the lesion.

26.21 Cryosurgery. A prone position is helpful in examining and treating plantar lesions.

26.22 Cryosurgery. Here liquid nitrogen is delivered with a cryospray gun. Note the 2- to 3-mm zone of freeze around the lesion.

26.23 Cryosurgery. Note the wart on the surface of a hemorrhagic blister that appeared 24 hours after treatment. 512

Part Three • Derm atologic Procedures

Po st o p e rat ive Co urse an d Wo un d Care • Mild to moderate swelling may occur at the lesion site. • A blister or blood blister may form within 24 hours and resolves in 2 to 7 days (FIG. 26.23). • The lesion site may be cleansed with soap and water during the exudative stage. • The lesion site starts to dry at the end of the exudative stage and then sloughs. • A crust, which loosens spontaneously, commonly occurs.

HELPFUL HINTS • It is best to underfreeze lesions; they can be retreated at a later date. • For anxious children, a topical anesthetic such as EMLA cream (eutectic mixture of local anesthetics) can be

26.24 Cryosurgery. Application with a Cryogun apparatus. Freezing the lesion at a right angle may lessen the pain.

applied under occlusion 1 hour before cryosurgery to decrease the discomfort associated with the procedure. • Alternative delivery methods that can help minimize pain are shown in Figures 26.24 and 26.25. (See also FIGS. 21.24 and 21.25.)

26.25 Cryosurgery. Treatment of a cutaneous horn with a hemostat that has been immersed for 30 seconds in liquid nitrogen. This simple, relatively painless procedure causes very little collateral damage to the surrounding skin.

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Mo h s’ Micro gra p h ic Su rger y BASICS • Mohs’ micrographic surgery is a microscopically controlled method of removing skin cancers that allows for controlled excision and maximum preservation of normal tissue.

Ad van t ag e s • Most reliable method in determining adequate margins • Cure rate of 98% to 99% for basal cell carcinomas • Preserves the maximum amount of normal tissue around the cancer Disad van t ag e s • Time-consuming • Expensive • May require extensive reconstruction of surgical wounds

A

In d icat io n s Mohs’ surgery is best suited for: • Recurrent basal and squamous cell carcinomas, particularly those on the face • Excessively large (more than 2 cm) or invasive carcinomas • Carcinomas within an orifice (e.g., ear canals or nostrils) • Carcinomas in locations where preservation of normal tissue is extremely important (e.g., tip of the nose, ala nasi, eyelids, ears, lips, glans penis) • Carcinomas in locations known to have a high rate of recurrence (e.g., ala nasi, nasal labial folds, medial canthi, pinnae of the ears, postauricular sulcus) • Morpheaform or sclerotic (desmoplastic) basal cell carcinoma • Lesions of the finger or penis

B

TECHNIQUE • Tissue is excised in a circular pie-shaped fashion (FIG. 26.26 A); then it is systematically mapped and examined by means of frozen sections. • While the patient waits in the examining room, tissue is submitted to a histotechnician for the surgeon to review (FIG. 26.26 B). • Excisions are repeated in the areas proven to be cancerous until a complete cancer-free plane is reached (FIG. 26.26 C). Several stages may be necessary.

C 26.26 A, B an d C Mohs’ micrographic surgery. A: First stage of excision of lesion (image courtesy of Michael J. Mulvaney, M.D.). B: The excised tissue is color-coded and then evacuated by frozen section. (Image courtesy of Michael J. Mulvaney, M.D.) C: A second stage of excision is performed, because the first section had positive margins. (Image courtesy of Michael J. Mulvaney, M.D.)

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• Surgical wounds may be left to heal by secondary intention or corrected by plastic reconstructive procedures (FIG. 26.26 D).

Wo un d Care an d He alin g • Infections after simple skin surgery are unusual. • Administration of systemic antibiotics is generally unnecessary. • Meticulous hemostasis during surgery is essential. • Small amounts of necrosis normally occur in wound healing. • Hemostasis induced by electrosurgery, suture ligature, or cautery always produces tissue necrosis. • Wound healing is delayed when necrosis is extensive. • Hemostasis can be achieved with a pressure dressing, which is applied for 24 hours. • When wounds are closed with a considerable amount of tension or if the patient has been taking steroids, the wound should be closed with sutures that are nonabsorbable and buried (nylon or Prolene) or have prolonged tensile strength (polydioxanone, Dexon, Vicryl). Under the former conditions, skin sutures may be left in place for longer periods of time. • External splinting using tape provides additional support until the tensile strength of the wound increases after suture removal. • Exercise that stretches the skin should be avoided to minimize spreading of the scar.

D 26.26 D Mohs’ micrographic surgery. Primary closure after the second tissue excision was found to be free of malignancy. (Image courtesy of Michael J. Mulvaney, M.D.)

Dre ssin g s an d Wo un d Man ag e m e n t • For small ellipses, dry, sterile gauze covered with paper tape may be all that is necessary. • An occlusive dressing or pressure dressing should be applied, if necessary, to prevent postoperative bleeding. • After 24 hours, the patient can remove the dressing and compress the wound with tap water or hydrogen peroxide. The hydrogen peroxide mechanically softens the wound and removes any debris. • A topical antibiotic such as bacitracin is applied to the surface of the wound before applying a clean, occlusive dressing. • Patients repeat this procedure daily at home until the wound is covered with fresh epidermis. • Patients are advised to return for follow-up if there is any pain, swelling, tenderness, purulent drainage, discharge, or bleeding of the wound. • Postoperative pain usually is negligible, and patients are advised to call the surgeon should any pain occur.

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P ART F O U R

Derm atologic Disorders in Special Population s

C H AP T ER

27

Special Considerations in the Skin of Pediatric and Elderly Patients

OVERVIEW An individual’s age, as well as gender and ethnic background, often influences the presence and severity of various skin disorders. This chapter provides a thumbnail description of dermatologic concerns in pediatric and elderly patients that are

not discussed in previous chapters. It is intended to complement the earlier descriptions of common skin disorders and to present some less common conditions and rare skin diseases that may affect a patient seeking medical attention from any health care provider.

TO SEE LARGER IMAGES, GO TO THE WEB SITE AT www.g o o d h e art sskin d iso rd e rs.co m .

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Ped ia t ric Sk in Diso rd ers BASICS • The overwhelming majority of pediatric skin disorders that present to pediatricians, family practitioners, and dermatologists consist of acne, atopic dermatitis, diaper rash, con-

genital lesions, warts, molluscum contagiosum, as well as a multitude of viral, bacterial, and idiopathic rashes. • Common as well as various rare dermatoses and congenital lesions are briefly summarized in TABLE 27.1.

Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS CONDITION

DESCRIPTION

MANAGEMENT

Superficial hemangioma (formerly called “strawberry” or capillary hemangioma)

Benign proliferation of endothelial cells that starts as macule and grows into dome-shaped papule or nodule Most often followed by spontaneous involution (“graying”)

Observation or treatment with intralesional or systemic steroids, or laser ablation, especially if lesions compromise function

Deep hemangioma (formerly called “cavernous” hemangioma)

Deep dermal and subcutaneous red to violaceous nodule; regression often incomplete

Observation or treatment with intralesional, systemic steroids, or laser ablation, especially if lesions compromise function

Macular stains (“angel’s kisses,” “salmon patches”)

Red macules located on forehead, eyelids, nose, or upper lip Most often regress by 2 years of age

None indicated

IMAGE

continued on page 521

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Stork bites

Red macules on back of neck Persist in 25% of adults

None indicated

Nevus flammeus (port-wine stain)

Congenital malformation of blood vessels Usually appears at birth

Laser therapy

Nevus spilus (speckled lentiginous nevus)

Tan patches characterized by numerous darker macules or papules

Surgical excision for cosmetic reasons only

IMAGE

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Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Becker’s nevus (pigmented hairy nevus)

Pigmented hairy nevus that is located over chest, shoulder, or back Often appears at puberty

None; surgical excision or laser ablation for cosmetic reasons only

Nevus sebaceous

Congenital hamartoma, with plaques on head or neck Thickens at puberty Small risk of malignant degeneration, mainly to basal cell carcinoma

Excision

Nevus lipomatosis

Solitary or grouped proliferation of fatty tissue Lesions are asymptomatic, soft, skincolored to yellow papules, nodules, or plaques, with predilection for upper thighs, pelvic, lumbar, and buttock areas

Surgical excision for cosmetic reasons only

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Epidermal nevi

Congenital hamartomas with various presentations: verrucous, inflammatory, linear, multiple, or comedonal

Excision, observation, or cryotherapy, with topical steroids for inflammatory type, topical retinoids for comedonal type

Mongolian spots

Macular, flat, blue or blue-gray skin markings that appear at birth or shortly thereafter on the sacral area and back Most prevalent among Asians and African Americans Often fade spontaneously

None

Nevus of Ota

Gray-blue melanin pigmentation of sclera of the eye Seen in Japanese, as well as in Africans, African Americans, and East Indians

Laser therapy

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Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Acropustulosis of infancy

Recurrent crops of small pruritic vesicles that evolve into pustules Involves the palms and soles, most often in black newborns and infants Remits spontaneously

Topical steroids

Gianotti-Crosti syndrome (acrodermatitis papulosa)

Self-limited, sometimes pruritic exanthem associated with many viral agents and immunizations Pale, pink to fleshcolored papules (sometimes flattopped) in symmetric distribution on extremities

None

Urticaria pigmentosum

Multiple red-brown macules, usually on the trunk

Antihistamines and/or topical steroids, if symptomatic

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Solitary mastocytoma (the mastocytosis syndrome can involve multiple organs and become chronic; it is not discussed here)

Lesions become a wheal (urticate) when rubbed or stroked; this change is referred to as Darier’s sign, which is explainable on the basis of mast cell degranulation induced by physical stimulation Most cases resolve spontaneously Usually yellowbrown rubbery plaque that urticates or blisters (bullous urticaria pigmentosum) after rubbing Resolves spontaneously

No treatment necessary

IMAGE

B

C

Tinea amiantacea

Thick, adherent scale on scalp and in hair

Keratolytics, followed by topical steroids when scale is cleared

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Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Talon noir (tennis heel)

Self-limited, multiple, black petechiae of heel after minor trauma

Paring, protective heel pad

Pitted keratolysis

Pits in stratum corneum of soles; caused by prolonged occlusion, hyperhidrosis, and bacterial proteinase proliferation Malodorous

Topical erythromycin, clindamycin, or oral erythromycin Wearing cotton socks to prevent moisture buildup

Lichen striatus

Idiopathic linear inflammatory eruption Consists of papules that coalesce into linear, unilateral plaques that appear most often on extremities Resolves spontaneously

Topical steroids

Perianal streptococcal dermatitis (perianal cellulitis)

Affects children 3 to 4 years of age Caused by group A beta-hemolytic streptococci Bright pink to red erythema that extends 2 to 3 cm from anus; infrequently accompanied by itching, fissuring, pain, and mucoid discharge May become more of a cellulitis, with possible pain on defecation

Penicillin V combined with topical Bactroban (mupirocin) ointment or cream twice a day

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Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Juvenile xanthogranuloma

Occurs in infancy and early childhood Lesions composed of histiocytic cells; benign, smooth, firm, red-brown papules and nodules that change to yellow Resolves spontaneously

None necessary

Lichen nitidus

Occurs on thighs, arms, trunk, and genitalia Idiopathic, asymptomatic, small (1 to 2 mm), flat-topped, shiny, skin-colored papules

Topical steroids, if necessary

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Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Hyperhidrosis

Usually starts in early teen years Excessive sweating, particularly axillae, palms, and soles

Topical: Aluminum and zirconium antiperspirants Topical 20% aluminum chloride hexahydrate in absolute alcohol, anticholinergics, aldehydes, and tannic acid Iontophoresis Systemic: Oral anticholinergic medications Injection: botulinum toxin Surgical: Liposuction Sympathectomy

IMAGE

A

B

Subcutaneous fat necrosis of newborn

Firm, erythematous nodules and plaques on trunk, arms, buttocks, thighs, and cheeks in otherwise healthy infants Self-limited

None necessary

Lymphangioma circumscriptum

Congenital hamartoma of lymphatics Consists of small clusters of vesicles (“frog spawn”)

Surgical excision, laser ablation, cryosurgery, electrocautery, or sclerotherapy

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.1 DERMATOSES AND CONGENITAL LESIONS IN PEDIATRIC POPULATIONS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Acute hemorrhagic edema of infancy (Finkelstein’s disease)

Large, urticarial or annular, targetoid, purpuric plaques found primarily on face, ears, and extremities; presumably immune complex–mediated Self-limited

None necessary

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B

C

Staphylococcal scalded skin syndrome (SSSS)

Occurs mostly in neonates in neonatal or day care nurseries Toxin-mediated type of exfoliative dermatitis caused by toxigenic strains of Staphylococcus aureus Lesions range from localized bullous impetigo to extensive blistering and exfoliation

Dicloxacillin

Chapter 27 • Sp ecial Considerations in the Skin of Pediatric and Eld erly Patients

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Sk in Diso rd ers in t h e Eld erly See TABLE 27.2. BASICS • The consequences of aging are most obvious on the skin. • Genetics and sun exposure are the most important factors in determining the rate of aging and seem to influence susceptibility to certain types of disorders, including benign as well as precancerous and cancerous skin lesions.

Tab le 27.2 SKIN DISORDERS IN OLDER PATIENTS CONDITION

DESCRIPTION

MANAGEMENT

Solar elastosis (dermatoheliosis, cutis rhomboidalis nuchae)

Caused by chronic sun exposure; results from breakage and clumping of elastic fibers in skin and thickening of epidermis Skin looks older than chronologic age Skin becomes wrinkled, furrowed, and unevenly pigmented, and it may have yellow hue

Sun protection measures, tretinoin, chemical peels, and/or laser resurfacing

Favre-Racouchot syndrome

Chronic sun exposure results in multiple, bilaterally symmetric, open and closed comedones in periorbital and temporal areas

Comedone extraction or topical tretinoin

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.2 SKIN DISORDERS IN OLDER PATIENTS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Giant comedones

Commonly seen in elderly, particularly on the back Lesion is large dilated pore of epidermal inclusion cyst

Comedone extraction Excision

Nonspecific balanitis

Erythema, pruritus Erosions are seen primarily in uncircumcised males

Low-potency topical steroids, pimecrolimus, or tacrolimus Consider circumcision in recalcitrant cases

Genital lichen sclerosis (lichen sclerosis et atrophicus) in women

Chronic, idiopathic inflammatory dermatosis that results in white vulvar plaques with epidermal atrophy

Class 1 topical steroids Oral retinoids

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Tab le 27.2 SKIN DISORDERS IN OLDER PATIENTS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Genital lichen sclerosis (balanitis xerotica obliterans) in men

Chronic, idiopathic, sclerosing, inflammatory dermatosis of penis and prepuce

Class 1 topical steroids or topical testosterone Oral retinoids Circumcision or laser vaporization

Grover’s disease (transient acantholytic dermatosis)

Most often seen in elderly men Multiple pruritic, red, scaly, or eroded papules on trunk

High-dose vitamin A or high-potency topical steroids

Bullous pemphigoid

Autoimmune blistering disease characterized by numerous tense vesicles and bullae May begin with nonspecific pruritic eruption; caused by autoantibodies

Mild: class 1 topical steroids, combination of tetracycline and niacinamide Severe: prednisone, azathioprine, cyclophosphamide, mycophenolate mofetil, dapsone, or methotrexate

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Part Four • Derm atologic Disorders in Special Pop ulations

Tab le 27.2 SKIN DISORDERS IN OLDER PATIENTS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Pemphigus vulgaris

Autoimmune blistering disease characterized by numerous superficial (flaccid) vesicles and bullae of skin and mucous membranes Caused by autoantibodies

Prednisone, class 1 topical steroids, and intralesional steroids Steroid-sparing agents: azathioprine, cyclophosphamide, mycophenolate mofetil, dapsone, cyclosporine, and intravenous immune globulin

Onychogryphosis

Nail plate enlargement with increased thickening and marked curvature

Ongoing podiatric care and appropriate footwear

Fissured heels

Linear parallel epidermal fissures Painful when lesions involve dermis

Keratolytics, emollients, and occlusive dressings

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Tab le 27.2 SKIN DISORDERS IN OLDER PATIENTS (Continued) CONDITION

DESCRIPTION

MANAGEMENT

Nonepidemic Kaposi’s sarcoma

Affects older men of Mediterranean or eastern European origin Violaceous patches, plaques, and nodules, most often on lower extremities

None indicated for indolent lesions Radiation therapy, cryotherapy, or surgical excision or laser ablation, when indicated

Lupus vulgaris (cutaneous tuberculosis)

Solitary, slowly evolving, redbrown papules or plaques of head and neck

Isoniazid, rifampin, pyrazinamide, ethambutol, or streptomycin

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AP P EN D I X

A GENERIC NAME

Brand Names of Derm atologic Medications in Various Countries UNITED STATES

For acne and rosacea: Oral Minocycline Minocin

FRANCE

GERMANY

UNITED KINGDOM

Skid, Lederderm

Minocin

Cynomycin

Minocin

Vibramycin

Vibramycin

Doxt

Monomycin, Erythrocin Roaccutan

Erymax

Eltocin

Nudoxycycline Eryc

Roaccutane

Sotret Isotroin

Accutane, Clarus NA Metrocream, Metrolotion, Metrogel, Noritate Dalacin-T, Clindets, Clinda-T Erysol

Doxycycline hyclate Erythromycin

Vibramycin

Mestacine Mynocine Vibromycine

E-Mycin

Érythrocyne

13-cis retinoic acid

Sotret Claravis Amnesteen

Roaccutane

INDIA

CANADA

For acne and rosacea: Topical Azelaic acid Azelex Metronidazole Noritate, MetroGel, MetroCream

Skinoren Rosiced Rozagel

Skinoren Metrogel

Skinoren Rozex

Aziderm Metrogyl

Clindamycin

Cleocin-T

Dalacine T

Basocin

Dalacin T

ClindacA

Erythromycin

Emgel

Éryacné

Stiemycin

NA

Tretinoin

Retin-A

Aberel Effederm

Aknemycin, Stiemycine Eudyna, Airol

Retin-A

Retino-A

Adapalene

Differin

Différine

Differin

Differin

Adaferin

Tazarotene Benzoyl peroxide

Tazorac Oxy-5, Oxy-10

Zorac Panoxyl Éclaran

Zorac Benzaknen, PanOxyl

Zorac PanOxyl

Tacroz Benzac AC

Retin-A micro, Retin-A, Stieva-A, Vitamin A Acoid Differin, Differin-XP Tazorac Benoxyl, Benzac, Panoxyl, Solugel continued on page 536

535

GENERIC NAME

UNITED STATES

UNITED KINGDOM

INDIA

CANADA

NA

Sa6, Sa12

NA

FRANCE

GERMANY

Cold cream salycilé Daivonex

Dovonex

Daivonex

Dovonex

Daivobet

Squamasol, Psórimed Psorcutan, Daivonex Daivobet

Dovobet

Daivobet

Dovobet

Antifungals: Topical Terbinafine Lamisil

Lamisil

Lamisil

Lamisil

Lamisil

Ketoconazole

Nizoral

Nizoral

Nizoral

Tolnaftate Econazole Ciclopirox

Tinactin Spectazole Loprox

Sporilline Dermazol Mycoster

Terzolin, Nizoral Tonaftal Epi-Pevaryl Batrafen

Lamisil, Zimig Nizral

Tinaderm Ecostatin NA

Tinaderm NA NA

NA NA Loprox, Stieprox

Grisovin

GrisOD

NA

Lamisil

Lamisil Sporonox Diflucan

For psoriasis: Topical Salicylic acid Keralyt gel Calcipotriene

Dovonex

Calcipotriene/ Taclonex betamethasone dipropionate

Nizoral

Antifungals: Oral Griseofulvin Fulvacin-PG

Fulcine

Terbinafine

Lamisil

Lamisil

Likuden, Fulcin Lamisil

Itraconazole Fluconazole

Sporanox Diflucan

Sporanox Triflucan

Sempera Diflucan

Sporanox Diflucan

Lamisil, Zimig Sporanox Zocon, Fusys

Antihistamines Hydroxyzine Cyproheptadine Loratadine Cetririzine Doxepin

Atarax Periactin Claritin Zyrtec Sinquan

Atarax Périactine Clarytine Zyrtec Quitaxon, Sinquan

Atarax, AH3 Peritol Lisino, Lorano Zyrtec Aponal, Sinquan

Atarax Periactin Clarityn Zirtek Sinquan

Atarax Practin Lorfast Zyrtec Spectra

Atarax NA Claritin Reactine Sinequan

Rogaine

Regaine

Regaine

Regaine

Mintop

Rogaine

Propecia

Propécia

Propecia

Propecia

Finpecia

Propecia

Efudix

Efudix

Efudix

Flonida

Efudex

Nix Charlieu anti-poux Aphtiria

Infectopedicul

Lyclear

Permite

Nix, Kwellada-P

Jacutin

Quellada

NA

NA

Mectizan

Ivermectol

NA

Alopecia Minoxidil (topical) Finasteride

Antimitotic: Topical 5-Fluorouracil Efudex Carac Scabacides: Topical Permethrin Elimite Acticin Lindane

Kwell

Scabacides: Oral Ivermectin Stromectol

The brand name of this product is either unavailable or was not obtained at the time of publication.

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App enid x A • Brand Nam es of Derm atologic Medications in Various Countries

Patient Handouts in English and Spanish Acne Acne: How to Apply Duac Gel, BenzaClin Gel, and Benzamycin Gel Acne: How to Apply Topical Retinoids Alopecia Areata Athlete’s Foot (Tinea Pedis) Atopic Dermatitis Atypical Nevus (Mole) Basal Cell Carcinoma Burow’s Solution Contact Dermatitis Dry Skin (Xerosis) Fungal Nails (Onychomycosis) Genital Warts Granuloma Annulare Hair Loss (Androgenic Alopecia) Hand Eczema Head Lice Herpes Simplex Herpes Zoster (Shingles) Hives (Urticaria) Keratosis Pilaris (Rough Bumpy Skin) Lichen Planus Lyme Disease

Lyme Disease: Prevention Malignant Melanoma Melasma Molluscum Contagiosum Pityriasis Rosea Poison Ivy and Poison Oak (Rhus Dermatitis) Pseudofolliculitis Barbae (Razor Bumps) Psoriasis Rosacea Scabies Scalp Psoriasis: Scale Removal Seborrheic Dermatitis of the Face Seborrheic Dermatitis of the Scalp and Dandruff Short-Term Cortisone Therapy Soak and Smear Instruction Sheet Solar Keratosis (Actinic Keratosis) Squamous Cell Carcinoma Sun Protection Advice Tinea Capitis Tinea Cruris (Jock Itch) Tinea Versicolor Vitiligo Warts

Acn e What is acne? • There are two types of acne: • Comedonal acne (blackheads and whiteheads) • Inflammatory acne (papules and pustules, also known as “zits”) Who gets it? • Acne is the most common skin problem of teenagers, but it is not limited to that age group. • It can begin before adolescence in both sexes, or it can occur in adulthood, especially in women. • It tends to run in families. What causes it? • Reaction of the skin’s oil glands to sex hormones. Patients with acne usually have normal levels of these hormones, but their oil glands are more sensitive to them and sometimes produce increased amounts of oil. Certain bacteria beneath the skin, acting on the oil, form irritating substances. When the openings to the oil glands become clogged, these irritating substances lead to the formation of blackheads, whiteheads, pimples, or cysts. • Role of food. Foods do not cause acne; however, some people may occasionally find that certain foods, such as chocolate or greasy food, may make their acne worse. If these foods aggravate your acne, avoid them. • Role of dirt. Dirt does not cause acne, and a person with acne usually does not have to wash his or her face more than once or twice a day. Instead, wash your face daily with a gentle cleanser.

Acne: Mild

Acne: Moderate

What makes it worse? • Emotional stress may worsen acne and females often have acne flares before menstruating. • Picking and squeezing of pimples is damaging and can lead to scars. Myths and Facts About Acne Myth: Frequent facials are beneficial. Fact: Professional facials and at-home scrubs, astringents, and masks are generally not recommended because they tend to aggravate acne. Myth: Cosmetics, particularly oil-based preparations, clog pores and cause acne. Fact: Cosmetics probably pose much less of a problem to women’s skin than was previously thought. Their use rarely, if ever, causes acne. More commonly, cosmetics can be irritants and may cause contact dermatitis. Myth: Acne should disappear by the end of adolescence. Fact: Some women have acne that persists well past adolescence. Others have their first episode in their 20s or 30s. Myth: Acne is caused or worsened by certain foods, such as chocolate, sweets, and greasy “junk” food. Fact: Despite occasional personal anecdotes and persistent cultural myths, acne is probably not significantly influenced by diet. Myth: A dirty face worsens acne; therefore, scrubbing the face daily helps clear it up. Fact: Scrubbing and rubbing a face that has acne, particularly inflammatory acne, only serves to irritate and redden an already inflamed complexion and may actually make your acne look worse. Myth: Oily skin causes acne. Fact: Oily skin is more often a result of acne, which increases oil gland activity, rather than a cause.

Acne: Severe

Acn é ¿Qué es el acné? • Hay dos tipos de acné: • Acné superficial (comedón blanco, puntos negros y espinillas) • Acné profundo o inflamatorio (pápulas y pústulas, mejor conocidas como “granos”)

Acné: ligero

Acné: moderado

¿A quién le da acné? • El acné es uno de los problemas de la piel más común en adolescentes, pero no se limita a esa edad. • Puede comenzar antes de la adolescencia en ambos sexos o puede ocurrir en adultos, especialmente mujeres. • Tiende a recurrir en la misma familia. ¿Qué lo causa? • Las glándulas sebáceas de la piel reaccionan a las hormonas sexuales. Los pacientes con acné generalmente tienen niveles normales de hormonas, pero sus glándulas sebáceas son más sensibles y producen mayores cantidades de grasa. Ciertas bacterias bajo la piel actúan con la grasa para formar sustancias irritantes. Cuando las glándulas sebáceas se tapan, las sustancias irritantes forman puntos negros, espinillas, granos y quistes. • El rol de la comida. La comida no causa acné; sin embargo, el acné de algunas personas puede empeorar con ciertos alimentos como chocolate o comida grasosa. Si estos alimentos agravian su acné, evítelos. • El rol de la suciedad. La suciedad no causa acné, y una persona con acné generalmente no debe lavar su cara más de una o dos veces al día. Lavar la cara diariamente con un jabón suave es suficiente. ¿Qué lo empeora? • El estrés emocional puede empeorar el acné. Las mujeres suelen sufrir brotes de acné antes de menstruar. • Rascar o exprimir los granos es dañino y puede dejar cicatrices.

Acné: severo

Mitos y Realidades sobre el Acné Mito: Es benéfico hacerse faciales frecuentemente. Realidad: Los faciales profesionales o hechos en casa con mascarillas, astringentes, exfoliantes o “scrubs” faciales generalmente no se recomiendan porque tienden a agravar el acné. Mito: Los cosméticos, particularmente las preparaciones oleosas, tapan los poros y causan acné. Realidad: Los cosméticos son probablemente más inofensivos para la piel de lo que se pensaba. Su uso raramente causa acné. Sin embargo, pueden ser irritantes y causar dermatitis por contacto. Mito: El acné generalmente desaparece al final de la adolescencia. Realidad: Algunas mujeres tienen acné que persiste aún después de la adolescencia. Otras tienen el primer episodio de acné a los 20 o 30 años. Mito: El acné es causado o empeorado por ciertos alimentos como chocolate, dulces, y comida chatarra grasosa. Realidad: A pesar de la ocasional anécdota personal y los mitos culturales que persisten, el acné no es influenciado significativamente por su dieta. Mito: Una cara sucia empeora el acné; por lo tanto, lavar la cara tallándola ayuda a eliminarlo. Realidad: Tallar o sobar la piel con acné, particularmente acné inflamatorio, únicamente irrita y enrojece la complexión, que está inflamada de por sí, y ocasiona que el acné se vea aún peor. Mito: La piel grasosa causa acné. Realidad: Una piel grasosa no es la causa sino el resultado de acné, ya que el acné incrementa la actividad de las glándulas sebáceas.

Acn e: H o w t o Ap p ly Du a c Gel, Ben za clin Gel, a n d Ben za m ycin Gel Duac Gel contains benzoyl peroxide and clindamycin BenzaClin Gel* contains benzoyl peroxide (gel) and clindamycin (powder) Benzamycin Gel* contains benzoyl peroxide (gel) and erythromycin (powder) (requires refrigeration) *Sometimes these products come unmixed, and you or your pharmacist must combine the clindamycin or erythromycin powder with the benzoyl peroxide gel.

The following guidelines may be helpful: • Before applying the medication, wash your skin gently, rinse with warm water, and pat dry. Apply the gel in small, pea-sized amounts to all acne-prone areas once a day or as directed by your health care provider. Avoid your eyes, lips, and the corners of your mouth, which are often very sensitive. • As you are able to tolerate this, build up to once or even twice daily if you are not making too much progress on your acne. • These medications can be irritating to your skin. For that reason, avoid abrasive, harsh, or drying soaps and cleansers while using the products. • The benzoyl peroxide in these medications can bleach hair, sheets, towels, and clothing. To avoid the bleaching effect, wear an old T-shirt after applying the medication to acne on the back or chest. Also, make sure that the gel has completely dried before your treated skin touches towels, clothes, or bedding (towels, sheets, and pillow cases should be white). Dealing with side effects • Dryness of the treated areas can be expected and is usually mild. If your skin is visibly scaly, apply a nonoily moisturizer, such as Eucerin Daily Control & Care Moisturizer, Cetaphil Moisturizing Lotion, or Olay Oil-Free Active Hydrating Beauty Fluid. The moisturizer should be applied over the medicated gels so that you don’t prevent them from doing their job. • You may experience a mild burning sensation or reddening of the skin when you first start to use this medication. Irritation and burning are common but usually disappear in 2 to 3 weeks. • These products may also cause contact dermatitis (red, dry, inflamed, itchy skin) because of irritation or allergy. This can be treated with a cortisone cream such as a 1% hydrocortisone, which is available without a prescription. • If the preparation you’re applying causes a more severe reaction, stop using it altogether and call your health care provider. Tip • Be patient! Acne responds very slowly to treatment. It may take 4 to 6 weeks before you notice any real improvement. • These products are designed to treat existing acne and prevent future breakouts. To prevent new acne from forming, continue using the preparation for a while, even after your acne clears.

Có m o Ap lica r: Du a c Gel, Ben za clin Gel, y Ben za m ycin Gel Duac Gel contiene peróxido de benzoilo y clindamicina BenzaClin Gel* contiene peróxido de benzoilo (gel) y clindamicina (polvo) Benzamycin Gel* contiene peróxido de benzoilo (gel) y eritromicina (polvo) (requiere refrigeración) *A veces estos productos vienen sin mezclar, y usted o su farmaceuta debe combinar el polvo de clindamicina o eritromicina con el gel de peróxido de benzoilo.

Las siguientes pautas pueden ayudar: • Antes de aplicar el medicamento, lave la piel con cuidado, enjuague con agua tibia y seque con palmaditas delicadas. Aplique el gel en pequeñas cantidades -del tamaño de un guisante- en todas las áreas susceptibles a acné, una vez al día o como lo indique su médico. Evite tocar áreas sensibles como los ojos, labios y bordes de la boca. • Como vaya mejorando su tolerancia al medicamento, y si no ha visto suficiente progreso en su acné, puede incrementar el uso una o hasta dos veces al día. • Estos medicamentos pueden irritar su piel. Por esta razón, evite jabones o limpiadores abrasivos, fuertes, o secantes mientras use éstos productos. • El peróxido de benzoilo en éstos medicamentos puede desteñir cabello, sábanas, toallas, y ropa. Para evitar la decoloración de su ropa predilecta, use una camiseta vieja cuando aplique el medicamento sobre la espalda o el pecho. Asegúrese también de que el gel haya secado por completo antes de que las áreas tratadas de su piel toquen su ropa, toallas, o ropa de cama (las toallas, sábanas, y fundas de almohadas conviene que sean blancas). Cómo lidiar con los efectos secundarios • Puede haber un poco de resequedad en las áreas tratadas, pero es generalmente leve. Si su piel se vuelve visiblemente escamosa, aplique un humectante no grasoso como la crema humectante Eucerin Daily Control & Care, el líquido hidratante Olay Oil-Free Active Hydrating Beauty, o la loción humectante Cetaphil. La crema humectante debe ser aplicada después de aplicar el gel, para permitir que el medicamento surja efecto. • Puede sentir un ligero ardor o enrojecimiento de la piel cuando comience a usar el medicamento. La irritación y el ardor son comunes pero suelen desaparecer en dos o tres semanas. • Estos productos pueden ocasionar dermatitis por contacto (piel roja, seca, inflamada, o con comezón) debido a irritación o alergia. Si le ocurre, aplique una crema de cortisona, como hidrocortisona de 1%, la cual es disponible en farmacias sin necesidad de receta. • Si el producto que está aplicando le causa una reacción severa, deje de usarlo por completo y llame a su médico. Consejo • ¡Sea paciente! El acné responde muy lentamente al tratamiento. Puede tardar entre 4 a 6 semanas en demostrar una mejora. • Estos productos son diseñados para tratar su acné actual y prevenir futuros brotes. Para prevenir que se forme nuevo acné, continúe usando la preparación por un tiempo, aún después de que su acné se aclare.

Acn e: H o w t o Ap p ly To p ica l Ret in o id s What are topical retinoids? • Topical retinoids are medications that are derived from vitamin A. • They are the drugs of choice in people who have comedonal (blackhead and whitehead) acne, and they are also helpful in clearing inflammatory acne (papules and pustules, also known as “zits”). How do these medications work? • Retinoids work by making the skin shed more easily so that hair follicle plugs don’t build up and form blackheads and whiteheads. • In addition, retinoids help “plump up” the skin and make large pores less obvious.

THE TOPICAL RETINOIDS BRAND NAME

GENERIC NAME

Retin-A, Tretin-X Retin-A Micro Differin Tazorac

Tretinoin cream, gel Tretinoin microsphere gel Adapalene cream, gel, solution, and pledgets Tazarotene cream, gel

How should I apply these medications? • Apply small, thin, pea-sized amounts of the medication to clean, dry skin once a day, usually at bedtime or as otherwise instructed by your health care provider. • Apply the medication to all affected areas as well as to places that are acne-prone. How long do they take to work? • Within 6 to 8 weeks, you should notice improvement if you have been using the retinoid continuously. The peak of improvement most often occurs by 3 to 4 months, so give it a real chance to work. How do I deal with side effects? • All retinoids can cause some skin irritation during the first few weeks of use. You may have some discomfort, such as stinging or burning, and sometimes may experience mild redness and scaling of your skin. These reactions are to be expected, and they are an indication that the retinoid is working. • After several weeks, your skin generally gets used to the medication and the discomfort eases. If you are sensitive to the retinoid that your health care provider prescribed for you, you can take a number of steps to help ease the irritation: • Start off gradually. Begin by using it every other day, or even less often, until you get used to it. If you have extremely sensitive skin, try applying the retinoid for short periods, such as leaving it on for a few minutes and then washing it off. You can put it on for as little as 2 to 5 minutes. This tends to make it more tolerable, and it still will have positive effects as long as you stick with it. As your skin becomes accustomed to it, you can gradually increase how frequently you use it and how long you leave it on. Eventually you may be able to apply it every day and leave it on all day or overnight. • Use a moisturizer. If you develop scaly skin, apply a moisturizer generously in the morning. The moisturizer should be applied over any medication you apply at night or in the morning. (If you also use a sunscreen, apply it over the moisturizer.) Effective moisturizers are Oil of Olay, Nivea Ultra Moisturizing Creme, and Eucerin creams. • Use only emollient, nonirritating cleansers to wash your face when you’re using a topical retinoid. continued on page 8

Lo s Ret in o id es Tó p ico s y Có m o Ap lica rlo s ¿Qué son los retinoides tópicos? • Los retinoides tópicos son medicamentos derivados de la vitamina A. • Son el medicamento preferido para quienes tienen acné comedonal (puntos negros y espinillas) e inflamatorio (pápulas y pústulas, mejor conocidas como “granos”). ¿Cómo funcionan estos medicamentos? • Los retinoides exfolian la piel, lo cual previene que los poros se tapen y formen puntos negros y espinillas. • También ayudan a “rellenar” la piel y disimular los poros.

LOS RETINOIDES TÓPICOS MARCA

NOMBRE GENÉRICO

Retin-A, Tretin-X Retin-A Micro Differin Tazorac

Tretinoina crema, gel Tretinoina microsphere gel Adapalene crema, gel, solución, y compresas Tazarotene crema, gel

¿Cómo debo aplicar estos medicamentos? • Aplique pequeñas cantidades (del tamaño de un guisante), en capas delgadas a la piel limpia y seca una vez al día, normalmente antes de acostarse o como lo indique su médico. • Aplique el medicamento en todas las áreas afectadas o susceptibles al acné. ¿Cuánto tiempo tardan en surtir efecto? • Usted debe notar una mejoría entre 6 y 8 semanas si ha usado los retinoides continuamente. La mejora más notable ocurre a los 3 o 4 meses, por lo que sea paciente y déle una oportunidad de surtir efecto. ¿Cómo combatir los efectos secundarios? • Todos los retinoides pueden ocasionar algo de irritación en la piel durante las primeras semanas de uso. Las molestias que se pueden presentar son ardor, enrojecimiento, escamas, o sensación de quemazón. Estas reacciones indican que los retinoides están funcionando. Después de varias semanas, la piel se acostumbra al medicamento y las molestias se alivian. Si usted es sensible a los retinoides que su médico le recetó, puede hacer lo siguiente para aliviar la irritación: • Comience gradualmente. Empiece por usarlo un día si y un día no, o menos seguido, hasta que se acostumbre. Si tiene piel muy sensible, intente aplicar el retinoide durante periodos cortos, comenzando con un par de minutos (pruebe entre 2 y 5 minutos) y enjuagándolo. Esto suele hacerlo más tolerable, permitiéndole tener efectos positivos mientras continúe con el tratamiento. Cuando su piel se acostumbre, puede incrementar gradualmente la frecuencia con que lo aplica y el tiempo que lo deja puesto. Eventualmente va a poder ser capaz de aplicarlo diariamente y dejarlo puesto toda la noche. • Use un humectante. Si desarrolla escamas o despellejamiento, aplique un humectante generosamente en la mañana. El humectante debe ser aplicado sobre el medicamento, después de su tratamiento. (Si también usa bloqueador, aplíquelo sobre el humectante.) Las cremas Oil of Olay, Eucerin, y Nivea Ultra, son humectantes muy efectivos. • Use limpiadores emolientes, no irritantes, para lavar la cara cuando use retinoides tópicos.

continued on page 9

Continued from page 6

Tips • Despite the common misconception, there is no flare of acne in the first few weeks of treatment; rather, the “flare” is either caused by irritation from the medication or from the natural progression of your acne, so try to “ride it through” unless the irritation is really severe—at which point you should call your health care provider. • Retinoids may produce sun sensitivity. It’s true that the retinoids can make you become somewhat more susceptible to sunburn; however, this problem eases after the drug has been used for a month or two. • Applying the medications at bedtime is added insurance against your having problems with sun exposure the next day. • If you’re using a retinoid in sunny conditions, particularly if you have fair skin, just take simple sun-protective measures, such as avoiding the midday sun, applying a broad-spectrum sunscreen or sunblock (over the medication), and wearing a protective cap or hat. Recommendation: Do not use retinoids during pregnancy or breast-feeding.

Continued from page 7

Consejos • A pesar de lo que comúnmente se cree, no hay brotes de acné durante las primeras semanas del tratamiento. Cuando hay “brotes” se debe a que el medicamento está irritando, o al progreso natural de su acné. Intente tolerarlo. Si la irritación es muy severa no dude en llamar a su médico. • Los retinoides pueden provocar sensibilidad al sol. Es cierto que los retinoides pueden volverlo susceptible a quemarse con el sol; sin embargo, este problema disminuye después de un mes o dos de usar el medicamento. • Si aplica el medicamento al acostarse, esto le evita tener problemas con la exposición al sol al día siguiente. • Si necesita usar el retinoide en condiciones soleadas, particularmente si tiene piel clara, tome estas simples precauciones: evite el sol de medio día, aplique un bloqueador de amplio espectro (sobre el medicamento), y utilice un sombrero o gorra. Recomendación: No use retinoides durante el embarazo o la lactancia.

Alo p ecia Area t a What is alopecia areata (AA)? • AA is a common condition that results in the localized loss of hair on the scalp and possibly on other parts of the body. • Shedding of hair is often first discovered by a family member or a person’s hairdresser. What does it look like? • AA usually starts with one or more small, smooth, oval or round patches of hair loss. • Hairless spots are most often found on the scalp, but they can also appear on the eyebrows, eyelashes, and areas of the face that bear hair, such as the beard or mustache in men. • Sometimes the patches of hair loss become so large that they may involve the entire head or body. This can be very difficult to treat.

Alopecia areata

Who gets it? • AA most commonly affects young adults and children. • AA sometimes runs in families. What causes it? • AA is considered to be an autoimmune condition (“self-allergy”), because antibodies appear to be attacking the hair follicles. • These antibodies, which are carried by white cells (T cells), cause the growth of hairs to slow and the hairs themselves to become very small. The hairs go into a state resembling hibernation; however, they remain alive below the surface. • “Nerves” do not cause AA. How is it treated? • Frequently, hair grows back without any treatment; however, it can fall out again. • The regrowing hair is initially thin and sometimes white, but it usually returns to its normal color eventually. • Because mild cases of AA often result in spontaneous regrowth, therapy is often unnecessary. • The spots of hair loss may get bigger before the hair starts to regrow, or more of them may appear while the hair is regrowing. Neither of these conditions is cause for alarm. • The daily application of potent topical steroids, such as _______________________, may speed hair regrowth. For increased drug penetration, the topical steroid may be applied to the scalp and covered with a plastic shower cap that is left on overnight. • If necessary, injections of steroids (diluted cortisone) into the bare patches may be given every 6 to 8 weeks. • Other treatments for AA that is not responding include a medication such as ______________________.

Alopecia areata

Alopecia areata

Alo p ecia Area t a ¿Qué es alopecia areata (AA)? • AA es una condición muy común que resulta en la pérdida de cabello, tanto en el cabeza como en otras partes del cuerpo. • Generalmente un familiar o el estilista comienza a notar la pérdida del cabello.

Alopecia areata

¿Cómo es? • AA comienza con una o más áreas localizadas de pérdida de cabello. Estas áreas son usualmente pequeñas, lisas, y ovaladas o redondas. • Las áreas calvas generalmente se encuentran en la cabeza, pero también pueden aparecer en las cejas, pestañas y zonas velludas de la cara como la barba o el bigote. • A veces las áreas sin cabello son tan grandes que incluyen toda la cabeza o el cuerpo. Esto puede ser muy difícil de tratar. ¿A quién le da? • AA comúnmente afecta niños y jóvenes adultos. • AA puede ser un mal familiar.

Alopecia areata

Alopecia areata

¿Qué lo causa? • AA es considerada una condición autoinmune (“alergia propia”) porque los anticuerpos parecen atacar los folículos del cabello. • Estos anticuerpos, generalmente vinculados con las células blancas (células T), ocasionan lentitud en el crecimiento del cabello y los que llegan a crecer son cabellos muy pequeños y débiles. El cabello entra en un estado como de hibernación; sin embargo, siguen vivos bajo la superficie. • Los “nervios” no causan AA. ¿Cómo se trata? • Frecuentemente el cabello vuelve a crecer sin ningún tratamiento; sin embargo, se puede volver a caer otra vez. • El cabello que vuelve a crecer inicialmente es muy delgado y a veces blanco, pero eventualmente regresa a su color normal. • Dado que los casos leves de AA generalmente resultan en un espontáneo regreso del crecimiento del cabello, no es necesario someterse a una terapia. • Las áreas calvas pueden hacerse más grandes, crecer, o multiplicarse antes de que el cabello vuelva a crecer o mientras esta creciendo cabello nuevo. Ninguna de estas condiciones es causa para alarmarse. • La aplicación diaria de esteroides tópicos potentes como _______________________, puede acelerar el crecimiento del cabello. Para óptima penetración del esteroide tópico, aplíquelo al cuero cabelludo y cúbralo con una gorra de baño. Deje ambos puestos durante toda la noche. • Si llegara a ser necesario, hay inyecciones disponibles para aplicar esteroides con cortisona diluida a las zonas calvas. Se pueden aplicar cada 6 a 8 semanas. • Otros tratamientos disponibles para AA incluyen medicamentos como _____________________.

At h let e’s Fo o t

(Tin ea Ped is)

What causes athlete’s foot? • Athlete’s foot is a very common superficial skin infection caused by a fungus. Those pervasive TV commercials are evidence of just how widespread this problem is. • The fungus that causes athlete’s foot is not very contagious, but it tends to grow in a warm, moist, sweaty environment such as that found in shoes or sneakers.

Who gets it? • It’s seen mostly in men and teenage boys but is not unusual in women. What does it look like? • There are two main types of athlete’s foot: the acute toe web infection, the most common type, and the “moccasin” or “dry” type.

Athlete’s foot (tinea pedis) between the toes

The acute toe web infection • Peeling and sometimes cracking (“fissures”) of the skin between the toes, usually the last two toes, are apparent. • Sometimes the infection appears as small blisters. • Itching or burning and sometimes pain may occur. • The infection may also be associated with an unpleasant odor. • The peeling and cracking can spread to neighboring toes if the fungus is not treated.

Treatment of acute toe web infection • Topical antifungal over-the-counter medications such as Nizoral, Lamisil, Lotrimin, Micatin, and Tinactin are usually very effective. • If necessary, a prescription topical antifungal medication such as _________may be given to you by your health care provider. • Wetness, oozing, or cracking of the skin between the toes may be soothed and dried by using Burow’s solution. • Burow’s solution is applied as wet compresses for 10 minutes twice a day until the oozing stops. (Burow’s solution can be obtained without a prescription.) • Topical antifungals such as ________ are applied after soaking with Burow’s solution.

Prevention of acute toe web infection • Decreasing wetness and friction helps. Frequent changes of socks, the use of absorbent powders such as Zeasorb-AF or baby cornstarch, and drying the area with a hair dryer after bathing are preventive. • The fungus that causes athlete’s foot is found almost everywhere, so taking special precautions to avoid it may not be worth the effort. Nonetheless, many dermatologists recommend daily washing of the feet, thorough drying between the toes, avoidance of tight footwear, wearing absorbent cotton or synthetic socks, and using antifungal powders in the shoes.

The “moccasin” or “dry” type • This scaly, sometimes reddish condition appears on the soles of the feet, often both feet. Sometimes it involves the palms; possibly only one hand is affected. • It’s usually not very itchy, but sometimes the skin thickens and cracks and becomes painful. • The infection can also involve the toenails; these infections are more difficult to treat. • Be aware that these symptoms and a similar appearance can be a result of other causes such as psoriasis or eczema.

Treatment of the “moccasin” or “dry” type • Treatment, if necessary, generally requires

an oral antifungal agent ___________________, in addition to topical agents such as ________________. • This type of athlete’s foot is more difficult to cure than the acute toe web infection. • Recurrence is common after therapy and can lead to long-term infection.

such

as

Keep in mind • Rashes of the feet are not always fungal infections! • In fact, if a child under the age of 12 has what appears to be athlete’s foot, it’s probably another skin condition such as eczema.

Chronic tinea pedis

Pie d e At let a

(Tin ea Ped is)

¿Qué causa el pie de atleta? • El pie de atleta es una infección superficial de la piel muy común, ocasionada por un hongo. Todos esos comerciales de televisión son evidencia de lo abundante que es éste problema. • El hongo que causa el pie de atleta no es muy contagioso, pero suele crecer en un ambiente cálido, húmedo y con sudor, que es típico de zapatos y tenis.

¿A quién le da? • Se ve con frecuencia en hombres y adolescentes, pero no es raro que se presente en mujeres.

¿Cómo es? Pie de atleta (tinea pedis) entre los dedos

• Hay dos tipos de pie de atleta: la infección aguda entre los dedos de los pies, la más común, y la de “mocasín” o “seca.”

Infección aguda entre los dedos de los pies • La piel se despelleja o se agrieta (“fisuras”) entre los dedos del pie, generalmente en los últimos dos dedos. • A veces la infección aparece como ampollas pequeñas. • Puede haber comezón, ardor, e inclusive dolor. • La infección puede ocasionar mal olor. • El despellejamiento y las grietas se pueden esparcir a los demás dedos del pie si no se trata el primer brote a tiempo.

Tratamiento de la infección aguda entre los dedos de los pies Tinea pedis crónica

• Lo más efectivo son los medicamentos antimicóticos tópicos (crema, pomada o talco) como Nizoral, Lamisil, Lotrimin, Micatin, o Tinactin, de venta en farmacias sin necesidad de receta médica. • Si llegara a ser necesario, su médico le puede recetar otro medicamento antimicótico tópico, como _________________. • Si tiene grietas, si siente humedad, o si le está saliendo líquido entre los dedos de los pies, puede usar solución de Burow para ayudar a secar y aliviar estos síntomas. • La solución de Burow se aplica en compresas húmedas durante 10 minutos, dos veces al día, hasta que el fluido se detenga. (Puede conseguir solución de Burow sin receta médica.) • Los antimicóticos tópicos como _______________ se aplican después de remojarse con solución de Burow.

Prevención de la infección aguda entre los dedos de los pies • Evitar que haya humedad y fricción en los pies es de mucha ayuda. Seque bien los pies con secadora de pelo después de bañarse. Una vez secos, use talcos absorbentes como Zeasorb-AF o talco para bebé y póngase un par de calcetines seco y limpio. Si humedece sus calcetines con frecuencia, procure cambiarlos durante el día. • El hongo que causa el pie de atleta se encuentra en todas partes, por lo que casi no valen la pena los esfuerzos por evitarlo. Sin embargo, muchos dermatólogos recomiendan que se lave los pies diariamente, que se asegure que los espacios entre los dedos estén bien secos, que evite usar calzado muy estrecho, que use calcetines absorbentes, y que use talco antimicótico en sus zapatos.

El tipo “seco” o de “mocasín” • Esta condición escamosa y a veces rojiza aparece en las suelas de los pies, generalmente en ambos. A veces aparece también en las palmas de las manos; en ocasiones afecta sólo una mano. • No da mucha comezón, pero la piel se endurece y se agrieta, y eso a veces es doloroso. • La infección puede incluir las uñas; estas infecciones son más difíciles de tratar. • Considere que estos síntomas se parecen mucho a los de psoriasis o eczema y puede haber confusión.

Tratamiento del tipo “seco” o de “mocasín” • El tratamiento, si es necesario, generalmente requiere un antimicótico oral como _________________, aunado a un medicamento tópico como ________________. • Esta clase de pie de atleta es más difícil de curar que la infección aguda entre los dedos de los pies. • Es común que la infección recurra aún después de la terapia y que se convierta en una infección de largo plazo.

Recuerde • ¡No todas las erupciones o sarpullidos en los pies son infecciones de un hongo! • De hecho, si un niño menor de 12 años tiene lo que parece ser pie de atleta, puede ser otra condición de la piel, como eczema.

At o p ic Der m a t it is What is atopic dermatitis? • Atopic dermatitis, which is sometimes called atopic eczema or hereditary eczema, is a very common, itchy, sensitive skin condition that runs in certain families. • It may flare up at times of stress or during the change of seasons, or it may just appear for no obvious reason. The problem frequently goes away by itself—in 40% to 50% of children— but it may return in adolescence or adulthood and possibly turn out to be a lifelong problem. Who gets it? • You, your child, or other family members may have one or more of the following symptoms in addition to the skin rash: dry, sensitive skin; allergies to medications, pollen, dust, house dust mites, ragweed, dogs, or cats; or other problems such as persistent runny nose, sinusitis, sneezing attacks, or chronic itchy or irritated eyes. Any one of these symptoms helps to suggest that atopic dermatitis is the cause of the chronic skin rash. • Other relatives (aunts, uncles, cousins, and grandparents) also may have similar symptoms. • Although most cases begin in childhood (often in infancy), atopic dermatitis may start at any age and has an unpredictable course. How is it treated? Topical steroids The foundation of treatment for atopic dermatitis is the application of topical steroids.

Atopic dermatitis

Atopic dermatitis

• Topical steroids are safe if used as directed and should be applied only for short periods of time, if possible, and only for active disease (i.e., itching and redness). • Topical steroids should be stopped when the skin is healed, and they should not be used to prevent future rashes. Noncortisone topical treatments • Tacrolimus (Protopic) ointment and pimecrolimus (Elidel), which contain no steroids, have been shown to reduce the symptoms of atopic dermatitis. • They may be used on a very nonregular basis in children older than 2 years of age. They are applied twice daily to limited areas where topical steroids should be used with caution, such as the eyelids, underarms, and genitals.

Atopic dermatitis

Other treatment measures • Sometimes oral steroids or antibiotics may be necessary. • Oral antihistamines such as hydroxyzine (Atarax) or the over-the-counter diphenhydramine (Benadryl) and chlorpheniramine (Chlor-Trimeton) probably won’t reduce itching, but they can be helpful if they bring about drowsiness or sleep. • Sun exposure, ideally in the early morning, may improve the condition. Is there a cure? • No, but atopic dermatitis can be kept under control, and sometimes it clears up by itself for long periods of time—sometimes permanently! How is it prevented? • Avoid or lessen exposure to possible trigger factors such as dry skin, irritants, harsh soaps, bubble baths, overheating, sweating, and allergens. • Avoid bathing every day. Bathing is fine for most infants but isn’t necessary. If your child has sensitive skin, it might be best to bathe him or her every other day. For some infants, daily baths can make the skin dry and irritated. Bathing can also cause flare-ups in infants with eczema. • Apply moisturizers, particularly in the dry winter months, immediately after bathing, to “trap” water in the skin. Suggested products include_____________ or _____________. • Use barrier creams such as ____________________________, which may work better than simple moisturizers in preventing atopic dermatitis.

Chronic atopic dermatitis

Der m a t it is At o p ica ¿Qué es la dermatitis atópica? • La dermatitis atópica, también conocida como eczema hereditario o atópico, es una condición muy común de la piel sensible, da mucha comezón y puede ser un mal de familia. • Puede brotar en tiempos de estrés o durante los cambios de estaciones, o puede aparecer sin ninguna razón. El problema frecuentemente desaparece por sí mismo—en 40% a 50% de los niños—pero puede regresar en la adolescencia o adultez y posiblemente volverse un problema de por vida. Dermatitis atópica

Dermatitis atópica

¿A quién le da? • Usted, sus hijos, u otros miembros de su familia pueden tener los siguientes síntomas aparte de erupciones en la piel o sarpullido: piel seca o sensible; alergias a medicamentos, polen, polvo, ácaros, ambrosía, perros, o gatos; otros problemas como sinusitis, ataques de estornudos, ojos crónicamente irritados y moqueado persistente. Cualquiera de estos síntomas sugiere que la causa del sarpullido en la piel es dermatitis atópica. • Otros familiares (tíos, primos, abuelos) pueden tener los mismos síntomas. • Aunque muchos casos comienzan en la infancia (a veces desde bebés), la dermatitis atópica puede comenzar a cualquier edad y tiene un curso impredecible. ¿Cómo se trata? Esteroides tópicos La base del tratamiento de la dermatitis atópica es la aplicación de esteroides tópicos. • Los esteroides tópicos se deben usar como se indica, únicamente por periodos de tiempo muy cortos si es posible, y solo para enfermedades activas (cuando hay comezón y rojez). • Los esteroides tópicos deben detenerse cuando la piel sane y nunca usarse para prevenir brotes futuros.

Dermatitis atópica

Tratamientos tópicos sin cortisona • Tacrolimus (Protopic) ungüento y pimecrolimus (Elidel), son medicamentos que no contienen esteroides y han reducido los síntomas de la dermatitis atópica. • Se pueden usar muy irregularmente en niños mayores de 2 años. Se aplican dos veces al día en áreas muy limitadas donde los esteroides tópicos se aplicarían con mucha precaución, como los párpados, las axilas, y los genitales. Otros tratamientos • A veces esteroides orales o antibióticos pueden ser necesarios. • Antihistamínicos orales como hydroxyzine (Atarax) o diphenhydramine (Benadryl) y chlorpheniramine (Chloro-Trimeton) probablemente no reduzcan la comezón, pero a veces ayudan porque tranquilizan o adormecen. • Algo de exposición al sol, idealmente temprano en la mañana, puede ayudar un poco.

Dermatitis atópica crónica

¿Hay una cura? • No, pero la dermatitis atópica se puede controlar. A veces desaparece por sí misma durante largos periodos y a veces desaparece—¡permanentemente! ¿Cómo se previene? • Evite o disminuya la exposición a factores que puedan causarla como: piel seca, irritantes, jabones duros, baños de burbujas, sobrecalentamiento, sudor, y alergenos. • Evite bañarse todos los días. El baño diario no es necesario para los bebés, y a veces puede secar o irritar la piel. Si su bebé tiene piel sensible conviene que lo bañe un día sí y un día no. El baño diario también puede causar brotes en bebés con eczema. • Aplique humectantes, particularmente en los meses secos del invierno, inmediatamente después de bañarse para “atrapar” el agua en la piel. Se sugieren productos como__________________ o __________________. • Use cremas “barrera” como ________________, que pueden ser mejores que los humectantes comunes para prevenir la dermatitis atópica.

At yp ica l Nevu s

(Mo le)

What is an atypical nevus? • An atypical nevus, also called a dysplastic nevus, atypical mole, or Clark’s nevus, is a benign skin growth. In plain English, it means “unusual mole.” • However, it does share some features with melanoma and can look like a melanoma—but it’s not a melanoma or a skin cancer. • Such atypical nevi are often inherited. What does it look like? An atypical nevus has some or all of the following features: • • • • •

It’s usually larger than a common mole. Its border is usually irregular and poorly defined. It usually has a flat appearance, but the center may be raised. It has an irregular coloration (tan, brown, black, pink, or red). In fact, it can look just like a melanoma.

Atypical nevus

Where is it seen on the body? • An atypical nevus is most often found on sun-protected areas—the trunk or upper legs and arms. • Generally, the face is spared. What does it mean if I have only one or two of them? • If you have a few atypical nevi and no family history of many atypical nevi or melanoma, you probably have little risk of developing a melanoma and should not necessarily be identified as being melanoma prone. • Still, you should learn how to perform self-examination of your skin, and your health care provider should perform a skin examination and watch for any changes in your moles. What does it mean if I have many of them? • The possibility that any particular atypical nevus developing into a melanoma cannot be determined exactly. • However, in some situations, atypical nevi are considered precursors to melanoma, as well as potential markers for someone who is at risk of developing melanoma. People are considered to have familial atypical mole syndrome (FAMS) if they meet the following three criteria: • A first-degree relative (e.g., parent, sibling, or child) or second-degree relative (e.g., grandparent, grandchild, aunt, uncle) with malignant melanoma • A large number of moles (nevi), often more than 50, some of which are atypical nevi • Moles that show certain features when examined under the microscope How is it treated? • The method chosen for treating a suspected atypical nevus depends on the purpose of removal. • If a melanoma is suspected, a complete excision (surgical removal) should be performed. • The wholesale removal of all atypical nevi is not generally considered a good idea. What can be done to prevent the development of melanoma? • Anyone who has many atypical nevi should avoid excessive sun exposure and routinely use a sunscreen with a sun protection factor (SPF) of 30 or greater. • Those people who meet the criteria for FAMS should examine their own skin every 2 to 3 months, in addition to having a full-body examination and regular screenings performed by a dermatologist. • High-risk patients and their families should be taught self-examination to detect changes in existing moles and be given printed material with photographs to help them recognize the features of malignant melanoma. Modified from an American Academy of Dermatology handout.

Atypical nevus

Nevu s At ip ico s

(Lu n a res)

¿Que es el nevus atípico? • El nevus atípico, también llamado nevus displásico, es un tumor benigno relativamente frecuente. Básicamente, es un “lunar inusual.” • Aunque comparte algunas características con el melanoma y puede verse como melanoma— no es melanoma ni cáncer de piel. • Estos lunares atípicos generalmente son heredados. ¿Cómo es? El nevus atípico tiene algunas—o todas—estas características: Nevus Atípico

• • • • •

Es más grande que un lunar común. Sus bordes son irregulares y mal definidos. Parece que es plano, pero el centro puede estar abultado. Su coloración es irregular (café claro, café oscuro, negro, rosa, o rojo). Parece melanoma.

¿En qué parte del cuerpo aparece? • El nevus atípico se encuentra comúnmente en áreas protegidas del sol—el tronco, los muslos, o los brazos. • Generalmente no aparece en la cara.

Nevus Atípico

¿Qué pasa si tengo uno o dos lunares atípicos? • Si tiene algunos lunares atípicos y su familia no tiene historia clínica de lunares atípicos o melanoma, usted tiene bajo riesgo de desarrollar un melanoma. • De cualquier manera, usted puede aprender a examinar su piel o puede acudir a su médico para un examen de piel que monitoree cualquier cambio en sus lunares. ¿Qué pasa si tengo muchos lunares atípicos? • La posibilidad de que un lunar atípico se convierta en melanoma no se puede determinar exactamente. • Sin embargo, en algunas situaciones, los lunares atípicos se pueden considerar precursores de melanoma o señales de que hay riesgo de desarrollar melanoma. Para considerar que alguien tiene Síndrome de Nevus Atípico Familiar (FAMS por sus siglas en Inglés) se necesita cumplir con las siguientes tres características: • Tener un pariente inmediato [padre, madre, hermano(a), hijo(a)] o de segundo grado [abuelo(a), tío(a), nieto(a)] con melanoma maligno • Tener muchos lunares (nevus), generalmente más de 50, y que algunos de ellos sean atípicos • Tener lunares que demuestran ciertas características cuando son examinados bajo el microscopio ¿Cómo se trata? • El método a elegir para quitar un lunar atípico sospechoso depende del propósito para eliminarlo. • Si se sospecha un melanoma, se debe hacer una extracción completa (escisión quirúrgica). • Quitarse todos los lunares atípicos de un jalón generalmente no se considera una buena idea. ¿Qué se puede hacer para prevenir el desarrollo de melanoma? • Cualquier persona con muchos lunares atípicos debe evitar la exposición excesiva al sol y usar regularmente un protector solar con SPF de 30 o más alto. • Las personas que cumplen con el criterio de FAMS deben examinar su propia piel cada 2 a 3 meses, aunado a vistas regulares con un dermatólogo para someterse a exámenes de cuerpo completo. • Los pacientes de alto riesgo y sus familias deben aprender a examinarse para detectar cambios en lunares existentes. Se les deben ofrecer folletos con fotografías que demuestren cómo reconocer las características del melanoma maligno. Modificado del folleto de la Academia Americana de Dermatología.

Ba sa l Cell Ca rcin o m a What is a basal cell carcinoma (BCC)? • BCC is the most common type of skin cancer. It’s often easily treated and cured in most cases. • Although BCC qualifies as a cancer, its harmful effects, if recognized and treated early, are usually minor. • BCC is usually very slow growing and rarely spreads (metastasizes), but it can cause serious local invasion and destruction if it’s ignored or treated inadequately. Who gets it? • A light complexion with poor tanning ability is a risk factor. • People who develop BCC often have a history of long-term sun exposure. • Other family members may also have a history of BCC.

Basal cell carcinoma

What does it look like? • It resembles a shiny “pimple” or sore that does not heal. • It’s usually a dome-shaped bump with a pearly appearance. • It may have a small scab on its surface. How is it diagnosed? • Diagnosis is generally made by a skin biopsy. How is it treated? • Most often, a simple minor office procedure called electrodesiccation and curettage is performed for small growths and for very superficial BCCs. • Surgical removal (excision) is the preferred method for larger tumors. • Micrographic (Mohs’) surgery may be the preferred method for recurrent or very large lesions. Mohs’ micrographic surgery is a microscopically controlled method of removing skin cancers that allows for controlled excision and maximum preservation of normal skin. Excisions are repeated in the areas proven to be cancerous until a completely cancer-free specimen is obtained. • Other treatment methods include the following: • Cryosurgery (“freezing”) with liquid nitrogen is a treatment option. • Radiation therapy is used for those patients who are physically debilitated or who are unable to undergo excisional surgery. • A topical cream known as Aldara is sometimes used to treat certain superficial types of BCCs. How do I avoid getting BCCs in the future? • Avoid exposure to sun. • Carefully plan outdoor activities before 10 a.m. and after 4 p.m. • Wear a broad-brimmed hat during outdoor activities, and use a sunscreen with a sun protection factor (SPF) of 15 or greater. • Learn skin self-examination, and have annual skin examinations performed by your dermatologist. What are some general preventive methods? • Sun avoidance measures: • Sunscreen • Hat with brim • Sunglasses with ultraviolet protection • Tinted windshields and side windows in cars • Protective clothing made of tightly woven or knitted fabrics that allows less sunlight to pass through is available. • Follow-up: after therapy, periodic skin examinations

Basal cell carcinoma

Basal cell carcinoma

Ca rcin o m a d e Célu la s Ba sa les ¿Qué es un carcinoma de células basales (CCB)? • El CCB es el cáncer de piel más común. Es muy fácil de tratar y se cura en la mayoría de los casos. • Aunque el CCB califica como cáncer, sus efectos dañinos son mínimos si se le reconoce y se trata temprano. • El CCB es muy lento en su crecimiento y raramente se esparce (metástasis), pero puede causar invasiones locales serias y destrucción si se le ignora o si no se le trata adecuadamente. Carcinoma de Células Basales

¿A quién le da? • Un factor de riesgo es tener una complexión clara que se quema al exponerse al sol. • La gente que desarrolla CCB generalmente tiene una larga historia de exposición al sol. • Otros miembros de la familia puede que hayan tenido historia de CCB. ¿Cómo es? • Parece un granito brilloso o una llaga que no sana. • Usualmente se ve como un brote abultado y aperlado. • Puede tener una pequeña costra en la superficie. ¿Cómo se diagnostica? • Generalmente el diagnóstico se hace con una biopsia de piel.

Carcinoma de Células Basales

Carcinoma de Células Basales

¿Cómo se trata? • Por lo regular, un proceso simple llamado electrodesecación y curetaje se realiza en la oficina, en brotes pequeños y en casos muy superficiales de CCB. • El método preferido para tumores más grandes es una extirpación quirúrgica (escisión). • La cirugía micrográfica de Mohs es el método preferido para lesiones recurrentes o mayores. Es un proceso microscópicamente controlado para extraer el cáncer de piel que permite una escisión precisa para preservar el máximo de piel normal. Las escisiones se repiten en las áreas cancerosas hasta que se obtiene un espécimen completamente libre de cáncer. • Otros tratamientos incluyen: • Criocirugia (“congelar”) con nitrógeno líquido—es una opción. • Terapia de radiación—para pacientes físicamente debilitados o incapaces de someterse a una cirugía. • Crema tópica Aldara—a veces ayuda a tratar ciertos tipos superficiales de CCB. ¿Cómo puedo evitar contraer CCB en el futuro? • Evite la exposición al sol. • Planee sus actividades al aire libre para antes de las 10 a.m. o después de las 4 p.m. • Use sombrero de ala ancha y use bloqueador solar con factor de protección (SPF) 15 o mayor. • Aprenda a examinar su piel y acuda a su dermatólogo para exámenes anuales. Métodos preventivos generales • Evite el sol con: • Bloqueador solar • Sombrero de ala ancha • Anteojos obscuros con protección ultravioleta • Parabrisas y ventanas entintados en su auto • Ropa que proteja contra el sol—con mangas largas y de tejido estrecho—se consigue fácilmente. • Seguimiento: después de su terapia, examine su piel periódicamente.

Bu ro w ’s So lu t io n What is Burow’s solution? • Burow’s solution is a topical antibacterial astringent preparation that helps “dry up” and control weeping, oozing, and infected skin. Where do I get it? • You can buy Burow’s solution (Domeboro, Bluboro, Boropak) in most chain pharmacies. It does not require a prescription. • It comes as a powder in packets or tablets that must be dissolved in water. How do I use it? • Mix one packet or tablet in an 8-ounce glass of water (about the size of a drinking glass). • Make a wet compress using a cloth or cotton swab moistened by the solution and place it over the affected skin area for 15 to 20 minutes. • Do this three to four times each day. • Apply a medication such as ____________________ and sterile dressings after the soaks, if recommended. • Use until all areas are no longer oozing. • Cool water may be more comfortable to use when treating itchy rashes such as poison ivy. Lukewarm water may be more comfortable for treating wintertime weeping eczema rashes and for drying the blisters of herpes zoster (shingles).

So lu cio n d e Bu ro w ¿Qué es la solución de Burow? • La solución de Burow es una preparación astringente tópica antibacterial que ayuda a “secar” y controlar la piel infectada que exude o segrega líquido. ¿Dónde la consigo? • Se puede comprar solución de Burow (Domeboro, Bluboro, Boropak) en casi todas las farmacias. No requiere receta médica. • Viene en polvo, en paquetes o tabletas que se deben disolver en agua. ¿Cómo se usa? • Disuelva un paquete o tableta en un vaso de agua (8 onzas son mas o menos el agua que cabe en un vaso de tamaño normal). • Haga una compresa húmeda usando un pedazo de tela o algodón mojado en la solución y póngala sobre el área de piel afectada durante 15 a 20 minutos. • Repita tres o cuatro veces al día. • Aplique el medicamento que le hayan recetado ____________________ y vendajes esterilizados tras aplicar las compresas, si se lo recomienda su médico. • Use hasta que la piel deje de exudar. • El agua fría es más confortable para tratar erupciones con comezón como la causada por hiedra venenosa. • El agua tibia es más confortable para tratar sarpullido o eczema que exuda en invierno o para secar las ampollas del herpes zoster.

Co n t a ct Der m a t it is What is contact dermatitis? • There are two types of contact dermatitis: allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD). • ACD is an inflammatory reaction caused by certain substances called allergens that come into contact with your skin. Common examples of ACD are poison ivy as well as reactions of the skin to jewelry and topical antibiotics such as neomycin. ACD reactions occur only in those people who are allergic to the substance. • ICD is also known as nonallergic contact dermatitis. Common examples of ICD are diaper dermatitis (diaper rash) and “dishpan hands.” ICD is often caused and worsened by soaps, detergents, and numerous chemicals found in the home and workplace; these all damage the skin after repeated contact. What are the TOP TEN allergens? • Nickel: found in jewelry, clasps, and metal buttons • Gold: found in jewelry • Balsam of Peru: included in perfumes and skin lotions • Thimerosal: used as preservative in local antiseptics and vaccines • Neomycin sulfate: found in first aid creams such as Neosporin and Polysporin • Fragrance mix: found in substances such as foods, cosmetics, perfumes, insecticides, and dental products • Formaldehyde: a preservative that is included in paper products, dry cleaning solvents, paints, and cosmetic products • Cobalt chloride: found in hair dyes and metals • Bacitracin: a topical antibiotic • Quaternium 15: a preservative often found in cosmetics and industrial agents

Contact dermatitis caused by nickel

Contact dermatitis caused by a watch

What does the rash of ACD and ICD look like? • In acute cases such as poison ivy or poison oak, the skin gets red and itchy and often develops blisters. • With long-term (chronic cases) exposure to the allergen, the skin becomes thickened, red, and scaly. • ICD may be characterized by dryness (scaling), cracking (fissuring), and redness. How is the cause determined? • The appearance of the skin rash and a careful history often serve as clues to the offending agent. • Your health care provider will ask about your daily habits and occupational exposures, so that any possible materials you may have been in contact with can be revealed. • If the allergen can’t be identified by the history or physical examination, patch testing may be necessary. This is a safe and painless procedure in which small amounts of the possible common allergens are applied to the skin on strips of tape and removed after two days. A positive test reveals a small red spot when the patches are removed. What can be done to prevent ACD and ICD? • ACD: The answer is fairly simple. Avoid the offending agent or minimize contact with it. • ICD: As with ACD, avoid the offending agent or minimize contact with it. Wearing protective gloves or using barrier creams is also helpful. How are ACD and ICD treated? • Treatment with topical or systemic corticosteroids may be warranted. • It may also be necessary to apply cool, moist compresses to blistered areas for a few days. • Moisturizers and special barrier creams are also recommended. continued on page 24

Contact dermatitis caused by rubber

Der m a t it is d e Co n t a ct o

Dermatitis de contacto causada por níquel

Dermatitis de contacto causada por un reloj

¿Qué es dermatitis de contacto? • Hay dos clases de dermatitis de contacto: dermatitis de contacto alérgica (DCA) y dermatitis de contacto irritante (DCI). • DCA es una reacción inflamatoria causada por ciertas sustancias llamadas alérgenas que entran en contacto con la piel. Algunos ejemplos comunes de DCA son la hiedra venenosa o las reacciones de la piel a cierta joyería o antibióticos tópicos como neomicina. Las reacciones de DCA le ocurren únicamente a personas alérgicas a esas sustancias. • DCI es conocida también como dermatitis de contacto no alérgica. Algunos ejemplos comunes de DCI son las rozaduras de pañal o las “manos de lavatrastos.” La DCI es generalmente causada y empeorada por jabones, detergentes, y otros químicos que se encuentran en el hogar o trabajo; todos ellos pueden dañar la piel con repetido contacto. ¿Cuáles son los diez principales alérgenos? • Níquel: se encuentra en joyería, broches, y botones de metal • Oro: se encuentra en joyería • Bálsamo de Perú: incluido en perfumes y cremas • Thimerosal: usado como preservativo en vacunas y antisépticos locales • Sulfato de Neomicina: presente en pomadas de primeros auxilios como Neosporin y Polysporin • Mezclas de fragancias: se encuentran en alimentos, cosméticos, perfumes, insecticidas, y productos dentales • Formaldehído: un preservativo que se usa en productos de papel, solventes de tintorería, pintura, y productos cosméticos • Cloruro de cobalto: se encuentra en tintes para el cabello y en metales • Bacitracin: un antibiótico tópico • Quaternium 15: un preservativo usado en cosméticos y agentes industriales ¿Cómo es la dermatitis de contacto? • En casos agudos como la hiedra venenosa o el roble venenoso, la piel enrojece, da comezón y a veces hay ampollas. • Con el tiempo, la piel se endurece, sigue rojiza, y desarrolla escamas con la exposición a largo plazo al alérgeno (casos crónicos). • La DCI se caracteriza por piel seca (escamas), agrietamiento (fisuras), y rojez.

Dermatitis de contacto causada por hule

¿Cómo se determina la causa? • La apariencia de la piel y una historia clínica adecuada proporcionan una idea de qué agente es la causa. • Su medico le preguntará sobre sus hábitos diarios y a lo que se expone en el trabajo, para revelar todos los materiales con los que haya estado en contacto. • Si el alérgeno no se puede identificar con la historia clínica o con el examen físico, puede ser necesario hacer una prueba de parche. Es un procedimiento inofensivo que no causa dolor: pequeñas cantidades de posibles alérgenos se aplican a la piel con trozos de cinta durante dos días. Un resultado positivo revela una mancha roja bajo la cinta con el alérgeno responsable. ¿Qué se puede hacer para prevenirla? • DCA: La respuesta es simple. Evite el agente responsable o minimice el contacto con él. • DCI: Al igual que DCA, evite el agente responsable, minimice el contacto con él. Puede ayudar si usa guantes protectores o cremas que actúen como barreras. ¿Cómo se trata? • Se puede requerir de tratamiento con corticosteroides tópicos o sistémicos. • También puede ser necesario aplicar compresas húmedas, frías, a las áreas con ampollas por unos días. • Se recomienda usar cremas barrera o lociones humectantes. continued on page 25

Continued from page 22

What is diaper rash? • Diaper rash is the result of overhydration of the skin that’s irritated by chafing, soaps and detergents, and prolonged contact with urine and feces (for example, when cloth diapers aren’t changed right away). Added to this wet environment is the occlusive effect of rubber or plastic diapers. • Diaper dermatitis may also be caused by, or intensified by, the presence of atopic dermatitis, seborrheic dermatitis, or a secondary yeast infection (Candida albicans). Helpful hints • Often when ACD is suspected, the problem is actually may be atopic dermatitis (a hereditary eczema). • If you or your child has atopic dermatitis, it’s more likely that ICD will develop as a result of the skin’s sensitivity and lessened barrier function.

Continued from page 23

¿Qué es la rozadura de pañal? • La rozadura de pañal es el resultado de sobre-hidratación de la piel irritada por jabones y detergentes, o contacto prolongado con orina y excremento (por ejemplo, cuando los pañales no se cambian de inmediato) y se añade al ambiente húmedo el efecto oclusivo de hule o plástico. • La dermatitis de pañal también puede ser causada o empeorada por la presencia de dermatitis atópica o seborreica, o una infección micótica secundaria (Candida albicans). Consejos • Cuando se sospecha DCA, el problema generalmente es dermatitis atópica (un eczema hereditario). • Si usted o su niño tiene dermatitis atópica, probablemente desarrolle DCI como resultado de la sensibilidad de la piel y la disminución de sus funciones de barrera.

Dr y Sk in

(Xero sis)

Measures to prevent and treat dry skin • Moisturizers do not add water to the skin, but they do help retain or “lock in” water that’s absorbed while you’re bathing or showering. • Many over-the-counter preparations are available, such as Aquaphor, Curel, Eucerin, Alpha Keri, Lubriderm, Moisturel, and Vaseline Petroleum Jelly. • Some are in ointment bases, cream bases, or lotions, and others contain alpha-hydroxy acids. The decision about which product to use involves personal choice, ease of application, cost, and effectiveness. • Ammonium lactate 12% (Lac-Hydrin) lotion or cream, which is available by prescription only, is very effective for scaly skin. AmLactin lotion or cream is a similar preparation that is available over the counter. As with moisturizers, these preparations work best when applied to damp skin. Tips • Take less frequent and shorter showers and baths, using lukewarm water. • Use mild soaps such as Dove, Basis, or a soap substitute such as Cetaphil Lotion. Avoid excessive use of any soap, especially on affected areas. • After bathing or showering, pat dry, preferably leaving some water on the skin surface, and then apply a moisturizer when the skin is still damp to help seal in the absorbed water. • The lubricating preparations may help prevent future breakouts, particularly in the dry winter months. • Self-adhesive bandages (e.g., Band-Aids) can help promote healing of fissures (cracks in fingers and heels). • If you have dry, sensitive hands, wear lined gloves while washing dishes. • Protect yourself from outdoor cold exposure by wearing garments such as gloves and hats. • Room humidifiers may be helpful. • Drinking large amounts of water is of little value.

Dry skin (xerosis)

Piel Seca

Piel seca (xerosis)

Medidas para prevenir y tratar la piel seca • Las cremas humectantes no añaden agua a la piel, pero ayudan a retener o “encerrar” el agua que su piel absorbió durante el baño. • Muchas preparaciones se venden en farmacias sin recetas médicas, como Aquaphor, Curel, Eucerin, Alpha Keri, Lubriderm, Moisturel, y Vaseline Petroleum Jelly. • Algunas de ellas son ungüentos, otras cremas o lociones y otras contienen alfa-hidroxiácidos. Para decidir cual producto usar se puede basar en su opinión personal, facilidad de aplicación, costo, y efectividad. • El lactato de amonio 12% (Lac-Hydrin) en loción o crema esta disponible sólo con receta médica, pero es muy efectivo para tratar piel escamosa. AmLactin en loción o crema es una preparación similar disponible sin receta médica. Al igual que los humectantes, éstas preparaciones funcionan mejor cuando se aplican acabando el baño, cuando la piel esta húmeda. Consejos • Tome baños menos frecuentes y más cortos, y use agua tibia. • Use jabones suaves como Dove o Basis, o un sustituto de jabón como Cetaphil Loción. Evite el uso excesivo de cualquier jabón, especialmente en las áreas afectadas. • Después de bañarse, no talle su piel fuerte con la toalla, séquela con palmaditas suaves, de preferencia dejándola algo húmeda, y aplique un humectante de inmediato para ayudar a sellar la humedad y que su piel absorba el agua. • Las preparaciones lubricantes pueden ayudar a prevenir futuros problemas, particularmente en los meses secos del invierno. • Las bandas adhesivas (curitas) pueden ayudar a sanar las pequeñas fisuras (aberturas de la piel en los talones o en los dedos). • Si tiene piel seca y manos sensibles, use guantes mientras lava los trastes. • Protéjase de la exposición al frío. Use guantes y gorros cuando salga. • Los humidificadores pueden ayudar también. • Tomar mucha agua no ayuda gran cosa.

Fu n ga l Na ils

(On ych o m yco sis)

What are fungal nails (onychomycosis)? • The term onychomycosis refers to an infection of the fingernails or toenails caused by various fungi. What causes it? • The major cause of onychomycosis are the fungi known as dermatophytes. • However, certain yeasts and molds may also be responsible. What does it look like? • Nail thickening and scale buildup under the nail are evident. • Nail discoloration (yellow, yellow-green, white, or brown). • Nail deformity may occur. • Onycholysis (nail plate elevation from the nail bed) may also occur.

F ungal nails (onychomycosis)

What are its symptoms? • Aside from footwear causing occasional physical discomfort and the appearance of unsightly nails, there are usually no symptoms. • It’s sometimes associated with chronic foot and palm fungus. • In patients with diabetes mellitus, fungal nails may infrequently act as an entry point for more serious bacterial infections of the lower leg. Who gets it? • It’s seen with advancing age, with rates as high as 30% in people 70 years and older. • It’s uncommon in children. F ungal nails (onychomycosis) How is it diagnosed? • Nail clippings or scale from under the nails are obtained. • The growth of dermatophyte, yeast, or mold on culture helps confirm the diagnosis. How is it treated? • Oral antifungal medications such as terbinafine (Lamisil) tablets, itraconazole (Sporanox) capsules, fluconazole (Diflucan) tablets, and griseofulvin (Gris-PEG) can be very effective in treating it; however, the chance that it will reappear is high. • The long-term cure rate is probably no greater than 40% to 50% with any of the above drugs. • Side effects are uncommon; however, certain baseline (pretreatment) liver function tests are usually performed by your health care provider and repeated while you are taking these medications. • Sporanox may also be used. The primary drawback to this drug is the risk of significant drug interactions. Make sure that your health care provider is aware of all the medications that you take. What are some other treatment methods? • Surgical removal of nails, which rarely results in a cure. • Topical therapy with lacquers, creams, and lotions, which are of little or no value in treating nail disorders because these agents don’t penetrate the nails enough. Helpful hints • Treatment with the newer oral antifungal agents is expensive and doesn’t always result in a cure. • Many molds and certain yeasts won’t respond to the oral antifungal medications. • Preexisting liver disease may be a reason not to take oral antifungal agents for nail fungus. • If you have a family history of nail fungus, it’s less likely to have a successful treatment outcome. Keep in mind Other common nail disorders that look like nail fungus include: • • • •

Psoriasis of the nails Bacterial infections such as Pseudomonas that can result in green-colored nails Onycholysis (nail plate elevation from the nail bed) without fungal involvement Nail injuries

Sp a n ish Na m e o f Co n d it io n ¿Qué es onicomicosis? • El término onicomicosis se refiere a una infección de las uñas de los pies o de las manos causada por varios hongos. ¿Qué lo causa? • La principal causa de onicomicosis son los hongos llamados dermatofitos. • Sin embargo, otros hongos y mohos pueden también ser responsables.

Uñas con hongos (onicomicosis)

¿Cómo es? • Se nota engrosamiento de la uña y acumulación de escamas bajo la superficie. • Cierta decoloración de la uña (amarillo, verdoso, blanco, o café). • La uña se puede deformar. • Puede haber despegamiento de la uña de su lecho (onicolisis). ¿Cuales son los síntomas? • Aparte de incomodidad o molestia con cierto calzado, o la apariencia desagradable de las uñas, generalmente no hay síntomas. • En ocasiones se asocia con hongos crónicos en las palmas de las manos o las plantas de los pies. • En pacientes con diabetes melitus, las uñas con hongos pueden servir como punto de entrada para infecciones bacteriales más serias en las piernas.

Uñas con hongos (onicomicosis)

¿A quién le da? • Se observa en edades avanzadas, con incidencia de hasta 30% en personas mayores de 70 años. • Es raro en niños. ¿Cómo se diagnostica? • Se obtienen muestras de las uñas o de las escamas debajo. • Un cultivo de dermatofitos, hongos o moho confirma el diagnostico. ¿Cómo se trata? • Los medicamentos antimicóticos orales como tabletas de terbinafine (Lamisil), cápsulas de itraconazole (Sporanox), tabletas de fluconazole (Diflucan), y griseofulvin (GrisPEG) pueden ser muy efectivos; sin embargo, la posibilidad de reincidencia es alta. • La probabilidad de curar la onicomicosis a largo plazo con los medicamentos mencionados es de 40% a 50%. • Es raro que haya efectos secundarios; sin embargo, su médico le hará exámenes básicos (antes y después del tratamiento) para monitorear la función del hígado. • Se puede usar Sporanox. El principal problema con este tratamiento es que interfiere con otros medicamentos. Asegúrese de informar a su doctor sobre todas las medicinas que usted toma. ¿Hay otros tratamientos? • Extracción quirúrgica de las uñas, pero esto raramente elimina el problema. • Terapia tópica con lacas, cremas y lociones, las cuales no son muy efectivas porque no penetran lo suficiente en la superficie de la uña. Consejos • El tratamiento con nuevos agentes antimicóticos orales es caro y no siempre curan por completo. • Muchos mohos y algunos hongos no responden a los medicamentos antimicóticos orales. • Si tiene problemas del hígado evite tomar medicamentos antimicóticos orales. • Si hay una historia clínica de uñas con hongos en su familia, sus probabilidades de curarlas por completo son muy bajas. Recuerde Otras enfermedades de las uñas que se pueden ver como hongos incluyen: • • • •

Psoriasis de las uñas. Infecciones bacteriales como pseudomonas, las cuales resultan en uñas color verde. Onicolisis (despegamiento de la uña de su lecho) sin hongos. Lesiones en las uñas.

Gen it a l Wa r t s What are genital warts? • Genital warts, also known as venereal warts or condyloma acuminatum, are a very common sexually transmitted disease. • These usually smooth or cauliflowerlike growths are seen in the vicinity of the penis, vagina, vulva, cervix, and anus. What causes them? • Genital warts are caused by a virus, the human papilloma virus (HPV). The type of HPV that causes genital warts is probably not the same subtype that causes the common wart. • It is thought that most genital warts are spread by sexual contact; however, recent evidence suggests that nongenital spread of the virus can also occur. • These warts have a fairly long incubation period and may appear several weeks or even years after sexual contact; thus, it is difficult to determine the origin of the infection in people who have had multiple sexual partners. Therefore, many infected persons are carriers of the virus and may never develop warts but still can transmit them to their sexual partners. • Mothers who have genital HPV can infrequently transmit genital warts to their infants during delivery.

Genital warts

How are they diagnosed? • The diagnosis of genital warts is often simple; however, when they are very small and difficult to see, they may be confused with normal structures of the skin. • Sometimes a skin biopsy is performed to confirm the diagnosis. • In women, evidence of the viral infection may be detected during a routine pelvic examination or a Pap smear. How are they treated? • Treatment is often difficult because no specific agent—antibiotic, antiviral, or otherwise— is available to actually destroy the virus. • The biggest problem is the tendency for the warts to recur, whichever method is used. It is impossible to predict who will have recurrences. Office treatment • Electrodesiccation uses a direct electric current to destroy the warts after local anesthesia is used. • Cryodestruction (“freezing”) uses liquid nitrogen. • Podophyllum is a liquid medication. • Dichloroacetic and trichloroacetic acids may be applied. • Laser therapy may be used to destroy the warts. • Interferon alpha is available as an injectable treatment. It is expensive, has more side effects, and may not offer any great advantage over the other treatments.

Genital warts

Perianal warts

Home treatment • Imiquimod (Aldara) and podofilox (Condylox) are medications that may be selfapplied. Both require a prescription. continued on page 32

Genital warts

Ver r u ga s Gen it a les ¿Qué son las verrugas genitales? • Las verrugas genitales, también conocidas como verrugas venéreas o condiloma acuminado, son una enfermedad muy común transmitida sexualmente. • Estas verrugas son generalmente lisas o con apariencia de coliflor y se presentan en el pene, la vagina, la vulva, el cervix y el ano.

Verrugas genitales

¿Qué las causa? • Las verrugas genitales son causadas por el virus de papiloma humano (VPH). Este tipo de VPH no es el mismo subtipo que ocasiona las verrugas comunes. • Se piensa que la mayoría de las verrugas genitales se contagian por contacto sexual; sin embargo, la evidencia reciente sugiere que también se puede contagiar sin contacto genital. • Estas verrugas tienen un periodo largo de incubación, pudiendo aparecer varias semanas o hasta años después del contacto sexual, lo que dificulta la habilidad de determinar el origen de la infección en personas que han tenido múltiples parejas sexuales. Aunado a esto, muchas personas infectadas son portadores del virus y aunque pueden nunca desarrollar las verrugas, pueden transmitirlas a sus parejas sexuales. • Las madres infectadas con el VPH rara vez transmiten verrugas genitales a sus bebés durante el parto. ¿Cómo se diagnostican? • El diagnóstico de verrugas genitales es simple; sin embargo, cuando son pequeñas y difíciles de ver se pueden confundir con estructuras normales de la piel. • A veces una biopsia de piel se realiza para confirmar el diagnóstico. • En mujeres, la evidencia de una infección viral se puede detectar durante un examen rutinario de pelvis o con el papanicolaou.

Verrugas genitales

Verrugas perianales

¿Cómo se tratan? • El tratamiento es difícil porque no hay un agente especifico antibiótico, antiviral, u otroque destruya el virus. • El mayor problema es su tendencia a recurrir, sin importar el método utilizado para eliminarlas. Es imposible predecir quién tendrá recurrencias. Tratamiento en la oficina • Electrodisecación es una corriente eléctrica directa para destruir las verrugas. Se usa anestesia local. • Criodestrucción “congela” las verrugas con nitrógeno líquido. • Podophyllum es un medicamento líquido. • Ácidos dicloroacetico y tricloroacetico se pueden aplicar. • Terapia láser se puede usar para destruir las verrugas. • Alfa interferón esta disponible como tratamiento inyectable. Es muy caro, tiene efectos secundarios y no tiene gran ventaja sobre los otros tratamientos. Tratamiento en casa • Imiquimod (Aldara) y podofilox (Condylox) son medicamentos que se puede aplicar por sí mismo, pero ambos requieren receta médica. continued on page 33

Verrugas genitales

En glish Na m e o f Co n d it io n Continued from page 30

How are they prevented? • Spread of warts can be lessened by the use of condoms; however, a condom may not cover all warts. • Recently, the Food and Drug Administration approved an HPV vaccine known as Gardasil. The vaccine provides protection against four types of HPV-associated cervical cancers and genital warts. It is approved for females from 9 to 26 years of age. • Because the vaccine doesn’t provide protection from all types of HPV, all women should continue to have regular Pap screenings to detect precancerous changes in the cervix. • In addition, women should also use all means at their disposal to prevent genital contact with HPV in the first place. What are the long-term consequences of HPV? • In many patients with HPV, the immune system keeps the virus under control or manages to eliminate it; however, a minority of people develop a persistent infection that doesn’t go away. • Over time, women with long-standing HPV are at higher risk of developing changes in the cells of the cervix. That condition can eventually progress to cervical cancer. Therefore, it is recommended that female partners of affected people be seen by a gynecologist.

Continued from page 31

¿Cómo se previenen? • El contagio de las verrugas se puede disminuir con el uso de condones; sin embargo, el condón puede no cubrir todas las verrugas. • La FDA recientemente aprobó una vacuna contra el VPH llamada Gardasil. Esta vacuna provee protección contra cuatro tipos de VPH asociados con cáncer cervical y verrugas genitales. Está recomendada para mujeres entre 9 y 26 años. • La vacuna no provee protección contra todos los tipos de VPH, por lo que todas las mujeres deben continuar sometiéndose a exámenes regulares de Papanicolaou para detectar cambios precancerosos en el cervix. • Adicionalmente, se recomienda que usen todos los métodos disponibles para evitar el contacto con el VPH. ¿Cuáles son las consecuencias a largo plazo de VPH? • Muchos pacientes con VPH tienen el virus bajo control gracias a su sistema inmune; sin embargo, una minoría desarrolla una infección persistente que simplemente no se cura. • Las mujeres que han tenido VPH durante mucho tiempo tienen mayor riesgo de desarrollar cambios en las células del cervix. Esta condición puede eventualmente desarrollar cáncer cervical. Por lo tanto, se recomienda que las mujeres cuyas parejas estén afectadas vean a un ginecólogo.

Gra n u lo m a An n u la re What is granuloma annulare? • Granuloma annulare is a raised, bumpy, often ring-shaped skin disorder that generally causes no symptoms. • It’s primarily a cosmetic problem, although some people tend to find its sudden appearance somewhat alarming. Who gets it? • It occurs more often in women than in men. • It’s not uncommon in children and young adults.

Granuloma annulare

What does it look like? • Most often it forms curious circles or semicircular skin-colored or red-colored bumps, which are often misdiagnosed as ringworm because the bumps (lesions) tend to be ringlike (clear in the center). • Although any part of the skin surface may be involved, lesions are most often symmetrically distributed on the backs of the hands, fingers, and feet. • In adults, especially women, lesions may also be found around the elbows. What causes it? • The cause is unknown, but it’s believed to be the result of an immune system reaction. • As far as we know, it’s not associated with any internal disease; however, research is ongoing to determine if there is a relationship between granuloma annulare and diabetes. How is it diagnosed? • The diagnosis is most often made by its appearance. • Sometimes a skin biopsy (a small sample of skin) is taken to confirm the diagnosis. What other skin rashes can it be confused with? • Tinea corporis (ringworm) • Whitish scale is present at the border of the ring(s). • Fungal examination is positive. • Erythema migrans rash of Lyme disease • The rings of this rash are larger than those associated with granuloma annulare. • The rash is often associated with a history of a tick bite. • The rash is self-limiting. What can I expect? • In very young children, it often disappears by itself (self-limiting). • In adults, it tends, more often, to be a long-lasting, chronic condition. How is it treated? • Because it often has no symptoms, treatment is not always necessary. • In fact, localized lesions on nonvisible skin in children are best left untreated. • If there is cosmetic concern, your health care provider may prescribe a topical steroid cream or steroid tape. • Another option is to have your health care provider inject a steroid medication directly into the lesions.

Granuloma annulare

Gra n u lo m a An u la r ¿Qué es el granuloma anular? • El granuloma anular es una enfermedad de la piel con protuberancias pequeñas y elevadas en forma de anillos, pero que generalmente no causa otros síntomas. • Es un problema principalmente cosmético, aunque algunas personas se alarman cuando aparece.

Granuloma anular

¿A quién le da? • Afecta a mujeres más frecuentemente que a hombres. • No es raro en niños o adolescentes. ¿Cómo es? • Generalmente presenta protuberancias circulares o semicirculares, de color piel o rojizas, comúnmente confundidas con tiña porque las lesiones tienen una apariencia anular con un centro claro. • Aunque puede afectar cualquier parte de la superficie de la piel, las lesiones comúnmente se distribuyen simétricamente sobre las manos, dedos y pies. • En adultos, especialmente mujeres, las lesiones pueden encontrarse alrededor de los codos.

Granuloma anular

¿Qué lo causa? • Se desconoce la causa, pero se cree que es el resultado de una reacción del sistema inmunológico. • Al parecer, no está asociado con enfermedades; sin embargo, se está investigando para determinar si existe una relación entre el granuloma anular y la diabetes. ¿Cómo se diagnostica? • Se diagnostica generalmente por su apariencia. • En ocasiones se toma una biopsia de piel (se extrae una pequeña muestra) para confirmar el diagnóstico. ¿Con qué se puede confundir? • Tinea corporis (tiña) • Tiene escamas blancas presentes en los bordes de los anillos. • Los exámenes muestran presencia de hongos. • Eritema migratorio—enfermedad de Lyme • Los aros de la enfermedad de Lyme son más grandes que los del granuloma anular. • Lyme se asocia con la mordedura de una garrapata. • La erupción es auto-limitante. ¿Qué puedo esperar? • En niños pequeños generalmente desaparece solo. • En adultos tiende a ser una condición crónica. ¿Cómo se trata? • Dado que no presenta síntomas, generalmente no requiere de tratamiento. • De hecho, en niños, es mejor dejar sin tratar las lesiones localizadas en áreas no visibles de la piel. • Si le preocupa la apariencia física, su doctor puede recetar una crema o cinta con esteroides tópicos. • Otra opción es pedir a su médico que inyecte un medicamento con esteroides en las lesiones.

H a ir Lo ss

(An d ro gen ic Alo p ecia )

What is androgenic alopecia? • Androgenic alopecia (AGA), also known as common baldness and male- or female-pattern alopecia, is an extremely common type of hair loss that becomes more noticeable as people age. • AGA isn’t a disease but a normal consequence of aging. What does it look like? • AGA usually produces two typical patterns of hair loss: • In men, the process usually begins in an M-shaped pattern on the front and top of the head (this is often referred to as male-pattern baldness). It usually begins in late adolescence. • In women, a thinning of the crown toward the front of the scalp occurs in a “Christmas tree” pattern (female-pattern baldness). The loss of hair is less obvious and tends to begin later in life than it does in men. • Hair loss may progress in both sexes but is often more extensive in men. Thus, in the end stages of AGA, many men have only a fringe of remaining hair, whereas women tend to maintain their hairline and do not become totally bald. What causes AGA? • AGA is genetically determined. It can be inherited from either the mother’s or father’s side of the family. • It’s caused by the action of an androgenic (male) hormone on hair follicles, which shortens the growth phase of the hair cycle, thus producing thinner, shorter hairs in a process known as miniaturization. How is AGA diagnosed? • The diagnosis of AGA is generally based on the pattern of baldness coupled with an absence of clues pointing to a specific disease or drug that may cause hair loss. • Your health care provider may wish to obtain blood tests if another reason for hair loss is suspected. What can be done about AGA? • Men • Minoxidil 5% solution and foam (Rogaine for Men), applied twice daily, may reduce shedding and may possibly contribute to some regrowth. • Finasteride (Propecia) is an antiandrogen. It is for the treatment of male pattern hair loss in MEN ONLY and should NOT be used by women or children. • Discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern. • Women • Minoxidil 2% solution (Rogaine for Women), applied twice daily, may reduce shedding and may possibly contribute to some regrowth. Regrowth may not be noted for at least 4 months. Continuing topical treatment with the drug is necessary indefinitely, because discontinuation of treatment produces a rapid reversion to the pretreatment balding pattern. • Women with excess androgen may benefit from antiandrogen medications, including oral contraceptives that lessen androgen production. • Men and women • Hair transplantation. This procedure involves moving hairs from areas such as the back of the scalp (donor sites) to thinning areas (recipient sites). • Scalp reduction. Less often, a surgical procedure known as scalp reduction is used to reduce the areas of hair loss.

Male-pattern alopecia

Female-pattern alopecia

Pérd id a d e Ca b ello

(Alo p ecia An d ro gén ica )

¿Qué es la alopecia androgénica? • La alopecia androgénica, o caída común del cabello, es muy común y se vuelve mas notable con la edad. • La alopecia no es una enfermedad, es una consecuencia normal de la edad.

Patrón de alopecia masculina

Patrón de alopecia femenina

¿Cómo es? • Hay dos patrones típicos de caída del cabello: • En hombres, el proceso generalmente comienza con un patrón en M en el área superior de la cabeza y ambos lados de la frente (a esto usualmente se le refiere como patrón de calvicie masculino). Suele comenzar al final de la adolescencia. • En mujeres, se afina el cabello desde la corona hacia la frente en un patrón de “árbol de Navidad” (patrón de calvicie femenino). La pérdida del cabello es menos obvia y tiende a comenzar en edades más avanzadas que en los hombres. • La pérdida del cabello progresa en ambos sexos, pero es más extensa en los hombres que en las mujeres. Por lo mismo, en las últimas etapas de la alopecia, muchos hombres retienen solamente un poco de cabello cuando las mujeres tienden a mantener la línea del cabello y no se vuelven completamente calvas. ¿Qué la causa? • La alopecia es genética. Se puede heredar tanto de la madre como del padre. • Es causada por la acción de una hormona androgénica (masculina) sobre los folículos del cabello. Esto acorta la fase de crecimiento en el ciclo del pelo, creando cabellos más cortos y finos en un proceso llamado miniaturización. ¿Cómo se diagnostica? • El diagnóstico de alopecia se basa generalmente en el patrón de calvicie, siempre y cuando no haya indicación de alguna enfermedad o droga que pueda causar la perdida del cabello. • Su médico puede requerir exámenes de sangre si sospecha que hay alguna otra razón para la pérdida del cabello. ¿Qué se puede hacer al respecto? • Hombres • Minoxidil 5% solución y espuma (Rogaine Para Hombres), aplicada dos veces al día, puede reducir la caída del cabello y posiblemente contribuir a nuevo crecimiento. • Finasteride (Propecia) es un antiandrógeno. Este medicamento trata únicamente el patrón de calvicie masculino en HOMBRES SOLAMENTE. No debe usarse en mujeres o niños. • Si descontinúa el tratamiento, el proceso de calvicie regresa de inmediato. • Mujeres • Minoxidil 2% solución (Rogaine Para Mujeres), aplicada dos veces al día, puede reducir la caída del cabello y posiblemente contribuir a nuevo crecimiento. Puede que no note el nuevo crecimiento en los primeros 4 meses, pero es necesario continuar el tratamiento con el medicamento tópico indefinidamente, porque si lo descontinúa provocará una rápida reversión al patrón de calvicie. • Las mujeres con exceso de andrógeno pueden beneficiarse de ciertos medicamentos antiandrógenos, incluyendo los anticonceptivos orales que disminuyen la producción de andrógeno. • Ambos • Transplante de cabello. Este procedimiento involucra mover algunos cabellos de áreas remotas, como la nuca o las zonas laterales (zonas donadoras) e implantarlos en áreas con menos cabello. • Reducción del cuero cabelludo. En raras ocasiones, se utiliza un proceso quirúrgico llamado cirugía de reducción de cuero cabelludo para reducir las áreas calvas.

H a n d Eczem a What is hand eczema? • A hand rash (eczema) caused by exposure to irritating or allergy-producing substances is called contact dermatitis. This is sometimes called “dishpan hands.” • When there is no evidence of an outside cause for hand eczema, the diagnosis is most likely atopic hand eczema. Who gets it? • Some people develop a hand rash from overexposure to irritating substances (e.g., hairdressers, cement workers), whereas others develop a contact dermatitis or allergic reaction from allergenic substances (e.g., latex gloves in health care personnel). • Other people who have such hand rashes have inherited this tendency. Often they, or other family members, have a similar problem with their hands. Also, asthma, hay fever, sinus problems, and other allergies tend to run in the family. What does it look like? • Often the hands are dry, sensitive, scaly, and red. • The fingers and palms may develop fissures (splits). • Sometimes the eczema may consist of blisters on the fingers or palms that look like little bubbles. This is referred to as dyshidrotic eczema.

Hand eczema

Hand eczema

What are the symptoms? • The hands can be very itchy. • Split fingers and palms can be painful and very sensitive to things such as citrus fruits. How is it diagnosed? • Careful history taking is important. • Possibly, patch testing with chemicals or substances that might be the source of the rash may also be used. How is it treated? • Usually a prescription topical steroid cream or ointment such as __________________ is prescribed to be applied once or twice daily. This medication should not be applied to the face. • Stubborn cases may require covering the medicated preparation with plastic wrap (e.g., Saran Wrap), which is held in place with tape or by wearing vinyl gloves. This helps the medicine penetrate the skin and is left on overnight or for several hours. This occlusion, or wrapping, should only be done under direction of your health care provider. (Occlusion with superpotent topical steroids should not be attempted, unless otherwise directed.) • If the rash involves only one or two fingers, only these fingers need be treated in this manner. • Alternatively, Cordran Tape may have been prescribed. This tape is impregnated with a steroid and is helpful for occlusive therapy when treating small areas such as the fingers. • Topical steroids are safe if used as directed and should be applied only for short periods, if possible, and only against active disease (i.e., with itching and redness). • Use of topical steroids should be stopped when the skin is healed, and the steroids should not be used for prevention of future rashes. • Severe cases are sometimes treated with antibiotics and oral or injectable cortisone. • Other medications that contain no steroids, such as ________________________, have been shown to reduce the symptoms and help prevent hand eczema. continued on page 40

Hand eczema

Hand eczema caused by atopic dermatitis

Eczem a en la Ma n o ¿Qué es eczema de la mano? • Es una erupción en la mano (eczema) causada por exposición a sustancias irritantes o que producen alergias llamada dermatitis de contacto. A veces se le llama “tiña de las manos.” • Cuando no hay evidencia de causas externas para el sarpullido, el diagnóstico es eczema atópico de la mano.

Eczema de la mano

Eczema de la mano

¿A quién le da? • A algunas personas les da eczema de mano cuando se sobreexponen a sustancias irritantes (como peluqueros o albañiles), otras desarrollan dermatitis de contacto o reacciones alérgicas a sustancias alérgenas (como guantes de látex en la comunidad médica). • Otras personas con eczema de mano la heredaron. En ocasiones otros miembros de la familia tienen problemas similares en las manos, o incluso otras condiciones como asma, fiebre, sinusitis u otras alergias. ¿Cómo es? • Las manos se ponen secas, sensibles, escamosas, y rojas. • Los dedos y las palmas desarrollan fisuras (cortadas). • A veces el eczema consiste de ampollas que parecen burbujitas en los dedos o en las palmas. Esto se conoce como eczema dishidrótico. ¿Cuáles son los síntomas? • Comezón en las manos. • Cortaduras dolorosas en los dedos y en las palmas, muy sensibles a cítricos. ¿Cómo se diagnostica? • Es importante notar la historia médica. • Se pueden hacer exámenes de parches para probar cuales sustancias o químicos pudieran causar el eczema.

Eczema de la mano

Eczema de la mano por dermatitis atópica

¿Cómo se trata? • Generalmente se recetan cremas esteroides tópicas o ungüentos como ______________ que se aplican una o dos veces al día. Este medicamento no se debe aplicar en la cara. • En casos difíciles la piel untada con medicamento se debe cubrir con envoltura de plástico (como Saran Wrap) o con guantes de vinilo. Esto ayuda al medicamento a penetrar la piel y debe dejarse puesto toda la noche o por lo menos varias horas. Esta envoltura se debe hacer bajo la dirección de su médico. (No intente cubrir su piel con esteroides tópicos superpotentes a menos que se lo indique su médico.) • Si la erupción sólo afecta uno o dos dedos, solamente medique los dedos afectados. • Hay una cinta llamada Cordran que su médico le puede recetar. Esta cinta viene impregnada con un esteroide y ayuda a tratar áreas pequeñas como los dedos. • Los esteroides tópicos deben usarse como se indica, por periodos de tiempo muy cortos, y únicamente sobre las áreas afectadas (las que tienen comezón y rojez). • El uso de esteroides tópicos debe detenerse en cuanto la piel sana y nunca deben usarse como medida preventiva. • Los casos severos a veces requieren de antibióticos y cortisona oral o inyectable. • Otros medicamentos sin esteroides, como __________, pueden disminuir los síntomas y ayudar a prevenir eczema en la mano. continued on page 41

Continued from page 38

Is there a cure? • If hand eczema is caused by an outside irritant or allergic reaction, those agents should be avoided and eliminated; however, there is no known cure for chronic hand eczema that doesn’t have an external cause. • The good news is that there are excellent ways to treat chronic hand eczema, and the condition does seem to get better as people age. What can be done to help prevent hand eczema? • Use lukewarm water, mild cleansers, or soap substitutes. • Use only mild, moisturizing soaps such as Dove or nonsoap cleansers such as Cetaphil Lotion. • Try to avoid using soap on red or itchy skin (many people mistakenly believe that “good soaps” may actually help red, itchy, inflamed skin). • Avoid latex gloves and use protective vinyl gloves at work and at home. • Use protective cotton-lined gloves while washing dishes or performing other similar tasks. Thin, white, cotton gloves come in boxes and are sold in photography stores (for handling negatives). • Use moisturizers liberally (especially in the cold, dry months). • Wear gloves in cold weather. • Use self-adhesive bandages (e.g., Band-Aids), which are helpful in healing fissured (cracked) fingers. • Avoid any materials that are known to cause your particular hand dermatitis.

Continued from page 39

¿Hay una cura? • Si el eczema en la mano es causado por un irritante o una reacción alérgica, evite/ elimine el contacto con esos agentes; sin embargo, no hay cura para el eczema crónico sin causa externa. • Hay métodos excelentes para tratar el eczema de mano crónico y mejora mucho con el paso del tiempo. ¿Qué se puede hacer para prevenir el eczema en la mano? • Use agua tibia, jabones suaves, o sustitutos de jabón. • Use jabones humectantes suaves como Dove o limpiadores sin jabón como la loción Cetaphil. • Evite usar jabón en piel roja o con comezón (mucha gente cree que los “jabones buenos” ayudan a desinflamar, pero no es cierto). • No use guantes de látex, mejor use guantes protectivos de vinilo en su casa y en el trabajo. • Use guantes protectivos con forro de algodón mientras lava los trastes, la ropa o hace la limpieza. Hay guantes de algodón, delgados y blancos que vienen en cajas y se venden en tiendas de fotografía para manejar los negativos. • Use cremas humectantes (especialmente en los meses fríos y secos del invierno). • Use guantes en climas fríos. • Use vendas adhesivas (curitas), para ayudar a sanar las fisuras (cortaduras) en los dedos. • Evite cualquier material que sepa que le causa irritación en las manos.

H ea d Lice What are head lice? • Head lice are an infestation caused by the tiny insect Pediculosis humanus capitis, which is about the size of a sesame seed. • The condition is spread from human to human. • Head lice are not known to transmit any disease. Who gets the condition? • Epidemics of head lice are most commonly seen in schoolchildren. • It occurs more often in females than in males. • It is unusual in African-Americans. What does it look like and what are its symptoms? • Crusts and scabs caused by scratching are sometimes seen on the scalp. • Nits (eggs) may be cemented to individual hairs. Nits are attached to the base of a hair shaft when the egg is first laid, and as the hair grows, they remain cemented to the hair as it lengthens. • Itching is the main symptom, but some children with head lice may not itch at all. How is it diagnosed? • Knowledge of an epidemic at school generally alerts parents or school nurses to look for evidence of lice. • White nits may be very obvious on a background of darker hair. It is difficult to find living lice. • A hair may be plucked by your health care provider and examined for nits using the low power of a microscope. How is it treated? • Removal of nits with a fine-tooth comb is possible after the hair is soaked in a vinegar solution; this helps soften the cementing substance that attaches the nit to the hair. • Shaving scalp hair is not necessary. First-line treatments • Products such as Nix Creme Rinse, Rid, and Acticin may be obtained without a prescription. • These agents all contain low concentrations of permethrin; they are very effective at killing adult lice and nymphs but not as effective at killing nits. Resistance of head lice to these agents has been growing. • How to use these products: • Wash the hair with a nonmedicated shampoo and towel dry, apply the preparation as a cream rinse, allow it to remain in place for 10 minutes, and then thoroughly rinse the hair. • Because these agents do not destroy nits totally, a second application (using the same technique) often is recommended 7 to 10 days after the first treatment. • An old-fashioned treatment technique is to use petrolatum, such as Vaseline Petroleum Jelly. Petroleum jelly is quite messy and hard to remove, but it is an inexpensive and sometimes effective method that smothers the lice and nits. Apply it to the entire scalp and leave it on overnight under a shower cap. continued on page 44

Pio jo s ¿Qué son los piojos? • Son una infestación causada por el pequeño insecto llamado Pediculosis humanus capitis, que es del tamaño de un ajonjolí. • Esta condición se transmite de persona a persona. • Los piojos no transmiten ninguna enfermedad. ¿Quién tiene esta condición? • Las epidemias de piojos son comúnmente vistas en niños de edad escolar. • Ocurren con más frecuencia en mujeres que en hombres. • Son raros en Americanos Africanos. ¿Cómo son y cuales son los síntomas? • Hay costras y heridas, dejadas al rascarse, en el cuero cabelludo. • Puede haber pequeños huevos de piojos (liendres) sujetados a los cabellos. Cuando se pone el huevo, éste se adhiere a la base del cabello y se queda pegado al pelo mientras crece. • El síntoma principal es comezón, pero algunos niños con piojos nunca la sienten. ¿Cómo se diagnostica? • Cuando hay una epidemia, la escuela alerta a la enfermera del colegio y a los padres para que busquen evidencia de piojos en los niños. • Los huevos blancos son muy obvios vistos en cabellos oscuros, pero es difícil ver piojos vivos. • Su doctor puede arrancar un pelo para examinarlo con un microscopio buscando los huevecillos. ¿Cómo se tratan? • Se puede remojar el cabello en vinagre para suavizar el pegamento de los huevos y usar un peine fino para quitarlos. • No es necesario rasurar la cabeza. Tratamientos de primera instancia • Algunos productos como Nix Creme Rinse, Rid, y Acticin se pueden comprar sin receta médica. • Todos estos productos contienen bajas concentraciones de permetrina; son muy efectivos para matar piojos adultos y pequeños, pero no tanto para matar los huevos. Los piojos han desarrollado una creciente resistencia a la permetrina. • Cómo usar estos productos: • Lave el cabello con un shampoo no medicado, séquelo con una toalla y aplique la preparación como si fuera acondicionador en crema. Manténgalo por 10 minutos y enjuague bien. • Estos productos no siempre destruyen las liendres completamente, por lo que una segunda aplicación (usando la misma técnica) es recomendable entre 7 a 10 días después del primer tratamiento. • Un tratamiento anticuado es el uso de petrolato, como Vaselina. Es difícil de quitar pero es barato y es efectivo para asfixiar los piojos y liendres. Aplique a todo el cuero cabelludo, cúbralo con una gorra de baño y déjelo puesto toda la noche. continued on page 45

Continued from page 42

For resistant cases, your health care provider may prescribe one of the following medications: • Ovide (malathion lotion) • This agent is considered the most effective treatment for head lice. It is both a pediculicide and an ovicide. • Caution: Ovide is flammable. Keep treated areas that are wet with this product away from open flames and electric heat sources such as hair dryers. • How to use Ovide: • Apply the lotion to dry hair in a quantity sufficient to wet hair and scalp. • Massage it into the scalp and leave it on for 8 to 12 hours. Do not use heat (e.g., hair dryers, hot curlers) to dry the lotion. • Rinse the hair and remove the nits with a fine-toothed (nit) comb. • Repeat the treatment in 7 to 10 days if lice are still present. • Elimite Cream (5% permethrin) • This is available as prescription 5% cream. • Leave it on overnight under an occlusive shower cap. • Repeat the treatment in 1 week to destroy any remaining eggs. • The latest treatment is a heating device called the LouseBuster, which looks like a hair dryer. It apparently kills lice eggs and living adult lice.

Continued from page 43

En casos difíciles, su doctor puede recetar alguno de los siguientes medicamentos: • Loción de Ovide (malatión) • Este producto es un pediculicida y ovicida y se considera el tratamiento más efectivo contra los piojos. • Precaución: La Loción de Ovide es inflamable. Mantenga las áreas tratadas con este producto fuera del alcance de fuego, flamas y fuentes de calor eléctrico como secadoras de pelo. • Cómo usar la Loción de Ovide: • Apliquela sobre el cabello seco hasta que humedezca el cuero cabelludo y todo el pelo por completo con la loción. • Dé un masaje al cuero cabelludo y deje la loción puesta entre 8 y 12 horas. No use calor (secadoras de pelo, tenazas o rizadores) para secar el cabello. • Enjuague bien y peine el cabello con un peine de dientes finos para eliminar las liendres. • Repita el tratamiento entre 7 a 10 días después si los piojos persisten. • Crema Elimite (5% permetrina) • Este producto en crema con 5% está disponible con receta médica. • Aplique y déjela puesta toda la noche con gorra de baño. • Repita el tratamiento en una semana para destruir huevos persistentes. • El último tratamiento es un aparato llamado LouseBuster, que parece una secadora de pelo. Aparentemente mata tanto a los piojos adultos como a los huevos o liendres.

H erp es Sim p lex What is herpes simplex? • The herpes simplex virus (HSV) causes small, fluid-filled blisters on a red base on almost any part of the body. The most common location is on the edge of the upper or lower lip; there the blister is often referred to as a “cold sore” or “fever blister.” • After the primary infection heals, the virus retreats to nerve cells, where it goes into a resting, or dormant, phase. HSV remains dormant until it’s reactivated by precipitating factors or triggers, such as sun exposure, menstrual cycles, fever, common colds, and emotional stress. What are its symptoms? • The sores may be painful, and their physical appearance may be embarrassing.

Herpes simplex virus type 1

What causes it? • Herpes is caused by two types of viruses: HSV-1 and HSV-2. HSV-1 • HSV-1 causes the vast majority of nongenital infections. • Most people contract HSV-1 in infancy or childhood, most of the time without their realizing it. • This highly contagious virus is spread by direct contact with the skin of family members or friends who already have the virus.

Herpes simplex virus type 1

HSV-2 • HSV-2 causes genital herpes, although HSV-1 can also infect genital skin. • This disease is also highly contagious, especially when the blisters are active. It becomes noncontagious when the blisters are all crusted over. • It’s most commonly—but not always—sexually transmitted. What types of infection are caused by HSV? There are two kinds of infections: primary and recurrent. Herpes simplex virus type 2 Primary HSV • The primary infection may go unnoticed (subclinical infection), but when it does cause symptoms, it’s often more severe than a recurrent infection. It may result in swollen glands and fever. • After a primary infection heals, HSV stays in the body and moves to nerve cells, where it remains in a resting state. Recurrent HSV • The blisters may never recur or may reappear in the same area. • Recurrent infections tend to be milder than primary infections. • They can be set off (reactivated) by a variety of situations in different people. • Some people may have recurrences that are infrequent, or they may have them once per month. • One or 2 days before blisters appear, there is often tingling, itching, numbness, or pain in the area. This is called the prodrome. • Over time, recurrences decrease in frequency, and they often stop altogether. How is HSV treated? Topical therapy • Topical Zovirax ointment, Denavir cream, and Abreva cream are not very effective treatments. • The discomfort of oral HSV can be lessened by applying cold soaks as well as over-thecounter “-caine” products such as Benzocaine or Lanacane. continued on page 48

H erp es Sim p le

(“Fu ego s”)

¿Qué es herpes simple? • El virus del herpes simple (HSV) causa ampollas pequeñas, llenas de líquido, sobre una base roja en casi cualquier parte del cuerpo. La ubicación más común es en la orilla de los labios, ya sea superior o inferior; ahí, comúnmente se le conoce como un “fuego,” “úlceras” o “ampollas febriles.” • Una vez que la infección primaria sana, el virus se retira a las células del nervio, donde entra en una fase inactiva y permanece latente. El HSV permanece latente hasta que se reactiva gracias a factores que lo precipitan o lo disparan, como exposición al sol, ciclos menstruales, fiebre, gripa, o estrés emocional. Virus del herpes simple, tipo 1 ¿Cuáles son los síntomas? • Las ampollas son dolorosas y su apariencia física puede ser vergonzosa. ¿Qué lo causa? • El herpes es causado por dos clases de virus: HSV-1 y HSV-2.

Virus del herpes simple, tipo 1

HSV-1 • HSV-1 causa la gran mayoría de infecciones no genitales. • Mucha gente contrae HSV-1 en su infancia, generalmente sin darse cuenta. • Este virus es altamente contagioso y se esparce a través del contacto directo con la piel de miembros de la familia o amigos que poseen el virus. HSV-2 • HSV-2 causa herpes genital, aunque HSV-1 también puede infectar la piel genital. • Esta enfermedad también es muy contagiosa, especialmente cuando las úlceras están activas. Se vuelve no contagiosa cuando las úlceras cicatrizan. • Comúnmente—pero no siempre—es sexualmente transmitido. ¿Qué tipo de infecciones son causadas por el HSV? Hay dos tipos de infecciones: primaria y recurrente.

Virus del herpes simple, tipo 2 HSV primario • La infección primaria puede no ser notada al principio (infección subclínica), pero cuando causa síntomas es generalmente más severa que una infección recurrente. Puede resultar en glándulas inflamadas y fiebre. • Cuando la infección primaria sana, el HSV permanece en el cuerpo y se establece en las células de los nervios, donde permanece latente. HSV recurrente • Las ampollas pueden no regresar, pero pueden reaparecer en la misma área. • Las infecciones recurrentes tienden a ser menos severas que las infecciones primarias. • Pueden ser reactivadas por una variedad de situaciones en distintas personas. • Algunas personas tienen recurrencias infrecuentes o una vez al mes. • Uno o dos días antes de que las ampollas aparezcan hay sensación de hormigueo, comezón, adormecimiento o dolor en el área. Esto se llama pródromo (síntoma preliminar). • Al pasar el tiempo, las recurrencias disminuyen en frecuencia y pueden cesar por completo. ¿Cómo se trata el HSV? Terapia tópica • El ungüento tópico Zovirax y las cremas Denavir y Abreva no son muy eficientes como tratamientos. • El malestar del HSV oral puede aliviarse aplicando compresas frías o productos farmacéuticos que terminan en “caína” como Benzocaína o Lanacaína. continued on page 49

Continued from page 46

Oral therapy • Recurrent (episodic) HSV. Treatment should begin during the prodrome, because this can often stop the blisters from erupting. • Oral antiviral medications such as Famvir and Valtrex are most effective. Take the medication in a dosage of ____ for ___ day(s). • You can carry the pills with you and take them at the first sign of symptoms. This is easy for women, but often men have nothing in which to carry the pills, so men should use a pill carrier or a key chain carrier. • Persistent or frequent recurrent HSV. For suppression, take the medication in a dosage of _____ daily. Some facts about genital HSV • Condoms may be helpful to prevent the transmission of HSV to sexual partners. • Many people are not aware that they have the infection and may be asymptomatic carriers. • A pregnant woman who has active HSV may pass on the infection to her infant at the time of delivery. • A recurrence that arises many years later may be mistaken for a primary episode, leading to unjust accusations about the origin of the herpes infection. • Also, women who have had genital HSV are more likely to have cervical cancer, and they should have yearly Pap smears. A point to remember Most cases of HSV-1 and at least some cases of HSV-2 are not sexually transmitted.

Continued from page 47

Terapia oral • HSV recurrente (episodios). Debe comenzarse con el pródromo, para así evitar que surjan las úlceras. • Las medicinas antivirales orales como Famvir y Valtrex son las más efectivas. Tome el medicamento en dosis de ________ por _________ día(s). • Puede tener las píldoras con usted para poderlas tomar a la primera señal de síntomas. Esto es fácil para mujeres que cargan bolsa, pero los hombres pueden usar un pastillero o un botecito en su llavero. • HSV recurrente, persistente, o frecuente. Para suprimirlo, tome el medicamento en dosis de _____ diariamente. Datos sobre el HSV genital • El uso de condones puede ayudar a prevenir la transmisión del HSV a sus parejas sexuales. • Mucha gente no sabe que tienen la infección y pueden ser portadores asintomáticos. • Una mujer embarazada que tiene HSV activo puede pasarle la infección al bebé durante el parto. • Una recurrencia que surge muchos años después puede llegar a ser malinterpretada como un episodio primario, ocasionando acusaciones injustas sobre el origen de la infección. • Las mujeres que han tenido HSV genital son propensas a tener cáncer cervical, por lo que es importante que se sometan al examen del Papanicolaou una vez al año. Algo que recordar La mayoría de los casos de HSV-1 y algunos casos de HSV-2 no son transmitidos sexualmente.

H erp es Zo st er

(Sh in gles)

What is herpes zoster? • Herpes zoster (shingles) is caused by varicella-zoster virus (VZV), which is the same virus that causes varicella (chickenpox). VZV first occurs as chickenpox, which is usually seen in childhood; later it returns as herpes zoster, caused by reactivation of the same virus. • Reactivation as shingles may be associated with illness or occur with no obvious cause. Why is it sometimes so painful? • The pain of herpes zoster is thought to be a result of the nerve damage caused by the virus spreading to the skin.

Herpes zoster

What does it look like? • Usually blisters occur in a characteristic pattern that “wraps” around one side of the body. • Although herpes zoster can affect any area of the body, it is most commonly found on the side of the chest, on one side of the face, on the lower back, or on an arm or a leg. • Sometimes there can be eye involvement. This may pose a risk to vision and must be promptly evaluated and treated. How is it treated? Pain control is generally the main concern. Oral medications • A progressing herpes zoster eruption is often treated with antiviral drugs. Valacyclovir (Valtrex), famciclovir (Famvir), and acyclovir are all most effective when given within 72 hours of the appearance of the zoster rash. These drugs have very few side effects. • Oral corticosteroids are sometimes used in combination with oral antiviral drugs for severe infections. Topical therapy • Burow’s solution is a soothing astringent preparation that helps dry up and control weeping, oozing, and infected skin. • Where do I get Burow’s solution? • Burow’s solution (Domeboro, Bluboro, Boropak) is available in most chain pharmacies. It does not require a prescription. • It may come as a powder in packets or as tablets that must be diluted. • How do I use Burow’s solution? • Dissolve one packet or tablet in an 8-ounce glass of cool or lukewarm water. • Make a wet compress using a cloth or cotton swab moistened by the solution and leave it in place for 15 to 20 minutes. Do this three to four times each day. • Discontinue the soaks when the oozing and any signs of infection have disappeared. Pain management • Over-the-counter pain medications, such as aspirin, acetaminophen (Tylenol), and nonsteroidal anti-inflammatory drugs such as Motrin, Advil, and Aleve are helpful in mild, self-limited cases. • A topical ointment, Zostrix, which contains capsaicin, an extract of pepper, sometimes helps control the pain. This ointment can be obtained without a prescription. • If the pain is not controlled by these measures, prescription-strength medication may be necessary. Discuss this with your health care provider. continued on page 52

Herpes zoster

H erp es Zo st er ¿Qué es herpes zoster? • El herpes zoster es causado por el virus varicela-zoster (VVZ), el mismo virus que causa varicela (viruela loca). Primero se manifiesta como varicela en la infancia y después regresa como herpes zoster, cuando se reactiva el virus. • Su reactivación como herpes zoster puede asociarse con una enfermedad o presentarse sin causa aparente.

Herpes zoster

¿Por qué es tan doloroso? • Se piensa que el dolor causado por el herpes zoster se debe al daño neurológico (nervios) causado por el virus cuando se extiende a la piel. ¿Cómo es? • Generalmente las ampollas o pápulas se presentan en el patrón característico donde se “envuelven” en un lado del cuerpo. • Aunque el herpes zoster puede afectar cualquier área del cuerpo, por lo común se encuentra en un lado del pecho, en un lado de la cara, en la espalda baja, en un brazo o en una pierna. • A veces puede presentarse en los ojos. Esto puede arriesgar la visión, por lo que debe ser evaluado y tratado de inmediato.

Herpes zoster

¿Cómo se trata? Generalmente el principal objetivo es controlar el dolor. Medicamentos orales • Una erupción progresiva de herpes zoster se medica con antivirales. Valaciclovir (Valtrex), famciclovir (Famvir) y el aciclovir genérico son los más efectivos si se administran dentro de las primeras 72 horas de la erupción de las pápulas. Estos medicamentos tienen muy pocos efectos secundarios. • Los corticoesteroides orales a veces se usan en combinación con antivirales orales para tratar infecciones severas. Terapia tópica • La solución de Burow es una preparación astringente que calma y ayuda a secar y controlar las secreciones y la piel infectada. • ¿Dónde consigo solución de Burow? • La solución de Burow (Domeboro, Bluboro, Boropak) está disponible en cualquier farmacia y no requiere receta médica. • Se puede conseguir en polvo, en paquetes o tabletas que deben ser diluidas. • ¿Cómo uso la solución de Burow? • Disuelva un paquete o tableta en un vaso de agua fría o tibia. • Moje una compresa de algodón o tela en la solución y aplíquela en el área afectada durante 15 a 20 minutos. Repita tres o cuatro veces al día. • Suspenda la aplicación de compresas cuando las secreciones se detengan y desaparezcan las señales de infección. Cómo manejar el dolor • Los analgésicos comunes como aspirina o acetaminofen (Tylenol), y los antiinflamatorios sin esteroides como Motrin, Advil, y Aleve pueden ayudar en casos leves. • El ungüento tópico Zostrix contiene capsaicin, un extracto de pimienta que puede ayudar a controlar el dolor y se consigue sin receta. • Si estos medicamentos no ayudan con el dolor, su médico puede recetar algo más fuerte en caso de ser necesario. continued on page 53

Continued from page 50

Things to keep in mind • Postherpetic neuralgia (PHN) is defined as pain persisting for more than 1 month after the rash of the initial herpes zoster lesions. • PHN may also develop after a pain-free interval. • The frequency of PHN increases with age. It is unusual in people younger than 50 years of age. • Patients with herpes zoster can transmit VZV as chickenpox to people who have not already been infected with the virus. Is there any way to prevent it? • A VZV vaccine (Zostavax) is now available. There appears to be a significant reduction in the appearance and severity of herpes zoster and PHN in people who are inoculated. • The vaccine is recommended for people older than 60 years of age. • The vaccine is not for everyone, and you should discuss it with your health care provider.

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Datos que recordar • La neuralgia post-herpética (NPH) se define como dolor que persiste más de un mes después de haber tenido las lesiones iniciales de herpes zoster. • NPH también se puede desarrollar después de un intervalo sin dolor. • La frecuencia de NPH aumenta con la edad. Es muy raro que ocurra en personas menores de 50 años. • Los pacientes con herpes zoster pueden transmitir VVZ como varicela a las personas que no hayan sido expuestas al virus anteriormente. ¿Hay manera de prevenirlo? • La vacuna contra VVZ (Zostavax) está disponible. Hay una notable reducción en la aparición y severidad del herpes zoster y NPH en la gente inoculada. • Se recomienda vacunar a mayores de 60 años. • La vacuna no es para cualquiera. Conviene que lo discuta con su médico.

H ives

(Ur t ica ria )

What are hives? • Hives, known medically as urticaria, are very common. • They are reddish, itchy swellings called “wheals” that last for a few hours before fading away. New ones may develop as old ones fade. When hives are forming, they usually are very itchy, and they may also sting. • There may be deep swelling (angioedema) around the eyes, lips, and tongue. • They “migrate around,” never occurring in the same place. • They may be classified as acute or chronic. • Acute hives last for fewer than 6 weeks. • Chronic hives last longer than 6 weeks. What causes acute hives? • Very often, a definite cause is never found. • However, there may be an obvious cause such as an acute viral infection, a reaction to a drug, or an insect bite. • The most common drugs that may cause acute hives are antibiotics (especially penicillin and sulfa drugs), pain medications (such as aspirin and ibuprofen), narcotics, radiocontrast dyes, diuretics (“water pills”), and opiates (such as codeine). • The most common foods that are associated with hives are milk, wheat, eggs, chocolate, shellfish, nuts, fish, and strawberries. Also, food additives and preservatives such as salicylates and benzoates may be responsible. • Rarely, a severe life-threatening allergic reaction known as anaphylaxis, which requires immediate medical attention, can occur. What causes chronic hives? • The cause is usually unknown; however, chronic hives may, very infrequently, be a sign of an underlying illness. • In 85% to 90% of patients, the cause is unknown. • Emotional stress may trigger recurrences. • Chronic hives also may be caused by physical stimuli such as pressure, cold, heat, sunlight, or exercise. Such hives are called physical urticarias. Who gets hives? • Between 10% and 20% of people have at least one episode of hives in their lifetime. What should be done to determine the cause? • Tell your health care provider about all of the medications (including oral contraceptives) and vitamins that you are taking. • Unfortunately, routine blood tests are of little or no value in determining the cause of chronic hives. • Allergy testing is expensive, and often tests are positive for allergies that have nothing to do with hives. What can be done to treat and prevent them? • If possible, the cause of the hives should be found and eliminated. • The mainstay of treatment for chronic hives is the use of oral antihistamines. • Systemic steroids (cortisone) are sometimes used for short periods to “break the cycle” of chronic hives. • People with severe reactions should consider wearing a medical alert bracelet that describes their problem. • Aspirin-containing compounds, ibuprofen, and narcotics, which are all histamine-releasing agents, may aggravate both acute and chronic types of hives. They should be avoided. • Tight clothing and hot baths and showers should be avoided, particularly in people who have a physical urticaria. • If all else fails, a diary of daily foods eaten may be kept, followed by elimination of foods and food additives. This is rarely successful.

Hives

Hives with swelling of eyelids

Ur t ica ria

Urticaria

Urticaria con hinchazón de los párpados

¿Qué es la urticaria? • La urticaria es muy común. • La urticaria consta de inflamaciones rojas que dan comezón, mejor conocidas como “ronchas” o “sarpullido,” y dura unas cuantas horas antes de desaparecer. Nuevas ronchas pueden desarrollarse mientras desaparecen las previas. Cuando la urticaria se forma suele haber comezón y puede también sentirse ardor. • Puede haber inflamación (angioedema) en los entornos de los ojos, los labios, y la lengua. • La urticaria “emigra,” nunca ocurre en el mismo lugar. • Puede ser clasificada como aguda o crónica. • La urticaria aguda dura menos de 6 semanas. • La urticaria crónica dura más de 6 semanas. ¿Qué causa urticaria aguda? • Muchas veces no hay una causa definitiva. • Sin embargo, puede haber una causa obvia como una infección viral aguda, o una reacción a una droga o picadura de insecto. • Las medicinas que con más frecuencia causan urticaria aguda son los antibióticos (especialmente penicilina y sulfamida), analgésicos (como aspirina o ibuprofeno), narcóticos, colorantes de contraste, diuréticos, y opiatos (como codeína). • Los alimentos que comúnmente se asocian con urticaria son leche, trigo, huevos, chocolate, nueces, mariscos, pescados y fresas. Los aditivos y preservativos tales como salicilatos y benzoatos también pueden ser responsables. • En raras ocasiones puede ocurrir una reacción alérgica severa llamada anafilaxis, que requiere de atención médica inmediata o puede ser mortal. ¿Qué causa urticaria crónica? • La causa generalmente es desconocida; sin embargo, la urticaria crónica puede, en ciertos casos, ser un síntoma de una enfermedad subyacente. • En 85% a 90% de los pacientes, la causa es desconocida. • El estrés emocional puede incitar recurrencias. • La urticaria crónica puede ser causada por estímulos físicos como presión, frío, calor, luz de sol o ejercicio. Esta se llama urticaria física. ¿A quién le da urticaria? • Entre 10% y 20% de la gente tiene por lo menos un episodio de urticaria en su vida. ¿Qué debe hacerse para determinar la causa? • Déle a su médico una lista con todas las medicinas (incluyendo anticonceptivos) y vitaminas que esté tomando. • Desafortunadamente, un examen de sangre de rutina no tiene casi ningún valor para determinar la causa de urticaria crónica. • Las pruebas de alergias son caras, y generalmente salen positivas para alergias que no tienen nada que ver con la urticaria. ¿Qué se puede hacer para tratar y prevenir la urticaria? • Si es posible, encontrar y eliminar la causa. • El principal tratamiento para controlar la urticaria crónica es medicarla con antihistaminas. • Los esteroides sistémicos (cortisona) se usan a veces durante periodos cortos para “romper el ciclo” de la urticaria crónica. • La gente con reacciones severas deben considerar usar el brazalete MedicAlert, describiendo su problema. • Los compuestos de aspirina que contienen ibuprofeno y narcóticos, todos agentes que liberan histamina, pueden agravar la urticaria tanto aguda como crónica y deben ser evitados. • Quien sufre de urticaria debe evitar bañarse con agua caliente y usar ropa pegada, especialmente la urticaria física. • Si nada de esto ayuda, puede mantener un diario de los alimentos que consume diariamente, seguido por una eliminación gradual de aditivos y ciertos alimentos. Esto a veces ayuda.

Kera t o sis Pila ris

(Ro u gh , Bu m p y Sk in )

What is keratosis pilaris? • Keratosis pilaris (scaly, bumpy hair follicles) is a common, harmless condition that looks and feels like “goose bumps.” • It runs in families, especially families that tend to have hay fever, asthma, sinusitis, some allergies, or a skin condition known as atopic dermatitis (hereditary eczema). • It’s usually worse during the winter months. What does it look like? • Tiny, rough, whitish, red, or tan spiny bumps usually first appear during the teen years. The bumps give the skin a sandpaperish texture. • The bumps are distributed in a gridlike pattern. • When the bumps are red, keratosis pilaris is often confused with acne. • The condition is also known as “allergic bumps,” because the bumps are often seen in people who have allergies or eczema.

Keratosis pilaris

Where does it appear? • Most commonly, keratosis pilaris is seen on the outer areas of the upper arms, the upper back, and sometimes the chest, thighs, the sides of the face, and even the buttocks. What can be done about it? • Unfortunately, there’s no cure or easy treatment; however, the roughness can be lessened by applying certain moisturizers, exfoliating or barrier creams, or lotions such as ___________________. • You can’t rub it off!

Keratosis pilaris

Qu era t o sis Pila ris

(Piel Co n Gra n o s Ásp ero s)

¿Qué es la queratosis pilaris? • La queratosis pilaris (folículos capilares escamosos y abultados) es una condición común e inofensiva que se ve y se siente como “piel de gallina.” • Se da en familias que suelen sufrir asma, fiebre, sinusitis, alergias, o dermatitis atópica, una condición de la piel conocida como eczema hereditario. • Generalmente empeora durante los meses del invierno.

Queratosis pilaris

¿Cómo es? • Los granitos ásperos generalmente aparecen durante la adolescencia. Estos granitos dan a la piel una textura como de lija. • Los granitos se presentan en un patrón cuadriculado. • Cuando los granitos son rojos, la queratosis pilaris se confunde con acné. • Esta condición también se conoce como “granitos alérgicos” porque los granitos se presentan en personas que sufren de alergias o eczema. ¿Dónde aparece? • La queratosis pilaris se ve comúnmente en las áreas externas de los brazos, la parte superior de la espalda, a veces en el pecho, los muslos, los lados de la cara y hasta los glúteos.

Queratosis pilaris

¿Qué se puede hacer? • Desafortunadamente no hay cura ni tratamiento; sin embargo, la aspereza se puede aliviar aplicando cremas humectantes, exfoliantes o barrera, o lociones como ___________________. • ¡No se va a quitar restregándolo!

Lich en Pla n u s What is lichen planus? • Lichen planus is a relatively uncommon disorder involving an itchy, inflammatory rash (lesions) on the skin or, sometimes, in the mouth. Who gets it? • It generally affects middle-aged adults. • It’s unusual in children. What causes it? • The exact cause is unknown, but it’s probably related to an allergic or immune reaction. • It’s been known to develop after exposure to certain medications, dyes, and other chemical substances.

Lichen planus

Where does it occur on the body? • Lesions are usually located on the inner areas of the wrists, legs, torso, or genitals. Sometimes they can be spread all over the skin. • Less commonly, the nails and hair are involved. What does it look like? • Reddish-purple bumps or spots occur on the skin. • White patches appear in the mouth—inside the cheeks, on the tongue, or the gums. What are its symptoms? • Itching in the location of lesions can be mild or absent, or it can be quite severe. • Oral lesions can be sore or painful, but most often they cause no discomfort. • Other symptoms may include nail ridges and hair loss. What diseases are associated with it? • Lichen planus may be associated with several other disorders, most notably hepatitis C. What can I expect? • The first episode of lichen planus may last for weeks to months, and the disorder may come and go for years. • It’s generally not harmful and may disappear with treatment. • Very infrequently, long-standing mouth ulcers may develop into oral cancer. How is it diagnosed? • A diagnosis may be made on the basis of the way your skin or mouth lesions look. • A skin lesion biopsy or biopsy of a mouth lesion may be necessary to confirm the diagnosis. • Additional blood tests may be done to rule out hepatitis C. How is it treated? • The goal of treatment is to reduce symptoms and speed healing of the skin lesions. If symptoms are mild, no treatment may be needed. • Treatments may include potent topical steroids. • Oral steroids such as prednisone may be prescribed in stubborn cases. • Steroids may be injected directly into a lesion. • Ultraviolet light therapy may be beneficial in some cases. • Other treatments include the following. • For mouth lesions, lidocaine mouth washes may numb the area temporarily and make eating more comfortable. • Topical immunomodulators such as Protopic ointment (tacrolimus) are sometimes effective for oral lesions. • Topical retinoic acid cream (a form of vitamin A) is also used to treat oral symptoms.

Lichen planus

Liq u en Pla n o ¿Qué es liquen plano? • El liquen plano es una enfermedad poco común que causa erupciones (lesiones) inflamadas con comezón en la piel o en la boca. ¿A quién le da? • Generalmente afecta a adultos de edad media. • Es rara en niños. Liquen plano

¿Qué lo causa? • Se desconoce la causa precisa, pero es probable que esté relacionada a una reacción alérgica o inmune. • Se sabe que se desarrolla después de una exposición a ciertos medicamentos, tintes, y otras sustancias químicas. ¿En qué parte del cuerpo aparece? • Las lesiones generalmente se localizan en las áreas internas de las muñecas, piernas, torso, o genitales. A veces pueden estar propagadas por toda la piel. • Es menos común, pero a veces también afectan las uñas y el cabello.

Liquen plano

¿Cómo es? • Granos o manchas rojizas-moradas en la piel. • Manchas blancas en la boca—en la lengua, en las encías, o en el interior de las mejillas. ¿Cuáles son los síntomas? • La comezón en el área de las lesiones puede ser moderada, inexistente o muy severa. • Las lesiones orales pueden doler o arder, pero generalmente no molestan. • Otros síntomas incluyen surcos en las uñas y pérdida de cabello. ¿Qué enfermedades se asocian con el? • El liquen plano se puede asociar con otras enfermedades, pero más notablemente con hepatitis C. ¿Qué puedo esperar? • El primer episodio puede durar semanas o meses, y la enfermedad puede ir y venir durante años. • Generalmente no es dañina y puede desaparecer con tratamiento. • En raras ocasiones las úlceras bucales persistentes pueden desarrollar cáncer oral. ¿Cómo se diagnostica? • Se puede diagnosticar con la apariencia de las lesiones en la piel o en la boca. • Puede ser necesario tomar una biopsia de las lesiones para confirmar el diagnóstico. • Adicionalmente, se pueden tomar exámenes de sangre para descartar hepatitis C. ¿Cómo se trata? • La meta del tratamiento es aliviar los síntomas y acelerar la curación de las lesiones. Si los síntomas son leves, puede que no necesiten tratamiento. • El tratamiento puede incluir esteroides tópicos potentes. • En casos persistentes, se pueden recetar esteroides orales como prednisona. • Los esteroides se pueden inyectar directamente en la lesión. • La terapia de luz ultravioleta puede ayudar en algunos casos. • Otros tratamientos incluyen: • En lesiones bucales, enjuagues de lidocaína adormecen el área temporalmente para poder comer. • Los inmunomoduladores tópicos como el ungüento Protopic (tacrolimus) a veces son efectivos en lesiones orales. • La crema tópica de ácido retinoico (una forma de vitamina A) también ayuda a los síntomas orales.

Lym e Disea se What is Lyme disease? • It is a noncontagious illness caused by bacteria known as Borrelia burgdorferi. • It’s spread by the bite of an infected tick, Ixodes scapularis, commonly known as the deer tick. However, not all deer ticks are infected with the bacteria that cause the disease. Who gets it? • Anyone can get the disease. What does the tick look like? • In its nymphal (immature) stage, the tick is about the size of a poppy seed or the period at the end of this sentence. What are the symptoms of the disease? • Early symptoms include an expanding, red, ringlike rash that may appear around the area of the tick bite. • The rash can resemble a bull’s-eye with a clearing center and a distinct red ring around it. • Sometimes many round rings can occur with or without the clear center. • Other early symptoms may include flulike symptoms, such as tiredness, headache, fever, and achy muscles and joints. • Late symptoms may include arthritis, neurologic problems, and heart problems. How soon do symptoms appear? • Early symptoms of Lyme disease usually occur within the first month of the tick bite. • Late symptoms can occur several weeks to several months later. How is it diagnosed? • Lyme disease may be difficult to diagnose because the symptoms can mimic many other disorders. • Blood tests can be helpful in the diagnosis of Lyme disease but should not be used exclusively. Doctors may perform blood tests to examine for antibodies of the bacteria. • Lyme antibodies can be absent early in the course of a Lyme disease infection, so a negative test result may be misleading. How is it treated? • It is easily treated when detected in the early stages. Treatment with oral antibiotics, such as doxycycline or amoxicillin, for a few weeks are often effective. • Intravenous antibiotic treatment may be necessary for patients with late symptoms of Lyme disease. • Sometimes treatment is ineffective in the late stages, which underscores the importance of early diagnosis and treatment. How can it be prevented? • People cannot develop immunity to Lyme disease, and a person who has already been treated for the disease can contract it again if reinfected. • No human vaccine is currently available. • See the handout “Prevention of Lyme Disease.”

Lyme disease rash

Lyme disease, tick

En fer m ed a d d e Lym e ¿Qué es la enfermedad de Lyme? • Es una enfermedad no contagiosa causada por la bacteria Borrelia burgdorferi. • Se adquiere con la mordida de una garrapata infectada, Ixodes scapularis, comúnmente conocida como garrapata de venado. Sin embargo, no todas las garrapatas de venado están infectadas con la bacteria que causa la enfermedad. ¿A quién le da? • Cualquier persona puede contraer la enfermedad. Enfermedad de Lyme, sarpullido ¿Cómo es la garrapata? • En la etapa inmadura, la garrapata es del tamaño de una semillita o del punto al final de este enunciado.

Enfermedad de Lyme, garrapata

¿Cuáles son los síntomas de la enfermedad? • Los primeros síntomas son erupciones o sarpullido rojizo como aro alrededor del área de la mordedura de la garrapata. • El sarpullido se ve como un tiro al blanco, con un centro claro y un circulo rojo alrededor. • A veces hay varios anillos de sarpullido sin el centro claro. • Otros síntomas tempranos incluyen cansancio, dolor de cabeza, fiebre y dolor de músculos y coyunturas, como gripa. • Síntomas tardíos pueden incluir artritis, problemas neurológicos o problemas cardiacos. ¿Cuándo se presentan los síntomas? • Los primeros síntomas de la enfermedad de Lyme generalmente aparecen durante el primer mes a partir de la mordida de la garrapata. • Los síntomas tardíos pueden ocurrir varias semanas o varios meses después. ¿Cómo se diagnostica? • La enfermedad de Lyme es difícil de diagnosticar porque los síntomas se parecen a otras enfermedades. • El doctor puede pedir exámenes de sangre para buscar anticuerpos contra la bacteria, lo que ayuda a diagnosticar la enfermedad de Lyme. • No se deje guiar exclusivamente por el resultado de los exámenes de sangre: los anticuerpos de Lyme pueden estar ausentes al principio de la infección, por lo que un resultado negativo puede estar equivocado. ¿Cómo se trata? • Es fácil de tratar si se detecta en las etapas tempranas. Los tratamientos con antibióticos orales, como doxiciclina o amoxicilina por unas semanas, son generalmente efectivos. • Los tratamientos con antibióticos por vía intravenosa pueden ser necesarios para los pacientes con síntomas tardíos de la enfermedad de Lyme. • A veces el tratamiento es ineficiente en las etapas tardías, por lo que es importante diagnosticar y tratar la enfermedad lo más temprano posible. ¿Cómo se puede prevenir? • No se puede desarrollar inmunidad a la enfermedad de Lyme, y una persona que ya ha sido tratada y curada puede contraerla otra vez si se vuelve a infectar. • No hay vacuna disponible. • Ver el folleto “Prevención de la Enfermedad de Lyme.”

Lym e Disea se: Preven t io n What is Lyme disease? • See the handout “Lyme Disease.” What can I do to prevent it? • Lyme disease can be prevented by avoiding contact with ticks or by removing them before they can transmit disease. • When working or playing outside in areas that ticks inhabit—tall grass and weeds, scrubby areas, woods, and leaf litter—walk in the center of trails to avoid tall grass and brush. • Keep your lawn mowed, cut overgrown brush, and clear any leaf litter away from your home. • Wear long-sleeved shirts and long pants. Create a “tick barrier” by tucking your pants into your socks or boots. • Apply a DEET- or permethrin-containing product to clothing, especially pants from knees to cuffs. • Use tick or flea repellents on your dogs and cats. How can I find ticks on myself or members of my family? • You’ll be able to spot ticks more easily if you wear light-colored clothing, which improves the chance of seeing ticks before they attach to the skin. • Examine the skin very carefully (especially thighs, groin, arms, underarms, legs, and scalp) after being outdoors. • The likelihood of infection is related to the amount of time the tick is attached. Infection is much less likely when ticks have been attached for less than 24 hours. • If you see a tick, remove it promptly. How should I remove ticks when I find them? • Using tweezers, grasp the tick as close to your skin as possible and gently lift it away, pulling gradually with steady pressure. Don’t yank the tick out. Try not to squeeze the tick during removal because you may inject infectious material into the bite. • If the tick doesn’t come off easily, twist the tweezers using a corkscrewlike motion. • Various “folk” methods for removing ticks such as holding a lit cigarette against it or covering it with Vaseline are not good ideas.

Preven cio n d e la En fer m ed a d d e Lym e ¿Qué es la enfermedad de Lyme? • Ver el folleto “Enfermedad de Lyme” ¿Qué puedo hacer para prevenirla? • La enfermedad de Lyme se puede prevenir evitando el contacto con garrapatas o eliminándolas antes que transmitan la enfermedad. • Cuando trabaje o juegue afuera, en áreas donde viven las garrapatas—terrenos con pastos, yerbas, arbustos y hojarascas o bosques—vaya por el centro del camino para evitar los pastizales altos. • Mantenga su jardín podado, corte los arbustos crecidos, y deshágase de las hojas secas. • Use mangas largas y pantalones. Haga una “barrera contra garrapatas” metiendo sus pantalones en sus calcetines o botas. • Aplique DEET -o un producto con permetrín- a su ropa, especialmente desde las rodillas hasta los tobillos de sus pantalones. • Aplique repelentes de pulgas y garrapatas a sus perros y gatos. ¿Cómo puedo encontrar garrapatas en mi o en mi familia? • Es mas fácil si usa ropa de color claro, porque mejora la oportunidad de ver las garrapatas antes de que se adhieran a la piel. • Examine la piel cuidadosamente (especialmente los muslos, la ingle, los brazos, axilas, piernas, y cuero cabelludo) después de haber estado afuera. • La posibilidad de infección está relacionada a la cantidad de tiempo que la garrapata lleve adherida. La probabilidad de infección es menor cuando las garrapatas llevan menos de 24 horas en el cuerpo. • Si ve una garrapata, elimínela de inmediato. ¿Cómo debo quitar las garrapatas cuando las encuentre? • Usando pinzas, sujete firmemente la garrapata lo más cerca a su piel como le sea posible. Levántela suavemente, jalando con cuidado, gradualmente, con presión estable. No la arranque. Trate de no apachurrarla cuando la esté quitando porque puede inyectar líquido infeccioso en la picadura. • Si la garrapata no sale fácilmente, trate de darle vuelta a las pinzas como si fuera sacacorchos o tirabuzón. • No es buena idea tratar de eliminar las garrapatas con “costumbres populares” como acercándoles un cigarro prendido o untándoles Vaselina.

Ma lign a n t Mela n o m a What is malignant melanoma (MM)? • MM is a cancer of pigment-producing cells (melanocytes). • Malignant melanoma is one of the only skin diseases that can be fatal if it’s ignored. • Therefore, early recognition and prompt removal of a melanoma can save a life. Who gets it? • People who are at greatest risk for developing melanoma have the following characteristics: • Age older than 20 years • Light complexion, with an inability to tan and a history of sunburns • Numerous moles, changing moles, or atypical moles • Personal or family history of melanoma • MM is rare in dark-skinned persons; however, when it does occur, it tends to occur on the hands and feet. What does it look like? • Superficial spreading melanoma (SSM), the most common type, may arise on normal skin or in a preexisting mole. • The SSM lesions may conform to some or all of the “ABCD” criteria for melanoma, in which the primary lesion is an elevated plaque that displays: A Asymmetry B Border that is irregular or notched C Color that is varied (brown, black, pink, blue–gray, white, or mixtures of these colors) D Diameter that is greater than 6 mm (diameter of a pencil eraser) E Evolution, or change in a pre-existing lesion. Any change—in size, color, elevation, or any new symptoms such as itching, bleeding, or crusting.

Melanoma. This mole has an irregular shape and color and is larger than a pencil eraser.

Melanoma. The legs are a common location for melanoma in women.

Where do melanomas occur on the body? • The most common sites are the upper back, lower legs, chest, and back. • The arms and legs are more common sites in women. • The trunk is the more common site in men. What can be done to prevent the development of melanoma? • Be aware of the warning signs of MM, which include new, changing, or unusual moles. • If you have many unusual moles, avoid unnecessary sun exposure and routinely use a sunscreen with an SPF (sun protection factor) of 15 or greater. • If you are at high risk (i.e., have a personal or family history of melanoma), examine your skin every 2 to 3 months to detect changes in existing moles. In addition, have a fullbody examination and regular screenings performed by a dermatologist. Anyone with a history of melanoma needs lifelong skin surveillance. • Your family should learn self-examination techniques. • Family members should also be given printed material with photographs to help them recognize the features of malignant melanoma. • It is necessary that all family members be examined. • Protect children from sun exposure beginning at an early age.

Melanoma. The chest, back, and shoulders are common locations for melanoma in men.

Melanoma. This is an early in situ melanoma.

Mela n o m a Ma lign o ¿Qué es el melanoma maligno (MM)? • MM es un cáncer de células que producen pigmento (melanocitos). • El melanoma maligno es una de las pocas enfermedades de la piel que puede ser fatal si se ignora. • Por lo tanto, diagnosticarlo temprano y extraer el melanoma a tiempo puede salvar la vida.

Melanoma. Este lunar es de forma y color irregular y es más grande que la goma de un lápiz.

Melanoma. En mujeres es común que los melanomas se presenten en las piernas.

¿A quién le da melanoma maligno? • La gente con más riesgo de desarrollar melanoma tiene las siguientes características: • Edad superior a los 20 años • Complexión clara, no se broncea sino que se quema o arde con el sol • Muchos lunares, lunares que cambian o lunares atípicos • Historia personal o familiar de melanoma • El MM es raro en gente morena o de piel obscura; sin embargo, cuando ocurre, suele aparecer en manos y pies. ¿Cómo es un melanoma? • El melanoma de extensión superficial (SSM), el tipo más común, puede aparecer en piel normal o en un lunar preexistente. • Las lesiones SSM suelen seguir algunas o todas las características “ABCD” del melanoma, en el cual la lesión primaria es una placa elevada que muestra: A Asimetría B Bordes irregulares o serrados C Color que varía (café, negro, rosa, azul–gris, blanco, o mezclas de estos colores) D Diámetro mayor de 6 mm (como la goma de un lápiz) E Desarrollo o cambios en lesiones preexistentes cualquier cambio en; color tamaño, desarrollo o cualquier neuvo sintoma como sangrado. ¿En qué partes del cuerpo ocurren los melanomas? • Los sitios más comunes son la espalda, el pecho y las extremidades inferiores. • Los brazos y piernas son los sitios más comunes en las mujeres. • El torso es el sitio más común en los hombres.

Melanoma. En hombres es común encontrar los melanomas en el pecho, la espalda y los hombros.

Melanoma. Este es un melanoma (in situ) temprano.

¿Qué se puede hacer para prevenir el desarrollo del melanoma? • Tome conciencia de las señales de advertencia del MM, que incluyen lunares nuevos, cambiantes, o anormales. • Si tiene muchos lunares inusuales, evite exponerse al sol innecesariamente y use bloqueador de sol con factor de protección solar (SPF) 15 o más alto, regularmente. • Si usted es de alto riesgo (por ejemplo, ha tenido melanoma o su familia tiene historia clínica de melanoma) examine su piel cada 2 o 3 meses para detectar cambios en sus lunares. Adicionalmente, hágase un examen de cuerpo entero y visite a su dermatólogo para que le haga revisiones regulares. Cualquiera que tenga historia de melanoma necesita supervisar su piel de por vida. • Su familia debe aprender las técnicas de auto examen. • Los miembros de la familia deben recibir material impreso con fotografías que les ayuden a reconocer los rasgos del melanoma maligno. • Es necesario que todos los miembros de la familia se examinen. • Proteja a los niños de la exposición del sol desde una edad temprana.

Mela sm a What is melasma? • Melasma is a type of skin darkening (hyperpigmentation) that is seen most commonly on the face. • It may develop during pregnancy, while taking birth control pills, or during menopause. Sometimes it appears for no obvious reason. Who gets it? • Melasma most commonly occurs in women during their reproductive years, particularly in women who have darker complexions and live, or were born, in a sunny climate. • It’s seen most often in Asia, the Middle East, South America, Africa, and the Indian subcontinent. • In North America, it’s most common among Hispanics, African-Americans, and immigrants from countries in which it’s very common.

Melasma

What does it look like? • Tan or brown spots are seen mainly on the cheeks, jaw, forehead, nose, chin, and above the upper lip. What can I expect? • During pregnancy, the darkening of the skin often appears in the second and third trimesters and usually fades after the end of pregnancy. • It also tends to fade when oral contraceptives are stopped or when sunlight is avoided. (Exposure to sunlight makes it worse.) • However, it may remain for many years or even for life. How is it treated? • Treatment of melasma involves a combination approach with one or more bleaching agents and a cosmetic for camouflage. In addition, sun avoidance and the use of sunblocks are very important. • Bleaching creams are readily available over the counter. Preparations such as the lowstrength Ambi and Esoterica contain 2% hydroquinone. • Stronger preparations are available by prescription only. Some contain sunblock, a topical steroid, Retin-A, vitamins C and E, and/or glycolic acid. • Other lightening agents, such as azelaic acid and kojic acid, may be used in addition to hydroquinone. These have been found to help lighten melasma. • All of these preparations should be applied twice a day to areas of darkening only. Slow but gradual lightening is to be expected. • This treatment requires patience during the many months in which lightening agents must be applied. • Without the strict avoidance of sunlight, successful treatments for melasma are doomed to failure. • Sunscreens are essential. They should be broad spectrum, which means that they should protect against both ultraviolet A and ultraviolet B rays. Those containing opaque physical blockers such as titanium dioxide and zinc oxide are preferred over chemical sunscreens because of their broader protection. They should be used on a daily basis, whether or not it is sunny. • Chemical peels, microdermabrasion, and laser procedures have also been used to treat melasma.

Melasma

Mela sm a ¿Qué es Melasma? • Melasma es un tipo de oscurecimiento de la piel (hiperpigmentación) visto comúnmente en la cara. • Se puede desarrollar durante el embarazo, al tomar píldoras anticonceptivas, o durante la menopausia. A veces aparece sin razón obvia.

Melasma

¿A quién le da? • Melasma le ocurre comúnmente a las mujeres en años reproductivos, particularmente a las de complexión oscura que nacieron o viven en climas soleados. • Se ve con regularidad en Asia, el Medio Oriente, Sudamérica, África, e India. • En Norteamérica es mas común en la comunidad Hispana, Afroamericana, y en inmigrantes de los países donde es común. ¿Cómo es? • Son manchas cafés en las mejillas, mandíbula, frente, nariz, barbilla, y sobre el labio superior.

Melasma

¿Qué puedo esperar? • Durante el embarazo, el oscurecimiento de la piel sucede en el segundo y tercer trimestre, desapareciendo al final del embarazo. • También suele desaparecer cuando se dejan de tomar los anticonceptivos orales o cuando se evita la luz del sol. (La exposición al sol empeora las manchas.) • Sin embargo, puede permanecer por varios años o por el resto de la vida. ¿Cómo se trata? • El tratamiento de melasma involucra la combinación de uno o más agentes blanqueadores y cosméticos para camuflaje. Es importante usar bloqueador solar y evitar la exposición al sol. • Ciertas cremas blanqueadoras están disponibles en farmacias sin receta médica. Las preparaciones como Ambi y Esotérica contienen 2% hidroquinona. • Las preparaciones más fuertes solamente están disponibles con receta médica. Algunas contienen un bloqueador solar, un esteroide tópico, Retin-A, vitaminas C y E, y/o ácido glicólico. • Otros agentes blanqueadores como el ácido azelaico y el ácido kójico se pueden usar además de la hidroquinona. Estos ayudan a aclarar la melasma. • Todas estas preparaciones se deben aplicar dos veces al día a las áreas oscuras solamente. Espere una aclaración lenta y gradual. • Este tratamiento requiere paciencia durante los muchos meses que se debe aplicar el tratamiento. • Si no evita estrictamente el sol, los tratamientos no van a funcionar. • Los bloqueadores de sol son esenciales. Deben ser de espectro amplio, o sea que deben proteger contra los rayos ultravioleta A y ultravioleta B. Es preferible usar los que contienen bloqueadores opacos como dióxido de titanio y óxido de zinc porque ofrecen más protección. Deben usarse diariamente, aunque no esté soleado. • Los “peels” químicos y los procedimientos de microdermabrasión, o láser también se usan para tratar melasma.

Mo llu scu m Co n t a gio su m What is molluscum contagiosum (MC)? • MC is a common superficial viral infection of the outer layer of skin. • MC produces something like warts; however, a different virus is involved. Who gets it? • Young, healthy children (infants and preschoolers) • HIV-positive patients • Young, healthy adults who are sexually active and who are not HIV positive Molluscum contagiosum What causes it? • MC is caused by a poxvirus. How does it spread? • MC is spread by skin-to-skin contact. • The little “bumps” are spread by picking and rubbing. What does it look like? • MC consists of dome-shaped, shiny or waxy bumps with a central white core. Are there any symptoms? • MC can be itchy. Where does it occur? • MC often appears on the face, including the eyelids. It also is seen in the armpits and on the arms and legs and sometimes on the chest and back. • In young children, MC can appear in areas of the skin that have eczema. • MC may also occur on the lower abdomen, on the inner thighs, and on the genitalia and pubic area in children and adults. How is it treated? Office treatment • The “bumps” may be frozen lightly with liquid nitrogen applied with a cotton swab (Q-Tip) or a “freezing gun.” • A blistering agent, such as cantharidin, may be applied carefully with a toothpick to each bump every 3 to 4 weeks. • Burning and scraping (electrodesiccation and curettage) may be necessary for stubborn MC lesions. Home treatment • A liquid wart medicine such as salicylic acid (Duofilm), which you can buy without a prescription, is applied carefully. It should be applied with a toothpick only to the center of the “bump.” • The eyelid area should not be treated using this method! • A little irritation usually occurs. If the area becomes too irritated, stop using the Duofilm for a day or two and then use it again when the irritation disappears. • Your health care provider may prescribe another topical or oral medication such as ______________ to try. Things to keep in mind • It is also an option not to treat this condition, especially in very young children, and just wait for it to go away on its own. • But, of course, if you do that, you run the risk that it will spread further—possibly spreading MC to other children.

Molluscum contagiosum

Mo lu sco Co n t a gio so ¿Qué es el molusco contagioso (MC)? • El MC es una infección viral superficial común de las capas externas de la piel. • El MC produce algo similar a las verrugas, pero es un virus distinto al de las verrugas. ¿A quién le da MC? • Niños pequeños y sanos (bebés y preescolares). • Pacientes seropositivos. • Adultos jóvenes y sanos, sexualmente activos, aunque no sean seropositivos. Molusco contagioso ¿Qué lo causa? • El MC es causado por un virus de la familia pox-virus. ¿Cómo se contagia y se esparce? • El MC se contagia por el contacto de la piel. • Los “granitos” se esparcen al rascarlos o frotarlos. ¿Cómo es un molusco contagioso? • El MC ocasiona pápulas o nódulos de aspecto aperlado o encerado y en forma de domo, con un núcleo central blanco. Molusco contagioso ¿Hay síntomas? • Puede haber comezón. ¿Dónde ocurre? • El MC generalmente aparece en la cara, incluyendo los párpados. También surge en las axilas, los brazos, las piernas, y a veces en el pecho o espalda. • En niños, el MC puede ocurrir en áreas de la piel donde hay eczema. • El MC también puede presentarse en el abdomen bajo, el interior de los muslos, o en los genitales y zonas púbicas, tanto en niños como en adultos. ¿Cómo se trata? Tratamiento en el consultorio • Las pápulas o nódulos pueden congelarse con nitrógeno líquido aplicado con un hisopo (Q-Tip) o con una “pistola para congelar.” • Un agente cauterizante como cantharidin, se puede aplicar cuidadosamente con un palillo o mondadientes sobre cada granito cada 3 o 4 semanas. • Puede ser necesario quemar o raspar (por electrocauterización o curetaje) las lesiones persistentes. Tratamiento en la casa • Puede aplicar con cuidado un medicamento líquido para verrugas como ácido salicílico (Duofilm), disponible en farmacias sin necesidad de receta. Debe aplicarlo con un palillo o mondadientes en el centro de la pústula. • ¡No aplique este medicamento en el área de los párpados! • Generalmente ocurre un poco de irritación. Si el área se torna muy irritada, deje de usar el Duofilm por uno o dos días y úselo de nuevo cuando la irritación desaparezca. • Su médico le puede recetar otro tratamiento oral o tópico como ______________ para que lo pruebe. Recuerde • Puede optar por no tratar esta condición, especialmente en niños pequeños, y esperar a que el MC desaparezca por sí mismo. • Por supuesto, si elige no tratar el MC, corre el riesgo de que la enfermedad se extienda a más áreas de la piel y de que contagie a otros niños.

Pit yria sis Ro sea What is pityriasis rosea? • Pityriasis rosea, which means “fine pink scale,” is a self-limiting rash that occurs most often in the spring and fall. Who gets it? • Although it may occur at any age, it is seen mostly in young adults and older children. What causes it? • The cause is unknown; however, the occasional clustering of cases and seasonal appearances suggest that a virus is responsible. A single outbreak tends to bring about lifelong immunity, although repeat cases have been reported. • Despite the prevailing opinion that pityriasis rosea is caused by an infectious agent, it does not appear to be contagious; household contacts and schoolmates usually do not develop the rash. What does it look like? • Typically, pityriasis rosea often begins with the larger “herald” or “mother” patch, a scaly rash that may be confused with a fungus (“ringworm”). • The herald patch is followed in several days to 2 weeks by many oval or elliptic red patches with fine, thin scale on their surface. These spots are smaller than the “herald” patch. • These new patches appear on the trunk, neck, arms, and legs in an “old-fashioned bathing suit” distribution, and they tend to give a so-called “Christmas tree” pattern on the trunk. • Patches in very dark-skinned people may not have the typical pink color of pityriasis rosea and may appear darker than the surrounding skin. What are its symptoms? • Itching is usually absent or mild, but it may be severe in a small minority of patients. • The rash usually fades within 6 to 8 weeks. • Second or third episodes are very rare. How is it diagnosed? • The diagnosis is usually made by a dermatologist or by your own health care provider. • Infrequently, the rash may involve the groin or underarms (inverse pityriasis rosea). • Other rashes that resemble pityriasis rosea can occur in association with many drugs. • The dermatologist may order blood tests, scrape your skin, or take a sample of your skin (skin biopsy) if necessary to help make the diagnosis. How is it treated? • Treatment is often unnecessary in most cases, because pityriasis rosea usually clears up on its own. • Occasionally, anti-inflammatory medication such as a corticosteroid cream may be prescribed to relieve any itching. • Sunlight exposure may speed up the clearing of the rash. • If the rash lasts beyond the typical 8 to 12 weeks, you should be seen by a dermatologist.

Pityriasis rosea

Pityriasis rosea

Pit iria sis Ro sa d a ¿Qué es la pitiriasis rosada? • Pitiriasis rosada significa “fina escama rosa” y es un sarpullido que se auto-limita, ocurriendo generalmente en la primavera y otoño. ¿A quién le da? • Aunque puede ocurrir a cualquier edad, se ve principalmente en jóvenes y niños.

Pitiriasis rosada

Pitiriasis rosada

¿Qué la causa? • La causa se desconoce; sin embargo, las apariciones por temporadas y la agrupación de casos sugieren que puede ser un virus. Un brote de la enfermedad tiende a proporcionar inmunidad, aunque ha habido casos que reportan relapsos. • Aunque la opinión general es que la pitiriasis rosada es causada por un agente infeccioso, parece no ser contagiosa; familiares y amigos generalmente no son afectados. ¿Cómo es? • La pitiriasis rosada habitualmente comienza con una placa “heráldica” grande, o “mácula madre,” un sarpullido escamoso que se puede confundir con un hongo (“tiña”). • A la placa heráldica le siguen durante los siguientes días o semanas varias placas ovales o elípticas rojas, con escamas finas y delgadas en la superficie. Estas áreas son más pequeñas que la placa heráldica. • Estas nuevas áreas de sarpullido aparecen en el torso, cuello, brazos y piernas, distribuidas como un “traje de baño anticuado,” y tienden a crear un patrón como de “árbol de Navidad” en la espalda. • Estas áreas en gente de piel oscura no se ven del color rosa típico de la pitiriasis, pudiendo verse más oscuras que la piel que las rodea. ¿Cuáles son los síntomas? • Puede haber algo o nada de comezón, o ser muy severa en algunos pacientes. • El sarpullido generalmente desaparece entre 6 a 8 semanas. • Es muy raro que halla segundos o terceros episodios. ¿Cómo se diagnostica? • Su dermatólogo o doctor puede hacer el diagnóstico. • El sarpullido raramente aparece en la ingle o axilas (pitiriasis rosada invertida). • Otros sarpullidos que se parecen a la pitiriasis rosada pueden ocurrir en asociación con algunas drogas. • Su dermatólogo puede ordenar exámenes de sangre, raspado de piel o tomar una muestra (biopsia), si lo considera necesario para el diagnóstico. ¿Cómo se trata? • En la mayoría de los casos no es necesario tratar la pitiriasis porque tiende a aliviarse por si misma. • Ocasionalmente se pueden recetar cremas antiinflamatorias medicadas con corticoesteroides para aliviar la comezón. • La exposición al sol puede acelerar la desaparición del sarpullido. • Si el sarpullido dura más de las típicas 8 a 12 semanas, consulte un dermatólogo.

Po iso n Ivy a n d Po iso n Oa k

(Rh u s Der m a t it is)

What is rhus dermatitis? • In the United States, the main causes of rhus dermatitis are poison ivy and poison oak. • Poison ivy is found throughout the country. • Poison oak is found more commonly in the western part of the country. • Poison sumac, another cause, is found only in woody, swampy areas. • In the eastern United States, it occurs mainly in the spring and summer. • In the western and southeastern United States, where outdoor activity is common all year, it may occur in any season. How is it acquired? • The plants’ invisible oils may reach the skin through direct contact. • Contact may also occur through garden tools, pet fur, golf clubs, or the smoke of a burning plant. What does the rash look like? • The typical rash consists of intensely itchy lines of red bumps (papules) and blisters where the plant has brushed against the skin. The rash typically occurs 2 days after contact with the plant. • Generally, exposed areas of the body are affected first. The rash may later involve covered areas that have come into contact with the plant oil.

Poison ivy

Poison ivy in the spring

How is it diagnosed? • The diagnosis of rhus dermatitis is based on history of exposure and the typical location of the rash. • Further spread of the rash is believed to occur through the bloodstream and not by touching, rubbing, or scratching the skin. This spread may occur within 5 to 7 days after the initial exposure, and the resulting rash may last for 3 weeks or more. How is it treated? • A limited eruption and mild itching may be relieved by the following: • Cool baths or showers and cool compresses such as frozen vegetable packages may help lessen the itching. • Calamine lotion is useful. • Oral antihistamines such as Benadryl are helpful, particularly at bedtime. • In severe cases with widespread eruption and marked itching: • An oral or injectable cortisone may be necessary. How can I avoid getting it? • To prevent rhus dermatitis, you should learn to recognize its plants: “leaves of three, let them be.” • If you come into contact with the plant or its oil, you should wash with soap and cold water as soon as possible. All exposed clothing should be laundered. Helpful hints • The rash is not contagious; you can’t spread the rash to others or spread it on yourself by touching the blisters or fluid. • If your work or hobbies result in frequent exposure to poisonous plants, try a barrier cream such as Ivy Shield or StokoGard before exposure.

Poison ivy in the fall

Poison oak

Derm a t it is Po r Rh u s

Hiedra venenosa

(H ied ra Ven en o sa y Zu m a q u e o Ro b le Ven en o so )

¿Qué es la dermatitis por rhus? • En los Estados Unidos, las principales causas de dermatitis por rhus son la hiedra venenosa y el zumaque o roble venenoso. • La hiedra venenosa se encuentra en todo el país. • El roble venenoso se encuentra comúnmente en el oeste del país. • El zumaque venenoso existe solo en áreas boscosas o pantanosas. • En el este de los Estados Unidos ocurre principalmente en la primavera y el verano. • En el oeste y el sureste de los Estados Unidos, donde las actividades al aire libre son comunes todo el año, puede ocurrir en cualquier estación. ¿Cómo se adquiere? • Los aceites invisibles de las plantas penetran la piel al contacto directo con ellas. • Puede haber contacto indirecto por medio de herramientas de jardinería, palos de golf, mascotas, o el humo cuando se queman las plantas.

Hiedra venenosa en la primavera

¿Cómo es? • El sarpullido brota en líneas de pápulas rojas con mucha comezón y ampollas donde la planta tocó la piel. Esto ocurre a los 2 días del contacto con la planta. • Generalmente, las áreas del cuerpo que estuvieron expuestas son afectadas primero. El sarpullido después se esparce a otras áreas cubiertas que hayan tenido contacto con los aceites de la planta. ¿Cómo se diagnostica? • El diagnostico de dermatitis por rhus se basa en que haya habido exposición a plantas y a la ubicación típica del sarpullido. • Se cree que el esparcimiento del sarpullido se debe a las corrientes sanguíneas, no por tocar, frotar o rascarse la piel. El esparcimiento ocurre entre 5 a 7 días después de la exposición inicial, y puede durar 3 semanas o más.

Hiedra venenosa en el otoño

Roble venenoso

¿Cómo se trata? • Un sarpullido limitado con poca comezón se puede aliviar con lo siguiente: • Bañarse con agua fría y aplicar compresas frías (como por ejemplo bolsas de verduras congeladas) alivian la comezón. • La loción de calamina también ayuda. • Los antihistamínicos orales como Benadryl son muy benéficos, particularmente a la hora de dormir. • En casos severos con más erupciones y mucha comezón: • Puede ser necesario prescribir cortisona oral o inyectable. ¿Cómo se previene? • Para prevenir la dermatitis por rhus, aprenda a reconocer las plantas: “si tiene de hojas tres, no las toques.” • Si llega a tocar la planta o sus aceites, lávese bien con jabón y agua fría de inmediato. También lave toda la ropa que fue expuesta a la planta. Consejos • El sarpullido no es contagioso; no puede pasarle las erupciones a nadie ni esparcirlas por su cuerpo con tocar las ampollas o el fluido. • Si su trabajo o sus pasatiempos requieren que se exponga frecuente a plantas venenosas, póngase una crema barrera como Ivy Shield o StokoGard antes de salir.

Pseu d o fo llicu lit is Ba rb a e

(Ra zo r Bu m p s)

What is pseudofolliculitis barbae (PFB)? • In some men with curly hair, the area under the chin, upper neck, or cheeks can be subject to an uncomfortable cluster of bumps known as “papules,” which can make shaving very difficult. • These bumps can really become itchy and painful, and they may scar and heal with dark spots. • The term “folliculitis” simply refers to any inflammation or infection of hair follicles. PFB is more commonly called “razor bumps.” How does it develop? • A curly hair grows from a sharply curved hair root. When shaved, the hair is left with a sharp point. As this hair grows, it makes a “U-turn,” and the sharp tip curves back and pierces the skin. • On the other hand, when hairs are cut too closely, they sometimes grow underneath the skin.

Pseudofolliculitis barbae (razor bumps)

Who gets it? • Most African-American people have curved hair follicles, and their cut hair may be sharply pointed. • If aimed toward the body, this cut hair can grow right back into the skin. How can it be prevented? General advice • Don’t pluck hairs because new hairs will again grow from below and penetrate a site that is already inflamed. • Allow your hairs to grow long enough so they will not grow back into the skin. • The key is to reduce the closeness of the shave so that you lessen the chance of ingrown hairs. Hairs cut too short are at risk of curling into the skin while growing and causing more razor bumps. Razor shaving • Avoid a close shave by using a guarded razor. Two recommended products are the PFB Bump Fighter or the Aveeno PFB Bump Fighter Razor. Both of these products should be available at your local drug store. • Soften your hairs before shaving. Try shaving after you take a warm shower. Steaming helps soften your beard. Washing your face before shaving removes oil and causes hairs to become more erect, making them easier to cut. Lather the beard area with a nonirritating, lubricating shaving gel such as Aveeno Therapeutic Shave Gel, Edge, or a benzoyl peroxide–containing prescription shaving foam such as Benzashave. • Use shaving gels to hydrate your hairs and to provide lubrication between the razor blades and your skin. • Shave with downward strokes; “go with the grain.” Shaving in the same direction that the hair lies (typically down) results in less pull on the hairs and less tendency to cut them too short. • Minimize repeat shaving strokes. Repeated shaving may result in hairs being cut too short. • Don’t stretch the skin during shaving, because this leads to a closer shave and increases the chances of producing ingrown hairs. • Don’t shave on a daily basis if you don’t have to. Electric shaving • Using an electric razor with gentle pressure is another method that reduces the closeness of the shave. continued on page 76

Pseudofolliculitis barbae (razor bumps)

Pseu d o fo licu lit is Ba rb a e

(“Irrit a ció n d e Ra su ra d o ra ”)

¿Qué es pseudofoliculitis barbae (PFB)? • En algunos hombres de cabello rizado, el área bajo la barba, las mejillas, o sobre el cuello puede desarrollar granos o “pápulas” incómodos y dolorosos que pueden dificultar la rasurada. • Estos granos pueden ser muy dolorosos y dar comezón, y al cicatrizar dejar manchas oscuras. • El termino “foliculitis” simplemente se refiere a la inflamación o infección de los folículos capilares. PFB se conoce comúnmente como “irritación de rasuradora.”

Pseudofoliculitis barbae (irritación de rasuradora)

¿Cómo se desarrolla? • Un vello rizado se origina de una raíz que es curvada. Al rasurarlo, el vello adquiere un extremo filoso. Cuando este vello crece, da vuelta “en U” y el extremo filoso se incrusta en la piel. • Por otro lado, cuando los vellos se rasuran demasiado cortos, tienden a crecer bajo la piel. ¿A quién le da? • Muchos Americanos Africanos tienen foliculos curvos y el vello rasurado tiene extremos filosos. • Cuando el vello crece hacia la dirección del cuerpo, se reinserta en la piel.

Pseudofoliculitis barbae (irritación de rasuradora)

¿Cómo se puede prevenir? Consejos generales • No arranque el vello porque uno nuevo crecerá otra vez desde abajo y penetrará el sitio inflamado. • Permita que el vello crezca lo suficiente para no reinsertarse en la piel. • La clave es: no rasurar el vello al extremo; así se elimina la incidencia de vellos incrustados. Los vellos que se rasuran muy cortos tienen el riesgo de rizarse hacia la piel mientras crecen y causar más granos irritantes. Rasurado con rastrillo • Evite rasurar al extremo usando una rasuradora con protector. Dos productos recomendables son: PFB Bump Fighter o Aveeno PFB Bump Fighter Razor. Estos productos están disponibles en farmacias. • Suavice los vellos antes de rasurar. Trate de afeitarse después de bañarse con agua caliente. El vapor ayuda a suavizar la barba. Si lava la cara antes de afeitarse, esto ayuda a eliminar aceites y eriza los vellos, lo que facilita cortarlos. Use crema de afeitar lubricante como Aveeno Therapeutic Shave Gel, Edge, o una espuma con peróxido de benzoilo como Benzashave. • Use gel para afeitar para hidratar el vello y proveer lubricación entre las navajas y su piel. • Afeite con movimientos hacia abajo; “con el crecimiento del vello.” Al afeitar en la misma dirección que crece el vello (generalmente hacia abajo) jala menos el vello y evita cortarlo muy cerca. • Minimice las veces que pasa el rastrillo. Cuando se rasura una y otra vez, afeita el vello muy corto. • No estire la piel mientras se afeita porque corta el vello muy cercano a la piel, incrementando la posibilidad de ocasionar que crezca hacia adentro. • No se rasure diariamente si no es necesario. Rasurado eléctrico • Si usa una maquina de afeitar eléctrica con presión suave puede reducir lo cercano de su afeitado. continued on page 77

Continued from page 74

Mechanical method • A curled hair can be flipped up before it has a chance to plunge into the skin by using a fine needle or toothpick to gently lift it before reentry. Medications • A prescription benzoyl peroxide such as BenzaClin gel may work very well for you. • An over-the-counter benzoyl peroxide such as eOxy-5 may also be effective. Other methods of hair removal Many methods are available for temporary or permanent hair removal, including the following: • Chemical depilatories: depilatories remove hair from the surface of the skin. For PFB, chemical depilatories such as Magic Shave and Royal Crown Powders are effective in removing and softening hairs. These products dissolve the hairs but can be too strong and cause chemical burns on facial skin. • Removing hairs permanently: techniques of permanent epilation include electrolysis, thermolysis, and laser epilation.

Continued from page 75

Método manual • Un vello rizado se puede reversar antes de que se incruste en la piel, levantándolo con una aguja o palillo. Medicamentos • Un gel medicado con peróxido de benzoilo como BenzaClin puede funcionar. • eOxy-es un peróxido de benzoilo efectivo que se vende sin receta médica. Otros métodos para eliminar vello Hay varios métodos disponibles para eliminar el vello temporalmente o permanentemente: • Depilatorios químicos: eliminan el vello de la superficie de la piel. Para PFB, los depilatorios químicos como Magic Shave y Royal Crown en polvo son eficientes para eliminar y suavizar los vellos. Estos productos disuelven el vello pero pueden ser muy fuertes y dejar quemaduras en la piel de la cara. • Depilación permanente: las técnicas de depilación permanente incluyen electrólisis, termólisis, y epilación láser.

Pso ria sis What is psoriasis? • Psoriasis is a red and scaly chronic skin condition of unknown cause. Who gets it? • About 30% of people with psoriasis have a family history of the condition. • It affects 1% to 2% of the world’s population. • Psoriasis most frequently begins in the second or third decade of life, but it can first be seen in infants or in elderly persons. Psoriasis on the elbows What causes it? • The exact cause is unknown; however, we do know that psoriatic lesions (spots) result from an increase in epidermal cell division. What does it look like, and where on the body does psoriasis occur? • Thickened, reddened, silvery or whitish, scaly patches can vary from only a few small bumps known as papules to larger plaques that cover large areas of the body. • Psoriasis tends to be remarkably symmetric. (It tends to look almost the same on both sides of the body.) • Fortunately, it usually spares the face. • Psoriasis is most commonly located on the: • Large joints: elbows, knees, and knuckles. • Palms and soles. • Body folds: the underarms, under the breasts, the anus and genital region, and the groin. This body fold type of psoriasis is referred to as inverse psoriasis. • Trunk. Lesions may be small, guttate (teardrop-shaped), or large plaques. • Scalp and ears. • Nails. Involvement of nails is very common in patients with psoriasis. What are its symptoms? • Psoriasis generally is symptom-free but can become quite itchy and uncomfortable, particularly during acute flare-ups or when it involves the scalp or skin fold regions. • A person who has psoriasis is mainly concerned about the appearance of his or her skin. • Psoriatic arthritis occurs in about 7% of patients who have psoriasis.

Psoriasis on the buttocks

Psoriasis on the scalp

What makes it worse? • Emotional stress, such as anxiety and depression, is believed to worsen psoriasis. • Certain drugs and excess alcohol may also play roles. What is the usual course of psoriasis? • Psoriasis has an unpredictable, waxing and waning course. It has no known cure. • In its mildest forms, psoriasis is an incidental finding. It may consist of nail pitting or mildly red, scaly patches on the elbows or knees. • During episodes of physical illness or pregnancy, psoriasis may worsen or suddenly clear. • The condition tends to improve during the summer and worsen during the colder times of the year. This fluctuation is probably a result of the positive influence of sunlight on psoriasis. continued on page 80

Psoriasis affecting the nails

Pso ria sis ¿Qué es la psoriasis? • La psoriasis (o mal de pintas) es una condición crónica, de origen desconocido, que ocasiona que la piel se torne rojiza o escamosa.

Psoriasis en los codos

¿A quién le da psoriasis? • Alrededor de 30% de la gente afectada tiene historia clínica de psoriasis en la familia. • Afecta del 1% al 2% de la población del mundo. • La psoriasis usualmente comienza en la segunda o tercera década de la vida, pero también afecta a niños y ancianos. ¿Qué la causa? • La causa exacta se desconoce; sin embargo, se sabe que las lesiones de psoriasis (manchas) ocurren por un incremento en la división de células epidérmicas.

Psoriasis en los glúteos

Psoriasis en el cuero cabelludo

¿Cómo es la psoriasis y en qué parte del cuerpo ocurre? • Son lesiones escamosas, gruesas, rojizas, grisáceas o blancuzcas que varían entre pequeñas ronchas como pápulas, o como placas más grandes que cubren áreas extensas del cuerpo. • La psoriasis suele ser notablemente simétrica (se ve casi igual en los dos lados del cuerpo.) • Afortunadamente, suele evitar aparecer en la cara. • La psoriasis comúnmente se encuentra en: • Las articulaciones grandes: codos, rodillas, y nudillos. • Las palmas de las manos y las suelas de los pies. • Los pliegues del cuerpo: las axilas, bajo el busto, el ano, la región genital y la ingle. Esta clase de psoriasis que afecta los pliegues de la piel se llama psoriasis invertida o psoriasis de pliegues. • Tronco. Estas lesiones pueden ser pequeñas, lesiones guttata (en forma de lágrima), o placas extensas. • El cuero cabelludo y las orejas. • Las uñas. Es muy común ver que las uñas estén afectadas en pacientes con psoriasis. ¿Cuáles son los síntomas? • La psoriasis es generalmente asintomática, pero se puede volver muy incómoda cuando hay comezón, particularmente durante brotes severos o cuando se presenta en el cuero cabelludo o en los pliegues del cuerpo. • Una persona con psoriasis se preocupa principalmente por la apariencia de su piel. • La Artritis Psoriásica ocurre en un 7% de los pacientes que tienen psoriasis.

Psoriasis afectando a las uñas

¿Qué lo empeora? • El estrés emocional, la ansiedad y la depresión, pueden empeorar la psoriasis. • Ciertas drogas y exceso de alcohol también pueden influir. ¿Cuál es el curso usual que sigue la psoriasis? • La psoriasis aumenta y disminuye, tomando cursos impredecibles. Hasta ahora no se sabe la cura. • En su forma más austera, la psoriasis es un encuentro incidental. Puede consistir de hendiduras en las uñas o zonas escamosas rojizas en los codos o rodillas. • Puede agraviarse o desaparecer de repente durante episodios de enfermedad o embarazo. • Suele mejorar durante el verano y empeorar en los tiempos de frío. Esta fluctuación probablemente ocurre por la influencia positiva que tiene la luz del sol sobre la psoriasis. continued on page 81

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How is it diagnosed? • Dermatologists can usually easily recognize it by simply examining the skin. • Other helpful diagnostic features include family history of psoriasis. • If necessary, other tests, such as a skin biopsy or fungal examinations, can be performed to rule out other conditions. How is it treated? • Topical corticosteroids. The use of a very potent topical steroid applied for a limited period, followed by a less-potent topical steroid for maintenance, has become a popular method for treating psoriasis. • Topical vitamin D • Dovonex (calcipotriene ointment, cream, and solution) is often used in combination with topical steroids. • Taclonex combines vitamin D and a topical steroid. • Topical immunomodulators such as Protopic ointment and Elidel cream are sometimes used to treat inverse psoriasis. • Other topical treatments. Topical retinoids and topical tar preparations are less often used. • Ultraviolet light therapy • Natural sunlight sometimes slows the growth of psoriasis. People with psoriasis all over their bodies may be treated with light boxes that expose most of their body to ultraviolet light. • Ultraviolet light therapy plus oral treatments is used when a person who has psoriasis is not responding to topical therapies or ultraviolet light treatment alone. • Diets. Special diets do not seem to help in any way. • Newer approaches to psoriasis therapy. There are many new biologic agents that are currently available for the treatment of psoriasis and psoriatic arthritis. The National Psoriasis Foundation provides information about the latest treatments for psoriasis, educational pamphlets, and information about self-help and discussion groups (800-723-9166).

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¿Cómo se diagnostica? • Los dermatólogos pueden reconocerla fácilmente en cuanto examinan la piel. • Si hay historia clínica de psoriasis en la familia, esto puede ayudar a determinarlo. • Si fuera necesario, puede hacerse exámenes tales como una biopsia de piel o una prueba para detectar infecciones micóticas para eliminar otras posibilidades. ¿Cómo se trata? • Corticoesteroides tópicos. Un método popular hoy en día es aplicar un esteroide tópico potente durante un periodo de tiempo limitado, seguido de un esteroide tópico menos fuerte, como mantenimiento. • Vitamina D tópica • Dovonex (calcipotriene ungüento, crema, y solución) se usa en combinación con esteroides tópicos. • Taclonex combina vitamina D y un esteroide tópico. • Inmunomoduladores tópicos como el ungüento Protopic y la crema Elidel se usan para tratar la psoriasis invertida. • Otros tratamientos tópicos. Los retinoides y las preparaciones de alquitrán son menos comunes. • Terapia de luz ultravioleta. La luz de sol natural a veces entorpece el crecimiento de la psoriasis. Las personas infestadas con psoriasis en todo el cuerpo pueden ser tratadas con exposición a luz ultravioleta. • Terapia de luz ultravioleta con tratamientos orales. Cuando la psoriasis no responde a la terapia tópica por sí misma, o a la luz ultravioleta sola, se complementa el tratamiento con medicamentos orales. • Dietas. Las dietas especiales generalmente no ayudan. • Nuevos enfoques en la terapia de psoriasis. Hay varios agentes biológicos nuevos actualmente disponibles para el tratamiento de la psoriasis y la artritis psoriásica. La Fundación Nacional de Psoriasis provee folletos educativos e información sobre los últimos tratamientos de psoriasis y sobre grupos de discusión y autoayuda (800-723-9166).

Ro sa cea What is rosacea? • Rosacea is a skin condition that is frequently mistaken for acne. In fact, as recently as the 1980s, rosacea was referred to as acne rosacea. • Rosacea is a common condition with no known cause or cure. Who gets it? • Rosacea develops later in life than acne, usually between 30 and 50 years of age. • It occurs most commonly in fair-skinned people of northern European ancestry, particularly those of Celtic descent. What does it look like? • Rosacea consists of red pimples (papules), pus pimples (pustules), and small blood vessels (telangiectasias). Where does it appear? • Rosacea is typically seen on the forehead, nose, cheeks, and chin (the so-called flush or blush areas of the face). What are its symptoms? • Rosacea is mainly a cosmetic problem, although a burning sensation can sometimes be bothersome. • It can also involve the eyes and eyelids, which may require treatment by an eye doctor. What makes it worse? • Sun exposure often triggers flares of rosacea. • Excessive washing of the face may also aggravate rosacea. • Irritating cosmetics are another factor that can worsen it. In some people, the following factors may aggravate rosacea: • Excess alcohol ingestion • Emotional stress • Spicy foods, smoking, or caffeine How is it treated? • Topical therapy • Noritate cream or MetroGel is used once daily. It is applied in a thin film to all rosaceaprone areas. • Other topical medications include ___________ and should be applied ____________. • Oral therapy • Your health care provider may also prescribe an oral antibiotic such as _________________. • Surgical treatment • Special light treatments and lasers are sometimes effective for the persistent redness that remains even after the inflamed pimples and papules are controlled.

Rosacea

Ro sá cea ¿Qué es la rosácea? • Rosácea es una enfermedad de la piel que frecuentemente se confunde con acné. De hecho, aún hasta 1980 se le conocía como acné rosácea. • Rosácea es un padecimiento común cuya causa o cura aún no se conoce.

Rosácea

¿A quién le da rosácea? • La rosácea se desarrolla más tarde en la vida que el acné, generalmente entre los 30 y 50 años de edad. • Comúnmente ocurre en gente de piel clara con ascendencia del norte de Europa, particularmente de linaje Celta. ¿Cómo es la rosácea? • La rosácea presenta granitos rojos (pápulas), erupciones con pus (pústulas), y pequeños vasos sanguíneos (telangiectasia). ¿Dónde aparece? • La rosácea se presenta por lo regular en la frente, nariz, mejillas, y barbilla (las zonas de la cara donde uno comúnmente se sonroja al avergonzarse). ¿Cuáles son los síntomas? • La rosácea es un problema de naturaleza principalmente cosmética, aunque a veces puede presentar una molesta sensación de ardor. • También puede involucrar los ojos y párpados; de ser así, debe ser tratado por un médico oftalmólogo. ¿Qué la empeora? • La exposición al sol puede ocasionar un brote de rosácea. • Lavarse la cara excesivamente también puede agravar la rosácea. • Otro factor que la empeora es el uso de cosméticos que irritan la piel. En algunas personas, los siguientes factores pueden agraviar la rosácea: • Ingestión de alcohol en exceso • Estrés emocional • Comer alimentos picantes o con muchas especias, fumar, o tomar cafeína ¿Cómo se trata? • Terapia tópica • Crema Noritate o MetroGel una vez al día. Se aplica en capas finas a las áreas susceptibles de rosácea. • Otros medicamentos tópicos incluyen _________ y deben ser aplicados ___________. • Terapia oral • Su médico le puede recetar un antibiótico oral como _________________, • Tratamiento quirúrgico (cirugía) • Hay tratamientos especiales de luz o láser que a veces son efectivos para tratar la rojez que persiste aún después de controlar los granos y pápulas inflamados.

Sca b ies What is scabies? • Scabies is a very itchy skin condition. • Children and adults rarely have lesions (itchy spots) above the neck. • Infants, however, tend to have more widespread involvement, including the face and scalp, and especially the palms and soles. • The main symptom of scabies is itching, particularly at night. What causes it? • Scabies is caused by a very small mite, about 0.4 mm in length, that can barely be seen by the human eye. How is it spread? • Scabies is almost always caught from another person, usually another family member or someone else with whom you have come into close contact. • It has nothing to do with dirt or poor personal hygiene. Where does the rash occur? • The itchy rash of scabies is most often located between the fingers, on the sides of the hands and feet, wrists, umbilicus (belly button), waistband area, armpits, ankles, buttocks, and groin. How is it treated? • Use permethrin (Elimite and Acticin) • Elimite and Acticin both contain permethrin cream 5%. • A prescription is required. • Thirty grams (half a tube) of medication are enough for an adult. • Follow these instructions • After a warm bath, apply a thin layer of Elimite or Acticin to all skin surfaces from head to toe (including the palms and soles and scalp in small children), and leave it on for 8 to 12 hours, usually overnight. • Wash it off the next morning. • Your health care provider may prescribe an oral medication known as ivermectin in very stubborn cases. • If instructed by your health care provider, have other family members and contacts treated at the same time. • Make sure that all bed linens and intimate undergarments are washed in hot water after treatment is completed. • Generally, only one treatment is necessary; however, a second treatment is often recommended in 4 to 5 days, especially in long-standing cases and in infants with scabies of the palms and soles. What should I expect after treatment? • It is normal to continue itching for days or even weeks after treatment, but the itching is usually less intense. • Call your health care provider if you or your child is not better. • Do not continue to apply the prescription medications unless otherwise instructed.

Scabies

Sa r n a

(Esca b io sis)

¿Qué es la sarna (escabiosis)? • La escabiosis, mejor conocida como sarna, es una enfermedad de la piel que ocasiona mucha comezón. • Los niños y adultos raramente presentan lesiones (áreas con comezón) arriba del cuello. • Los bebés, sin embargo, suelen presentarla en más áreas, incluyendo la cara, el cuero cabelludo, y especialmente las palmas de las manos y las suelas de los pies. • El principal síntoma de sarna es comezón, particularmente en la noche. Sarna (escabiosis)

¿Qué la causa? • La sarna es ocasionada por un ácaro muy pequeño, de aproximadamente 0.4 mm de largo, y casi no se puede ver a simple vista. ¿Cómo se contagia? • La sarna casi siempre se contrae a través de otra persona, generalmente un miembro de la familia o alguien con quien tenga contacto próximo. • No tiene nada que ver con suciedad o mala higiene personal. ¿Dónde ocurre? • La sarna generalmente se encuentra entre los dedos, a los lados de las manos y pies, en las muñecas, el ombligo, el área de la cintura, las axilas, los tobillos, los glúteos, y la ingle. ¿Cómo se trata? • Use permethrin (Elimite y Acticin) • Las cremas Elimite y Acticin contienen 5% de permethrin. • Necesita receta médica. • Treinta gramos (medio tubo) de medicamento es suficiente para un adulto. • Siga estas instrucciones • Después de un baño tibio, aplique una delgada capa de Elimite o Acticin a todas las superficies afectadas de la piel (incluyendo las palmas, suelas y cuero cabelludo en niños pequeños), y déjelo puesto entre 8 y 12 horas, preferentemente durante la noche. • Lo puede quitar lavándolo a la mañana siguiente. • Su médico puede recetar un medicamento oral como ivermectin en casos difíciles. • Su médico puede sugerir que el resto de la familia y sus contactos usuales se traten al mismo tiempo. • Asegúrese de que toda su ropa, la ropa de cama y la ropa íntima se laven bien con agua caliente cuando termine el tratamiento. • Generalmente sólo un tratamiento es necesario; sin embargo, un segundo tratamiento puede ser recomendado en 4 o 5 días, especialmente en casos persistentes y en bebés con sarna en las palmas y las suelas. ¿Qué puede suceder después del tratamiento? • Es normal que continúe la comezón durante días o incluso semanas después del tratamiento, pero es generalmente menos intensa. • Llame a su médico si no hay mejoría. • No continúe aplicando el medicamento más allá de lo recetado, a menos de que lo indique su médico.

Sca lp Pso ria sis: Sca le Rem o va l If your health care provider has diagnosed scalp psoriasis or “sebopsoriasis,” it’s often necessary to remove thickened scale to allow the medications to get to where the action is— your scalp. Scale may be removed as often as necessary, usually two to three times per week at the beginning, and, later, whenever the scale builds up again. Here’s how: • Wash your hair with your favorite shampoo and rinse thoroughly. • Then, while your scalp is still damp, apply Keralyt gel or Salex cream only to the thickened scaly areas. Both Keralyt and Salex are prescription 6% salicylic acid preparations. • After applying the Keralyt or Salex, cover your head with a shower cap and leave it on overnight, or leave it on while you are awake for several hours (whichever is more convenient for you). • Shampoo the area again. (You’ll note Keralyt gel is very messy and greasy, and it will take some time to remove it.) • You may now apply other recommended medication(s) such as ____________________ and/or __________________. • Use the scale removal method if the scale builds up again.

Scalp psoriasis: Scale removal

Pso ria sis Del Cu ero Ca b ellu d o : Elim in a cio n d e Esca m a s Si su médico le ha diagnosticado psoriasis del cuero cabelludo o “sebopsoriasis,” suele ser necesario quitar las escamas gruesas para permitir que el medicamento llegue a la zona afectada—su cuero cabelludo. Las escamas deben ser eliminadas tan frecuentemente como sea necesario; generalmente dos o tres veces por semana al principio, y después, tan seguido como se vuelvan a formar.

Psoriasis del cuero cabelludo: Eliminación de escamas

Cómo quitar las escamas: • Lave el cabello con su shampoo favorito y enjuague bien. • Mientras el cuero cabelludo sigue húmedo, aplique el gel Keralyt o la crema Salex únicamente a las áreas escamosas. Tanto Keralyt como Salex son preparaciones de 6% ácido salicílico que requieren receta médica. • Después de aplicar ya sea Keralyt o Salex, cubra la cabeza con una gorra de baño y déjela puesta toda la noche. También la puede usar durante el día, por varias horas (escoja la situación más conveniente para usted). • Vuelva a lavar con shampoo. (Notará que el gel Keralyt suele ser grasoso y dificultoso, requiere de tiempo para eliminarlo.) • Puede proceder a aplicar otros medicamentos recomendados tales como ________________________ y/o ______________________. • Repita el método de eliminación de escamas si vuelven a brotar.

Seb o r rh eic Der m a t it is o f t h e Fa ce What is seborrheic dermatitis? • Seborrheic dermatitis (dermatologists call it “seb derm” for short) is an inflammatory skin condition of unknown cause. It’s a very common problem that’s mostly cosmetic in nature but can sometimes be a little itchy. It tends to come and go. There’s no cure, but the good news is that it can be treated easily. • Seborrheic dermatitis occurs in those skin areas that have the greatest number of sebaceous (oil-producing) glands—the scalp and face—as well as other areas that are mentioned below. • The condition tends to reappear from time to time, and it may first be seen at any age, but it most often first appears in people from ages 20 to 50.

Seborrheic dermatitis

What does it look like? • Facial seborrheic dermatitis is sometimes just scaly, just red, or both scaly and red. It can be itchy and can produce a burning sensation. It’s really like having “dandruff” with redness (inflammation) on your face. Sometimes it’s greasy because your oil glands are working overtime. In fact, what everybody thinks of as “dandruff” is often really seborrheic dermatitis. Where does it occur? • The face and scalp. Facial seborrheic dermatitis tends to occur on the sides of the nose, the eyebrows, behind the ears, in the ear canals, and sometimes the forehead, cheeks, and along the border of the scalp. It can also appear on the beard and mustache area in men. Many people have it on both the face and the scalp. • Other areas of the body. Seborrheic dermatitis can also be seen in the middle of the chest, under the arms, breasts, groin, where it is referred to as intertrigo. It can even pop up on your belly button. What can I expect? • Although there’s no real cure for seborrheic dermatitis, sun exposure often improves it; at other times, sunlight seems to worsen it. More often, it tends to act up in the dry, cold winter months. It is also commonly aggravated by scratching and emotional stress. How is it treated? By your health care provider, who may prescribe: • A fairly strong cortisone medication such as __________________. You should apply a tiny amount once or twice daily as necessary. Regular long-term use of such steroid medications should be avoided, especially on the face, under the arms, and on the breasts or groin. They are for short-term use only! • A nonsteroidal immunosuppressant drug such as ______________________________. • A special antiyeast preparation such as ___________________. There is recent evidence that seborrheic dermatitis may be triggered by a yeast organism. In fact, the regular use of an anti-yeast shampoo such as prescription or over-the-counter (OTC) Nizoral shampoo or prescription Loprox shampoo or gel will often keep the dermatitis under control, not only on the scalp, but elsewhere. By yourself: • Facial seborrheic dermatitis is relatively easy to treat, because the rash tends to respond quickly to very low strength topical cortisone creams such as Cortaid 1%, Cortizone-10, or generic hydrocortisone 1%, all of which can all be purchased without a prescription. • Also, it can be treated by topical OTC antifungal creams such as Lotrimin (clotrimazole) and Spectazole (econazole), which are usually used to treat athlete’s foot.

Seborrheic dermatitis

Der m a t it is Seb o r reica

Dermatitis seborreica

¿Qué es la dermatitis seborréica? • La dermatitis seborréica es una inflamación de la piel. Es un problema muy común, de origen desconocido. Aunque es un problema principalmente cosmético, puede ocasionar un poco de comezón. Suele ir y venir y no tiene cura, pero su tratamiento es muy sencillo. • La dermatitis seborréica ocurre en las áreas de la piel con la mayor cantidad de glándulas sebáceas (que producen grasa): el cuero cabelludo y la cara. También se puede presentar en otras áreas. • Este padecimiento suele aparecer por primera vez entre los 20 y 50 años de edad, y continúa reapareciendo ocasionalmente. ¿Cómo es la dermatitis seborréica? • La dermatitis seborréica facial puede ser escamosa, roja, o escamosa y roja. Puede dar comezón y puede arder. Es como tener “caspa” con una inflamación rojiza en la cara. A veces es grasosa porque las glándulas sebáceas están trabajando de más. De hecho, cuando la gente cree que tiene “caspa,” es generalmente dermatitis seborréica.

Dermatitis seborreica

¿Dónde se presenta la dermatitis seborréica? • La cara y el cuero cabelludo. La dermatitis seborréica facial suele presentarse en los lados de la nariz, en las cejas, tras las orejas, en los canales auditivos, y a veces en la frente, las mejillas, y los bordes del cuero cabelludo. También puede presentarse en la barba y el bigote de los hombres. Mucha gente la tiene tanto en la cara como en el cuero cabelludo. • Otras partes del cuerpo. La dermatitis seborréica también aparece en el medio del pecho, en las axilas, busto e ingle, y se le conoce como intértrigo. Puede salir hasta en el ombligo. ¿Qué puedo esperar? • Aunque no hay cura para la dermatitis seborréica, la exposición a la luz del sol a veces ayuda a mejorarla y a veces parece empeorarla. Generalmente suele brotar en los meses de invierno secos y fríos. Rascarse las áreas afectadas o sufrir estrés emocional la agravian. ¿Cómo se trata? Por su médico, quien puede recetar: • Un medicamento fuerte de cortisona como __________________. Aplique una pequeña cantidad una o dos veces al día, como sea necesario. Evite utilizar medicamentos de esteroides regularmente o por periodos largos, especialmente en la cara, axilas, busto o ingle. ¡Deben ser usados muy poco tiempo! • Un medicamento inmunosupresivo sin esteroides como ________________________. • Una preparación antimicótica especial como ___________________. Hay evidencia reciente que la dermatitis seborréica puede ser disparada por un organismo micótico (hongo). De hecho, el uso regular de un shampoo antimicótico (OTC) como el shampoo Nizoral, o el shampoo o el gel Loprox (algunos de ellos sólo se venden con receta médica) mantienen la dermatitis bajo control, no sólo en el cuero cabelludo sino en todas partes. Por usted mismo: • La dermatitis seborréica facial es relativamente fácil de tratar porque las erupciones reaccionan rápidamente a la cortisona tópica, como las cremas Cortaid 1%, Cortizone-10, o la hidrocortisona genérica de 1%, cuya venta no necesita receta médica. • También se puede tratar con cremas antimicóticas (OTC) como Lotrimin (clotrimazole) y Spectazole (econazole) las cuales generalmente se usan para tratar el pié de atleta.

Seb o r rh eic Der m a t it is o f t h e Sca lp a n d Da n d r u ff What are seborrheic dermatitis and dandruff? • Seborrheic dermatitis of the scalp (dermatologists call it “seb derm” for short) is a very common problem that is mostly cosmetic but can sometimes be very itchy, annoying, and embarrassing. • It first occurs after puberty on those skin areas that have the greatest number of oil glands—most commonly the scalp and face. • It tends to reappear from time to time. • Common dandruff is a very mild type of seborrheic dermatitis. It consists of white flakes (scales) and none of the redness or inflammation that is usually seen in more severe cases. What are the symptoms? • Flaking, redness, and excessive itching of the scalp may indicate the presence of seborrheic dermatitis. Mild, patchy scaling to widespread, thick, scabs may be evident. • Some people also have seborrheic dermatitis on the face, where it tends to appear on the nose, eyebrows, behind the ears, in the ear canals, and sometimes on the forehead, cheeks, and along the border of the scalp. It may also appear in the central chest and genital region. How is it treated? • To treat seborrheic dermatitis on the scalp, your health care provider may prescribe a strong cortisone foam, lotion, gel, or solution medication such as __________________. These medications should be used only when necessary, and long-term use should be avoided. • A special scale-removing preparation such as ______________________ may also be useful. • An antiyeast shampoo such as ___________________ is often helpful, because there is evidence that seborrheic dermatitis may be triggered by a yeast organism in some people. • In fact, the regular use of an antiyeast shampoo such as prescription or over-the-counter Nizoral shampoo or prescription Loprox shampoo or gel sometimes keeps seborrheic dermatitis under control, not only on the scalp but elsewhere on the body. • You should continue using the antifungal shampoo after the seborrheic dermatitis has cleared up; it keeps the yeast population under control. Important tips • You might actually not have seborrheic dermatitis; rather, you might actually have a sensitive skin condition that looks just like seborrheic dermatitis. This is known as atopic dermatitis, a type of eczema, which often arises on the back portion of your scalp and can be very itchy. • Whether you have seborrheic dermatitis or eczema, if you have a dry, itchy scalp, go easy with shampoos! • Keep in mind that most shampoos are detergents, and that’s what helps them to get so foamy and clean your scalp. • A harsh detergent cleans your scalp, but it can really irritate skin that’s already red, scaly, and inflamed. Although it’s true that many shampoos are medicated, the benefit from the medication can be far outweighed by the detergent effect of the shampoo. Special instructions ________________________________________________________________________ ________________________________________________________________________

Seborrheic dermatitis of the scalp and dandruff

Derm a t it is Seb o r reica d el Cu ero Ca b ellu d o y Ca sp a

Dermatitis seborreica del cuero cabelludo y caspa

¿Qué es la dermatitis seborreica y la caspa? • La dermatitis seborreica del cuero cabelludo (los dermatólogos la llaman “seb derm” en inglés) es un problema muy común, principalmente cosmético, pero puede ocasionar mucha comezón y ser irritante y vergonzoso. • Comienza a ocurrir tras la pubertad en las áreas de la piel con más glándulas sebáceas— el cuero cabelludo y la cara. • Tiende a recurrir, reaparece de vez en cuando. • La caspa común es un tipo muy leve de dermatitis seborreica. Se presenta como partículas blancas (escamas) sin la rojez ni la inflamación que acompañan a los casos más severos. ¿Cuáles son los síntomas? • Si hay escamas, rojez, o comezón excesiva, esto indica la presencia de dermatitis seborreica. Puede haber desde un descarapelado ligero en zonas pequeñas hasta un área grande de costras gruesas. • Algunas personas tienen dermatitis seborreica en la cara, donde tiende a aparecer en la nariz, cejas, tras las orejas, en los canales del oído, y a veces en la frente, las mejillas, y el borde del cuero cabelludo. También puede aparecer en el área central del pecho o, la región genital. ¿Cómo se trata? • Para tratar la dermatitis seborreica en el cuero cabelludo, su doctor puede recetar una cortisona fuerte ya sea en espuma, loción, gel, o solución medicada como _________________________. Estos medicamentos deben usarse únicamente cuando es necesario y a corto plazo. Evite usarlos durante periodos prolongados. • Una preparación especial para eliminar escamas como _____________________ puede ser útil. • Un shampoo antimicótico como _____________ puede ayudar porque hay evidencia de que en algunas personas la dermatitis seborreica fue provocada por un hongo. • De hecho, el uso regular de shampoos antimicóticos como Nizoral o Loprox mantienen la dermatitis seborreica bajo control, no solo en el cuero cabelludo pero en todo el cuerpo. • Debe continuar usando el shampoo antimicótico aun cuando la dermatitis seborreica se haya eliminado; mantienen la población de hongos bajo control. Consejos importantes • Puede ser que usted no tenga dermatitis seborreica; puede ser que usted tenga una condición de piel sensible que parece dermatitis seborreica. Se le conoce como dermatitis atópica, un tipo de eczema que suele aparecer en la parte posterior del cuero cabelludo y puede dar mucha comezón. • Ya sea que usted tenga dermatitis seborreica o eczema, si tiene resequedad y comezón en el cuero cabelludo, reduzca el uso del shampoo! • Recuerde que muchos shampoos contienen detergente, que es lo que limpia su cabello y hace tanta espuma. • Un detergente fuerte limpia su cabello, pero puede irritar la piel inflamada, escamosa o rojiza. Aunque es cierto que muchos shampoos están medicados, el beneficio del medicamento no se compara con el daño que causa el detergente del shampoo. Instrucciones especiales ________________________________________________________________________ ________________________________________________________________________

Sh o r t -Ter m Co r t iso n e Th era p y What is short-term cortisone? • Short-term cortisone (STC)—most often prednisone—is an oral steroid medication that is often used to treat severe acute self-limiting inflammatory disorders such as poison ivy, poison oak, other types of acute dermatitis, allergies, asthma, and drug reactions. • STC involves taking a starting dose that is tapered down (or leveled) over a few days to 3 weeks. How is it taken? • STC is usually taken as a single dose with meals or right after meals to avoid an upset stomach. • It can be stopped any time without withdrawal problems. What are its side effects? • Minor complaints can include sleeplessness, mood swings, stomach upset, a sense of fullness, short-term weight gain, and a sense of well-being. Persons with severe previous psychologic problems may be more affected. • Do not confuse STC with long-term usage, which does have significant risks. How does it affect other medications or diseases? • STC can raise blood sugar in people with diabetes. It can also raise blood pressure and eye pressure (glaucoma). • Drug interactions are uncommon, but blood thinner effects may change. • STC can aggravate infections, especially tuberculosis. • STC must not be taken if herpes infection of the eye is present. • HIV-positive patients may require simultaneous antibiotics. • Avascular necrosis is a rare but severe side effect of STC. It is a disease resulting from the temporary or permanent loss of the blood supply to the bones. Without blood, the bone tissue dies and causes the bone to collapse. The relationship to STC is disputed and not proven. The risk is extremely low, and most patients who take corticosteroids for years do not develop avascular necrosis. DOSING SCHEDULE Name of drug:____________________ Strength: ________________________ Monday _________________________

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Tera p ia d e Co r t iso n a a Co r t o Pla zo ¿Qué es la cortisona a corto plazo? • La cortisona de corto plazo—generalmente prednisona—es un medicamento oral con esteroides que se usa para tratar enfermedades inflamatorias auto-limitantes agudas o severas como hiedra venenosa, roble venenoso, otros tipos de dermatitis aguda, alergias, asma, y reacciones hacia ciertas drogas. • Se toma una dosis inicial que se disminuye gradualmente (o se nivela) durante algunos días o hasta tres semanas. ¿Cómo se toma? • Se toma en una única dosis con alimentos, o acabando de comer, para evitar molestias estomacales. • Se puede suspender en cualquier momento sin provocar síndrome de abstinencia. ¿Cuáles son los efectos secundarios? • Algunos efectos incluyen insomnio, cambios de humor, estómago revuelto, sensación de estar satisfecho, aumento de peso a corto plazo, y sensación de bienestar. Las personas con previos problemas psicológicos severos pueden ser más afectadas. • No confunda el uso de esteroides a corto plazo con el uso de esteroides a largo plazo, ya que ellos si conllevan riesgos importantes. ¿Cómo afecta a otros medicamentos o enfermedades? • Puede elevar los niveles de azúcar en la sangre en personas con diabetes. También puede elevar la presión sanguínea o de los ojos (glaucoma). • Es raro que interactúe con otros medicamentos, pero puede alterar los efectos de anticoagulantes. • Puede agravar infecciones, especialmente tuberculosis. • No se debe tomar si se tiene una infección de herpes en los ojos. • Los pacientes con VIH pueden necesitar antibióticos simultáneamente. • La necrosis avascular es un raro pero posible efecto secundario. Esta enfermedad resulta de la pérdida del suministro de sangre a los huesos, temporal o permanente. Sin sangre, el tejido de los huesos muere y el hueso se colapsa. La relación entre la necrosis avascular y los esteroides de corto plazo está bajo disputa y no se ha probado. El riesgo es extremadamente bajo y muchos pacientes que toman corticosteroides por años no desarrollan necrosis avascular. PROGRAMA PARA DOSIFICAR Nombre del medicamento: _____________________________ Dosis: _____________________________ Lunes __________________________

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So a k a n d Sm ea r In st r u ct io n Sh eet How does the “soak and smear” technique work? • This treatment is both messy (find an old pair of pajamas!) and time consuming but can lead to a rapid improvement in even a day or two. It works on many types of itchy skin problems such as eczema, poison ivy, and, sometimes, psoriasis. • The soaking allows water to get into the skin and moisturize it. Soaking also allows the anti-inflammatory cortisone ingredient in the ointment to penetrate more deeply into the skin. • The smearing of the ointment traps the water in the skin because water cannot move out through greasy materials. What steps are involved? In general Usually, do the soaking and smearing for 2 to 3 days. The treatments are best done at night because the greasy ointment applied to the skin gets on pajamas (instead of on daytime clothes), and the ointment is on the skin during sleep. The number of nights of soaking and smearing depends on how severe your (or your child’s) skin condition is and how long it takes to get it under control. • Soak in a bathtub using lukewarm, plain water for 20 minutes (use a timer) at night, then, without drying the skin, immediately smear the skin with a thin film of the steroid ointment containing __________________ for ____ days as directed. • If you have no bathtub or are unable to use a tub, take a long shower (again, lukewarm) and follow it by applying the steroid ointment to the wet skin. Then cover the affected area(s) with a cool, water-soaked towel and leave it on the skin for half an hour or so. • In the morning, you can apply _____________________ cream to the most troublesome areas, if necessary. For localized problems of hands, feet, or other body parts • Soak the affected areas continuously in a pan or basin of lukewarm water for 20 minutes at night and follow with the smearing of the steroid ointment containing _____________ as described above. • After the problem is under control, the soaks at night can be stopped and you can apply _____________________ cream in the morning, if necessary. A word about soap Even using a mild soap every day in the shower or bath can further dry out and irritate the skin by removing its natural oils. Unless otherwise instructed, you should avoid using any soap on red, inflamed, itchy skin.

In st r u ccio n es Pa ra Rem o ja r y Un gir ¿Cómo funciona la técnica de “remojar y ungir”? • Este tratamiento es sucio (¡póngase un viejo par de pijamas!) y toma tiempo, pero da buenos resultados en uno o dos días. Alivia muchas clases de problemas de la piel con comezón, como eczema, hiedra venenosa, y a veces psoriasis. • El remojar permite que el agua entre a la piel y la hidrate. También ayuda al ingrediente antiinflamatorio del ungüento de cortisona a penetrar profundamente en la piel. • El untar la pomada sobre la piel después de remojarla, atrapa el agua en la piel porque no puede moverse a través de materiales oleosos. ¿Qué pasos hay que seguir? En general Remoje y unte por 2 o 3 días. Los tratamientos son más efectivos cuando se aplican de noche porque el ungüento grasoso está en contacto con su piel mientras duerme y termina embarrado en la pijama (en lugar de en su ropa de día). El número de noches que hay que remojar y untar depende de la severidad de la condición de la piel y cuánto tiempo toma controlarla. • Remoje el cuerpo en una bañera de agua tibia durante 20 minutos (use un reloj) por la noche. Al terminar, sin secarse, unte de inmediato una capa delgada del ungüento con esteroides ____________ por ____ días o como lo indique su médico. • Si no tiene bañera y no puede usar una tina, tome un largo baño en regadera (con agua tibia) y al terminar aplique el ungüento sobre la piel mojada. • Cubra las áreas afectadas con una toalla remojada en agua fría y déjela sobre la piel durante aproximadamente media hora. • En la mañana, puede aplicar _____________________ en crema a las áreas más problemáticas, si es necesario. Para problemas localizados en las manos, pies y otras partes del cuerpo • Remoje las áreas afectadas en una tinaja o recipiente con agua tibia durante 20 minutos en la noche y unte la pomada de esteroides _______________ como se describió previamente. • Cuando el problema esté controlado, puede dejar de remojarse en la noche y simplemente aplicar la crema ________ en la mañana, si es necesario. Un detalle sobre el jabón El uso diario de jabón, aunque sea un jabón muy suave, puede resecar e irritar la piel al eliminar los aceites naturales. Sería conveniente que evitara usar cualquier jabón sobre las áreas rojas, inflamadas, o con comezón, a menos que su médico le indique lo contrario.

So la r Kera t o sis

(Act in ic Kera t o sis)

What are solar keratoses? • Solar keratoses, also known as actinic keratoses, are the most common sun-related skin growths. • A solar keratosis is benign (nonmalignant); however, it does—if left untreated—have the potential to develop into a type of skin cancer, squamous cell carcinoma. • An estimated 1 in 20 lesions eventually turns into squamous cell carcinoma. • The good news is that the squamous cell carcinomas that develop from these solar keratoses are a very slow-growing, unaggressive type of skin cancer, and the prognosis is usually excellent. Distant metastasis (spread) is extremely rare.

Solar keratosis on the nose

What do they look like? • They usually appear as crusty, “dry,” scaly bumps that are typically rough-textured and sandpaperlike to the touch. • Sometimes they are skin colored, reddish, or yellowish. They may also be tan or dark brown in color (pigmented solar keratosis). • They can gradually enlarge, thicken, and become more elevated and form “cutaneous horns” (they resemble a horn of an animal and often arise on the ears). Where do they appear? • Solar keratoses are most often seen on a background of sun-damaged skin or on any area that’s repeatedly exposed to the sun. • They appear mainly on the face, especially on the nose, temples, forehead, and sometimes on or around the lips. They also commonly arise on the top of the forearms and hands. • In men, they are commonly noted on the bald areas of the scalp, the tops of ears, and the sun-exposed areas of the neck. • In women, they also may occur on the legs. Who gets them? • Solar keratoses are seen in people who are fair-skinned, burn easily, and tan poorly. • They are more common in men, particularly those who work in outdoor occupations, such as farmers, sailors, and gardeners, and those who participate in outdoor sports. • The rate of occurrence is highest in Australia and in the Sun Belt of the United States. Solar keratoses are rare in dark-skinned people.

Solar keratoses

Solar keratoses on the scalp

What causes them? • The development of solar keratoses is related directly to cumulative sun exposure. What are the symptoms? • Solar keratoses usually don’t cause any symptoms, but they may become tender or irritated. How are they diagnosed? • Very small solar keratoses are more easily felt than seen. They feel like gritty bumps. • Larger ones are diagnosed by dermatologists based on their appearance or a skin biopsy. How are they treated? Treatment involves destruction of solar keratoses. continued on page 98

Cutaneous horn overlying a solar keratosis

Qu era t o sis So la r

Queratosis solar en la nariz

¿Qué es la queratosis solar? • La queratosis solar, también conocida como queratosis actínica, es una de las condiciones de la piel más comunes relacionadas a la exposición al sol. • La queratosis solar es benigna (no maligna); sin embargo, si no se trata, tiene el potencial de desarrollarse y convertirse en un tipo de cáncer de piel llamado carcinoma escamocelular. • Alrededor de 1 de cada 20 lesiones eventualmente se convierte en carcinoma escamocelular. • Los carcinomas escamocelulares que se desarrollan de la queratosis solar crecen muy lentamente, son un cáncer de piel no agresivo y su prognosis es generalmente excelente. Rara vez ocurre una metástasis distante (esparcimiento). ¿Cómo es la queratosis solar? • Habitualmente aparecen como protuberancias escamosas, parecidas a costras, “secas,” con una textura rasposa, como de lija, cuando se toca. • Generalmente son de color piel, rojizas o amarillentas, pero pueden tener un tinte moreno o café oscuro (queratosis solar pigmentada). • Pueden crecer gradualmente, engrosar, volverse más elevadas y formar “cuernos cutáneos” (parecen cuernos de animales y usualmente aparecen en las orejas).

Queratosis solar ¿Dónde aparece? • La queratosis solar se ve comúnmente en el fondo de la piel dañada por el sol o en áreas que están regularmente expuestas al sol. • Aparecen principalmente en la cara, especialmente en la nariz, sien, frente, y labios. También aparecen sobre los antebrazos y las manos. • En hombres se notan en áreas calvas de la cabeza, sobre las orejas y en las áreas del cuello expuestas al sol. • En mujeres también pueden verse en las piernas. Queratosis solar en el cuero cabelludo

¿A quién le da queratosis solar? • Gente de piel clara que se quema fácil y le cuesta trabajo broncearse. • Son mas comunes en hombres, particularmente quienes trabajan al aire libre como granjeros, jardineros, marineros y deportistas. • La incidencia más alta es en Australia y en el “cinturón solar” de los Estados Unidos. Es muy raro que le de a gente de piel oscura. ¿Qué la causa? • El desarrollo de la queratosis solar esta directamente relacionado a la acumulación de exposición al sol.

Cuerno cutáneo sobre una queratosis solar

¿Cuáles son los síntomas? • Usualmente es asintomática, pero puede presentarse con un poco de irritación o sensibilidad. ¿Cómo se diagnostica? • Los casos pequeños son más fáciles de sentir que de ver. Se sienten como granitos arenosos. • Los dermatólogos pueden diagnosticar los casos más grandes basados en su apariencia o con una biopsia de piel. ¿Cómo se trata? El tratamiento involucra la destrucción de la queratosis solar. continued on page 99

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Office treatment Destructive methods include the following: • Liquid nitrogen (“freezing”) is applied to individual solar keratoses for 3 to 5 seconds. • Biopsy, followed by electrocautery of individual lesions, or electrocautery alone. Home treatment Topical chemotherapy (you need a prescription) • Application of a 5-fluorouracil cream (5-FU) may be used when solar keratoses are too numerous to treat individually. Topical 5-FU treatment can be likened to using a “smart bomb,” in which the “bomb”—in this case 5-FU—targets only the “enemy”—the rapidly growing abnormal cells. • Topical Aldara (imiquimod) cream or Solaraze (diclofenac) may also be self-administered. Other methods that are less often used include: • Photodynamic therapy • Chemical peels and laser skin resurfacing How do I prevent them? • Prevention begins with limiting sun exposure. • Use a broad-spectrum sunscreen with an SPF (sun protection factor) of 30 or higher. • Wear a wide-brimmed hat. • Wear clothing that covers arms and legs.

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Tratamiento en el consultorio Los siguientes son métodos destructivos: • Nitrógeno líquido (para “congelar”) es aplicado a lesiones individuales cada 3 a 5 segundos. • Biopsia mas electrocauterización de las lesiones individuales, o electrocauterización solamente. Tratamiento en casa Quimioterapia tópica (necesita receta médica) • Puede aplicar una crema de 5-fluorouracil (5-FU) cuando hay demasiadas lesiones y no se puede tratarlas individualmente. El tratamiento tópico 5-FU es como usar una “bomba inteligente,” donde la “bomba”—el 5-FU—ataca únicamente al “enemigo”—las células anormales. • La crema tópica Aldara (imiquimod) o Solaraze (diclofenac) también puede usarse en casa. Otros métodos menos usuales incluyen: • Terapia fotodinámica • “Peels” químicos y regeneración láser ¿Cómo la prevengo? • Comience por prevenir su exposición al sol. • Use un bloqueador de amplio espectro con factor de protección solar (SPF) de 30 o más alto. • Use sombreros de ala ancha. • Use ropa que cubra piernas y brazos.

Sq u a m o u s Cell Ca rcin o m a What is squamous cell carcinoma (SCC)? • SCC is the second most common type of skin cancer. What does it look like? • It usually looks like a scaly or crusty bump. • It also can appear as a nonhealing sore or ulcer. Where does it appear? • It’s most often seen on sun-damaged skin. It’s found mainly on sun-exposed areas—the face, especially the nose, the temples and forehead, and the lips. • It’s also commonly noted on the bald areas of the scalp and the tops of ears in men, the top of the forearms and hands, and the sun-exposed areas of the neck. • In addition, it may also occur on any area that is repeatedly exposed to the sun. • It may occur on the legs in women. Who gets it? • Because SCC is related to sun exposure, it’s noted more frequently in those with a greater degree of outdoor activity. It is seen in people who are fair-skinned, burn easily, and tan poorly. • It’s more common in men, particularly those who work in outdoor occupations, such as farmers, sailors, and gardeners, and those who participate in outdoor sports. Where does it come from? • In most cases, it arises in a solar keratosis, a precancer also known as an actinic keratosis. • Causes other than sun exposure include the following: • Radiation exposure • Tanning parlors, exposure to psoralens with ultraviolet A (PUVA) phototherapy • Exposure to coal tar • Immunosuppression by medications or disease such as HIV How is it diagnosed? • Diagnosis is generally made by shave or excisional biopsy. How is it treated? • Most often, a simple minor office procedure called electrodesiccation and curettage is performed for small growths and for very superficial SCCs, known as squamous cell carcinoma in situ. • Surgical excision is the preferred method for larger tumors. • Micrographic (Mohs’) surgery may be the preferred method for recurrent or very large lesions. Mohs’ surgery is a microscopically controlled method of removing skin cancers that allows for controlled excision and maximum preservation of normal skin. Excisions are repeated in the areas proven to be cancerous until a completely cancer-free specimen is obtained. • Other treatment methods include the following: • Cryosurgery (freezing) with liquid nitrogen • Radiation (x-ray) therapy, which is used for those patients who are physically debilitated or who are unable, or refuse, to undergo excisional surgery continued on page 102

Squamous cell carcinoma

Squamous cell carcinoma

Ca rcin o m a d e Celu la Esca m o sa ¿Qué es el carcinoma de célula escamosa (CCE)? • Es el segundo tipo más común de cáncer de piel. ¿Cómo es? • Generalmente se ve como un bultito escamoso o con costra. • También puede parecer una llaga o úlcera que no sana.

Carcinoma de célula escamosa

Carcinoma de célula escamosa

¿Dónde aparece? • Comúnmente se ve en piel dañada por el sol. Se encuentra en áreas expuestas al sol—la cara, especialmente la nariz, la frente, y los labios. • También se presenta en las áreas calvas del cuero cabelludo en hombres, y sobre las orejas, los antebrazos, las manos y las áreas del cuello expuestas al sol. • Puede ocurrir en cualquier área que se expone al sol regularmente. • También puede aparecer en las piernas de las mujeres. ¿A quién le da? • El CCE esta relacionado a la exposición al sol, por lo tanto se nota frecuentemente en gente que pasa tiempo al aire libre. Se encuentra en gente de piel clara, que se quema fácilmente en lugar de broncearse. • Es mas común en hombres, particularmente quienes trabajan afuera como granjeros, marineros, jardineros y deportistas. ¿De dónde viene? • En la mayoría de los casos se presenta como queratosis solar, un pre-cáncer también conocido como queratosis actínica. • Aparte de exposición al sol, otras causas incluyen: • Exposición a radiación • Salones de bronceado, exposición a fototerapia psoralen ultravioleta A (PUVA) • Exposición a alquitrán o brea de carbón • Inmunosupresión por medicamentos o enfermedad como el VIH ¿Cómo se diagnostica? • El diagnóstico se realiza con una biopsia de escisión o rasurado. ¿Cómo se trata? • Para crecimientos pequeños y CCE muy superficiales llamados “in situ” generalmente se realiza un proceso simple en la oficina llamado electrodisecación y curetaje. • La escisión quirúrgica se reserva para tumores más grandes. • La cirugía micrográfica de Mohs se prefiere para lesiones recurrentes o muy grandes. Es un proceso microscópicamente controlado para extraer el cáncer de piel que permite una escisión precisa para preservar el máximo de piel normal. Las escisiones se repiten en las áreas cancerosas hasta que se obtiene un espécimen completamente libre de cáncer. • Otros tratamientos incluyen: • Criocirugía (“congelar”) con nitrógeno líquido • Terapia de radiación (rayos X) para pacientes físicamente debilitados, incapaces de someterse a una cirugía o que se rehúsan a ser operados. continued on page 103

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How is it prevented? • Sun avoidance measures: • Sunscreen • Hat with brim • Sunglasses with UV protection • Tinted windshields and side windows in cars • Protective clothing made of tightly woven or knitted fabrics that allows less sunlight to pass through • Follow-up: after therapy, periodic skin examination months after treatment Keep in mind • Sometimes SCCs are considered more risky than basal cell carcinomas and so must be treated more carefully, and patients must be watched more closely afterward. • Also, certain types of SCCs, particularly the larger and deeply penetrating ones and those found next to or on mucous membranes, are considered more dangerous and must be treated more thoroughly. • Many people who say they “never go out in the sun” get SCCs, too; 5 minutes of sun a day adds up over 30 or 40 years.

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¿Cómo se previene? • Evite el sol con: • Bloqueador solar • Sombrero de ala ancha • Anteojos obscuros con protección UV • Parabrisas y ventanas entintados en su auto • Ropa que proteja contra el sol—las mangas largas y los tejidos estrechos bloquean el sol • Seguimiento: después de su terapia, examine su piel periódicamente. Recuerde • A veces los CCE se consideran más riesgosos que los carcinomas de células basales, por lo que hay que tratar las lesiones con cuidado y se debe observar muy bien al paciente. • Algunos tipos de CCE, particularmente las lesiones más grandes o profundas y las que se encuentran cerca de membranas mucosas, se consideran más peligrosas y se deben tratar con detenimiento. • Muchas gentes que dicen que “nunca salen al sol” tienen CCE; 5 minutos de sol al día sobre 30 o 40 años se van acumulando.

Su n Pro t ect io n Ad vice Anyone with a family history of skin cancer and people who have very fair skin that never tans but always burns should apply a sunscreen. In addition to skin cancer, long-term sun exposure can cause wrinkles, age spots, and “broken” (dilated) blood vessels, and it can make the skin look older. The following are recommendations modified from those of the Skin Cancer Foundation: • Avoid sun exposure during the hours between 10 a.m. and 4 p.m., when the sun is strongest. • Wear protective headgear such as a hat with a wide brim or a baseball cap; wear longsleeved shirts and long pants. • Apply a sunscreen at least 30 minutes before sun exposure. Use a sunscreen with a sun protection factor (SPF) of 15 or greater to prevent burning. For sunscreens to work best, they should be reapplied every 2 to 3 hours, especially after swimming, toweling off, or sweating. • Apply sunscreens even on cloudy, hazy days. • Be aware of reflected light from sand, water, or snow. Ultraviolet (UV) rays can still bounce off these surfaces. Beach umbrellas and other kinds of shade are a good idea, but they do not provide full protection. • Choose a waterproof sunscreen. Remember, even water-resistant sunscreens should be reapplied often, about every 2 hours. • Apply sunscreen generously and evenly so as not to miss any areas of sun-exposed skin. Keep sunscreen out of your eyes. If it makes your eyes sting, make sure you use a pure, so-called “chemical-free” product on your face; however, such “chemical-free” products generally require more rubbing to get them to disappear. • Choose a broad-spectrum sunscreen that blocks both ultraviolet B (UVB, the burning rays) and ultraviolet A (UVA, the more penetrating rays that promote wrinkling and aging). • Excellent choices for infants and young children are Neutrogena Sensitive Skin UVA/UVB SPF 30 and Vanicream (SPF 15). Both are “chemical-free,” opaque, physical sunscreens that contain titanium dioxide or zinc oxide, which block, reflect, or scatter UV energy. They provide good coverage, are waterproof, and cause fewer allergic reactions than other sunscreens. • Be aware that moisturizers that contain built-in sunscreens usually have a lower SPF. When tested against one another, all name-brand sunscreens performed well, so choose one based on such factors as feel, absorbency, and price. Gel (alcohol)-based products disappear into the skin quickly. Each dermatologist has his or her own favorite, but you should experiment until you find your own favorite. Mexoryl-containing sunscreens from LaRoche-Posay (brand name Anthelios) have a better UVA-blocking capability than traditional sunscreens. This sunscreen may be used by anyone but may be especially helpful for people with sun-sensitive diseases such as lupus or “sun poisoning” (polymorphous light eruption), or those taking medications that make them sun sensitive. continued on page 106

Co n sejo s Pa ra Pro t ejerse Co n t ra el So l Cualquier persona que tenga una historia clínica familiar de cáncer en la piel o que tenga piel clara, que en lugar de broncearse se quema con facilidad, debe aplicarse bloqueador solar. Aparte del cáncer en la piel, la exposición prolongada al sol causa arrugas, manchas, “rompimiento” de los vasos sanguíneos (se dilatan) y que la piel envejezca. Las siguientes son recomendaciones de la Fundación de Cáncer en la Piel, modificadas: • Evite exponerse al sol durante las horas entre 10 a.m. y 4 p.m., cuando el sol es más fuerte. • Cubra su cabeza con sombreros de ala ancha, gorras o cachuchas; use camisas de manga larga y pantalones o faldas largas. • Aplique bloqueador por lo menos 30 minutos antes de exponerse al sol. Use un bloqueador con factor de protección solar (SPF) 15 o más alto para prevenir quemaduras. Para que el bloqueador pueda cumplir su función, reaplique cada 2 a 3 horas, especialmente después de nadar, secarse con la toalla, o sudar. • Aplique bloqueador aún en días nublados. • Tome nota que la luz del sol se refleja en la arena, con el agua, o en la nieve. Los rayos ultravioleta (UV) rebotan en estas superficies. Las sombrillas de playa y otros techos que proveen sombra son una buena idea, pero no proveen protección completa. • Escoja un bloqueador a prueba de agua. Recuerde que incluso los bloqueadores que resisten el agua deben ser reaplicados con regularidad, por ejemplo, cada dos horas. • Aplique el bloqueador generosamente y espárzalo bien, no se salte ningún área de la piel que se exponga al sol (como las orejas o los dedos de los pies). Evite el contacto con los ojos. Si le arden los ojos, escoja un producto “chemical-free” (libre de químicos) para su cara; estos productos generalmente requieren que los frote más para que desaparezcan. • Escoja un bloqueador de amplio espectro que bloquee tanto los rayos ultravioleta B (UVB, los que queman) como los rayos ultravioleta A (UVA, los que penetran para arrugar y envejecer la piel). • Tanto Neutrogena Sensitive Skin (piel sensible) UVA/UVB (SPF 30) como Vanicream (SPF 15) son excelentes productos para bebés y niños pequeños. Ambos son libres de químicos, opacos, y contienen dióxido de titanio u óxido de zinc que bloquean, reflejan, o dispersan la energía UV. Cubren bien, son resistentes al agua, y causan menos reacciones alérgicas que otros bloqueadores. • Note que las cremas hidratantes que contienen bloqueador solar generalmente tienen muy bajo SPF. Los bloqueadores solares han sido examinados a fondo y todas las marcas tuvieron buenos resultados, así que escoja uno basado en textura, absorción, y precio. Los productos en gel, con base de alcohol, desaparecen en la piel rápidamente. Cada dermatólogo tiene su bloqueador favorito, pero usted puede experimentar con varios hasta que uno le agrade. Los bloqueadores que contienen Mexoryl de LaRoche-Posay (marca Anthelios) tienen mejor protección contra los rayos UVA que los bloqueadores tradicionales. Este bloqueador puede ser usado por cualquiera, pero es especialmente benéfico para gente con enfermedades sensibles al sol como lupus, fotosensibilidad (erupciones polimorfas), o que tomen medicamentos que los hacen sensibles al sol. continued on page 107

Continued from page 104

F urther advice • Avoid tanning beds! The UV light from tanning beds causes skin cancer and wrinkling. UVA light goes deep in the skin and contributes to photoaging, causing wrinkling, brown spots, leathery skin, and skin cancer. • Keep infants out of direct sunlight. • Teach children about sun protection at a young age. • Wear UV-blocking sunglasses. • Most clothing absorbs or reflects UV rays. However, lighter colored and loosely knit fabrics as well as wet clothes that cling to the skin do not offer much protection. The tighter the weave, the more sun protection the clothing offers. • If you tan easily, you may use a sunscreen with a lower SPF number. • Lips are also sun sensitive, so use special lip-coating sunscreens that have a waxy base. • You can use self-tanning preparations that dye the skin (self-tanning lotion and spray products), but be aware that they offer very little sun protection, unless they are combined with a sunscreen. • Certain drugs can make you more likely to burn, such as tetracycline and doxycycline, diuretics (“water pills”), and certain oral antidiabetic medications. • Remember, there is no such thing as a healthy or safe tan!

Continued from page 105

Más consejos • ¡Evite ir a salones de bronceado! La luz UV de las camas de bronceado causan cáncer en la piel y arrugas. La luz UVA penetra profundamente en la piel y contribuye al fotoenvejecimiento, causando arrugas, manchas cafés, piel con aspecto de cuero, y cáncer. • Mantenga a los bebés alejados de los rayos directos del sol. • Instruya a los niños a protegerse del sol desde una edad temprana. • Use anteojos de sol que bloqueen rayos UV. • Mucha ropa absorbe o refleja los rayos UV, sin embargo, la ropa de colores claros, tejida con puntos anchos, o mojada y pegada a la piel, no ofrece mucha protección. Los tejidos o tramas estrechos ofrecen más protección. • Si se broncea con facilidad, puede usar un bloqueador con menor número de SPF. • Los labios también son sensibles al sol. Use protectores de labios con bases de cera y bloqueador solar. • Puede usar lociones de auto-bronceado para pigmentar su piel (hay productos en crema, loción, y aerosol), pero recuerde que no ofrecen protección solar, los tiene que combinar con un bloqueador. • Ciertos medicamentos como la tetraciclina y doxiciclina, los diuréticos, y ciertos medicamentos orales contra la diabetes pueden facilitar que su piel se queme con el sol. • ¡Recuerde, no hay tal cosa como un bronceado saludable o seguro!

Tin ea Ca p it is What is tinea capitis? • Tinea capitis, or “ringworm” of the scalp, which is sometimes referred to as “wigworm,” is a superficial fungal infection of the hair shaft that most commonly appears in young children. What does it look like? • Inflamed, scaly, often hairless patches, mimicking “cradle cap,” are especially common in infancy. • Toddlers may have a scaling rash with many round areas, without hair. Tinea capitis What are its symptoms? • Itching, rubbing, and possible hair loss occur. • Tender lumps known as kerions may also occur. Who gets it? • In the United States, young African-American children are most often affected. • Trichophyton tonsurans is, by far, the most common fungus that causes this condition. Other fungi such as Microsporum audouinii, which is spread from human to human, and Microsporum canis, which is spread from animals (cats and dogs), are more often seen in white children. Tinea capitis Is it contagious? • Yes, tinea capitis is very contagious and is generally spread by person-to-person contact. In fact, some adults exposed to a child with tinea capitis have been shown to be carriers. • The fungus has also been isolated from objects such as hairbrushes and pillows. How is it diagnosed? • Hairs may be gently plucked as samples for a fungal culture, or plucked hairs or scale may be obtained with gentle brushing with a toothbrush. This is done to confirm the diagnosis. • In the past, a special black light known as a Wood’s light was a valuable screening tool to diagnose tinea capitis easily, but it has lost its usefulness, because nowadays most cases are caused by fungi that do not fluoresce. How is it treated? • Oral antifungal medications are very effective in treating and curing tinea capitis. • Topical therapy is of little or no value, although an antifungal shampoo such as ketoconazole may be used by the infected person and contacts to prevent reinfection and spread. • Griseofulvin • In children, oral treatment with a liquid suspension of griseofulvin is the mainstay of therapy. • Griseofulvin should be given with milk or food, which increases its absorption. It should be continued until your child is cured, generally in 6 to 8 weeks. Some children may require longer therapy. What are some newer treatments? • Itraconazole (Sporanox) and terbinafine (Lamisil) are newer oral medications and can be used in some cases of in which griseofulvin is not effective. • In children reluctant to swallow tablets, there is a new “child-friendly” Lamisil. This can be sprinkled on the food of a child who may not like to take medicine. Helpful hints • An itchy, scaly rash with or without hair loss is not always “ringworm.” • A fungal culture or fungal hair analysis may be necessary before treatment is given. • Other common causes of an itchy, scaly scalp in children include atopic dermatitis (eczema) or seborrheic dermatitis. Alopecia areata is another cause that may be responsible for hair loss.

Tiñ a Ca p it is ¿Qué es la tiña capitis? • Tiña capitis, o tiña del cuero cabelludo, es una infección micótica superficial del cabello que aparece comúnmente entre la infancia y la pubertad. ¿Cómo es? • Se presenta en parches inflamados, con escamas, en ocasiones sin pelo, parecidos a la “costra láctea,” especialmente en la infancia. • Los niños pequeños pueden tener un sarpullido con muchas áreas circulares, sin pelo. Tiña capitis

¿Cuáles son los síntomas? • Es posible que haya comezón, prurito, y pérdida de cabello. • Puede desarrollar lesiones inflamatorias exudativas con áreas de cicatrices tipo kerion. ¿A quién le da? • En los Estados Unidos, los más afectados son niños Afroamericanos. • El Trichophyton tonsurans es, por mucho, el hongo más común que causa esta condición. Otros hongos como el Microsporum audouinii, que se contagia de persona a persona, y el Microsporum canis, que se contagia por animales (perros y gatos), son vistos principalmente en niños caucásicos.

Tiña capitis con kerion

¿Es contagiosa? • Sí, la tiña capitis es muy contagiosa y generalmente se pasa de persona a persona por contacto. De hecho, algunos adultos expuestos a niños con tiña capitis son portadores. • El hongo se ha encontrado en objetos como cepillos y almohadas. ¿Cómo se diagnostica? • Con pinzas se puede extraer una muestra de cabello para un cultivo micótico, o se puede tomar una muestra de las escamas delicadamente con un cepillo de dientes. Con esto se confirma el diagnóstico. • Antes se usaba luz negra para diagnosticar la tiña capitis porque permitía ver el hongo, pero ya no es útil porque la mayoría de los casos hoy en día son causados por hongos que no son fluorescentes. ¿Cómo se trata? • Los medicamentos orales antimicóticos son muy efectivos para tratar y curar la tiña capitis. • La terapia tópica casi no ayuda, aunque la persona infectada (y quien este en contacto con ella) puede usar un shampoo antifungal como ketoconazol, para prevenir contagio o reinfección. • Griseofulvina • En niños, la terapia principal es un tratamiento oral con griseofulvina en suspensión líquida. • La griseofulvina se debe tomar con leche o comida para aumentar la absorción. Se debe continuar la terapia hasta que el niño se cure, y puede tardar de 6 a 8 semanas o más. ¿Cuáles son los nuevos tratamientos? • Itraconazole (Sporanox) y terbinafine (Lamisil) son medicamentos orales que se pueden usar en algunos casos si la griseofulvina no funciona. • Para niños que no toman pastillas, hay un nuevo Lamisil “infantil.” Se puede espolvorear sobre la comida del niño si no quiere tomar medicina. Consejos • Un parche con prurito o escamas o comezón, no siempre es tiña, haya o no pérdida de cabello • Puede ser necesario hacer un cultivo micótico o un análisis de hongos del cabello para poder prescribir un medicamento. • Otras causas comunes de comezón o escamas en el cuero cabelludo de niños incluyen la dermatitis atópica (eczema) o seborreica. La alopecia areata es otra causa posiblemente responsable de la pérdida de cabello.

Tin ea Cr u ris ( Jo ck

It ch )

What is tinea cruris? • Tinea cruris is a very common superficial skin infection caused by a fungus. Those everpresent TV commercials are evidence of just how widespread this rash is. • The fungus tends to grow in a warm, moist, sweaty environment such as that found in the groin, buttocks, and upper thighs. The pubic area may also be involved. • The rash tends to spare the scrotal area and penis. If these areas are involved, other conditions such as psoriasis or eczema should be considered. Who gets it? • It’s seen mostly in men and teenage boys but is not unusual in women. • The fungus that causes tinea cruris is not very contagious, and the likelihood of its spread between sexual partners appears to be very small. What are the symptoms? • Itching or burning and sometimes pain may occur. • The infection may also be associated with an unpleasant odor. • Redness, scaling, and sometimes cracking (“fissures”) of the skin may be apparent. How is it treated? • Topical antifungal over-the-counter medications such as Nizoral, Lamisil, Lotrimin, Micatin, and Tinactin are usually very effective. • If necessary, a prescription topical antifungal medication such as __________________ may be given to you by your health care provider. • Wetness, oozing, or cracking of the skin may be soothed and dried by using Burow’s solution, which can be obtained without a prescription. Burow’s solution is applied as wet compresses for 10 minutes twice a day until the oozing stops. • The topical antifungal is applied after soaking with Burow’s solution. Systemic (oral) antifungal therapy may be necessary in cases that do not respond to topical therapy or for extensive chronic recurrent tinea cruris. How can it be prevented? • Decreasing wetness and friction helps. Try the following methods: • Frequent changes of underwear and avoidance of tight underpants or boxer shorts • Absorbent powders such as Zeasorb-AF or baby cornstarch • Avoidance of soap to affected areas during itchy, red periods • Thorough “pat” drying or using a hairdryer Keep in mind • Rashes of the groin are not always fungal infections! • The symptoms and a similar rash may be a result of other causes. • In fact, if a child under the age of 12 has what appears to be tinea cruris, it’s probably another skin condition such as eczema.

Tinea cruris

Tiñ a Cr u ra l

(“Tiñ a In gu in a l”)

¿Qué es la tiña crural? • La tiña crural es una infección de la piel muy común, causada por un hongo. Todos esos comerciales de TV son evidencia de lo abundante que es. • El hongo tiende a crecer en ambientes cálidos, húmedos, y con sudor, como el que se encuentra en la ingle, los glúteos y los muslos. También puede incluir el área púbica. • El sarpullido tiende a evitar el escroto y el pene. Si existen molestias en éstas áreas, se deben considerar otras condiciones como psoriasis o eczema. Tiña crural

¿A quién le da? • Se ve generalmente en hombres y adolescentes pero no es inusual en mujeres. • El hongo que causa la tiña crural no es muy contagioso, y la posibilidad de que se pase entre parejas sexuales es mínima. ¿Cuáles son los síntomas? • Puede haber comezón o ardor y a veces dolor. • La infección se puede asociar con un olor desagradable. • Puede haber rojez, escamas y a veces agrietamiento (“fisuras”) en la piel. ¿Cómo se trata? • Los medicamentos antimicóticos tópicos como Nizoral, Lamisil, Lotrimin, Micatin, y Tinactin normalmente son muy efectivos. • Si fuera necesario, su doctor puede recetar otro antimicótico tópico como __________________. • La solución de Burow alivia las molestias cuando hay humedad, exudación, o fisuras en la piel y se puede conseguir sin receta médica. La solución de Burow se aplica en compresas mojadas durante 10 minutos, dos veces al día. • El antimicótico tópico se aplica después de haber aplicado la solución de Burow. Puede ser necesario recetar una terapia antimicótica sistémica (oral) en casos extensos, crónicos, recurrentes de tiña crural o que no responden a la terapia tópica. ¿Cómo se puede prevenir? • Reducir la humedad y la fricción ayuda. Trate los siguientes métodos: • Cambie frecuentemente su ropa interior y evite usarla muy estrecha o pegada. • Use talcos absorbentes como Zeasorb-AF, de bebé, o de almidón de maíz. • Evite usar jabón en las áreas afectadas mientras estén rojas y ardan o den comezón. • Seque bien el área, pero delicadamente con suaves “palmaditas” de la toalla o con secadora de pelo. Recuerde • ¡No todos los sarpullidos en la ingle son infecciones micóticas! • Los síntomas y una rozadura similar pueden atribuirse a otras causas. • De hecho, si un niño menor de 12 años tiene algo que parece tiña crural, probablemente es otra condición de la piel, como eczema.

Tin ea Versico lo r What is tinea versicolor? • Tinea versicolor, also known as pityriasis versicolor, is a very common, harmless, noncontagious yeast infection of the skin. • It’s not considered contagious because the yeast is a normal inhabitant of just about everybody’s skin. What does it look like? • Light or dark spots or patches can be seen scattered on the chest, back, abdomen, and upper arms. The skin discoloration varies from white to pink to red, tan, brown, or even black. A fine, dustlike scale often covers the spots. • People who have tinea versicolor often complain that the involved skin fails to tan in the summer and that sometimes it is a little itchy. • Tinea versicolor becomes more noticeable in the summer because your skin’s warmth and moisture help the yeast grow. Also, as the rest of your skin tans in the sun, lighter spots become more noticeable, especially against a background of dark skin. • The spots tend to fade in cool weather.

Tinea versicolor: White

Can it be cured? • Tinea versicolor may last for years and finally disappear on its own. Tinea versicolor: Faun How is it treated? By your health care provider • Obtain the prescription-strength shampoo or lotion ______________, if you have received a prescription. • Use this medication to form a lather all over, including beyond the affected areas. • Let soak for about 10 minutes and then rinse off in the shower. • Do this for 3 or 4 weeks and: • After showering and using the prescribed shampoo, use a prescription antifungal cream, lotion, or spray such as _________________, which you also may have received from your health care provider. Apply it to all affected spots. Do this for 3 or 4 weeks, too. • It’s also a good idea to repeat this routine before the next warm season or before taking a tropical vacation. (It’s a good idea to note this on your calendar.) • To treat stubborn cases, sometimes your health care provider will prescribe an oral antifungal medication such as ________________, which you take for _______ days; however, this does not prevent recurrences. On your own • Sometimes, you can clear tinea versicolor by using shampoos such as Nizoral or Head & Shoulders. • Make a lather with these shampoos all over, as described above. • After showering, apply an antifungal preparation such as miconazole (Micatin), clotrimazole (Lotrimin), or Lamisil. • All of these preparations are available over the counter; you don’t need a prescription. • Do this for 3 or 4 weeks, as described above. What you can expect • The scale of this rash disappears after a few treatments, but it may take months for your skin to return to its normal color. • This slow return of color is part of the usual healing process and does not mean that the treatment has failed.

Tinea versicolor: Tan

Tiñ a Versico lo r ¿Qué es la tiña versicolor? • La tiña versicolor, también conocida como pitiriasis versicolor, es una infección micótica de la piel, muy común, inofensiva, y no es contagiosa. • No se considera contagiosa porque el hongo (un tipo de levadura) es habitual de la piel.

Tiña versicolor: Blanca

¿Cómo es la tiña versicolor? • Parches de color claro u oscuro se pueden ver esparcidos en el pecho, la espalda, el abdomen, y los brazos. La decoloración de la piel varía de blanca a rosácea a rojiza, o de morena a café y hasta negra. A veces hay escamas finas como polvosas sobre las manchas. • Quienes tienen tiña versicolor se quejan de que la piel afectada no se broncea con el sol y que a veces hay comezón. • La tiña versicolor se nota más en el verano porque el calor y la humedad promueven el crecimiento del hongo en la piel. También porque cuando la piel se broncea, las manchas claras se vuelven más notables contra el nuevo color oscuro del resto de la piel. • Las manchas generalmente se desvanecen cuando el clima enfría. ¿Se puede curar? • La tiña versicolor puede durar años y finalmente desaparecer por si misma.

Tiña versicolor: Cervato ¿Cómo se trata? Por su médico • Obtenga un shampoo o loción medicado como ______________, bajo receta médica. • Use este medicamento para crear una espuma y aplique a todas las áreas, incluso las que no estén afectadas. • Deje la espuma puesta por 10 minutos y enjuague en la regadera. • Haga esto durante 3 o 4 semanas. • Después de bañarse con el shampoo medicado, use una crema, loción o aerosol antimicótico como _________________, que probablemente también le recetó su médico. Aplique a las áreas afectadas. Haga esto durante 3 o 4 semanas también. • Conviene repetir esta rutina antes de la próxima temporada de calor o antes de ir de vacaciones a la playa. (Sería buena idea anotarlo en su calendario). • Para tratar casos difíciles, su medico puede recetar un medicamento oral antimicótico como ____________, que puede tomar por ____ días; sin embargo, esto no previene que reincida.

Tiña versicolor: Canela

Por su parte • A veces puede tratar la tiña versicolor usando shampoos como Nizoral o Head & Shoulders. • Haga espuma, aplique a todas las áreas, y déjela puesta durante 10 minutos, como se describió anteriormente. • Después de bañarse y enjuagarse, aplique una crema como miconazol (Micatin), clotrimazol (Lotrimin), o Lamisil. • Todos estos productos los puede comprar en cualquier farmacia sin necesidad de receta médica. • Este proceso también debe durar entre 3 o 4 semanas. Lo que puede esperar • Las escamas de las zonas afectadas desaparecen tras un par de tratamientos, pero pueden pasar meses antes de que la piel recobre su color normal. • El tardado regreso del color es parte del lento proceso de curación; sin embargo, no significa que el tratamiento esté fallando.

Vit iligo What is vitiligo? • Vitiligo is a skin condition characterized by white patches resulting from a loss of skin pigment. Who gets it? • Vitiligo affects 1% to 2% of the world’s population. Thirty percent of these people report a family history of the disorder. • It’s infrequently associated with certain autoimmune diseases, and your health care provider may suggest that you have certain blood tests.

Vitiligo

What causes it? • Although the cause of vitiligo is still unknown, one theory is that it results from the body’s immune system making antibodies to its own pigment cells. These antibodies attack the pigment-producing cells of the skin (melanocytes). What does it look like? • Occasionally, the spots may have various shades of color and may include dotlike “islands” of repigmentation. Such repigmentation “islands” are a good sign—they mean that the skin is recruiting new pigment cells from the hair follicles and trying to repigment itself. • In dark-skinned people, pigment loss may be observed at any time of year, whereas in light-skinned people, the white spots may be most obvious in the summer, because the tanning effects of the summer sun can intensify the contrast between the light and dark skin. How is it treated? • Topical corticosteroids are occasionally helpful in promoting repigmentation. • Recently, the application of tacrolimus or pimecrolimus ________ twice daily has shown some promising results in repigmentation of vitiligo. • Special cosmetic makeup that’s formulated to match a person’s normal skin color (e.g., Dermablend or Covermark) or self-tanning products that contain dihydroxyacetone, such as ___________________, may be very effective at hiding the white spots. • Sunscreens can be used to avoid deepening the contrast between normal skin and lesions and to protect the light-colored patches, which are sensitive to the sun.

Vitiligo

Vit íligo ¿Qué es vitíligo? El vitíligo es una enfermedad de la piel caracterizada por parches blancos que resultan de la pérdida de pigmento en la piel.

Vitíligo

¿A quien le da vitíligo? • El vitíligo afecta del 1% al 2% de la población del mundo. Treinta por ciento de estas personas reportan que ha habido vitíligo en la familia. • A veces se asocia con enfermedades autoinmunes, por lo que su médico puede sugerir exámenes de sangre. ¿Qué lo causa? • Aunque la causa del vitíligo es desconocida, una de las teorías es que lo ocasiona el sistema inmunológico. El sistema inmunológico crea anticuerpos que atacan a las células que producen pigmento (melanocitos).

Vitíligo

¿Cómo es el vitíligo? • Ocasionalmente las manchas tienen variaciones en color y pueden incluir “islas” o puntos de repigmentación. Estas “islas” son buenas señales—significa que la piel está reclutando nuevas células para crear pigmento y se está repigmentando a sí misma. • En gente morena o de piel oscura, la pérdida de pigmento se nota en cualquier época del año; pero en gente de piel clara, las manchas blancas se comienzan a notar durante el verano, cuando gracias a la exposición al sol o al bronceado, se intensifica el contraste entre la piel normal y la que le falta pigmento. ¿Cómo se trata? • Los corticoesteroides tópicos ocasionalmente ayudan a promover la repigmentación. • Recientemente, la aplicación de tacrolimus o pimecrolimus ________ dos veces al día ha tenido resultados positivos de repigmentación en vitíligo. • El maquillaje cosmético especial formulado para igualar el color de la piel (como Dermablend o Covermark) o productos de autobronceado que contienen dihydroxyacetone como _____________ pueden ser muy efectivos para disimular las manchas blancas. • Los bloqueadores del sol se pueden usar para evitar obscurecer el resto de la piel y que no se note tanto el contraste y para proteger a los parches claros, que son muy sensibles al sol.

Wa rt s What are warts? • Warts are skin growths caused by a viral infection in the outer layer of skin. • Warts are very common, particularly in children. An estimated 20% of school-age children at some time have at least one wart. • In children, warts tend to disappear over a period of several months to years, but sometimes they can be very stubborn and resistant to many types of treatment. • In many adults, warts often prove even more difficult to destroy. What causes them? • All warts are caused by a type of virus, the human papillomavirus HPV.

Warts

What do they look like? Their appearance depends on their location. • Common warts generally grow on the hands and fingers and around the nails. They are frequently seen on the knees and elbows, especially in children. They usually have a bumpy, cauliflowerlike appearance. • Plantar (not “planter’s”) warts are located on the soles of the feet. When they grow in clusters, they are known as mosaic warts. Plantar warts often have “black dots.” • Flat warts are small, smooth, skin colored, and flat. In children, they are most often seen on the face. In adults, they are seen on the legs in women and on the face in both sexes. Shaving tends to spread them. How are they treated? The choice of one or more of the following methods of treatment depends on: the type of wart, the location of the wart(s), and the age of the patient. Home treatment Peeling agents that contain salicylic acid • These are available in over-the-counter products such as Duofilm, Occlusal, and Compound W. Also, 40% salicylic acid plasters that are cut to the size of the wart are available. These preparations provide the best treatment for small children in whom warts often disappear on their own. • For best results, the affected area should be hydrated first by soaking it in warm water for five minutes before applying the medication. • It’s also a good method for plantar warts—one that’s painless, inexpensive, and doesn’t require office visits.

Filiform (threadlike) warts

F lat warts

Office treatment Freezing (cryotherapy with liquid nitrogen) • Liquid nitrogen is applied with a cotton swab or with a cryotherapy “freezing gun.” • Freezing is best for warts on hands. • It’s fast, and many warts can be treated on each visit; however, it can be painful and may require many office visits. Burning and scraping (light electrocautery and blunt dissection) • This method is best for warts on the knees, elbows, and backs of the hands. • The pain is bearable in most adults, but it requires local anesthesia and may cause scarring.

Plantar warts

Other office treatments • Lasers, blistering chemicals (“bug juice”), and acids are just a few of many treatments that are being used to treat warts. • There have been reports of the successful use of Aldara cream on flat warts, some common warts, and plantar warts. You need a prescription for Aldara cream. continued on page 118

Plantar warts (mosaic)

Ver ru ga s ¿Qué son las verrugas? • Las verrugas son crecimientos causados por una infección viral en las capas superficiales de la piel. • Las verrugas son muy comunes, particularmente en niños. Alrededor de 20% de niños en edad escolar han tenido por lo menos una verruga. • En los niños las verrugas suelen desaparecer después de algunos meses o años, pero a veces son muy obstinadas y resistentes a los tratamientos. • En los adultos, las verrugas son aún más difíciles de eliminar. Verrugas ¿Qué causa verrugas? • Todas las verrugas son causadas por el virus del papiloma humano (HPV o papilomavirus). ¿Cómo son las verrugas? Su apariencia depende de su ubicación. • Verrugas comunes—generalmente crecen en las manos y dedos y alrededor de las uñas. Se ven frecuentemente en las rodillas y en los codos, especialmente en niños. Generalmente son brotes abultados con apariencia de coliflor. • Verrugas plantares—se localizan en las suelas de los pies y a veces tienen puntitos negros. Cuando crecen en grupos se les llama verrugas en mosaico. • Verrugas planas—son pequeñas, lisas, del color de la piel, y planas. En niños aparecen comúnmente en la cara. En adultos, aparecen en las piernas de las mujeres y en la cara en ambos sexos. Suelen esparcirse cuando se afeitan. Verruga filiforme (como de hilo)

¿Cómo se contagian y cómo se evitan? Aún si nunca besa a nadie, nunca saluda de mano a nadie, nunca camina descalzo, y decide vivir en una burbuja, aún así puede contraer una verruga. ¿Cómo se tratan? La elección de uno o más de los siguientes métodos de tratamiento depende de: la clase de verruga, su ubicación, y la edad del paciente.

Verrugas planas

Verrugas plantares

Verrugas plantares (mosaico)

Tratamiento en casa Agentes que contienen ácido salicílico • Estos productos están disponibles en farmacias sin necesidad de receta médica: Duofilm, Occlusal, y Compound W. También hay parches con 40% ácido salicílico que se cortan al tamaño de la verruga. Estos tratamientos son los mejores para niños pequeños en quienes las verrugas generalmente desaparecen por sí mismas. • Para mejores resultados, el área afectada debe ser hidratada primero: remójela en agua tibia durante 5 minutos antes de aplicar el medicamento. • También es un buen método para las verrugas plantares—sin dolor, barato, y no requiere de consulta médica. Tratamiento en el consultorio Congelamiento (crioterapia con nitrógeno líquido) • El nitrógeno líquido se aplica con un hisopo o por medio de crioterapia. • El congelamiento es el mejor para las verrugas en las manos. • Es rápido y se pueden tratar muchas verrugas en una visita; sin embargo, puede ser doloroso y puede requerir de varias visitas. Quemado y raspado (electrocauterización y disección) • Este método es mejor para las verrugas en las rodillas, codos, y manos. • El dolor es tolerable para muchos adultos, pero requiere de anestesia local y puede dejar cicatrices. continued on page 119

Continued from page 116

How do I know when the warts are gone? When they don’t come back. How do you get warts and how do you avoid spreading warts to others? Never shake hands! Never kiss anyone! Never walk barefoot! Live in a bubble! And you still can get ‘them and spread them. Wart facts • As you can see, the numerous treatments that are used for warts are testimony to the fact that we don’t have any definite “cure” for them. • More often than not, warts tend to “cure” themselves over time. • The hero of successful wart treatment is usually the last person to treat the wart or the last person to recommend a treatment before the wart goes away. • The “wart hero” may have been a wart charmer, a hypnotist, or a person who recommended a folk medicine, such as the application of garlic or aloe vera, or even . . . a dermatologist!

Continued from page 117

Otros tratamientos en el consultorio • Los lásers, químicos que ampollan, y ácidos, son algunos de los muchos tratamientos que se usan contra las verrugas. • Ha habido reportes del uso exitoso de la crema Aldara en verrugas planas, algunas verrugas comunes, y verrugas plantares. Necesita de una receta médica para conseguir la crema Aldara. ¿Cómo sé que las verrugas se eliminaron? Cuando no regresan. ¿Cómo sé contraen verrugas y cómo sé evita tener verrugas y transmitiralas? ¡Nunca estreche manos! ¡Nunca dese a nadie! ¡Nunca camine desalzo! ¡Viva aislado! Y aun asi las puede contraer transmitiralas. Datos sobre las verrugas • Como puede ver, los numerosos tratamientos utilizados contra las verrugas son testimonio de que no sabemos en definitiva como “curarlas.” • Generalmente, son las verrugas mismas las que suelen “curarse” a sí mismas con el tiempo. • El héroe, el mejor curador de verrugas, es generalmente la última persona que vio al paciente o que recetó el último medicamento antes de que la verruga desapareciera por sí misma. • Por lo tanto, el “héroe de la verruga” puede haber sido un charlatán, un hipnotista, un curandero que recetó aplicar ajo o aloe vera, o incluso hasta . . . ¡un dermatólogo!

Index Note: Page numbers followed by “f” indicate figure, and “t” indicate table.

A ABCDE criteria, 414–416, 414f–417f Acantholytic dermatosis, transient, 532t Acanthosis, 49 Acanthosis nigricans, 286–287, 286f, 287f benign, 286–287 in diabetics, 286f, 287f, 460, 460f malignant, 287 Acetaminophen, for herpes zoster, 165 Acetic acid (vinegar) for green nail syndrome, 262 as topical therapy, 13 Acitretin (Soriatane) for atopic hand eczema, 70 for exfoliative dermatitis, 490 for lichen planus, 125 for psoriasis, generalized plaque, 99 for Reiter’s syndrome, 484 Acne from Agent Orange, 48 classification of, 23 comedo in, 24, 25f “cystic,” 26, 27f–28f from dioxins, 48 drug-exacerbated, 48 drug-induced, 48 endocrinopathic, 48 epidemiology of, 23 general points on, 38 hyperpigmentation from, 284, 284f macules in, 25f neonatal, 48 nodular, 26, 27f–28f nodules in, 25f, 26, 27f overview of, 23 papules in, 24, 25f papulopustular, 26 pustules in, 24, 25f scars from, 27f from steroids, 133 Acne, adolescent, 24–29 clinical manifestations and sequelae of, 28, 28f diagnosis of, 28 hyperpigmentation after, 28, 28f vs. keratosis pilaris, 29, 29f lesions in distribution of, 28 inflammatory, 25f–27f, 26 noninflammatory (comedonal), 25f, 26, 27f myths vs. facts on, 24 overview of, 23

pathophysiology of, 24, 24f–25f scars from, 27f severity of, 26, 27f–28f Acne, postadolescent (adult-onset), 38–40, 39f Acne conglobata, 26, 27f–28f “Acne cosmetica,” 38 Acne excoriée des jeunes filles, 48, 48f Acneiform conditions/eruptions, 23 classification of, 23 drug-induced, 298, 301, 301f from topical steroids, 16, 16f Acne inversa, 48 Acne keloidalis, 235, 235f Acnelike disorders, 23 Acne management, adolescent, 29–37 comedo extraction, 35 compliance in, 37 corticosteroid injection, intralesional, 35 general principles in, 29 goals in, 29 laser and light therapy, 35–36 points to remember on, 36 rollercoasting in, 37 systemic antibiotics, oral, 32–34 chemical peels, office-based, 36 hormonal, 34 overview of, 32 retinoids (isotretinoin), oral, 34–35 trimethoprim-sulfamethoxazole, 34 topical therapies alpha- and beta-hydroxy acids, 32 antibiotic-benzoyl peroxide combination, 31–32, 31t antibiotics, topical, 31, 31t azelaic acid, 32 benzoyl peroxide, 29–30, 30t multi-ingredient products, 32 over-the-counter, 32 retinoids, topical, 30–31, 30t, 37 retinols, 32 Acne rosacea. See Rosacea Acne vulgaris. See Acne, adolescent Acral lentiginous melanoma, 420–421, 420f, 421f Acrochordons, 375–376, 375f, 376f Acrodermatitis chronica atrophicans (ACA), 345 Acrodermatitis papulosa, 524t Acropustulosis of infancy, 524t Acrosclerosis, 477, 477f Actinic cheilitis, 396, 396f

Actinic keratosis. See Solar keratosis Actinic purpura, 313, 313f Acute cutaneous lupus erythematosus (ACLE), 466 Acute hemorrhagic edema of infancy, 529t Acyclovir (Zovirax) for erythema multiforme from herpes simplex, 312 for herpes simplex, 159–160 for herpes simplex, HIV-associated, 440 for herpes simplex genitalis, 331 for herpes zoster, 165 for herpes zoster, HIV-associated, 441, 441f for oral hairy leukoplakia, HIV-associated, 452 for varicella, 196 Adalimumab (Humira), for exfoliative dermatitis, 490 Adenoma sebaceum, 493, 493f Adolescent acne. See Acne, adolescent Adrenocorticotropic hormone, acnelike lesions from, 48 Adult-onset acne, 38–40, 39f Aerosols, 15 Agent Orange, acne from, 48 Albendazole, for cutaneous larva migrans, 362 Alcohol for jellyfish sting, 359 for Portuguese man-of-war sting, 359 Alefacept (Amevive), for generalized plaque psoriasis, 100 Alitretinoin (Panretin), for HIV-associated Kaposi’s sarcoma, 446 Allergens. See also specific allergens allergic contact dermatitis from, 65–66, 65f, 66f on atopic dermatitis, 59 top ten, 66 Allergic contact dermatitis, 63–66. See also Contact dermatitis other forms of, 65–66, 65f rhus dermatitis, 50, 50f, 63–65, 63f Alopecia androgenic, 215–217, 215f, 216f (See also Androgenic alopecia) central centrifugal cicatricial, 229, 229f diffuse, 222–226 anagen effluvium, 225, 225f senescent alopecia, 226 telogen effluvium, 222–224, 222f

Alopecia (continued) frontal fibrosing, 229 hot-comb, 229, 229f scarring, 227–232 (See also Scarring alopecia) senescent, 226 traction, 230, 230f Alopecia areata, 218–221, 218f–220f basics of, 218 clinical manifestations of, 219, 219f diagnosis of, 219 differential diagnosis of, 220, 220f helpful hint on, 221 lesion distribution in, 219, 219f lesions in, 218, 218f management of, 220 pathogenesis of, 218 points to remember on, 221 vs. tinea capitis, 178, 178f Alopecia totalis, 218 Alopecia universalis, 218 Alpha-hydroxy acid for adolescent acne, 32 for melasma, 283 Aluminum acetate. See Burow’s solution (aluminum acetate, Domeboro) 5-Aminosalicylic acid, for pyoderma gangrenosum, 487 Amitriptyline for brachioradial pruritus, 292 for postherpetic neuralgia, 166 Ammonium lactate (Lac-Hydrin, AmLactin) for asteatotic eczema, 76, 296 for HIV-associated drug eruptions, 454 for xerosis, 296 Amorolfine nail lacquer, for onychomycosis, 186 Amoxicillin for adolescent acne, 33 for Lyme disease, 348 for rosacea, 44 Amyopathic dermatomyositis, 475 Anabolic steroids, acne from, 48 Anagen effluvium, 225, 225f Anagen phase, 237, 237f Androgenic alopecia, 215–217 basics of, 215 clinical manifestations of, 216 diagnosis and differential diagnosis of, 216 female-pattern, 215, 215f, 216f hair loss in, 215 lesions and lesion distribution in, 216 male-pattern, 215, 215f management of, 217 pathogenesis of, 215 points to remember on, 217 Androgens, acne from, 48 Angel’s kisses, 520t Angiofibromas, 384, 384f Angiokeratomas, 390, 390f

538

Index

Angiolipoma, 380, 380f Angiomas, 389–390, 389f Annular lesions, 11, 11f Anogenital warts, 321–327 basics of, 321 clinical manifestations of, 323 vs. condyloma latum of secondary syphilis, 325, 334f diagnosis of, 323, 323f differential diagnosis of, 324–325, 324f–325f, 390f vs. giant condyloma acuminatum, 325, 325f helpful hints in, 326 HIV-associated, 444 lesion distribution in, 322, 322f lesions in, 321–322, 321f, 322f management of, 325–326, 325f, 327t vs. pearly penile papules, 324, 324f points to remember in, 326 risk factors in, 321 vs. vestibular papillae, 324, 324f Anthralin, short-contact therapy with (SCAT), for psoriasis in children, 102, 103 guttate, 102, 103 of palms and soles, 110 Anthralin, topical for alopecia areata, 220 for psoriasis localized plaque, 96 of palms and soles, 110 Antiandrogens. See also specific agents for adolescent acne, 34 for androgenic alopecia in women, 217 for hirsutism, 242 for postadolescent acne, 40 Antibiotics. See specific agents and types Antibiotics, oral for adolescent acne, 32–34 for autoeczematized eruption from stasis dermatitis, 86 for postadolescent acne, 39 for rosacea, 43–44 Antibiotics, systemic for atopic hand eczema, 70 for impetiginization from stasis dermatitis, 86 Antibiotics, topical, for adolescent acne, 31, 31t with benzoyl peroxide, 31–32, 31t Anticonvulsants, hypersensitivity syndrome from, 300 Antiepileptic drugs, on acne, 48 Antifungal/corticosteroid combination, topical, prolonged application of, 17 Antifungals, 170t–171t. See also specific agents and disorders Antihistamines. See also specific agents for drug eruptions, 301 for drug eruptions, HIV-associated, 454

for insect bites and stings, 343 for lichen simplex chronicus, 74 for “neurotic” excoriations and factitia, 77 for pruritus of unknown origin, 291 for rhus dermatitis, 62 Antimalarials. See also specific agents oral hyperpigmentation from, 253, 253f Antiseborrheic shampoos, 81. See also specific agents Aphthous stomatitis, 7, 7f, 244–246, 244f, 245f vs. herpes labialis, 158, 158f HIV-associated, 453, 453f Aquagenic pruritus, 292 Aquagenic urticaria, 307, 308 Aquaphor ointment, for diaper dermatitis, 62 Arciform lesions, 11, 11f Arthritis from Lyme disease, 345 psoriatic, 113, 113f Arthritis mutilans, 113, 113f Arthropod bite reaction, vs. purpura, 317, 317f Artificial nails, nail dystrophy from, 273, 273f Aspirin for herpes zoster, 165 for Kawasaki’s syndrome, 214 for necrobiosis lipoidica diabeticorum, 459, 459f Asteatotic eczema, 76, 76f, 294–295, 294f, 295f Atazanavir (Reyataz), for HIV-associated lipoatrophy, 456 Athlete’s foot. See Tinea pedis (athlete’s foot) Atopic cheilitis, 8, 8f Atopic dermatitis, 51–59 allergen removal on, 59 “allergic shiners” in, 54, 55f associated dermatoses with, 56, 56f asthma and, 51–52 basics of, 51–52, 51f, 52f clinical manifestations and complications of, 56 Dennie–Morgan lines in, 54, 55f diagnosis of, 56 vs. diaper dermatitis, 61, 61f differential diagnosis of, 56 of fingernails, 55f follicular, 53f hyperlinear palmar creases in, 54, 55f hypopigmentation in, 279, 279f lesions in adolescent and adult, 53–54, 53f–55f childhood, 52f, 53 infantile, 51f, 53 with lichenification, 9, 9f of lips, 8, 8f, 54f of nape of neck, 54f

vs. Paget’s disease of the breast, 426, 426f pathogenesis of, 52 periorbital, 55f prevention of, 58–59 vs. psoriasis, 93, 93f scrotal, 55f vs. tinea pedis, 169, 169f vulvar and inguinal, 55f xerosis from, 295–296, 295f Atopic dermatitis, hand, 67–70 basics of, 67 diagnosis of, 68 differential diagnosis of, 69, 69f “dry,” 55f, 68, 68f factors in recurrences of, 68 management of, 70 “wet,” 67, 67f Atopic eczema. See Atopic dermatitis Atopic hand eczema. See Atopic dermatitis, hand Atrophic plaques, 4, 4f Atrophie blanche, vs. purpura, 318, 318f Atrophy, skin, from topical steroids, 16, 16f Atypical nevus, 370–371, 370f Autoeczematization, 84, 85f Axillary freckling, 491, 491f Azathioprine (Imuran) for atopic hand eczema, 70 for cutaneous sarcoidosis, 482 for dermatomyositis, 476 for purpura, 319 for pyoderma gangrenosum, 487 Azelaic acid for adolescent acne, 32 for perioroficial dermatitis, 32t for rosacea, 43, 44t Azithromycin for adolescent acne, 34 for chancroid, 337 for granuloma inguinale, 339 for Lyme disease, 348 for rosacea, 44

B Bacillary angiomatosis HIV-associated, 447, 447f vs. HIV-associated Kaposi’s sarcoma, 445f Back, itchy interscapular, 79 Bacterial exanthems, 207–214 Kawasaki’s syndrome, 211–213, 212f, 213f overview of, 207 scarlet fever, 208–209, 208f toxin-mediated streptococcal and staphylococcal disease, 210 Bacterial infections, superficial, 126–134. See also specific infections folliculitis, 130–133, 130f–133f furunculosis, 134, 134f impetigo, 127–129, 127f–129f

overview of, 126 Staphylococcus aureus, 126 Balanitis candidal, 188 nonspecific, 79, 531t Balanitis xerotica obliterans, 532t Balsam of Peru, allergic contact dermatitis from, 66 Basal cell carcinoma (BCC), 407–411 basics of, 407 clinical manifestations of, 409 diagnosis and differential diagnosis of, 410 helpful hints on, 411 lesion distribution in, 409, 409f lesions in, 407–408, 407f–408f management of, 411 morpheaform, 410, 410f points to remember on, 411 superficial, 410, 410f Base, 13 Bathing trunk nevi, 368, 368f Becaplermin (Regranex), for diabetic neuropathic ulcers, 460, 460f Becker’s nevus, 522t Beclomethasone dipropionate (Vanceril), for aphthous stomatitis, 245 Bee sting, 341–343, 341f Behçet’s syndrome, aphthous stomatitis in, 244, 244f Benign pigmented purpura (BPP), 314–315, 314f, 319 Benign skin neoplasms, 363–391. See also specific neoplasms atypical nevus, 370–371, 370f chondrodermatitis nodularis chronica helicis, 381–382, 381f, 382f cysts, 378–379, 378f, 379f fibrous and vascular lesions, 383–384 dermatofibromas, 383–384, 383f fibrous papules (angiofibromas), 384, 384f hypertrophic scars and keloids, 385–388, 385f–387f lipoma, 380, 380f melanocytic nevi, 364–369, 364f–368f overview of, 363 sebaceous hyperplasia, 377, 377f seborrheic keratosis, 372–374, 372f–374f skin tags, 375–376, 375f, 376f vascular lesions, 389–390 angiomas, 373f, 389–390, 389f, 390f management of, 390 pyogenic granuloma, 391, 391f spider telangiectasias, 390, 390f Benign vascular lesions, 389–390 angiomas, 373f, 389–390, 389f, 390f management of, 390 pyogenic granuloma, 391, 391f spider telangiectasias, 390, 390f, 433, 433f

Benoquin, for vitiligo vulgaris, 278 Benzathine penicillin G, for primary syphilis, 333 Benzoyl peroxide, for adolescent acne, 29–30, 30t with antibiotic, 30, 31–32, 31t Bergamot lime oil, phytophotodermatitis from, 285, 285f Berloque dermatitis, 285, 285f Beta-hydroxy acid, for adolescent acne, 32 Betamethasone dipropionate lotion (Diprosone), for seborrheic dermatitis, 81 Betamethasone valerate (Luxiq foam), 95t for seborrheic dermatitis, 81, 82t Bichloracetic acid, for anogenital warts, 327t Biologic therapies. See specific agents Biopsy, skin, 501–504, 502f–504f. See also Skin biopsy Biotin, for brittle nails, 260 Bismuth (Pepto-Bismol), oral hyperpigmentation from, 253, 253f Bite line, normal, vs. lichen planus, 125, 125f Bites, insect, 341–343, 341f, 342f Black hairy tongue, 252, 252f Blackhead, 24, 25f, 26, 27f Bleach for eczema, 57 for green nail syndrome, 262 Bleomycin, for warts, 148 Blisters, large. See Bullae Blue nevi, 367, 367f Body lice, 355–357 Boils, 134, 134f Bourneville’s disease, 493–494, 493f Bowen’s disease, 401–402, 401f, 402f cutaneous horn in, 394f, 395 vs. psoriasis, 93 Brachioradial pruritus, 292 Breslow’s measurement, 413, 413t Brittle nails, 260, 260f Broadband UVB. See UVB (ultraviolet light B) Bullae, 3, 3f Bullosis diabeticorum, 459–460, 459f Bullous disease, diabetic, 459–460, 459f Bullous eruptions, drug-induced, 298 Bullous impetigo, 6, 6f Bullous pemphigoid, 532t Burow’s solution (aluminum acetate, Domeboro), 13 for atopic hand eczema, 70 for cutaneous candidiasis, 189 for eczema, 57, 58 for erythema multiforme from herpes simplex, 312 for herpes simplex, 159 for herpes zoster, 165 for paronychia, acute, 266 Index

539

Burow’s solution (continued ) for rhus dermatitis, 62 for stasis dermatitis, 85 for tinea pedis, interdigital, 170 Buschke-Löwenstein, scleroderma of, 461

C Café au lait spots, 491, 491f Calamine lotion, for rhus dermatitis, 62 Calcineurin inhibitors, 17 Calcipotriene–betamethasone (Dovonex–Taclonex), 95t for localized plaque psoriasis, 95t, 96 Calcipotriene (Dovonex), 95t for inverse psoriasis, 108 for psoriasis localized plaque, 95t, 96 of palms and soles, 110 scalp, 105 for scleroderma, 479 Calcitriol, for scleroderma, 479 Calcium hydroxyapatite microspheres (Radiesse), for HIV-associated lipoatrophy, 456 Campbell De Morgant spots, 389, 389f Candidal balanitis, 188 Candidal diaper dermatitis, 188 Candidal folliculitis, 188 Candidal intertrigo, 188, 188f Candidal paronychia, 189, 267 Candidal vulvitis, 188 Candidal vulvovaginitis, 188 Candidiasis cutaneous, 188–189, 188f, 189f in diabetics, 460, 460f vs. inverse psoriasis, 106, 107f oral (thrush), 189, 251 HIV-associated, 452–453, 452f Canker sore. See Aphthous stomatitis Cantharidin (Cantharone) for molluscum contagiosum, 153–154 for warts, 148 Capillary hemangioma, 520t Capsaicin for brachioradial pruritus, 292 for notalgia paresthetica, 292 Carbuncle, 134 Carmol 40 Gel, for onychomycosis, 186 Carotenemia, 288, 288f Catagen phase, 237, 237f Caustic agents, for warts, 148 Cavernous hemangioma, 520t Caviar spots, 390, 390f Ceftriaxone for chancroid, 337 for Lyme disease, 348 Cefuroxime, for Lyme disease, 348 Cellulitis perianal, 526t with stasis dermatitis, 84, 84f

540

Index

Central centrifugal cicatricial alopecia (CCCA), 229, 229f Cephalexin for eczema, with coexisting infection, 57 for folliculitis decalvans, 231 for hidradenitis suppurativa, 138 for impetiginization from stasis dermatitis, 86 Cephalosporins. See also specific agents for adolescent acne, 34 for furunculosis, 134 for paronychia, 266 for scarlet fever, 209 Cercarial dermatitis, 360 Cetaphil lotion, for diaper dermatitis, 62 Cetirizine (Zyrtec) for drug eruptions, 302 for urticaria and angioedema, 309 Chancroid, 336–337, 336f Charcoal, activated, for pruritus of unknown origin, 291 Cheilitis, atopic, 8, 8f Chemical folliculitis, 133 Chemical leukoderma, vs. vitiligo vulgaris, 277, 277f Cherry angiomas, 389, 389f Chickenpox (varicella), 3, 3f, 194–196, 194f Children, skin disorders in. See Pediatric skin disorders Chloasma (melasma), 282–283, 282f Chloracne, 48 Chlorambucil, for pyoderma gangrenosum, 487 Chlorhexidine gluconate, for HIVassociated oral candidiasis, 453 Chlorine bleach for eczema, 57 for green nail syndrome, 262 Chloroquine (Aralen) for discoid lupus erythematosus, 473 for drug-induced lupus, 470 Cholestyramine (Questran), for pruritus from liver disease, 291 Cholinergic urticaria, 307, 308 Chondrodermatitis nodularis chronica helicis, 381–382, 381f, 382f Chronic cutaneous lupus erythematosus (CCLE), 466, 472–473, 472f hair loss from, 227–228, 228f Chronic eczematous dermatitis, 50 Cicatricial alopecia. See Scarring alopecia Ciclopirox (Loprox, Penlac Nail Lacquer) for onychomycosis, 186 for psoriasis, scalp, 105 for seborrheic dermatitis, 81, 82t for tinea pedis, interdigital, 170, 170t for tinea versicolor, 192, 192t Cimetidine (Tagamet) for molluscum contagiosum, 154 for urticaria and angioedema, 309 for warts, 148

Ciprofloxacin for chancroid, 337 for granuloma inguinale, 339 for hidradenitis suppurativa, 138 for Pseudomonas (hot tub) folliculitis, 132, 132f 13-cis-Retinoic acid (Accutane) for adolescent acne, oral, 32, 34–35 for exfoliative dermatitis, 490 for Reiter’s syndrome, 484 Clarithromycin, for rosacea, 44 Clark’s levels, 414, 414t Clark’s nevus, 370–371, 370f Clavus, vs. plantar wart, 144, 144f Cleansers, soap-free, for diaper dermatitis, 62 Clindamycin for adolescent acne, 31, 31t, 34 for hidradenitis suppurativa, 137 for MRSA impetigo, 129 Clindamycin plus benzoyl peroxide (DenzaClin, Duac gel) for adolescent acne, 30, 31–32, 31t for pseudofolliculitis barbae, 234 Clobetasol, 95t for alopecia areata, 220 for cutaneous larva migrans, 362 for eczema, 57 for granuloma annulare, 121 for nummular eczema, 72 for paronychia, 268 for rhus dermatitis, 62 for seborrheic dermatitis, 81, 82t Clobetasol propionate for psoriasis of palms and soles, 110 scalp, 105 for seborrheic dermatitis, 81, 82t Clotrimazole (Lotrimin) for cutaneous candidiasis, 189 for inverse psoriasis, 176 for oral candidiasis, HIV-associated, 453 for paronychia, chronic, 268 for perlèche, 248 for tinea pedis, interdigital, 170, 170t for tinea versicolor, 192, 192t Coal tar for localized plaque psoriasis, 96 for seborrheic dermatitis, 81, 82t Cobalt chloride, allergic contact dermatitis from, 66 Colchicine, for purpura, 319 Cold urticaria, 307–308, 307f Colloidal oatmeal agents (Aveeno), for rhus dermatitis, 62 Comedo (comedone) in acne, 24, 25f in adolescent acne, 25f, 26, 27f Comedo extraction, 35, 508, 508f Common warts (verruca vulgaris), 141–142, 141f, 145f. See also Warts, nongenital

Compound melanocytic nevi, 366, 366f Compressive therapy, for stasis dermatitis, 85 Condyloma acuminatum. See Anogenital warts Condyloma latum of secondary syphilis, vs. anogenital warts, 325, 334f Configuration of lesions, 12, 12f Confluent and reticulated papillomatosis, 286, 286f Congenital adrenal hyperplasia (CAH), hirsutism in, 239 Congenital hairy nevus, 368, 368f Congenital melanocytic nevi, 368, 368f Connective tissue diseases, 466–479 cutaneous lupus erythematosus acute, 466 chronic, 466, 472–473, 472f subacute, 466, 470–471, 470f, 471f dermatomyositis, 475–476, 475f, 476f drug-induced lupus, 469–470 neonatal lupus erythematosus, 474, 474f scleroderma and morphea, 477–479, 477f, 478f systemic lupus erythematosus, 466–469, 466f–468f Contact dermatitis, 60–67, 69f allergic, 63–66 other forms of, 65–66, 65f rhus dermatitis, 50, 50f, 63–65, 63f diaper, 60–62, 61f drug-induced, 298, 301f eczematous reaction pattern in, 9, 9f hyperpigmentation from, 284, 284f irritant, 60–62, 60f, 61f vs. inverse psoriasis, 106, 107f vs. tinea pedis, 169, 169f Contraceptives, oral for androgenic alopecia in women, 217 for hirsutism, 242 for postadolescent acne, 39–40 Cordran tape. See Flurandrenolide (Cordran tape) Corn (clavus), vs. plantar wart, 144, 144f Corticosteroid injection, intralesional. See also specific agents for acne keloidalis, 235 for adolescent acne, 35 for alopecia areata, 220 for aphthous stomatitis, 245 for central centrifugal cicatricial alopecia, 230 for cutaneous lupus erythematosus, hair loss from, 228 for cutaneous sarcoidosis, 482 for discoid lupus erythematosus, 473 for hidradenitis suppurativa, 137 for hypertrophic scars, 386–387 for keloids, 386–387, 387f for lichen planopilaris, alopecia from, 229

for necrobiosis lipoidica diabeticorum, 459, 459f for “neurotic” excoriations and factitia, 77 for postherpetic neuralgia, 166 for prurigo nodularis, 75 for psoriasis, localized plaque, 95t, 96 for psoriatic nails, 112 for pyoderma gangrenosum, 487 for sarcoidosis of scalp, 231 for scleroderma, 479 Corticosteroids for hidradenitis suppurativa, 137 for lichen planus, 125 for rhus dermatitis, 62 Corticosteroids, intramuscular. See also specific agents for rhus dermatitis, 62 Corticosteroids, oral, for cutaneous sarcoidosis, 482 Corticosteroids, systemic. See also specific agents acnelike lesions from, 48 for allergic contact dermatitis, 66 for atopic hand eczema, 70 for autoeczematized eruption from stasis dermatitis, 86 for chronic cutaneous lupus erythematosus, hair loss from, 228 for erythema nodosum, 480, 480f for herpes zoster, 165 for lichen planopilaris, alopecia from, 229 for lichen planus, 125 for purpura, 319 for rhus dermatitis, 62 Corticosteroids, topical, 95t. See also specific agents for acne keloidalis, 235 for alopecia areata, 220 for aphthous stomatitis, 245 for asteatotic eczema, 76 for atopic dermatitis, 296 for atopic hand eczema, 70 for central centrifugal cicatricial alopecia, 230 for cradle cap, 81 for diaper dermatitis, 62 for eczematous dermatitis, nonspecific, 76 for exfoliative dermatitis, 101 for granuloma annulare, 121 for guttate psoriasis, 102 for lichen planus, 125 for lichen simplex chronicus, 74 for “neurotic” excoriations and factitia, 77 for nummular eczema, 72 for prurigo nodularis, 75 for psoriasis localized plaque, 94–96, 95t scalp, 105 for pyoderma gangrenosum, 487 for rhus dermatitis, 62

for sarcoidosis of scalp, 231 for seborrheic dermatitis, 81 for stasis dermatitis, 85–86 for vitiligo vulgaris, 277 Coxsackievirus A16, hand-foot-and mouth disease from, 197–198, 197f “Cradle cap,” 79, 81 Creams, 13, 15 Creeping eruption, 361–362, 361f CREST syndrome, 477–479, 477f, 478f Crowe’s sign, 491, 491f Crusted scabies, 352, 352f, 449f Crusts, 6, 6f Cryosurgery (liquid nitrogen), 511–513, 511f–513f for cutaneous larva migrans, 362 for filiform warts, 149, 149f for flat warts, 148 for Kaposi’s sarcoma, HIV-associated, 446 for molluscum contagiosum, 153 for mucous cyst, oral, 256 for solar keratosis, 397 for warts, 147, 149 Cryptococcosis, disseminated, vs. HIVassociated molluscum contagiosum, 443, 443f Curettage, 510, 510f Cushing’s syndrome, hirsutism in, 239 Cutaneous candidiasis, 188–189, 188f, 189f in diabetics, 460, 460f Cutaneous dental sinus tract, 257, 257f Cutaneous horn, 393, 394f, 395 Cutaneous larva migrans, 361–362, 361f Cutaneous lupus erythematosus acute, 466 chronic, 466, 472–473, 472f hair loss from, 227–228, 228f subacute, 466, 470–471, 470f, 471f Cutaneous neurofibromas, 491, 491f Cutaneous sarcoidosis, 10, 10f, 481–482, 481f Cutaneous T-cell lymphoma. See Mycosis fungoides Cutaneous tuberculosis, 534t Cutaneous vasculitis, 316–317, 316f Cutis rhomboidalis nuchae, 530t Cyclophosphamide (Cytoxan) for dermatomyositis, 476 for purpura, 319 Cyclosporine (Neoral, Sandimmune) for atopic dermatitis, 58 for atopic hand eczema, 70 for dermatomyositis, 476 for exfoliative dermatitis, 490 for lichen planopilaris, alopecia from, 229 for psoriasis generalized plaque, 99 of palms and soles, 110 for psoriatic nails, 112 Index

541

Cyproheptadine (Periactin), for urticaria and angioedema, 309 Cyproterone (acetate) for hirsutism, 242 for postadolescent acne, 40 Cyst, 378–379, 378f, 379f definition and description of, 5, 5f digital mucous (myxoid), 268–269, 268f, 269f epidermoid, 5, 5f oral mucous cyst, 256, 256f odontogenic sinus, 257, 257f punch biopsy to remove, 509, 509f “Cystic” acne, 26, 27f–28f

D Dandruff. See Seborrheic dermatitis Dapsone for chronic cutaneous lupus erythematosus, hair loss from, 228 for drug-induced lupus, 470 for lichen planopilaris, alopecia from, 229 for purpura, 319 for pyoderma gangrenosum, 487 for subacute chronic lupus erythematosus, 471 Darier-Roussy nodules, 481 Deep hemangioma, 520t Dental sinus tract, cutaneous, 257, 257f Depo-Provera, on acne, 40 Dercum’s disease, 380 Dermal melanocytic nevi, 366, 366f Dermal reaction patterns, 10, 10f Dermatitis. See also specific types atopic, 51–59 Berloque, 285, 285f cercarial, 360 contact, 60–67 definition of, 49 diaper, 60–62, 61f, 188 eczematous, 49 (See also Eczema) nonspecific, 77 vs. psoriasis, 93, 93f, 104, 104f, 105f secondary nail dystrophy in, 265, 265f exfoliative, 101, 101f, 300, 487–490, 488f hand, chronic, 67–70 (See also Atopic dermatitis, hand) neurodermatitis, 76–77, 77f perianal streptococcal, 526t perioral (perioroficial), 44t, 46, 46f phytophotodermatitis, 285, 285f rhus, 50, 50f, 63–65, 63f seborrheic, 78–82 (See also Seborrheic dermatitis) stasis (gravitational), 83–86 (See also Stasis dermatitis) steroid use/abuse/misuse, 46, 46f Dermatofibromas, 383–384, 383f Dermatographism, 11, 11f, 307, 307f Dermatoheliosis, 530t

542

Index

Dermatomyositis, 475–476, 475f, 476f on nails, 271, 271f Dermatophytid, 174 Dermatosis papulosa nigra, 373–374, 374f Desloratadine (Clarinex), for urticaria and angioedema, 309 Desonide (DesOwen), 95t for diaper dermatitis, 62 for eczema, 57 for perlèche, 248 for seborrheic dermatitis, 81, 82t for stasis dermatitis, 86 Desoximetasone (Topicort), 95t for psoriasis, scalp, 105 for seborrheic dermatitis, 82t Desquamation, 6, 6f Diabetic bullous disease, 459–460, 459f Diabetic dermopathy, 461, 461f Diabetic neuropathic ulcers, 460, 460f Diagnostic and therapeutic procedures, 497–515 comedo extraction, 508, 508f cryosurgery, 511–513, 511f–513f (See also Cryosurgery (liquid nitrogen)) electrodesiccation and curettage, 510, 510f Mohs’ micrographic surgery, 514–515, 514f, 515f overview of, 497 potassium hydroxide (KOH) test, 498–500, 498f–500f punch biopsy to remove cysts, 509, 509f simple elliptic excision, 505–507 basics of, 505 technique in, 505–506, 505f undermining technique in, 506, 506f wound closure in, 507, 507f skin biopsy, 501–504 punch biopsy, 503–504, 504f scissor (snip) biopsy and excision, 502–503, 503f shave biopsy and shave removal, 501–502, 502f Diaper dermatitis, 60–62, 61f, 188 Dichloroacetic acid, for warts, 148 Diclofenac sodium (Solarase), for solar keratosis, 397 Dicloxacillin for eczema, with coexisting infection, 57 for furunculosis, 134 for hidradenitis suppurativa, 138 for impetiginization from stasis dermatitis, 86 for paronychia, acute, 266 Diffuse alopecia, 222–226 anagen effluvium, 225, 225f basics of, 222 points to remember on, 222 senescent alopecia, 226 telogen effluvium, 222–224, 222f Digital mucous (myxoid) cyst, 268–269, 268f, 269f

Dinitrochlorobenzene (DNCB), for warts, 148 Diode laser, for adolescent acne, 36 Dioxins, acne from, 48 Diphencyprone, for warts, 148 Diphenhydramine (Benadryl) for aphthous stomatitis, 245 for drug eruptions, 302 for eczema, 58 for urticaria and angioedema, 309 Dipyridamole, for necrobiosis lipoidica diabeticorum, 459, 459f Discoid lupus erythematosus (DLE), 466–469, 467f, 472–473, 472f “Dishpan hands,” 60 Disseminated granuloma annulare, 461 Docosanol (Abreva), for herpes simplex, 159 Dog tick, 348, 348f Donovanosis, 339 Doxepin (Sinequan), for urticaria and angioedema, 309 Doxycycline for acne, 48t for adolescent acne, 33 for bacillary angiomatosis, HIVassociated, 447 for hidradenitis suppurativa, 137 for lichen planopilaris, alopecia from, 229 for Lyme disease, 348 for lymphogranuloma venereum, 338 for rosacea, 43t, 44, 48t for syphilis, primary, 333 Drospirenone, for postadolescent acne, 39 Drug eruptions, 297–302. See also specific types basics of, 297–298 clinical manifestations of, 300–301 diagnosis and differential diagnosis of, 301 exanthematous, 298, 298f HIV-associated, 454, 454f lesion distribution in, 300 lesions in, 298–302, 298f–300f management of, 301 overview of, 297 skin reactions in, 298, 298f urticarial, 298, 298f Drug-exacerbated acne, 48 Drug-induced acne, systemic, 48 Drug-induced hirsutism, 239 Drug-induced hypertrichosis, vs. hirsutism, 241, 241f Drug-induced lupus, 469–470 Drug photosensitivity, 298, 299f Drug rash, 10, 10f Ducto-therapy, 146, 146f Dyshidrotic eczema, vs. acute vesicular tinea pedis, 173, 173f Dysplastic nevus, 370–371, 370f

E Econazole (Spectazole), 170t for paronychia, chronic, 268 for seborrheic dermatitis, 81, 82t Eczema, 49–86 acute, 9, 9f, 49–50, 50f asteatotic, 294–295, 294f, 295f atopic dermatitis, 51–59 (See also Atopic dermatitis) atopic hand, 67–70 (See also Atopic dermatitis, hand) chronic, 9, 9f, 49–50, 50f contact dermatitis, 60–67 (See also Contact dermatitis) definition of, 49 follicular, 12, 12f histopathology of, 49 historical background on, 49 hyperpigmentation from, 284 management of, 57–59 nonspecific eczematous dermatitis, 77 nummular, 11, 11f vs. psoriasis, 93, 93f seborrheic, 78–82 (See also Seborrheic dermatitis) stasis dermatitis (See Stasis dermatitis) subacute, 9, 9f, 49–50, 50f terminology for, 49 variants of, 71–77 asteatotic eczema, 76, 76f lichen simplex chronicus, 73–74, 73f “neurotic” excoriations and factitia, 76–77, 77f nonspecific eczematous dermatitis, 76 nummular eczema, 71–72, 71f, 72f prurigo nodularis, 75, 75f Eczema herpeticum, 159, 159f Eczematous dermatitis. See also Eczema nonspecific, 77 vs. psoriasis, 93, 93f vs. psoriasis, scalp, 104, 104f, 105f secondary nail dystrophy in, 265, 265f Eczematous reaction patterns, 9, 9f Edema, vascular, 10, 10f Efalizumab (Raptiva), for psoriasis generalized plaque, 100 of palms and soles, 110 Eflornithine hydrochloride (Vaniqa) for hirsutism, 242 for pseudofolliculitis barbae, 234 Elastic, allergic contact dermatitis from, 65, 65f Elderly, skin disorders of, 530t–534t bullous pemphigoid, 532t Favre-Racouchot syndrome, 530t fissured heels, 533t genital lichen sclerosis in men, 532t in women, 531t giant comedones, 531t Grover’s disease, 532t

Kaposi’s sarcoma, nonepidemic, 534t lupus vulgaris, 534t nonspecific balanitis, 531t onychogryphosis, 533t pemphigus vulgaris, 533t solar elastosis, 530t Electrocautery, for rosacea, 44 Electrodesiccation, 510 EMLA (eutectic mixture of lidocaine and prilocaine), for herpes simplex genitalis, 331 Emollient foams, 13 Endocrine diseases, cutaneous manifestations, 458–461 acanthosis nigricans, 286f, 287f, 460, 460f cutaneous candidiasis, 460 diabetic bullous disease, 459–460, 459f diabetic neuropathic ulcers, 460, 460f necrobiosis lipoidica diabeticorum, 458–459, 458f other findings in diabetics, 286f, 287f, 460–461, 460f–461f Endocrinopathic acne, 48 Endogenous eczema. See Atopic dermatitis Eosinophilic folliculitis HIV-associated, 451 pustular, 133 Ephelides, 2, 2f vs. junctional melanocytic nevi, 365, 365f Epidermal nevi, 523t Epidermoid cysts, 5, 5f, 378–379, 378f Epinephrine for insect bites and stings, 343 for urticaria and angioedema, 310 Erosio interdigitalis blastomycetes, 188 Erosions, 7, 7f Eruptive xanthomas, 464–465, 464f in diabetics, 461 Erythema for hidradenitis suppurativa, 137 vascular, 10, 10f Erythema craquelé, 295, 295f Erythema infectiosum, 199–200, 199f Erythema migrans of Lyme disease, 344–349, 344f, 345f. See also Lyme disease vs. granuloma annulare, 121, 121f vs. tinea corporis, 182, 182f Erythema multiforme, 311–312, 311f in pregnancy, 434 Erythema multiforme major, 311–312, 311f drug-induced, 298, 300 oral lesions from, 247, 247f, 311f Erythema multiforme minor, 311–312, 311f drug-induced, 298 oral lesions from, 246, 246f Erythema nodosum, 480, 480f drug-induced, 298, 300 in pregnancy, 434, 434f

Erythemotelangiectatic rosacea, 42 Erythroderma, exfoliative, 101, 101f, 300, 487–490, 488f Erythromycin for adolescent acne, 33 benzoyl peroxide with, 30, 31–32, 31t topical, 31, 31t for bacillary angiomatosis, HIV-associated, 447 for chancroid, 337 for folliculitis decalvans, 231 for furunculosis, 134 for granuloma inguinale, 339 for hidradenitis suppurativa, 137, 138 for lymphogranuloma venereum, 338 for pseudofolliculitis barbae, 234 for scarlet fever, 209 Erythroplasia of Queyrat, 401, 401f Estrogen, for postadolescent acne, 39–40 Etanercept (Enbrel), for generalized plaque psoriasis, 99–100 Exanthematous drug eruptions, 298, 298f Exanthems, 207. See also specific types Excimer laser UVB. See UVB (ultraviolet light B) Excision scissor biopsy and, 502–503, 503f simple elliptic, 505–507, 505f–507f Excoriations, 8, 8f “neurotic,” 76–77, 77f, 290–291, 290f from scratching, 8, 8f Exfoliative dermatitis, 101, 101f, 300, 487–490, 488f Exfoliative erythroderma, 101, 101f

F Factitia, neurotic, 76–77, 77f, 290–291, 290f Famciclovir (Famvir) for erythema multiforme from herpes simplex, 312 for herpes simplex, 159–160 for herpes simplex genitalis, 331–332 for herpes zoster, 165 Familial atypical mole syndrome, 371 Familial hirsutism, 238, 238f Favre-Racouchot syndrome, 530t Fetal varicella syndrome, 196 Fexofenadine (Allegra), for urticaria and angioedema, 309 Fibroepithelial polyps, 375–376, 376f Fibroepithelioma, pedunculated, 375–376, 376f Fibroma oral, 254–255, 254f soft, 375–376, 376f Fibrous papules (angiofibromas), 384, 384f Fifth disease (erythema infectiosum), 199–200, 199f Filiform warts, 145, 145f. See also Warts, nongenital Index

543

Finasteride (Propecia) for androgenic alopecia, 217 for hirsutism, 242 Finkelstein’s disease, 529t Fire ant sting, 341–343 Fissured heels, 533t Fissures, 8, 8f Fixed drug eruptions, 298, 299f, 300f Flat warts (verruca planae), 144–145, 144f. See also Warts, nongenital Flea bite, 341–343, 341f Fluconazole (Diflucan), 171t for cutaneous candidiasis, 189 for onychomycosis, 186 for oral candidiasis, HIV-associated, 453 for tinea capitis, 181 for tinea pedis, chronic plantar, 173 for tinea versicolor, 192, 192t Fluocinonide (Lidex), 95t for atopic hand eczema, 70 for eczema, 57 for granuloma annulare, 121 for psoriasis, scalp, 105 for seborrheic dermatitis, 81, 82t Fluorinated compounds. See also specific compounds in children and elderly, 17 Fluoroquinolone, for impetiginization from stasis dermatitis, 86 5-Fluorouracil (5-FU, Efudex, Carac) for keratoacanthoma, 406 for solar keratosis, 397, 397f for warts, 148 Flurandrenolide (Cordran tape), 95t for granuloma annulare, 121 for lichen planus, 125 for nummular eczema, 72 for paronychia, chronic, 268 for prurigo nodularis, 75 for psoriasis, localized plaque, 95 for psoriatic nails, 112 “Flusher/blushers,” 42, 43 Flutamide for androgenic alopecia in women, 217 for hirsutism, 242 for postadolescent acne, 40 Fluticasone, 57, 95t Foams, 13, 15. See also specific agents Follicular degeneration syndrome, 229, 229f Follicular eczema, 12, 12f Follicular lesions, 12, 12f Follicular occlusion triad, 134, 134f Follicular prominence, 26, 27f Folliculitis, 130–134 basics of, 130 candidal, 188 chemical, 133 eosinophilic HIV-associated, 451 pustular, 133

544

Index

frictional, 133 fungal, 133 vs. hidradenitis suppurativa, 137, 137f hot tub, 132, 132f irritant, 133 perforating, 461 pruritic, 436 Pseudomonas (hot tub), 132, 132f staphylococcal, 130–132, 130f, 131f steroid-induced, 133, 133f tinea, 133 viral, 133 whirlpool, 132, 132f Folliculitis barbae, 4, 4f Folliculitis decalvans, 232, 232f Folliculitis keloidalis, 235, 235f Fordyce angiokeratomas, 390, 390f Fordyce spots, 258, 258f Formaldehyde allergic contact dermatitis from, 65, 66 for warts, 148 Formic acid, for warts, 148 Foscarnet for herpes simplex, HIV-associated, 440 for herpes simplex genitalis, 332 for herpes zoster, 165 for herpes zoster, HIV-associated, 441, 441f Fragrance mix, allergic contact dermatitis from, 66 Freckles definition and description of, 2, 2f vs. junctional melanocytic nevi, 365, 365f Freezing. See Cryosurgery (liquid nitrogen) Frictional folliculitis, 133 Frontal fibrosing alopecia, 229 Fungal folliculitis, 133 Fungal infections, superficial, 167–193. See also specific infections cutaneous candidiasis, 188–189, 188f, 189f onychomycosis (tinea unguium), 184–187 tinea capitis (ringworm), 177–180 tinea corporis (ringworm), 181–183 tinea cruris (jock itch), 74, 74f, 175–176, 175f, 176f tinea pedis (athlete’s foot), 168–174 Furunculosis, 134, 134f vs. hidradenitis suppurativa, 137, 137f

G Gabapentin, for brachioradial pruritus, 292 Garlic, for warts, 149 Garment nevi, 368, 368f Gels, 13, 15 Genital lichen sclerosis in men, 532t in women, 531t Geographic tongue, 249, 249f German measles (rubella), 203–204, 203f Gianotti-Crosti syndrome, 524t

Giant comedones, 531t Giant condyloma acuminatum, vs. anogenital warts, 325, 325f Giant pigmented hairy nevi, 368, 368f Gingivitis, pregnancy, 434 Gingivostomatitis, 156f Glutaraldehyde, for warts, 148 Glycolic acid for adolescent acne, 32 for melasma, 283 Gold allergic contact dermatitis from, 66 for drug-induced lupus, 470 for subacute chronic lupus erythematosus, 471 Gonadotropins. See also specific agents acne from, 48 Gonococcemia, disseminated, vs. purpura, 318, 318f Gottron’s papules, 475, 475f Gougerot-Carteaud disease, 286, 286f Granuloma annulare, 119–121 basics of, 119 clinical manifestations of, 120 diagnosis of, 120 differential diagnosis of, 121, 121f disseminated, 461 lesion distribution in, 120, 120f lesions in, 119, 119f management of, 121 pathophysiology of, 119 Granuloma gravidarum, 391 Granuloma inguinale, 339 Graves’ disease, 462–463, 462f, 463f Gravitational dermatitis, 83–86. See also Stasis dermatitis Green nail syndrome, 262, 262f vs. onychomycosis, 185, 185f Griseofulvin (Fulvicin, Grisactin, Gris-PEG), 170t for molluscum contagiosum, 154 for tinea capitis, 180 Group A beta-hemolytic streptococci (GABHS) impetigo from, 127 scarlet fever from, 208–209, 208f Grouped lesions, 12, 12f Grover’s disease, 532t Gums, in pregnancy, 434 Guttate psoriasis, acute in adults, 102, 102f in children, 103, 103f vs. pityriasis rosea, 117, 117f

H HAART, for HIV-associated Kaposi’s sarcoma, 446 Hair cycles of growth of, 214, 237–238, 237f, 238f in pregnancy, 433–434

texture and shape of, 214, 234f types of, 214 Hair follicle problems, 233–234, 233f, 234f Hair loss, from hair and scalp disorders, 214–235 acne keloidalis, 235, 235f alopecia areata, 218–221, 218f–220f (See also Alopecia areata) androgenic alopecia, 215–217, 215f, 216f (See also Androgenic alopecia) diffuse alopecia, 222–226 anagen effluvium, 225, 225f senescent alopecia, 226 telogen effluvium, 222–224, 222f overview of, 214 pseudofolliculitis barbae, 233–234, 233f, 234f scarring alopecia, 227–232 basics and pathogenesis of, 227 central centrifugal cicatricial alopecia, 229, 229f chronic cutaneous lupus erythematosus, 227–228, 228f clinical manifestations and course of, 227 folliculitis decalvans, 232, 232f lichen planopilaris, 228–229, 228f sarcoidosis, 231 traction alopecia, 230, 230f Hairy leukoplakia, oral, HIV-associated, 452, 452f Half-and-half nails, 273, 273f Halo nevi, 367, 367f Hand-foot-and-mouth disease, 197–198, 197f Hands atopic eczema of (See Atopic dermatitis, hand) chronic dermatitis of, 67–70 (See also Atopic dermatitis, hand) differential diagnosis for, 69, 69f Head lice, 355–357, 355f Heels, fissured, 533t Heliotrope rash, 475, 475f Hemangioma deep, 520t superficial, 520t Henoch-Schönlein purpura (HSP), 317 Herald patch, in pityriasis rosea, 115, 115f Herpes gladiatorum, 159 Herpes labialis primary, 156–157, 156f recurrent, 157–158, 157f, 158f Herpes simplex genitalis, 328–331, 328f, 330f clinical manifestations of, 329 complications of, 159f, 329 differential diagnosis of, 330, 330f grouped vesicles in, 12, 12f helpful hints on, 331 HIV-associated, 438–440, 439f

lesions distribution in, 328, 328f lesions in, 328, 328f, 438f, 439f management of, 330–331 points to remember on, 331 Herpes simplex virus (HSV), nongenital, 155–161 basics of, 155 diagnosis of, 157–158, 157f, 158b disseminated, 160 eczema herpeticum, 159, 159f extraorolabial, 159b grouped vesicles in, 12, 12f herpes gladiatorum, 159 herpetic sycosis, 160 herpetic whitlow, 159, 159f HIV-associated, 438–440, 438f lesions in, 156, 156f management of, 160–161 neonatal, 160 ocular, 160 orolabial primary, 156–157, 156f recurrent, 157–158, 157f, 158f pathophysiology of, 155 points to remember on, 161 Herpes viral folliculitis, 133 Herpesvirus type 6 (HHV-6), roseola infantum from, 201–202, 201f Herpes zoster, 9, 9f, 162–166 basics of, 162 clinical manifestations of, 164 complications of, 164 diagnosis of, 164 differential diagnosis of, 165 disseminated, 164, 441f herpes zoster ophthalmicus, 164, 164f HIV-associated, 441, 441f lesion distribution in, 163, 163f, 441f lesions in, 162–163, 162f management of, 165–166 points to remember in, 166 vaccination against, 166 Herpes zoster ophthalmicus, 164, 164f Herpes zoster vaccine, 166 Herpetic sycosis, 160 Herpetic whitlow, 159, 159f Hexacetonide, for rhus dermatitis, 62 Hidradenitis suppurativa, 48, 135–138 basics of, 135 diagnosis of, 136 differential diagnosis of, 137, 137f lesion distribution in, 136, 136f lesions and clinical manifestations of, 135, 136f management of, 137–138 pathophysiology of, 135 points to remember on, 138 Hirsutism, 236–242 basics of, 236 clinical manifestations of, 239 cycles of hair growth and, 237–238, 237f

diagnosis of, 240 differential diagnosis of, 241, 241f disorders in congenital adrenal hyperplasia, 239 Cushing’s syndrome, 239 drug-induced, 239 familial hirsutism, 238, 238f polycystic ovary syndrome, 238, 238f idiopathic, 239 lesions and lesion distribution in, 240 management of, 241–242 overview of, 236 pathogenesis of, 236–237 points to remember on, 242 in pregnancy, 433 Hirsutoid papules, 324, 324f Histoplasmosis, disseminated, vs. HIVassociated molluscum contagiosum, 443, 443f HIV, cutaneous manifestations of, 437–456 aphthous ulcers, 453, 453f bacillary angiomatosis, 447, 447f condyloma acuminatum, 444 drug eruptions, 454, 454f eosinophilic folliculitis, 451 herpes simplex, 438–440, 438f, 439f herpes zoster, 441, 441f Kaposi’s sarcoma, 445–446, 445f lipoatrophy (lipodystrophy), 455, 455f molluscum contagiosum, 442–443, 442f, 443f Norwegian scabies, 449–450, 449f, 450f oral candidiasis, 452–453, 452f oral hairy leukoplakia, 452, 452f overview of, 437 pruritus, 454, 454f psoriasis, 455 seborrheic dermatitis, 455 syphilis, 448, 448f Hookworm infestation, 361–362, 361f Hornet sting, 341–343 Hot-comb alopecia, 229, 229f Hot tub folliculitis, 132, 132f Human immunodeficiency virus (HIV). See HIV, cutaneous manifestations of Human papillomavirus (HPV) infection anogenital warts from, 321 (See also Anogenital warts) factors predisposing to, 140 nongenital warts from, 140 (See also Warts, nongenital) Hutchinson’s sign, 421, 421f Hydration, 14–15, 15f Hydrocortisone, topical, 95t for diaper dermatitis, 62 for eczema, 57 for inverse psoriasis, 176 for perlèche, 248 for scale/erythema in hypopigmentation, 280 for seborrheic dermatitis, 81, 82t Index

545

Hydrocortisone valerate for atopic hand eczema, 70 for diaper dermatitis, 62 for eczema, 57 for inverse psoriasis, 176 for seborrheic dermatitis, 81, 82t for stasis dermatitis, 86 Hydrogen peroxide, for black hairy tongue, 252 Hydroquinone (Melanex, Eldoquin Forte, Lustra), for melasma, 283 Hydroxychloroquine (Plaquenil) for chronic cutaneous lupus erythematosus, hair loss from, 228 for cutaneous sarcoidosis, 482 for dermatomyositis, 476 for discoid lupus erythematosus, 473 for drug-induced lupus, 470 for lichen planopilaris, alopecia from, 229 oral hyperpigmentation from, 253, 253f for sarcoidosis of scalp, 231 Hydroxyzine (Atarax) for drug eruptions, 301 for eczema, 58 for urticaria and angioedema, 309 Hyperhidrosis, 528t Hyperpigmentation, 282–288. See also specific disorders acanthosis nigricans, 286–287, 286f, 287f, 460, 460f after adolescent acne, 28, 28f Berloque dermatitis, 285, 285f carotenemia, 288, 288f confluent and reticulated papillomatosis, 286, 286f in eczema, 50, 50f melasma, 282–283, 282f phytodermatitis, 285, 285f poikiloderma of Civatte, 285, 285f postinflammatory hyperpigmentation, 287, 287f in pregnancy, 432, 432f Hypersensitivity reactions. See also Drug eruptions; specific agents and toxins from topical steroids, 16 Hypersensitivity syndrome, 300 Hypersensitivity vasculitis, 316 Hyperthermia, for warts, 149 Hyperthyroidism, 462–463, 462f, 463f Hypertrichosis, 236 drug-induced, vs. hirsutism, 241, 241f Hypertrophic scars, 385–388, 385f basics of, 385, 385f clinical manifestations and diagnosis of, 386 lesion distribution in, 386 lesions in, 385 management of, 386–387 pathogenesis of, 385 Hypertrophic solar keratosis, 393, 394f vs. keratoacanthoma, 406, 406f

546

Index

Hypnosis, for warts, 149 Hypomelanosis idiopathic guttate, 280, 280f other, 280, 280f Hypopigmentation, 275–281. See also specific disorders atopic dermatitis, 279, 279f basics of, 278 in eczema, 50, 50f idiopathic guttate hypomelanosis, 280, 280f other hypomelanosis, 280, 280f pityriasis alba, 279, 279f postinflammatory, 278–279, 279f vitiligo vulgaris, 275–278 (See also Vitiligo vulgaris) Hypothyroidism, 462–463

I Ichthyosis vulgaris, 56, 56f Idiopathic guttate hypomelanosis, 280, 280f Id reaction, 84, 85f, 174 Imiquimod (Aldara) for anogenital warts, 327t for basal cell carcinoma, 411 for keloids, 388 for molluscum contagiosum, 153, 443 for plantar warts, 148 for solar keratosis, 397 for squamous cell carcinoma, 403 for warts, 147 Immunization. See Vaccine Immunomodulators, topical, 17. See also specific agents for eczema, 57–58 Impetiginization, 6, 85, 85f, 127 from atopic hand eczema, 67 from stasis ulcers, 86 Impetigo, 127–129, 127f–129f Impetigo herpetiformis, 436 Inflammatory eruptions of unknown cause, 114–125. See also specific disorders granuloma annulare, 119–121, 119f–121f lichen planus, 122–125, 122f–125f overview of, 114 pityriasis rosea, 115–118, 115f–117f Inflammatory skin disorders, 483–484, 483–490, 483f exfoliative dermatitis, 487–490, 488f pyoderma gangrenosum, 485–487, 485f Reiter’s syndrome, 483–484, 483f Infliximab (Remicade) for exfoliative dermatitis, 490 for generalized plaque psoriasis, 100 for hidradenitis suppurativa, 138 Inguinal striae, from topical steroids, 16, 16f, 17

Insect bites, 341–343, 341f, 342f bullous, 4, 4f Intense pulsed light (IPL) for adolescent acne, 36 for rosacea, 44 Interdigital tinea pedis, 168–170, 168f, 169f, 170t–171t Interferon, for dermatomyositis, 476 Interferon- 2a, for drug-induced lupus, 470 Interferon- 2b for anogenital warts, 326 for drug-induced lupus, 470 Interferon induction, for warts, 147 Interscapular itchy back, 79 Intertrigo, irritant, vs. cutaneous candidiasis, 189, 189f Intertrigonous areas, 16f, 17 Intraepithelial squamous cell carcinoma, 401–402, 401f, 402f Intravenous gamma globulin for dermatomyositis, 476 for drug-induced lupus, 470 for streptococcal toxic shock syndrome, 210 Intravenous immune globulin (IVIG), for Kawasaki’s syndrome, 214 Inverse psoriasis, 74, 74f, 106–108, 106f, 107f vs. tinea cruris (jock itch), 176, 176f Iodides, for erythema nodosum, 480, 480f iPLEDGE program, 35 Iron supplementation, for telogen effluvium, 223 Irritant contact dermatitis (ICD), 60–62, 60f, 61f Irritant folliculitis, 133 Irritant intertrigo vs. cutaneous candidiasis, 189, 189f vs. inverse psoriasis, 106, 107f Isoniazid, acne from, 48 Isotretinoin (Accutane) for adolescent acne, 32, 34–35 for chronic cutaneous lupus erythematosus, hair loss from, 228 for eosinophilic folliculitis, HIV-associated, 451 for exfoliative dermatitis, 490 for lichen planopilaris, alopecia from, 229 for Reiter’s syndrome, 484 “Itchy back syndrome,” 79 Itraconazole (Sporanox), 171t for cutaneous candidiasis, 189 for eosinophilic folliculitis, HIV-associated, 451 for onychomycosis, 186 for paronychia, chronic, 268 for tinea capitis, 180 for tinea pedis, chronic plantar, 173 for tinea versicolor, 192, 192t

Ivermectin (Stromectol) for lice, 357 for Norwegian scabies, HIV-associated, 450 for scabies, 353, 353t Ixodes tick, 344, 348, 348f

J Jellyfish sting, 358–359, 358f Jock itch, 176–177, 176f, 177f Junctional melanocytic nevi, 364–365, 364f, 365f, 419f–421f, 421 vs. freckles, 365, 365f vs. solar lentigenes, 365, 365f, 419f, 420f Junctional nevus, of nail, 272, 272f Juvenile xanthogranuloma, 527t

K Kaposi’s sarcoma HIV-associated, 445–446, 445f nonepidemic, in elderly, 534t Kaposi’s varicelliform eruption, 159, 159f, 329 Kawasaki’s syndrome, 211–213, 212f, 213f Keloid, 3, 3f, 385–388, 385f–387f basics of, 385, 385f clinical manifestations and diagnosis of, 386 lesion distribution in, 386, 386f lesions in, 385 management of, 386–388, 387f pathogenesis of, 385 in pregnancy, 433, 433f Keratoacanthoma, 405–406, 405f, 406f Keratolytic agents, 95t. See also Salicylic acid, topical for cradle cap, 81 for seborrheic dermatitis, 81 Keratosis pilaris, 56, 56f vs. adolescent acne, 29, 29f Ketoconazole (Nizoral), 170t for cutaneous candidiasis, 189 for paronychia, 268 for perlèche, 248 for psoriasis, scalp, 105 for seborrheic dermatitis, 81, 82, 82t for tinea capitis, 180 for tinea pedis, interdigital, 170, 170t for tinea versicolor, 192, 192t Köbner reaction, 122f in psoriasis, 90, 90f, 104 in sunburn, 90, 90f Koenen’s tumors, 493 KOH test, 498–500, 498f–500f Koilonychia, 271, 271f Kojic acid, for melasma, 283 Kyrle’s disease, 461

L Labial melanotic macule, 252, 252f Lactic acid cream, for brittle nails, 260

Lactic-salicylic acid (Duofilm, Occlusal-HP), for flat warts, 148 Lanugo, 214 Laser therapy for adolescent acne, 35–36 for rosacea, 44 for warts, 147 Lemon oil, phytophotodermatitis from, 285 Lentigo maligna, 419, 419f Lentigo maligna melanoma, 419, 419f Leser-Trélat, sign of, 374 Lesions, 2–8. See also specific types and disorders configuration of, 12, 12f follicular, 12, 12f grouped, 12, 12f linear, 11, 11f primary, 2–5, 2f–5f (See also specific lesions) secondary, 6–8, 6f–8f (See also specific lesions) shape of, 11, 11f Leukocytoclastic vasculitis, 298, 300, 316–317 Leukoderma, chemical, vs. vitiligo vulgaris, 277, 277f Leukonychia striata, 270, 270f Leukoplakia oral, 250, 250f oral hairy, 251, 251f Leukotrichia, 275 L’homme rouge, 487–490, 488f Lice infestations, 355–357, 355f Lichenification atopic dermatitis with, 9, 9f in eczema, 50, 50f, 53f Lichen nitidus, 527t Lichenoid eruptions, drug-induced, 301 Lichen planopilaris, 228–229, 228f Lichen planus, 122–125, 250, 250f basics of, 122 clinical manifestations of, 123 clinical variants of, 124, 124f diagnosis of, 124 differential diagnosis of, 124–125, 124f hyperpigmentation from, 284, 284f lesion distribution in, 124, 124f lesions in, 122, 122f, 123f management of, 125 oral, 250, 250f other clinical findings with, 123 pathophysiology of, 122 point to remember on, 125 Lichen sclerosis, genital in men, 532t in women, 531t Lichen sclerosis et atrophicus, 531t Lichen simplex chronicus, 55f, 73–74, 73f vs. lichen planus, 124, 124f vs. psoriasis, 93, 93f vs. tinea cruris (jock itch), 175, 175f

Lichen striatus, 526t Lidocaine, topical (Xylocaine) for aphthous stomatitis, 245 for herpes simplex genitalis, 331 Lidocaine patches, for postherpetic neuralgia, 166 Light-induced urticaria, 307, 308, 308f Light therapy. See also UVA (ultraviolet light A); UVB (ultraviolet light B) for adolescent acne, 35–36 for rosacea, 44 Lindane (Kwell, Scabene) for lice, 357 for Norwegian scabies, HIV-associated, 450 for scabies, 353 Linea nigra, 432, 432f Linear lesions, 11, 11f Linezolid, for MRSA impetigo, 129 Lip disorders. See Oral disorders; specific disorders Lipid abnormalities, 464–465, 464f, 465f Lipoatrophy (lipodystrophy), HIVassociated, 455, 455f Lipodermatosclerosis, 84, 84f Lipodermosclerosis, with stasis dermatitis, 84, 84f Lipoma, 380, 380f multiple, 10, 10f Liquid nitrogen (cryosurgery). See Cryosurgery (liquid nitrogen) Lithium, on acne, 48 Livedoid vasculopathy, vs. purpura, 318, 318f Livedo reticulitis, 467, 467f Liver spot. See Solar lentigenes Löfgren’s syndrome, 482 Longitudinal ridging of nails, 260, 260f Loratadine (Claritin) for drug eruptions, 302 for urticaria and angioedema, 309 Lotions, 13, 15. See also specific types Lupus, drug-induced, 469–470 Lupus erythematosus acute cutaneous, 466 chronic cutaneous, 466, 472–473, 472f hair loss from, 227–228, 228f neonatal, 474, 474f subacute cutaneous, 466, 470–471, 470f, 471f systemic, 466–469, 466f–468f Lupuslike drug eruption, drug-induced, 301 Lupus pernio, 481–482, 481f Lupus vulgaris, 534t Lyme borreliosis. See Lyme disease Lyme disease, 344–349 basics of, 344 clinical manifestations of, 345 diagnosis of, 346 differential diagnosis of, 347, 347f erythema migrans rash of Index

547

Lyme disease (continued ) vs. granuloma annulare, 121, 121f vs. tinea corporis, 182, 182f helpful hints on, 349 lesion distribution in, 345 lesions in, 344–345, 344f, 345f management of, 348, 348f points to remember on, 349 vs. tinea corporis, 347, 347f vs. urticaria, acute, 347, 347f Lyme disease vaccine (LYMErix), 348 Lymphangioma circumscriptum, 528t Lymphogranuloma venereum, 338, 338f

M Macular stains, 520t Macule, 2, 2f, 25f “Maculopapule,” 3 Majocchi’s granuloma, 133 Majocchi’s purpura, 314, 314f Majocci’s granuloma, 182, 183 Malassezia furfur folliculitis from, 133 in tinea versicolor, 190 Malathion (Ovide), for lice, 357 Malignant neoplasms. See Premalignant vs. malignant neoplasms Mask of pregnancy, 432, 433f Mastocytoma, solitary, 525t Mastocytosis syndrome, 525t Measles (rubeola), 205–206 Median nail dystrophy, 264, 264f Melanocytic nevi, 364–369, 364f–368f basics of, 364 blue, 367, 367f compound, 366, 366f congenital, 368, 368f dermal, 366, 366f halo, 367, 367f junctional, 364–365, 364f, 365f, 419f, 420f management of, 369 Spitz, 367 Melanogenesis, 274 Melanoma, 412–424 basics of, 412–413 clinical manifestations of, 413–415 ABCDE criteria, 414–416, 414f–417f Breslow’s measurement, 413, 413t Clark’s levels, 414, 414t superficial spreading melanoma, 414–416, 414f–416f clinical variants of acral lentiginous melanoma, 420–421, 420f, 421f lentigo maligna and lentigo maligna melanoma, 419, 419f nodular melanoma, 418, 418f diagnosis of, 416, 416f differential diagnosis of, 417, 417f helpful hints on, 424

548

Index

lesion distribution in, 413 management of, 418, 422 points to remember in, 424 premalignant vs. malignant, 412–424 (See also Premalignant vs. malignant neoplasms) vs. seborrheic keratosis, 417, 417f Melanotic macule, labial, 252, 252f Melasma, 282–283, 282f, 432 Metformin (Glucophage), for hirsutism, 242 Methicillin resistant Staphylococcus aureus (MRSA), 126 impetigo from, 127 Methotrexate (Rheumatrex) for atopic hand eczema, 70 for cutaneous sarcoidosis, 482 for dermatomyositis, 476 for exfoliative dermatitis, 490 for psoriasis generalized plaque, 98–99 of palms and soles, 110 for psoriatic arthritis, 113, 113f for psoriatic nails, 112 for purpura, 319 for Reiter’s syndrome, 484 for scleroderma, 479 Metronidazole for perioroficial dermatitis, 44t for rosacea, 43, 44t Miconazole (Micatin, Zeasorb-AF powder, Monistat-Derm), 170t for cutaneous candidiasis, 189 for diaper dermatitis, Candida, 62 for inverse psoriasis, 176 for paronychia, 268 for tinea pedis acute vesicular, 174 interdigital, 170 for tinea versicolor, 192, 192t Microcomedo, 24, 25f Milia, 378–379, 379f Minocycline for acne, 48t for acne keloidalis, 235 for adolescent acne, 33 for hidradenitis suppurativa, 137–138 for lichen planopilaris, alopecia from, 229 for MRSA furunculosis, 134 for pseudofolliculitis barbae, 234 for rosacea, 43t, 44, 48t Minoxidil (Rogaine) for alopecia areata, 220 for androgenic alopecia, 217 hypertrichosis from, 241, 241f Mite, 350, 350f Mite infestation, 350–354. See also Scabies Mixed connective tissue disease, 475 Mohs’ micrographic surgery, 514–515, 514f, 515f

Molluscum contagiosum, 151–154 basics of, 151 clinical manifestations of, 152, 152f diagnosis of, 152–153, 152f, 153f differential diagnosis of, 153 helpful hints on, 154 HIV-associated, 442–443, 442f, 443f lesion distribution in, 151–152, 151f lesions in, 151, 151f management of, 153–154 points to remember on, 154 Mometasone (Elocon), for perlèche, 248 Mongolian spots, 523t Montelukast (Singulair), for urticaria and angioedema, 310 Morphea, 477–479, 477f, 478f Morpheaform basal cell carcinoma, 410, 410f. See also Basal cell carcinoma (BCC) Mosquito bite, 341–343 Mouth disorders. See Oral disorders; specific disorders Mucocele, oral, 256, 256f Mucous cyst, oral, 256, 256f Mucous patches of syphilis, tongue, 249, 249f Multiple atypical nevi, 370–371, 370f Mupirocin (Bactroban, Centany) for eczema, 57 for impetigo, 129 for perlèche, 248 Mycophenolate mofetil (CellCept) for drug-induced lupus, 470 for purpura, 319 Mycosis fungoides, vs. psoriasis, 94, 94f Myxedema lesions, pretibial, 462–463, 462f

N Naftifine (Naftin), 170t Nail curvature, increased transverse, 270, 270f Nail diseases and abnormalities, 259–273 common, 260–262 brittle nails (onychoschizia), 260, 260f green nail syndrome, 262, 262f longitudinal ridging (onychorrhexis), 260, 260f onycholysis, 261–262, 261f dermatomyositis, 271, 271f dystrophy from preformed artificial nails, 273, 273f half-and-half nails, 273, 273f infections, 266–269 digital mucous (myxoid) cyst, 268–269, 268f, 269f onychomycosis, 184–187 (See also Onychomycosis (tinea unguium)) paronychia, acute, 266, 266f paronychia, chronic, 267–268, 267f

inflammatory, 265 with eczematous dermatitis, 265, 265f psoriasis, 265, 265f junctional nevus, 272, 272f koilonychia, 271, 271f leukonychia striata, 270, 270f overview of, 259 pincer nails, 270, 270f sarcoidosis, 271, 271f subungual verruca, 272, 272f Terry’s nails, 272, 272f traumatic basics of, 263 median nail dystrophy, 264, 264f subungual hematoma, 263, 263f yellow nail syndrome, 270, 270f Nail dystrophy with eczematous dermatitis, 265, 265f median, 264, 264f from preformed artificial nails, 273, 273f Nails brittle, 260, 260f in pregnancy, 434 psoriasis of, 111–112, 111f, 112f vs. onychomycosis, 185, 185f Necrobiosis lipoidica diabeticorum (NLD), 458–459, 458f Neomycin sulfate, allergic contact dermatitis from, 65, 65f, 66 Neonatal acne, 48 Neonatal lupus erythematosus, 474, 474f Neoplasms benign skin (See Benign skin neoplasms) oral, 254–255, 254f, 255f (See also Oral disorders, neoplasms) premalignant vs. malignant (See Premalignant vs. malignant neoplasms) Neurocutaneous syndromes, 491–494 neurofibromatosis, 491–492, 491f tuberous sclerosis, 493–494, 493f Neurodermatitis, 76–77, 77f Neurofibromatosis, 491–492, 491f Neurontin (gabapentin), for postherpetic neuralgia, 166 Neuropathic ulcers, diabetic, 460, 460f Neurotic excoriations and factitia, 76–77, 77f, 290–291, 290f Nevus (nevi) atypical, 370–371, 370f Becker’s, 522t Clark’s, 370–371, 370f congenital hairy, 368, 368f dysplastic, 370–371, 370f epidermal, 523t junctional, of nail, 272, 272f melanocytic, 364–369, 364f–368f (See also Melanocytic nevi) multiple, 2, 2f pigmented hairy, 522t speckled lentiginous, 521t

Nevus araneus, 390, 390f Nevus flammeus, 521t Nevus lipomatosis, 522t Nevus of Ota, 523t Nevus pigmentosus, 281, 281f Nevus sebaceous, 522t Nevus spilus, 521t Nickel, allergic contact dermatitis from, 65, 65f, 66 Nitrogen mustard, for pyoderma gangrenosum, 487 Nodular acne, 26, 27f–28f Nodular amelanotic melanoma, 418, 418f Nodular melanoma, 418, 418f Nodules, 3, 3f acne, 25f, 26, 27f Darier-Roussy, 481 Nonpalpable purpura, 313–315, 313f, 314f benign pigmented, 314, 314f Majocchi’s, 314, 314f Schamberg’s, 314, 314f senile (actinic), 313, 313f Nonspecific balanitis, 531t Nonspecific eczematous dermatitis, 77 Nonsteroidal antiinflammatory drugs (NSAIDs) for erythema nodosum, 480, 480f for herpes zoster, 165 for psoriatic arthritis, 113, 113f for purpura, 319 for Reiter’s syndrome, 484 Norwegian scabies, 352, 352f, 449f HIV-associated, 449–450, 449f, 450f Notalgia paresthetica, 292, 292f Nummular eczema, 71–72, 71f, 72f vs. psoriasis, 93, 93f Nummular lesions, 11, 11f Nystatin for diaper dermatitis, 62 for oral candidiasis, HIV-associated, 453 for perlèche, 248

O Occlusion, 14, 15, 15f, 17 Ocular rosacea, 42, 42f Odontogenic sinus, 257, 257f Ofloxacin, for scarlet fever, 209 Oil of Bergamot, phytophotodermatitis from, 285, 285f Ointments, 15 Onychogryphosis, 533t Onycholysis, 261–262, 261f psoriatic, 111–112, 111f, 112f Onychomycosis (tinea unguium), 184–187 basics of, 184 clinical manifestations of, 184 diagnosis of, 184 differential diagnosis of, 185, 185f helpful hints on, 186 lesions in, 184, 184f management of, 186

points to remember on, 186 proximal white, 184, 184f vs. psoriatic nails, 112, 112f superficial white, 184, 184f Onychorrhexis, 260, 260f Onychoschizia, 260, 260f Oral candidiasis (thrush), 189, 251, 452–453, 452f Oral contraceptives. See also specific agents for postadolescent acne, 39–40 Oral disorders, 243–258. See also specific disorders cystic lesions, 256–257 mucous cyst, 256, 256f odontogenic sinus, 257, 257f erosions, blisters, fissures, ulcers, 244–248 aphthous stomatitis, 7, 7f, 244–246, 244f, 246f erythema multiforme major, 247, 247f erythema multiforme minor, 246, 246f perlèche, 248, 248f systemic lupus erythematosus, 247 neoplasms oral fibroma, 254–255, 254f pyogenic granuloma, 254, 254f solar keratosis, 155, 155f squamous cell carcinoma, 155, 155f venous lake, 254, 254f normal variants Fordyce spots, 258, 258f torus, 258, 258f overview of, 243 pigmentary changes black hairy tongue, 252, 252f drug-induced, 253, 253f labial melanotic macule, 252, 252f tongue erosions and ulcers, 249, 249f whitish plaques, 250–251 candidiasis (thrush), 189, 251, 452–453, 452f lichen planus, 250, 250f oral hairy leukoplakia, 251, 251f oral leukoplakia, 250, 250f Oral hairy leukoplakia, 251, 251f HIV-associated, 452, 452f Oral leukoplakia, 250, 250f Oral psoralen plus topical ultraviolet A (PUVA), for atopic hand eczema, 70 Oxiconazole (Oxistat), 170t

P Paget’s disease of the breast, 425–426, 425f, 426f Palmar erythema, in pregnancy, 433, 433f Palms, differential diagnosis for, 69, 69f Palpable purpura (PP), 316–317, 316f Papules, 2, 2f in acne, 24, 25f fibrous (angiofibromas), 384, 384f Index

549

Papules (continued) Gottron’s, 475, 475f hirsutoid, 324, 324f pearly penile, vs. anogenital warts, 324, 324f pruritic urticarial papules and plaques of pregnancy, 435, 435f Papulopustular acne, 26 Papulosquamous reaction pattern, 8f, 9 Parakeratosis, 49 Paraphenylenediamine, allergic contact dermatitis from, 65 Parapsoriasis, vs. psoriasis, 94 Paronychia acute, 266, 266f candidal, 189 chronic, 267–268, 267f vs. onychomycosis, 185, 185f Parvovirus B19, erythema infectiosum from, 199–200, 199f Patches, 2, 2f Pearly penile papules, vs. anogenital warts, 324, 324f Pediatric skin disorders, 520t–529t acropustulosis of infancy, 524t acute hemorrhagic edema of infancy, 529t Becker’s nevus, 522t deep hemangioma, 520t epidermal nevi, 523t Gianotti-Crosti syndrome, 524t hyperhidrosis, 528t juvenile xanthogranuloma, 527t lichen nitidus, 527t lichen striatus, 526t lymphangioma circumscriptum, 528t macular stains, 520t Mongolian spots, 523t nevus flammeus, 521t nevus lipomatosis, 522t nevus of Ota, 523t nevus sebaceous, 522t nevus spilus, 521t perianal streptococcal dermatitis, 526t pitted keratolysis, 526t solitary mastocytoma, 525t staphylococcal scalded skin syndrome, 529t stork bites, 521t subcutaneous fat necrosis of newborn, 528t superficial hemangioma, 520t talon noir, 526t tinea amiantacea, 525t urticaria pigmentosum, 524t Pediculosis, 355–357, 355f Pediculosis capitis, 355–357, 355f Pediculosis corporis, 355–357 Pediculosis pubis, 355–357 Pedunculated fibroepithelioma, 375–376, 376f

550

Index

Pemphigoid gestationis, 436, 436f Pemphigus vulgaris, 533t Penciclovir (Denavir), for herpes simplex, 159 Penetration, skin, 14–15, 15f Penicillin for scarlet fever, 209 for syphilis, HIV-associated, 448 Penicillinase-resistant antibiotics, for toxic shock syndrome, 210 Pentoxifylline (Trental), for necrobiosis lipoidica diabeticorum, 459, 459f Perforating folliculitis, 461 Perianal cellulitis, 526t Perianal streptococcal dermatitis, 526t Perioral (perioroficial) dermatitis, 44t, 46, 46f Periungual telangiectasias, 467, 475, 476f Perlèche, 248, 248f Permethrin (Nix Creme Rinse, RID, Acticin, Elimite) for lice, 357 for Norwegian scabies, HIV-associated, 450 for scabies, 353 Petechiae, 313, 433 Petrolatum, for lice, 357 Petrolatum zinc oxide, aluminum acetate solution (1-2-3 Paste), for diaper dermatitis, 62 Phenytoin, on acne, 48 Photocontact dermatitis, 285, 285f Photodynamic therapy (PDT) for adolescent acne, 36 for solar keratosis, 397 Phototherapy. See UVA (ultraviolet light A); UVB (ultraviolet light B) Phototoxic eruption, 298, 299f Phytodermatitis, 285, 285f Phytophotodermatitis, 285, 285f Pigmentary changes, oral black hairy tongue, 252, 252f drug-induced, 253, 253f labial melanotic macule, 252, 252f Pigmentary disorders, 274–288. See also specific disorders hyperpigmentation, 282–288 (See also Hyperpigmentation) hypopigmentation, 275–281 (See also Hypopigmentation) melanogenesis and, 274 overview of, 274 Pigmented hairy nevus, 522t Pigmented solar keratosis, 395, 395f Pilar cysts, 378–379, 378f Pimecrolimus (Elidel), 17 for aphthous stomatitis, 245 for atopic hand eczema, 70 for eczema, 58 for inverse psoriasis, 108 for lichen simplex chronicus, 74

for perlèche, 248 for seborrheic dermatitis, 82, 82t for vitiligo vulgaris, 277 Pincer nails, 270, 270f Pitted keratolysis, 526t Pityriasis alba, 279, 279f Pityriasis rosea, 115–118 basics of, 115 clinical manifestations of, 115–116, 116f diagnosis of, 116 differential diagnosis of, 117, 117f vs. guttate psoriasis, 102, 102f lesion distribution in, 115–116, 115f, 116f lesions in, 115, 115f management of, 118 pathogenesis of, 115 points to remember on, 118 Pityrosporum folliculitis, 133 Pityrosporum orbiculare, in tinea versicolor, 190 Pityrosporum ovale, in tinea versicolor, 190 Planar xanthomas, 464–465 Plantar tinea pedis, chronic, 172–173, 172f Plantar warts, 143–144, 143f, 144f, 150. See also Warts, nongenital Plaques, 4, 4f atrophic, 4f, 5 pruritic urticarial papules and plaques of pregnancy, 435, 435f whitish oral, 151f, 189, 250–251, 250f Plexiform neuromas, 491, 491f Podofilox (Condylox) for anogenital warts, 327t for molluscum contagiosum, HIV-associated, 443 Podophyllin for oral hairy leukoplakia, HIV-associated, 452 for warts, 148 Poikiloderma, 466f, 475 Poikiloderma of Civatte, 285, 285f Poison ivy/oak, 50, 50f, 63–65, 63f Polycystic ovary syndrome (PCOS), hirsutism in, 238, 238f Poly-L-lactic acid (Sculptra), for HIV-associated lipoatrophy, 456 Pompholyx, 67 Portuguese man-of-war sting, 358–359, 358f Port-wine stain, 521t Postadolescent acne, 38–40, 39f Postherpetic neuralgia (PHN), 164, 166 Postinflammatory hyperpigmentation, 287, 287f Postinflammatory hypopigmentation, 278–279, 279f Postinflammatory pigment alterations (PIPA), in eczema, 50, 50f Potassium hydroxide (KOH) test, 498–500, 498f–500f

Povidone-iodine (Betadine), for impetigo, 129 Prednisone. See also Corticosteroids for hidradenitis suppurativa, 137 for lichen planus, 125 for rhus dermatitis, 62 Pregnancy, 431–436 dermatoses of impetigo herpetiformis, 436 pemphigoid gestationis, 436, 436f pruritic folliculitis, 436 pruritic urticarial papules and plaques of pregnancy, 435, 435f pruritus gravidarum, 435 recurrent cholestasis of pregnancy, 436 normal changes, frequently seen connective tissue changes, 432, 433f erythema multiforme, 434 erythema nodosum, 434, 434f gums, 434 hair changes, 433–434 hyperpigmentation, 432, 432f nails, 434 pyogenic granuloma, 434, 434f vascular phenomena, 433, 433f overview of, 431 Pregnancy gingivitis, 434 Premalignant vs. malignant neoplasms, 392. See also specific neoplasms basal cell carcinoma, 407–411 extramammary Paget’s disease, 426–427, 426f keratoacanthoma, 405–406, 405f, 406f melanoma, 412–424 Paget’s disease of the breast, 425–426, 425f solar keratosis, 155, 155f, 393–398 squamous cell carcinoma, 155, 155f, 272, 399–404 Pre-rosacea, 42 Pretibial myxedema lesions, 462–463, 462f Primary lesions, 2–5, 2f–5f. See also specific lesions Procedures. See Diagnostic and therapeutic procedures; specific procedures Progestin, for postadolescent acne, 39 Progressive systemic sclerosis, 477–478 Propionibacterium acnes, 24 Protopic ointment. See Tacrolimus (Protopic ointment) Prurigo nodularis, 75, 75f Pruritic folliculitis, 436 Pruritic urticarial papules and plaques of pregnancy (PUPPP), 435, 435f Pruritus, 289–292 aquagenic, 292 brachioradial pruritus, 292 HIV-associated, 454, 454f notalgia paresthetica, 292, 292f overview of, 289 pruritus of unknown origin, 290–291, 290f

Pruritus gravidarum, 435 Pruritus of unknown origin, 290–291, 290f Pseudofolliculitis barbae, 233–234, 233f, 234f Pseudomonas folliculitis, 132, 132f Pseudomonas nail infection green nail syndrome, 262, 262f vs. onychomycosis, 185, 185f paronychia, 266 Psoralen plus topical ultraviolet A (PUVA). See also UVA (ultraviolet light A) for atopic hand eczema, 70 for psoriasis of palms and soles, 110 for vitiligo vulgaris, 277 Psoralen plus topical ultraviolet A (PUVA), for atopic hand eczema, 70 Psoriasis, 72f, 80f, 87–113 acute guttate in adults, 102, 102f in children, 103, 103f arthritis, 113, 113f in children, 103, 103f clinical manifestations of, 89–91, 90f diagnosis of, 91 differential diagnosis of, 91b epidemiology of, 87 exfoliative dermatitis, 101, 101f generalized plaque, 97–100 basics of, 97, 97f helpful hints on, 100 management of, 97–100 histopathology of, 89, 89f HIV-associated, 455 inverse, 74, 74f, 106–108, 106f, 107f vs. tinea cruris (jock itch), 176, 176f Köbner reaction in, 90, 90f lesion distribution in, 89 vs. lichen planus, 125, 125f localized plaque, 92–96 basics of, 92, 92f diagnosis of, 92, 94f differential diagnosis of, 93–94, 93f, 94f management of, 94–96, 95t nail, 111–112, 111f, 112f, 265, 265f vs. onychomycosis, 185, 185f overview of, 87–88 of palms and soles, 69f, 109–110, 109f of scalp, 104–105, 104f, 105f sebopsoriasis (seborrheisis), 78f, 79f, 89 vs. tinea corporis, 183, 183f vs. tinea pedis, 172, 172f Psoriasis vulgaris, 4, 4f Psoriatic arthritis, 113, 113f Psoriatic nails, 111–112, 111f, 112f Pubic lice, 355–357 Pulsed dye laser (PDL) for adolescent acne, 36 for rosacea, 44 Pulsed light and heat energy (LHE) therapy, for adolescent acne, 36

Punch biopsy, 503–504, 504f, 509, 509f Purpura, 313–319 basics of, 313, 313f differential diagnosis of, 317–318, 317f, 318f drug-induced, 298 helpful hint on, 319 management of, 319 nonpalpable, 313–315, 313f, 314f benign pigmented, 314–315, 314f, 319 Majocchi’s, 314, 314f Schamberg’s, 314, 314f senile (actinic), 313, 313f palpable, 316–317, 316f points to remember on, 319 from topical steroids, 16 Purpura annularis telangiectodes, 314, 314f Pustular folliculitis, 451 Pustular psoriasis of Von Zumbusch, 490 Pustules, 4, 4f, 24, 25f PUVA (psoralen plus topical ultraviolet A). See also UVA (ultraviolet light A) for atopic hand eczema, 70 for psoriasis of palms and soles, 110 for vitiligo vulgaris, 277 Pyoderma gangrenosum, 485–487, 485f Pyogenic granuloma, 254, 254f, 391, 391f in pregnancy, 434, 434f Pyrithione zinc for seborrheic dermatitis, 81, 82t as shampoo (Head & Shoulders), 192, 192t

Q Quadrivalent vaccine (Gardasil), for anogenital warts, 326 Quaternium-15, allergic contact dermatitis from, 65, 66 Queen Anne’s lace, phytophotodermatitis from, 285

R Ramsay Hunt syndrome, 164 Raynaud’s phenomenon, 467 Reaction patterns, 8–10, 8f–10f dermal, 10, 10f eczematous, 9, 9f papulosquamous, 8f, 9 subcutaneous, 10, 10f vascular, 10, 10f vesicobullous, 9, 9f Rebound rosacea, 16, 16f Recurrent cholestasis of pregnancy, 436 Reiter’s syndrome, 483–484, 483f Resorcinol, for adolescent acne, 32 Retinoic acid, for flat warts, 148 Retinoids. See also specific agents for exfoliative dermatitis, 490 oral for adolescent acne, 34–35 for drug-induced lupus, 470 Index

551

Retinoids (continued) for psoriasis of palms and soles, 110 for psoriatic nails, 112 for Reiter’s syndrome, 484 for subacute chronic lupus erythematosus, 471 topical, 95t for adolescent acne, 30–31, 30t, 37 Retinols. See also specific agents for adolescent acne, 32 Rhinophyma, 47, 47f Rhus dermatitis, 50, 50f, 63–65, 63f Ridging of nails, longitudinal, 260, 260f Rifampin for nasal impetigo, 129 plus cephalexin, for folliculitis decalvans, 231 plus clindamycin, for folliculitis decalvans, 231 for scarlet fever, 209 Ringworm tinea capitis, 177–180 tinea corporis, 181–183 Rituximab (Rituxan), for purpura, 319 Rollercoasting, 37 Rosacea, 41–45, 80f clinical manifestations of, 42, 42f diagnosis of, 42 differential diagnosis of, 42–43, 43f epidemiology of, 41 etiology of, 41 helpful hints on, 45 lesion distribution in, 42, 42f lesions in, 41–42, 42f management of, 43–45, 43t, 48t ocular, 42, 42f points to remember on, 45 rebound, 16, 16f from steroids, 46, 46f, 133 topical agents for, 44t triggers of, 45 Rosacea variants, 46–47, 46f Roseola infantum, 201–202, 201f Rotational therapy, for psoriasis generalized plaque, 99 localized plaque, 96 Rubella (German measles), 203–204, 203f Rubeola (measles), 205–206 Ruby spots, 389, 389f Russian hogweed, phytophotodermatitis from, 285

S Salactic film, for plantar warts, 148 Salicylic acid, topical (compound W, Duofilm, Keralyt, Mediplast, Salex) for adolescent acne, 32 for molluscum contagiosum, 153 for Norwegian scabies, HIV-associated, 450

552

Index

for plantar warts, 148 for psoriasis of palms and soles, 110 of scalp, 105 for seborrheic dermatitis, 81, 82t for warts, 146–147 Salicylic acid, transdermal (Trans-Ver-Sal), for flat warts, 148 Salmon patches, 520t Sarcoidosis cutaneous, 10, 10f, 481–482, 481f hair loss from, 231 on nails, 271, 271f Sausage finger deformity, 113, 113f Scabies, 350–354 basics of, 350 clinical manifestations of, 351, 351f clinical variants of, 352, 352f, 449f diagnosis of, 351f, 352, 352f, 449f helpful hints on, 354 lesion distribution in, 351, 351f lesions in, 350–351, 350f management of, 353, 353t mites in, 350, 350f pathogenesis of, 350, 350f points to remember on, 354 Scabs, 6, 6f Scales, 6, 6f, 50, 50f Scarlet fever, 208–209, 208f Scarring alopecia, 227–232 basics of, 227 central centrifugal cicatricial alopecia, 229, 229f chronic cutaneous lupus erythematosus, 227–228, 228f clinical manifestations and course of, 227 folliculitis decalvans, 232, 232f lichen planopilaris, 228–229, 228f pathogenesis of, 227 sarcoidosis, 231 traction alopecia, 230, 230f Scars acne, 27f hypertrophic, 385–388, 385f SCAT (short contact anthralin therapy) for guttate psoriasis, 102, 103 for psoriasis in children, 102, 103 for psoriasis of palms and soles, 110 Schamberg’s purpura, 314, 314f Scissor biopsy and excision, 502–503, 503f Sclerodactyly, 477, 477f, 478f Scleroderma, 477–479, 477f, 478f Scleroderma of Buschke-Löwenstein, 461 Scratching. See also Pruritus excoriation from, 8, 8f Seabather’s eruption, 359–360, 359f Sea lice, 359–360, 359f Sebaceous hyperplasia, 377, 377f Sebopsoriasis, 78f, 79f, 81, 89 Seborrheic dermatitis, 6, 6f, 78–82

basics of, 78 clinical manifestations of, 79 clinical variants of, 79 differential diagnosis of, 80–81, 80f distribution of, 79, 79f helpful hints on, 82 HIV-associated, 455 lesions and lesion distribution in, 78–79, 79f, 80f management of, 81, 82t pathogenesis of, 78 points to remember on, 82 vs. scalp psoriasis, 104, 104f, 105f Seborrheic eczema, 78–82. See also Seborrheic dermatitis Seborrheic keratosis, 372–374 basics of, 372 clinical variants of, 373–374, 373f, 374f diagnosis and differential diagnosis of, 373 helpful hint on, 374 lesion distribution in, 373, 373f lesions in, 372, 372f management of, 374 vs. melanoma, 417, 417f points to remember on, 374 Seborrheisis, 78f, 79f, 89 Secondary lesions, 6–8, 6f–8f. See also specific lesions Selenium sulfide (Selsun Blue), 170t for seborrheic dermatitis, 81, 82t for tinea capitis, 180 for tinea versicolor, 192, 192t Senescent alopecia, 226 Senile angiomas, 389, 389f Senile purpura, 313, 313f Septic vasculitis, vs. purpura, 318, 318f Sexually transmitted diseases (STDs), 320–339. See also specific diseases anogenital warts, 321–327 chancroid, 336–337, 336f granuloma inguinale (Donovanosis), 339 herpes simplex genitalis, 328–331 lymphogranuloma venereum, 338, 338f overview of, 320 syphilis, 332–335 Shagreen patch, 493 Shape of lesions, 11, 11f. See also specific lesions Shave biopsy and removal, 501–502, 502f Sign of Leser-Trélat, 374 Silver nitrate, for aphthous stomatitis, 245 Simple elliptic excision, 505–507 basics of, 505 technique in, 505–506, 505f undermining technique in, 506, 506f wound closure in, 507, 507f Skin biopsy, 501–504 punch biopsy, 503–504, 504f scissor (snip) biopsy and excision, 502–503, 503f

shave biopsy and shave removal, 501–502, 502f Skin neoplasms, benign. See Benign skin neoplasms Skin tags, 375–376, 375f, 376f Small vessel vasculitis, 313–315, 313f, 314f Smearing, 14f, 15 Snip biopsy and excision, 502–503, 503f Soaking, 14–15, 15f, 17 Sodium sulfacetamide for adolescent acne, 32 for perioroficial dermatitis, 44t for rosacea, 43, 44t Soft fibromas, 375–376, 376f Solar elastosis, 530t Solar keratosis, 155, 155f, 393–398 basics of, 393 clinical manifestations of, 396 diagnosis of, 396 differential diagnosis of, 396 helpful hints on, 398 hypertrophic, 393, 394f vs. keratoacanthoma, 406, 406f lesion distribution in, 395–396, 395f lesions in, 365f, 393–395, 393f–395f management of, 397, 397f pathogenesis of, 393 points to remember on, 398 Solar lentigenes, vs. junctional melanocytic nevi, 365, 365f, 419f, 420f Solar urticaria, 307, 308, 308f Solitary mastocytoma, 525t Solutions, 13, 15 Speckled lentiginous nevus, 521t Spider angiomas, 390, 390f Spider bite, 341–343, 343f Spider telangiectasias, 390, 390f, 467 in pregnancy, 433, 433f Spironolactone for adolescent acne, 34 for androgenic alopecia in women, 217 for hirsutism, 242 for postadolescent acne, 40 Spitz nevi, 367 Spongiosis, 49 Sporadic atypical nevi, 370 Squamous cell carcinoma, 399–404 vs. aphthous stomatitis, 245, 246, 246f basics of, 399 clinical manifestations of, 400–401, 401f clinical variants of intraepithelial squamous cell carcinoma, 401–402, 401f, 402f squamous cell carcinoma of mucous membranes, 402, 402f differential diagnosis of, 403 helpful hints on, 404 histopathology of, 399 vs. keratoacanthoma, 406, 406f lesion distribution in, 400 lesions in, 400, 400f

management of, 403 metastasis risk of, 399 oral, 155, 155f points to remember on, 404 subungual, 272 Squamous cell carcinoma of mucous membranes, 402, 402f Squaric acid dibutylester (SADBE), for warts, 148 Staphylococcal folliculitis, 130–132, 130f, 131f Staphylococcal scalded skin syndrome (SSSS), 529t Staphylococcus aureus infections, 126 furuncles, 134 impetigo, 127 paronychia, 266 scarlet fever, 208–209, 208f Stasis dermatitis, 83–86 basics of, 83 clinical manifestations of, 84, 84f, 85f differential diagnosis of, 84f, 85 lesion progression and distribution in, 83, 83f management of, 85–86 pathogenesis of, 83 Steroid-induced acne, 133 Steroid-induced folliculitis, 133, 133f Steroid-induced rosacea, 133 Steroids. See also Corticosteroids; Hydrocortisone; Prednisone acne from, 133 anabolic, acne from, 48 rosacea from, 133 Steroids, oral for pyoderma gangrenosum, 487 for Reiter’s syndrome, 484 Steroids, systemic for dermatomyositis, 476 for drug eruptions, 301 for exfoliative dermatitis, 490 for insect bites and stings, 343 for urticaria and angioedema, 309 Steroids, topical, 13–17, 95t. See also specific agents adverse effects of, 16, 16f with antifungals, 17 anti-inflammatory, 13 antimitotic, 13 for aphthous ulcers, HIV-associated, 453 for cutaneous larva migrans, 362 for cutaneous sarcoidosis, 482 delivery/percutaneous penetration of, 14–15, 15f for discoid lupus erythematosus, 473 for drug eruptions, HIV-associated, 454 for eczema, 57 for exfoliative dermatitis, 490 fluorinated, 14 general considerations with, 13–14 helpful hints on, 17

higher potency, 17 for jellyfish sting, 359 “long list” of, 18t–19t mechanism of action of, 13 for necrobiosis lipoidica diabeticorum, 459, 459f for neonatal lupus, 474 points to remember on, 17 for Portuguese man-of-war sting, 359 potencies of, 14 for pseudofolliculitis barbae, 234 for Reiter’s syndrome, 484 “rosacea” from, 46, 46f for scleroderma, 479 “short list” of, 18t for subacute chronic lupus erythematosus, 471 treatment note on, 17 Steroid use/abuse/misuse dermatitis, 46, 46f Stevens-Johnson syndrome drug-induced, 298, 300 oral lesions from, 247, 247f Sting bee, 341–343, 341f jellyfish, 358–359, 358f Portuguese man-of-war, 358–359, 358f Stomatitis, aphthous, 7, 7f, 244–246, 244f, 246f Stomatitis elixir, for HIV-associated aphthous ulcers, 453 Stork bites, 521t Strawberry hemangioma, 520t Streptococcal dermatitis, perianal, 526t Streptococcal toxic shock syndrome (STSS), 210 Streptococcus pyogenes, scarlet fever from, 208–209, 208f Stretch marks, in pregnancy, 432, 432f Striae, inguinal, from topical steroids, 16, 16f, 17 Striae gravidarum, 432, 432f, 433f Stucco keratoses, 373, 373f Subacute cutaneous lupus erythematosus, 466, 470–471, 470f, 471f Subcutaneous fat necrosis of newborn, 528t Subcutaneous reaction patterns, 10, 10f Subungual hematoma, 263, 263f Subungual verruca, 272, 272f Sulconazole (Exelderm), 170t Sulfur for adolescent acne, 32 for rosacea, 43 for scabies, 353 for seborrheic dermatitis, 81 Superficial bacterial infections, 126–134. See also specific infections folliculitis, 130–133, 130f–133f furunculosis, 134, 134f impetigo, 127–129, 127f–129f overview of, 126 Staphylococcus aureus, 126 Index

553

Superficial basal cell carcinoma, 410, 410f. See also Basal cell carcinoma (BCC) Superficial fungal infections, 167–193. See also specific infections cutaneous candidiasis, 188–189, 188f, 189f onychomycosis (tinea unguium), 184–187 overview of, 167 tinea capitis (ringworm), 177–180 tinea corporis (ringworm), 181–183 tinea cruris (jock itch), 74, 74f, 175–176, 175f, 176f tinea pedis (athlete’s foot), 168–175 tinea versicolor, 190–192, 190f, 191f, 192t Superficial hemangioma, 520t Superficial spreading melanoma (SSM), 414–415, 414f, 415f Superficial viral infections, 139–166 herpes simplex, nongenital, 155–161 herpes zoster, 162–166 molluscum contagiosum, 151–154 overview of, 139 warts, nongenital, 140–150 Swimmer’s itch, 360 Syphilis, 332–335 basics of, 332 congenital, 335 HIV-associated, 448, 448f latent, 335 primary, 330, 332–333, 333f vs. herpes simplex genitalis, 330, 330f secondary, 34f, 333–335, 333f condyloma latum of, vs. anogenital warts, 325, 334f mucous patches of, tongue, 249, 249f vs. pityriasis rosea, 117, 117f tertiary, 335 Systemic disease, cutaneous manifestations, 457–494. See also specific diseases connective tissue diseases, 466–479 (See also Connective tissue diseases; specific diseases) cutaneous sarcoidosis, 481–482, 481f endocrine diseases, 458–461 acanthosis nigricans, 286f, 287f, 460, 460f cutaneous candidiasis, 460 diabetic bullous disease, 459–460, 459f diabetic neuropathic ulcers, 460, 460f necrobiosis lipoidica diabeticorum, 458–459, 458f other findings in diabetics, 286f, 287f, 460–461, 460f–461f erythema nodosum, 480, 480f inflammatory skin disorders, 483–490 exfoliative dermatitis, 487–490, 488f pyoderma gangrenosum, 485–487, 485f Reiter’s syndrome, 483–484, 483f

554

Index

lipid abnormalities (xanthomas), 464–465, 464f, 465f neurocutaneous syndromes, 491–494 neurofibromatosis, 491–492, 491f tuberous sclerosis, 493–494, 493f overview of, 457 thyroid disease, 462–463, 462f, 463f Systemic lupus erythematosus, 247, 466–469, 466f–468f

T Tachyphylaxis (tolerance), 14 Tacrolimus (Protopic ointment), 17 for aphthous stomatitis, 245 for atopic hand eczema, 70 for eczema, 57–58 for inverse psoriasis, 108 for lichen planus, 125 for lichen simplex chronicus, 74 for perlèche, 248 for seborrheic dermatitis, 82, 82t for vitiligo vulgaris, 277 Talon noir, 526t Tar preparations for atopic dermatitis, 58 for localized plaque psoriasis, 96 Tazarotene (Tazorac), 95t for psoriatic nails, 112 Telangiectasias periungual, 467, 475, 476f spider, 390, 390f, 467 in pregnancy, 433, 433f Telogen effluvium, 222–224, 222f in pregnancy, 433 Telogen phase, 237, 237f Tennis heel, 526t Terbinafine (Lamisil), 170t–171t for inverse psoriasis, 176 for onychomycosis, 186 for tinea capitis, 180–181 for tinea pedis, chronic plantar, 173 for tinea versicolor, 192, 192t Terminal hair, 214 Terry’s nails, 272, 272f Tetracyclines for acne, 48t for adolescent acne, 32–33 for aphthous stomatitis, 245 for confluent and reticulated papillomatosis, 285 for folliculitis decalvans, 231 for hidradenitis suppurativa, 137 for MRSA impetigo, 129 for rosacea, 43t, 44, 48t for syphilis, primary, 333 Thalidomide for aphthous stomatitis, 245 for aphthous ulcers, HIV-associated, 453 for chronic cutaneous lupus erythematosus, hair loss from, 228 for drug-induced lupus, 470

for prurigo nodularis, 75 for subacute chronic lupus erythematosus, 471 Therapeutic procedures. See Diagnostic and therapeutic procedures Thiabendazole, for cutaneous larva migrans, 362 Thimerosal, allergic contact dermatitis from, 65, 66 Thrush, 189, 251, 452–453, 452f HIV-associated, 452–453, 452f Thymol in ethanol, for paronychia, 268 Thyroid disease, cutaneous manifestations of, 462–463, 462f, 463f Tick dog, 348, 348f Ixodes, 348, 348f Tinea amiantacea, 525t vs. tinea capitis, 179, 179f Tinea capitis, 177–180 basics of, 177 diagnosis of, 178 differential diagnosis of, 178–179, 178f, 179f helpful hints on, 180 lesions in, 177–178, 177f, 178f management of, 179–180 points to remember on, 180 Tinea corporis, 11, 11f, 72f, 181–183, 181f–183f basics of, 181 clinical manifestations of, 182, 182f diagnosis of, 182 differential diagnosis of, 182–183, 182f, 183f vs. granuloma annulare, 121, 121f vs. impetigo, 129, 129f lesion distribution in, 181 lesions in, 181, 181f vs. Lyme disease, 347, 347f management of, 183 point to remember on, 183 vs. psoriasis, 93, 93f tinea folliculitis from, 133 Tinea cruris (jock itch), 74, 74f, 175–176, 175f, 176f basics of, 175 clinical manifestations and diagnosis of, 175 differential diagnosis of, 175–176, 175f vs. inverse psoriasis, 106, 107f lesions and lesion distribution in, 175, 175f management of, 176 Tinea faciale, 181, 181f Tinea folliculitis, 133 Tinea gladiatorum, 128f Tinea incognito, 16, 182, 182f Tinea manuum, 69f Tinea pedis (athlete’s foot), 168–174 acute vesicular, 173–174, 173f antifungal drugs for, 170t–171t

basics of, 168 chronic plantar, 172–173, 172f interdigital, 168–170, 168f, 169f, 170t–171t Tinea unguium (onychomycosis). See Onychomycosis (tinea unguium) Tinea versicolor, 190–192 basics of, 190 diagnosis of, 191, 191f differential diagnosis of, 191, 191f, 488f lesions and lesion distribution in, 190, 190f management of, 192, 192t vs. pityriasis rosea, 117, 117f Tolerance, 14 Tolnaftate (Tinactin), 170t Tongue, black hairy, 252, 252f Tongue disorders. See Oral disorders; specific disorders Tongue erosions and ulcers, 249, 249f Topical steroid–induced “rosacea,” 46, 46f Topical therapy, 13–19. See also specific agents and therapies basics of, 13 immunomodulators (calcineurin inhibitors) as, 17 overview of, 13 steroids as, 13–17 (See also Corticosteroids, topical; Steroids, topical) vehicles in, 13 wet dressings in, 13 Torus, 258, 258f Torus platinus, 258, 258f Toxic epidermal necrolysis, 300, 300f HIV-associated, 454, 454f Toxic shock syndrome (TSS), 210 Toxin-mediated streptococcal and staphylococcal disease, 210 Traction alopecia, 230, 230f Transient acantholytic dermatosis, 532t Tretinoin (retinoic acid, Retin-A) for adolescent acne, topical, 31t for black hairy tongue, 252 for flat warts, 148 for melasma, 283 for molluscum contagiosum, HIVassociated, 443 for oral hairy leukoplakia, HIVassociated, 452 Triamcinolone acetate/acetonide (Kenalog), 95t for adolescent acne, 35 for atopic hand eczema, 70 for eczema, 57 for granuloma annulare, 121 for hidradenitis suppurativa, 137 for mucous cyst, oral, 256 for nummular eczema, 72 for psoriasis, scalp, 105

for stasis dermatitis, 86 for tinea pedis, acute vesicular, 174 Triamcinolone diacetate, for rhus dermatitis, 62 Trichloroacetic acid for anogenital warts, 327t for molluscum contagiosum, 154, 443 for warts, 148 for xanthelasmas of eyelids, 465 Trichotillomania, vs. alopecia areata, 220, 220f Trimethoprim-sulfamethoxazole (TMZ; Bactrim) for adolescent acne, 34 for granuloma inguinale, 339 for MRSA impetigo, 129 Tuberculosis, cutaneous, 534t Tuberous sclerosis, 493–494, 493f Tuberous xanthomas, 464–465, 465f Two-feet one-hand tinea pedis, 173, 173f Tzanck preparation, 157, 157f, 158b

U Ulcers, 7, 7f Unna’s boot, for stasis ulcers, 86 Urea lotion for atopic dermatitis, 296 for xerosis, 296 Urticaria vs. Lyme disease, 347, 347f vs. tinea corporis, 182, 182f wheals in, 5, 5f Urticarial drug eruption, 298, 298f Urticaria pigmentosum, 524t UV (ultraviolet light), for exfoliative dermatitis, 101 UVA (ultraviolet light A) for discoid lupus erythematosus, 473 for psoriasis generalized plaque, 98 of palms and soles, 110 for scleroderma, 479 UVB (ultraviolet light B) for discoid lupus erythematosus, 473 for drug eruptions, HIV-associated, 454 for eosinophilic folliculitis, HIVassociated, 451 for pityriasis rosea, 118 for pruritus of unknown origin, 291 for psoriasis generalized plaque, 97–98, 98 guttate, 102 for scleroderma, 479 for vitiligo vulgaris, 277

V Vaccine herpes zoster, 166 Lyme disease, 348 quadrivalent, for anogenital warts, 326 varicella, 196

Valacyclovir (Valtrex) for erythema multiforme from herpes, 312 for herpes simplex, 159–160 for herpes simplex genitalis, 331–332 for herpes zoster, 165 Varicella (chickenpox), 194–196, 194f Varicella immunoglobulin (VZIG), 196 Varicella vaccine (Varivax), 196 Varicella-zoster virus (VZV), 194–196, 194f Vascular diseases, 303–319. See also specific diseases erythema multiforme, 311–312, 311f overview of, 303 purpura, 214f, 313–315, 313f (See also Purpura) urticaria and angioedema, 304–310 acute vs. chronic urticaria in, 304 aquagenic urticaria, 307, 308 basics of, 304 cholinergic urticaria, 307, 308 clinical manifestations of, 306 cold urticaria, 307–308, 307f dermatographism, 307, 307f diagnosis of, 308 differential diagnosis of, 309 helpful hints on, 310 lesion distribution in, 306 lesions in, 305, 305f management of, 309 pathophysiology of, 304 physical urticarias, 307–308, 307f–308f points to remember on, 310 solar urticaria, 307, 308, 308f Vascular lesions, benign, 389–390 angiomas, 373f, 389–390, 389f, 390f management of, 390 pyogenic granuloma, 391, 391f spider telangiectasias, 390, 390f, 433, 433f Vascular phenomena, in pregnancy, 433, 433f Vascular reaction patterns, 10, 10f Vasculitic ulcers, 467, 467f, 468f Vasculitis, 316–317, 316f cutaneous, 316–317, 316f drug-induced, 298, 300 leukocytoclastic, 298, 300, 316–317 septic, vs. purpura, 318, 318f small vessel, 313–315, 313f, 314f ulcers in, 7, 7f Vehicles, 13 Vellus, 214 Venous lakes, 254, 254f, 373f, 389, 389f Venous stasis ulcer, with stasis dermatitis, 84, 84f Venous varices, 373f, 389, 389f Verruca, subungual, 272, 272f Verruca planae, 144–145, 144f. See also Warts, nongenital Index

555

Verruca vulgaris, 141–142, 141f, 145f. See also Warts, nongenital Vesicles, 3, 3f Vesicobullous reaction patterns, 9, 9f Vestibular papillae, vs. anogenital warts, 324, 324f Vinblastine, for HIV-associated Kaposi’s sarcoma, 446 Vinegar for green nail syndrome, 262 as topical therapy, 13 Viral exanthems, 193–206 erythema infectiosum (fifth disease), 199–200, 199f hand-foot-and-mouth disease, 197–198, 197f overview of, 193 roseola infantum, 201–202, 201f rubella (German measles), 203–204, 203f rubeola (measles), 205–206 varicella (chickenpox), 194–196, 194f Viral folliculitis, 133 Viral infections, superficial, 139–166. See also specific infections herpes simplex, nongenital, 155–161 herpes zoster, 162–166 molluscum contagiosum, 151–154 overview of, 139 warts, nongenital, 140–150 Vitamin B2, for brittle nails, 260 Vitamin D3, 95t. See also specific agents for localized plaque psoriasis, 95t, 96 Vitamin D3–steroid combination, topical, 95t. See also specific agents Vitiligo universalis, 275, 275f Vitiligo vulgaris, 2, 2f, 275–278 basics of, 275 clinical manifestations of, 276 diagnosis of, 276, 276f differential diagnosis of, 277, 277f helpful hints on, 278 lesion distribution in, 275, 275f lesions in, 275, 275f management of, 277–278, 278f

556

Index

pathogenesis of, 275 points to remember on, 278 vs. tinea versicolor, 191, 191f Vulvar papillomatosis, vs. anogenital warts, 324, 324f Vulvitis candidal, 188 nonspecific, 79 Vulvovaginitis, candidal, 188

W Warts, anogenital. See Anogenital warts Warts, nongenital, 140–150 basics of, 140 common warts (verruca vulgaris), 141–142, 141f, 145f filiform warts, 145, 145f flat warts (verruca planae), 144–145, 144f human papillomavirus infection in, 140 lesion distribution in, 141 lesions in, 140 management of, 145–149 in adults and immunocompromised, 146 alternative treatments in, 149 caustic agents in, 148 in children, 145–146 for common warts, 148 duct tape (ducto-therapy) in, 146, 146f electrocautery and blunt dissection in, 147 for filiform warts, 149, 149f for flat warts, 148 general principle of, 145–146 immunotherapy in, 147–148 liquid nitrogen cryotherapy in, 147, 149f for plantar warts, 148 salicylic acid in, topical, 146–147 vesicants in, 148 plantar warts, 143–144, 143f, 144f, 150 points to remember on, 150 subungual, 272, 272f

Wasp sting, 341–343 Wet dressings, 13 Wheals, 5, 5f Whirlpool folliculitis, 132, 132f Whitehead, 24, 25f, 26, 27f Whitish plaques, oral, 250–251 candidiasis (thrush), 189, 251, 452–453, 452f lichen planus, 250, 250f oral hairy leukoplakia, 251, 251f oral leukoplakia, 250, 250f Whitlow, herpetic, 159, 159f Winter eczema, 294–295, 294f, 295f

X Xanthelasma, 464–465, 464f Xanthogranuloma, juvenile, 527t Xanthoma palpebarum, 464–465, 464f Xanthomas, 464–465, 464f, 465f Xerosis, 293–298 asteatotic eczema, 294–295, 294f, 295f atopic dermatitis, 295–296, 295f definition and pathogenesis of, 294 overview of, 293 X-irradiation, superficial, for atopic hand eczema, 70

Y Yellow nail syndrome, 270, 270f

Z Zinc, for adolescent acne with benzoyl peroxide, 30 with erythromycin, 31t Zinc oxide ointment (Balmex, Desitin, A D ointment), for diaper dermatitis, 62 Zinc pyrithione for seborrheic dermatitis, 81, 82t as shampoo (Head & Shoulders), 192, 192t Zinc sulfate, for folliculitis decalvans, 231 Zostavax, 166