Proceedings of the Bockus International Society of Gastroenterology: Fourth Annual Meeting, Geneva, May 7-9, 1962 [Reprint 2016 ed.] 9781512813968

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PROCEEDINGS 1962

B O C K U S I N T E R N A T I O N A L SOCIETY OF G A S T R O E N T E R O L O G Y

Fourth Annual Meeting Geneva, May 7-9, 1962

PROCEEDINGS Rudolf W . Ammann, M.D. Editor

University of Pennsylvania Press Philadelphia

© 1964 by the Trustees of the University of Pennsylvania

Libran· of Congress Catalog Card Number: 63-22180

Published in Great Britain, India, and Pakistan by the Oxford University Press London, Bombay, and Karachi

7403 Printed in the United States of America

LIST OF MEMBERS AND GUESTS OF THE SWISS COMMITTEE

L i s t of M e m b e r s and guests of the Swiss C o m m i t t e e which organized the F o u r t h A n n u a l M e e t i n g of the B o c k u s I n t e r n a t i o n a l Society of G a s t r o e n t e r o l o g y

WISSMER—Chairman (Geneva) AMMANN—Editor of the Proceedings (Zurich) F E R N A N D B O R E R (Geneva) J A C Q U E S L A C I E R (Geneva) BERNARD

RUDOLPH

E x e c u t i v e Committee Meeting. F r o m left to r i g h t : J . E . B e r k , B . W i s s m e r , J . M. de la Vega, A. Wiebenga, H. L. B o c k u s , F . Mendes, J . L . A. R o t h , and R . Sifre.

PROGRAM

Program of the Fourth Annual Meeting of the Bockus International Society of Gastroenterology May 7-9, 1962, Geneva, Switzerland Official themes: Postgastrectomy and Postvagotomy Sequelae; Cancer of the Stomach Monday, May 7 9:00 A.M. Opening Introductory Remarks by Bernard Wissmer 9:15 A.M.—10:45 A.M.: Free Papers President: Bernard Wissmer Discussion opened by Henry L. Bockus 11:00 A.M. Guest Lecture Michel Demole, Geneva Erwin Rutishauser, Geneva 11:30 A.M.—1:00 P.M.: Free Papers President: Jose Maria de la Vega Discussion opened by Geraldo Siffert Tuesday, May 8 8:30 A.M.—10:00 A.M.: Symposium on Postgastrectomy and Postvagotomy Sequelae President: Adolf H. Wiebenga 10:00 A.M.—11:15 A.M.: Panel Discussion Moderator: Henry L. Bockus 11:15 A.M.—11:30 A.M.: Summary by Ernst H after, Zurich

Wednesday, May 9 8:30 A.M.—10:45 A.M.: Free Papers President: J. Edward Berk Discussion opened by Figueiredo Mendes 11:00 A.M.—11:30 A.M.: Progress Reports of the Research Committee President: J. Edward Berk 11:30 A.M.—1:00 P.M.: Business Meeting Place of Meeting: Hotel Richemond, Geneva Annual Dinner: Tuesday, May 8, 1962 at 7:00 P.M. Candlelight Banquet in the Castle of Oron

PREFACE

W h o in our society would have ventured to predict that a meeting comparable to the Brazilian Congress in Rio de Janeiro in 1960 would ever take place again. Those who were fortunate enough to attend the Geneva meeting, our Fourth Congress, under the presidency of Adolf Wiebenga (the Netherlands) know that this has come to pass. Less fortunate members who could not attend and have not heard from others, will, upon perusal of these proceedings, soon be convinced. This society, the "brain child" of Figuieredo Mendes, has indeed matured. A band of studious gastroenterologists from many nations brought together by common ties of training in Philadelphia and by a universal knowledge of one language—medicine, that greatest of all fraternities—and sparked by the Spirit of Brotherly Love, have now been welded firmly into a unique international society—all alumni of a great University. T h e Congress in Geneva was superb. T h e meetings to follow in years to come may be as successful, but none will surpass the Geneva conclave. Geneva and its environs is an ideal setting for such a gathering. T h e local chairman, Bernard Wissmer, was born to the role. T h e scientific assemblies functioned with an alacrity and perfection of rhythm seldom achieved in the deliberations of any scientific meeting. T h e directing influence of Wissmer was ever manifest. T h e organization of social events by the Wissmer defy adequate description. When will one ever forget the reception at the Palais Eyard, the trip along the beautiful shores of Lake Leman and through the Swiss Alps, the cocktails in the courtyard of the Castle of Gruyeres, the medieval pageantry and candlelight banquet in the Castle of Oron and the dancing and gaiety on the boat cruise on Lake Geneva. All this served to enhance that spirit of comaraderie for which our group are renowned. Financial support for the social and scientific sessions was obtained by Dr. Wissmer from pharmaceutical firms, friends and patients. T h e scientific program so well organized by Chairman Wissmer in collaboration with President Wiebenga and Secretary Roth is fully set forth in these proceedings. These colleagues merit a vote of sincere thanks for arranging this comprehensive array of fine papers and panel discussions. In addition to member participation, several close friends

Opening Ceremony at the R i c h e m o n d Hotel. F r o m left to right: James L. A. Roth, Secretary General; Bernard Wiesmer, Chairman; Adolf Wiebenga, President. and associates of members, eminent gastroenterologists and scientists, took part in the deliberations. T h e participation of scientists from Switzerland, friends of our members (including our guest lecturers, Professors Michael Demole and Erwin Rutishauser) , added f u r t h e r to the scientific worth of the meeting. T h e proceedings of this third congress of o u r society were edited by Dr. Rudolf A m m a n n (Zurich). Dr. Reis, the editor of the Brazilian proceedings will appreciate the n a t u r e of this task and I join with him in expressing our thanks for a task well done. A balance of the f u n d accumulated by Dr. Wissmer together with a contribution of the University of Pennsylvania made this publication possible. T h e University of Pennsylvania Press, through the efforts of Dean Paul Nemir of the Graduate School of Medicine, kindly agreed to the printing and publication of the volume. Once again at this Geneva meeting the purposes of our g r o u p have been fulfilled: (1) T h e exchange of medical knowledge on a worldwide basis and (2) the furtherance of international friendship and understanding.

I share with the members of our faculty a deep sense of pride and satisfaction for having had the opportunity of participatng in the training of the members of this splendid society and forming in this way lasting friendships of physicians from everywhere. H . L. Bockus.

FOREWORD

Now that our meeting is over, I feel somewhat like a father whose daughter has just been married. For a long time, I have raised that child, I watched her growing, then came the big ceremony with its excitement, and now all the guests have left and so has my child and I am alone with the faded flowers. But if I feel some melancholy, on the other hand I am deeply happy because never before had I realized that my family was so large and so closely bound. I want to say thank you with ail my heart to all of you who have told me or written to me to say how successful our meeting W2s. My dear friends, this success was yours. It was due to the unexpectedly large number of registrations coming from twenty-three different countries and to the outstanding quality of our guests. And it was due to the high scientific level of our working sessions (I can say so as I did not participate personally!). But I would like also to emphasize how much we owe to the generosity of the pharmaceutical companies (which are listed at the end of this book) and of a few anonymous private friends. T o all of them, a heartful thanks. I want to tell our President Adolf Wiebenga how wonderful it was to work with him, knowing that he was always backing my decisions and thinking in the same direction as I was. Dear Dr. Bockus, you are "our father," and we all know that without you, our Society would never have existed; once again, you have amazed us by your unbelievable youth and your constant and stimulating presence at the scientific sessions as well as on the dance floor. My last word will be for our friend Figueiredo Mendes, initiator of our Society. He can be proud to see how beautiful his generous idea has been progressing, and there is no doubt that our next meeting shall be even more successful. Geneva, May 1962 Bernard Wissmer, M. D. Chairman of the Swiss Committee. Vice-President.

INTRODUCTORY REMARKS

There is a well-known saying of the famous German cartoonist and poet Wilhelm Busch that goes: "Vater werden ist nicht schwer, Vater sein dagegen sehr" ("To become a father is not difficult, to be a father however is very difficult"). T h e same way be said of the editor. In both instances it lasts about nine months until the result of their efforts becomes evident. But finally the "child" of the editor is not his own product, the editor remains despite his efforts somewhat a step-father. These Proceedings are your work and are the result of your contributions made during the most interesting scientific session at our fourth meeting in Geneva. A great number of most interesting free papers have beeen presented and a great deal of time was spent in most stimulating discussion. We will not forget to thank our guests who added a great deal to the success of the meeting by their presentations. All these contributions are captured in this volume, a memory for all who attended and a report for those who were not able to join us. T h e publication of these Proceedings has become possible through the personal initiative of Dr. Paul Nemir and the generous offer of the University of Pennsylvania Press. T h e important support given to us by the different firms listed at the end of this volume is also acknowledged. T h e valuable cooperation of all colleagues providing their contributions for the Proceedings and the advice and encouragement of many friends were of great help. Our sincere thanks are expressed to all people who helped us in the editing and printing of the Proceedings. T h e third volume of the Proceedings is an additional document of the will and the ability of our society in trying to advance medical knowledge in gastroenterology by international exchange of ideas and to foster international understanding and friendship. T h e indoctrination by our great master Dr. Henry L. Bockus has given us a common background, one that forms the basis for starting investigative work in gastroenterology on a world-wide basis. T h e present volume of our Proceedings marks one more step in this direction. Let us however not forget that still greater and united efforts are necessary to reach the goal. Rudolf W. Ammann, M. D.

CONTENTS

CHAPTER I—FREE PAPERS

Recurrent Aphthous Stomatitis—R. C. Connelly Familial Recurring Polyserositis Manifested by Intestinal Ileus-7?. J. Priest, R. K. Nixon, and W. R. Eyler Physiological Considerations in Management of Duodenal U l c e r - G . McHardy T h e Problem of Intractable Duodenal Ulcer— 5. J. Stempien and A. E. Dagradi Gastric Tissue and Juice Changes in Gastric Ulcer. Reversible and Irreversible Lesions—E. Deutsch, H. J. Christian, and R. Hill Late Postgastrectomy Sequelae in Gastroduodenal Ulcer with Special Reference to Gastritis—/. Valencia-Parparcen Discussion Opened by Henry L. Bockus

19 22 28 40

49 56 63

CHAPTER II—FREE PAPERS

T h e Stomach in Laennec's Cirrhosis—G. Friozzi and J. D. Prospero Classification of Jaundice According to the New Concepts on Bilirubin Metabolism—/. M. Orellana-Alcalde Idiopathic Jaundice of Pregnancy—M. Velasco, J. Klinger, H. Alessandri, and R. Katz Amebic Abcess of the Liver— V. O. Tachdjian T h e Value of Pancreozymin in the Diagnosis of Biliary Tract Disease—D. C. H. Sun, C. A. Tattory, and J. K. Chen Chronic Pancreatitis—P. Bove Discussion Opened by Geraldo Siffert

71 75 81 87

96 106 121

CHAPTER III—SYMPOSIUM ON POSTGASTRECTOMY AND POSTVAGOTOMY SEQUELAE

Mechanisms of the Dumping Syndrome—F. Hernandez-Morales, R. A. Sifre, and A. Nigaglioni Mechanisms of Postgastrectomy Malnutrition—C. F. Hawkins Feeding Technics in the Management of Gastrectomized Patients—S. Krigun and I. Schor Some Considerations on the Gastrectomized Patient— J. J. Villalobos, J. Solis, L. Landa, and A. Palacios Postgastrectomy Acid Secretion— W. S. Haubrich Malignancy in the Postgastrectomy Remnant—D. L. Curb Morphologic Spruelike Changes of the Jejunal Mucosa Following Gastric Resection and Their Significance— R. Ammann and E. Pfenninger Postvagotomy Gastric Stasis—/. L. A. Roth, F. Vilardell, and H. A ffolter Panel Discussion—Moderator, Henry L. Bockus Summary of the Symposium—Ε. H after

125 128 135 142 150 158

164 175 182 197

CHAPTER IV—CARCINOMA O F T H E STOMACH AND O F T H E DIGESTIVE TRACT

Is the Carcinomatous Degeneration of Gastric Ulcer a Reality or an Illusion?—M. Demole (Guest Lecture) A Histogenetic Study of Carcinoma in Association with Gastric Ulcer—E. Rutishauser and P. Tschantz (Guest Lecture) Carcinoma of the Stomach. Clinical Aspects—R. S. Zarabozo, A. Ponce de Leon, J. Naves, and J. M. de la Vega Correlation of Exfoliative Cytology and Histopathology in Benign and Malignant Conditions of the Stomach— F. Vilardell, A. Valdes-Dapena, and G. N. Stein Experience with Declomycin-Induced Fluorescence of Gastric Sediment as a Diagnostic Test for Gastric Cancer J. E. Berk and S. M. Kantor An Experimental Study on the Use of Radiophosphorus for the Diagonsis of Gastric Cancer—/. AÍ. Job Epidemiology of Digestive Cancer in Colombia— / . A. ]acome Valderrama Discussion Opened by Figueiredo Mendes

202 209 215

225

234 240 245 254

CHAPTER V—FREE PAPERS

Incidence of Colonic Diverticulosis—F. P. Antia Peroral Biopsy of the Intestinal Mucosa in Some Intestinal Parasitosis (Necatoriasis+Strongyloidiasis) — S. Beker, J. Valencia-Par pareen, L. Carbonell, and P. R. Moneada Intestinal Parasitism in Colombia—A. Albornoz-Plata, J. Borrero, W. Rojas, E. Mejia-Ruiz, and A. Habib

261

265 271

Discussion Opened by Figueiredo

Mendes

280

CHAPTER VI—NOTICES

The Social Activities of the Fourth Meeting Officers of the Society List of Membership Acknowledgments

288 289 292 302

CHAPTER I FREE PAPERS

RECURRENT APHTHOUS STOMATITIS Richard, Campbell

Connelly*

Isolated vesico-ulcerative lesions of the mouth and tongue are common. When these lesions become numerous, widespread, and recurrent and are at times associated with diffuse inflammatory or membranous exudate they present a syndrome with serious dangers to health, comfort, and productivity. T h e term "recurrent aphthous stomatitis" seems to describe the pathology observed more accurately than others which have been used. T h e r e is at present no known cause, although bacterial infection, allergy, protozoan invasion, trauma, and hereditary factors have been implicated. T h e disease has been attributed to a virus infection, but the responsible virus has not yet been isolated or even identified and no antibodies have been demonstrated. However, Stark, Kibrick, and Weisberger 1 have presented evidence which they believe indicates that the causative factor of recurrent aphthous stomatitis is not the same as for herpes simplex. T h e first attack of aphthous stomatitis may occur in childhood and have a prodromal period of as much as 10 days, in which fever and malaise and excessive salivation are present. Vesicles appear on the buccal surface, on the tongue, and in the throat. T h e s e tend to rupture and form shallow ulcers with moderate or minimal inflammatory reaction about them. T h e y are frequently very painful and slow to heal. Generalized inflammation of the mouth resulting from invasion of other organisms may follow. T h e first attack, which may be subclinical in its manifestations, may be followed by latent infection persisting throughout life. T h i s carrier state, according to B l a n k and Rake, 2 is a common condition affecting 70 to 9 0 % of the population. T h e latent virus may be activated by numerous endogenous and exogenous factors which change the status of the affected tissues rendering them more susceptible to invasion or injury. Included in these factors are fatigue, mental strain, malnutrition, systemic disease including infections, physical, or chemical trauma. Endocrine factors seem to be associated • Bon Secours Hospital, Harper Hocpital Receiving Hospital and the Department of Medicine, Wayne State University, College of Medicine.

19

20

Richard

Campbell

Connelly

with the aphthous lesions since menstruation and menopause tend to coincide with exacerbation and pregnane)' with remissions. Emotional disturbances, such as anxiety, fear, and depression are commonly related to the onset and continuation of the ulcers. Sirkus, Church, and Kelleher 3 report recognizable mental abnormality in one-third of their patients with severe environmental and emotional stress preceding and development of ulcerations in 6 3 % of the females and 5 9 % of the males. Many characteristics of recurrent aphthous stomatitis resemble those of collagen diseases. T h i s is particularly true in the indolent response of the tissues to the invading agent or diseased area. T h e possibility of an auto-immune mechanism, triggered by physical or chemical factors, being involved in the recurring lesions is worthy of consideration. T h e existence of such an auto-immune tissue reaction in herpetic lesions is suggested by the studies of Good and Campbell 4 · 5 who produced herpetic encephalitis in rabbits previously inoculated with virus by the use of anaphylactic or histamine shock. Similarly, Schmidt and Rasmussen 8 report stress activation of latent encephalitis by repeated intramuscular injections of epinephrine. Hope for the eventual control of recurrent aphthous stomatitis lies in the development of a vaccine capable of producing adequate immunity early in life. Anderson and Kilbourne T have been able to immunize mice by intravenous and intraperitoneal inoculation with herpes simplex virus previously inactivated by exposure to ultraviolet irradiation. Neutralizing antibody in considerable concentration was demonstrated after inoculation, and the mice so immunized withstood subsequent challenge doses of live virus implanted directly into the cerebrum. If similar antibody against the organism producing recurrent aphthous stomatitis can be produced and a vaccine made available so that immunization can be carried out early in life, the control of this disease may be accomplished. In the meantime one must resort to the group of remedies which has been used with varying success. These include smallpox, typhoid, and other vaccination, application of silver nitrate and copper sulphate, estrogens, androgens, sulfonamides, antibiotics, steroids, vitamins, X-ray, and psychotherapy. T r u e love and Morris-Owen 8 have reported good results with local application of hydrocortisone hemisuccinate linguets. Sircus 9 conducted a double-blind study of the effect of lozenges and sedatives. He found that most medications were ineffective and only one-quarter of his subjects had a sustained remission with local application of steroids. W e have found that for the local treatment of the ulcers cauterization with a solution of trichloracetic acid on a cotton applicator after local anesthesia with pontocaine is effective. T h i s solution is more

Recurrent

Aphthous

21

Stomatitis

easily handled than silver nitrate or copper sulphate in solid form. Plain, lightly flavored, nonmedicated glycerine lozenges tend to make the patient more comfortable. Administration of hydroxychloroquine sulfate alone or in combination with steroids has been followed by reduction in the number of lesions. Arsenic should be avoided, we believe, since we have found evidence of heavy metal accumulation in patients years after its use. Continued use of sedatives, tranquilizers, and opiates presents problems in this long-term disease. A nutritious diet with supplemental vitamins is important. Irritating and allergenic foods should be avoided. T o combat malnutrition and electrolyte imbalance, forced feeding of a complete balanced diet in blended form by intubation with a small polyethylene tube and the use of the barron p u m p has been very effective. SUMMARY

1. T h e problem of recurrent aphthous stomatitis has been reviewed. 2. T h e r e is need for further search for the cause of the disease and a method of prevention. 3. Suggestions are made concerning additional effective measures in treatment. REFERENCES 1. STARK

λί.

M.,

KIBRICK,

S.,

and

WEISBERCER,

D.

Studies

on

recurrent

aphthae: evidence that herpes simplex is not the etiological agent, with further observations o n the i m m u n e responses in herpetic infections. J.

Lab. Clin. Med. 44:261

3.

4.

5. 6. 7.

8. 9.

(1954).

H. and R A K E , G . Herpes simplex, in Viral and Rickettsial Diseases of the Skin, Eye and Mucous Membranes of Man. Little, Brown, Boston, 1955, p. 43). SIRCUS, W . , CHURCH, R., and KELLEHER, J . Recurrent aphthous ulceration of the mouth. Quart. J. Med. 26:235 (1957). GOOD, R. Α., and CAMPBELL, B. Potentiating effect of anaphylactic and histamine shock u p o n herpes simplex virus infection in rabbits. Proc. Soc. Exper. Biol. 59:305 (1945). GOOD, R. A. and CAMPBELL, B. T h e precipitation of latent herpes simplex encephalitis by anaphylactic shock. Proc. Soc. Exper. Biol. 68:82 (1948) SCHMIDT, J. R., and RASMUSSEN, A. F., Jr. Activation of latent herpes simplex encephalitis by chemical means. J. Infect. Dis. 106:154 (1960). ANDERSON, W . Α . , and KILBOURNE, E. D . Immunization of mice with inactivated herpes simplex virus. Proc. Soc. Exper. Biol. 707:518 (1961). TRUELOVE, S. C . , and M O R R I S - O W E N , R. M. T r e a t m e n t of aphthous ulceration of the mouth. Brit. Med. J. 7:603 (1958). SIRCUS, W . T h e management of recurrent aphthous stomatitis. Brit. Med. J. 10:804 (1959).

2. BLANK,

FAMILIAL RECURRING POLYSEROSITIS MANIFESTED BY INTESTINAL ILEUS Robert

J. Priest,* Robert K. Nixon * and William R. Eyler*

Familial recurring polyserositis is one of the many disorders to be considered in the differential diagnosis of an acute abdomen. In this disease any serosal membrane may be affected in the same or different patients, although it most commonly presents as an acute peritonitis. Siegal in 1945 1 first described this entity as "benign paroxysmal peritonitis." Earlier case reports have been presumed to have been the same disease.2·3 Since then, the disorder has been found to be neither entirely benign 4 · 6 nor to be limited to the peritoneum.®·7·8 Any serosal surface may become inflamed, including the peritoneum, pleura, pericardium, meninges, or joints. A unique character of the disease is the chronic recurrence of these attacks, presenting in one or varying serosal areas of the body. The apparent periodicity of the episodes led Reimann® to include it among "periodic diseases." Many observers have noted that the attacks may have an apparent rhythm, but the time interval usually is irregular.®· 7 · 8 Several names have been added to the nomenclature of diseases, depending on the emphasis placed on varying aspects of the clinical spectrum. Heller 7 considered fever to be sine qua non and added the name "familial Mediterranean fever." Siguier et al.10 rejected "La Maladie Périodique" and described it as "so-called periodic disease." Mamou 1 1 suggested "Epanalepsie Méditerranéene," implying repeated attacks in persons of Mediterranean ancestry. Of several hundred patients with this disorder reported in the medical literature, practically all of the cases have been described in persons of Armenian, Arab, or Jewish ethnic origin. The Jewish non-Ashkenazi ethnic subgroup has a much higher incidence than among Jews whose parentage has not been of Sephardi or Oriental origin. Sohar et al.12 • Henry Ford Hospital, Detroit, Michigan.

22

Familial

Recurring

Polyserositis

23

concluded that the disease is a recessive disorder with an incidence of 1:2,720 in the non-Ashkenazi population of Israel. CASE REPORT

M. K., a ten-year-old boy of Armenian ancestry, had recurring episodes of swollen ankles from two to five years of age. Oral penicillin medication did not prevent the presumed manifestations of rheumatic fever. Episodes of severe abdominal pain with fever became frequent at irregular intervals. During his ninth year the longest period of time free from attacks was three weeks. His parents, grandparents, and younger sister had no history of similar disease. In September, 1960, the boy was hospitalized with X-ray evidence of pericardial effusion (Figure 1). Flattening of the T-waves in the

Figure 1. Pericardial effusion in a 10-year-old Armenian boy. precordial leads and reduced voltage was seen in the electrocardiogram. Fluoroscopically the heart shadow was massively enlarged with diminished pulsations and a right pleural effusion. His temperature!

24

Priest,

Nixoji,

Eyler

Figure 2. Same patient 2 weeks later, norma] heart. elevated to 103 degrees. T h e leucocyte count was 14,900. Blood cultures and throat cultures were negative for pathogenic organisms. Within 10 days the marked enlargement of the cardiac shadow had returned to normal (Figure 2). Similar episodes of fever and pericarditis recurred 1 and 2 months later. During the fourth month he was hospitalized with a dramatic ileus. Bowel movements had diminished for 6 days before hospital admission and he had vomited repeatedly for 2 days. His abdomen was diffusely tender to the lightest palpation or percussion. He complained of cramping pains throughout his belly. His white-blood-cell count was 39,250 and yet his fever did not go above 100 degrees except on one day to 102. T h e heart size was normal and a barium meal study of the small intestine was done. T h e barium entered a fluidfilled jejunum (Figure 3). During the succeeding ten days the boy required careful control of his blood electrolytes. A serum bilirubin of 9.6 mg. per cent was found to have returned to normal in 4 days. Severe abdominal tenderness, emesis, and hypoperistalsis gradually improved in the next 2 weeks.

Familial

Recurring

Polyserositis

25

Figure 3. Barium in fluid-filled, dilated jejunum. B a r i u m passed slowly t h r o u g h the small bowel. T h e marked distention of the u p p e r intestine persisted with a diameter of 4 cm. (Figure D u r i n g the past year the boy has been following a 20-gm. fat diet. H e has had only three m i n o r attacks of abdominal pain. One attack followed a dietary indiscretion while visiting his grandmother, similar to an episode described by Mellinkoff. 1 3 T h e value of dietary therapy remains in question however, because he has had two similar previous years with few a n d m i n o r attacks of polyserositis.

DISCUSSION

T h i s case report illustrates the spectrum of serosal involvement in one patient d u r i n g different episodes of recurring polyserositis. T h e patient's Armenian ancestry illustrated the ethnic selection. D u r i n g his lifetime he has had attacks of serositis involving joints, pericardium, pleura, and p e r i t o n e u m . T h e dramatic episode of ileus resolved u n d e r observation. Surgical intervention was not considered

26

Priest, Nixon,

Eyler

Figure 4 . Persisting ileus 1 0 days after Figure 3. because of awareness that the condition simulates an acute abdomen and has represented a pitfall for exploratory laparotomies. 14 Positive roentgen manifestations have included motor abnormalities in the small intestine. 15 T h e transit time of barium is delayed, sometimes considerably. T h e barium column is disconnected with fine strands of barium connecting the loops. The intestinal mucosa may appear thickened and residual barium leaves a snowflake pattern. Small bowel studies in the interval between the attacks are within normal limits. Laboratory and pathologic studies are not diagnostic. T h e pathogenesis of familial recurring polyserositis is unknown.

Familial

Recurring

27

Polyserositis 5

N e c r o p s y findings of amyloidosis have b e e n r e p o r t e d . T h e hyperfibrinogenemia d u r i n g attacks may be nonspecific® as a r e o t h e r labo r a t o r y findings, e.g., b i l i r u b i n e m i a a n d elevated s e d i m e n t a t i o n rate. Episodes of r e c u r r i n g polyserositis p r e s e n t i n g as ileus o r as p e r i t o n i t i s m u s t be recognized to avoid unnecessary a b d o m i n a l o p e r a t i o n s .

REFERENCES

1. SIECAL, S. Benign paroxysmal peritonitis. Ann. Int. Med. 23:1 (1945). 2. JANEWAY, T .

C.

and

MOSENTHAL, H .

O. A n

unusual

paroxysmal

syn-

drome, probably allied to recurrent vomiting, with a study of nitrogen metabolism. Trans. Asso. Am. Physicians 23:504 (1908). 3. COOKE, R. A. Gastrointestinal manifestations of allergy. Bull. N. Y. Acad. Med. 9:15 (1933). 4 CATTA&, R., and MAMOU, H. 14 cas de maladie périodique dont 8 compliqués de néphropathies, Bull. So. med. Hôp. Paris. 67:1104 (1951). 5 . H E L L E R , H . SOHAR, E . GAFNI, J . , a n d H E L L E R , J . A m y l o i d o s i s i n

familial

Mediterranean fever. Arch. Int. Med. 107:539 (1961). 6. PRIEST, R. J., and NIXON, R. K. Familial recurring polyserositis: a disease entity. Ann. Int. Med. 52:1253 (1959). 7. H E L L E R ,

H.

SOHAR,

E.,

and

SHERF,

L.

Familial

Mediterranean

fever

Arch. Int. Med. 102:50 (1958). 8. EHRENFELD, Ε . Ν . , ELIAKIM, M . , a n d RACHMILEWITZ, M . R e c u r r e n t

poly-

serositis (familial Mediterranean fever, periodic disease. Am. J. Med. 3 / : 107 (1961). 9. REIMANN, H. A. Periodic disease: periodic fever, periodic abdominalgia, cyclic neutropenia, intermittent arthralgia, angioneurotic edema, anaphylactoid purpura and periodic paralysis. J. A. M. A. 141:175 (1949). 10. SIGUIER, F., ZARA, M . , FUNCK-BRETANO, J . L., a n d LAGRUE, G .

Réflexions

sur la maladie dite périodique. Sem. Hôp. Paris. 29:3649 (1953). 11. MAMOU, H. La maladie périodique. Expansion Scientifique Française, Paris, 1956. 12. SOHAR, E., PRASS, M .

HELLER, J . , a n d

HELLER, H .

Mediterranean fever. Arch. Int. Med. 107:529 13. MELLINKOFF, S. M . ,

SCHWABE, A .

D.,

and

G e n e t i c s of

familial

(1961).

LAWRENCE, J .

S. A

dietary

treatment for familial Mediterranean fever. Trans. Assoc. Am. Physiol. 73:197

(1960).

14. NIXON, R. K., and PRIEST, R. J. Familial recurring polyserositis simulating acute surgical condition of the abdomen. New Eng. J . Med. 265:18

(1960).

15. EYLER, W . R . , N I X O N , R . K., a n d PRIEST, R . J . F a m i l i a l r e c u r r i n g

serositis. Am. J. Roentgen. 84:262 (1960) .

poly-

PHYSIOLOGIC CONSIDERATIONS IN MANAGEMENT OF DUODENAL ULCER Gordon

McHardy*

Gastric ulcer and duodenal ulcer are now generally conceded to be separate entities with significantly different genetic characteristics, etiology, pathogenesis, therapeutic responsiveness, and prognosis. T h e management of patient and disease advocated herein for duodenal ulcer is in part applicable to a benign gastric ulcer; it is not to be concluded, however, that the two lesions should be handled identically. T h e exact cause of duodenal ulcer remains obscure Available knowledge of the gastric secretory mechanism, especially as it pertains to the biochemistry of the parietal cell in the active transport of hydrogen, chloride, and potassium, ions is incomplete. Developments of interest and importance within the past decade include the revelation through electron microscopy of the morphology of the parietal cell in relation to its exocrine function. T h e recognition of the plasma proteins, the gastric proteases other than pepsin in various gastric secretions, has created interest in their ulcerogenic significance. T h e major stimulatory and inhibitory mechanisms for the control of gastric secretion have been ingeniously studied in the experimental animal, with partially confirmatory observations in humans, to establish conclusively the many contributing vagal processes, the humoral processes involving gastrin and histamine, and the inhibitory mechanisms arising in the duodenum. T h e chemical and physical characteristics of the gastric mucinous secretions are considered to be protective against peptic ulcer. T h e endocrine ulcerogenic tumors, the serotonin-reserpine complex relationship to gastric hypersecretion, the ulcerogenic potentiality of corticosteroids, parietal cell mass, and maximal histamine secretory response have all contributed to our physiologic knowledge of ulcer. These data permit a practical, although incomplete, physiologic therapeutic approach and discount the currently prevalent concept that the end result of both the medi• From the Department of Medicine, Louisiana State University Medicine and Browne-McHardy Clinic, New Orleans, Louisiana.

28

School

of

Physiologic

Considerations

in Management

29

cal and surgical management of ulcer is merely the natural eventuation of the disease. Discovery of the precise mechanism of production of ulcer would possibly establish more sound and effective protection in relation to alteration in mucosal resistance, if this single factor is the deciding issue. On the basis of our present knowledge, the other two contributng factors, abnormal secretion and abnormal motility, are obviously etiologically paramount and are susceptible to control in most instances by meticulous therapy. We should, therefore, dedicate our efforts toward a physiologic approach to management which can be rationalized, is practical, and can achieve a favorable prognosis, rather than subscribe to the nihilistic rejection of benefit, the ascription of any improvement to informal psychotherapy, or the scientific interpretation of animal evaluation without benefit of clinical application or experience. Initiation of therapy implies that we know the patient and the disease, i.e., that the patient has been carefully evaluated as to background, course of the ulcer, and associated or resultant anatomic, nutritional, physiologic, and psychic changes, as well as presence of related or unrelated diseases. Such investigative analysis should permit formulation of a therapeutic regimen which clinical experience dictates applicable and which can be modified to fit the social, economic, and occupational status of the patient. This analytic approach continues to survive the trial of time and the new remedies of many decades, permits the combination of pharmacologic, dietetic, psychotherapeutic, and surgical approaches to abnormal secretion and motility, and is most susceptible to physiologic interpretation and accomplishments. T h e entire therapeutic program must, however, be directed toward the following practical clinical principles and not toward physiologic laboratory measures of the results: 1. Assurance of satisfactory quiescence by management sustained adequately to permit healing of the segment that cannot be put at complete physiologic rest. An ulcer of many years' duration, with scarring and penetration, is an anatomic and not a functional entity. It cannot completely granulate in and epithelialize over in a period of a few weeks or months, if ever. 2. Prophylaxis against reactivation by adequate initial therapy and interval intensive management, as indicated, in the presence of greater liability to physical or emotional stress, infections, exposure to ulcerogenic agents, and seasonal factors. 3. Retreatment of reactivation as meticulously as of the initial illness, and awareness that recurrence and refractoriness may indicate endocrinopathy. Such occurrences are more prone to complication.

30

Gordon

McHardy

4. Recognition, intelligent interpretation, and proper medical or surgical management of complications to prevent chronic debilitation. 5. Avoidance of personality conflicts in patient or physician, in which the insight of either may permit the disease, with or without complication, to eventuate in emotional or physical disability or both. After thorough diagnostic appraisal, the experienced clinician, whose scope of contact with and responsibility to the patient is beyond that of a consultant, will tailor his therapy to the various issues in the individual patient. Sex, age, temperament, and occupation of the patient, the organic status of the disease in relation to complication and to associated disease, the interplay of psyche and soma, the emotional influences of financial problems, environment, and frustration, all can contribute to physiologic derangement. It is, therefore, requisite that the therapeutic program include certain basic and therapeutically susceptible physiologic considerations. Decisive factors in the pathogenesis of peptic ulcer that are available for such practical management include: 1. Secretion of hydrochloric acid and associated activation of pepsin. 2. Gastric motility and emptying, with the accompanying neutralizing, inhibiting, or stimulating influence. 3. Mucous secretion, its importance in physical and chemical protection, and its removal by acidification. 4. Psychogenesis of stress-induced secretory, motor, and vascular abnormalities. 5. Ulcerogenic agents that act by secretory stimulation, mucous depletion, or mucosal damage. 6. Endocrinopathies and their susceptibility, presently limited to surgical correction. T h e significance of ulcerogenic agents is obscured by their avoidance or by protective activity when their use is mandatory. Admittedly, such phenomena as mucosal vulnerability, host resistance, genetic factors, and blood-group association cannot be adequately analyzed. Surgical correction of endocrinopathies or revomal of their end organ must be sought. Thus, in the absence of complications, medical management should be concerned primarily with methods of favorably altering gastric acid secretion and motor activity. T h e influences on gastric secretion and motility are overlapping, probably inseparable and, in the analysis of their behavior, often seem to be contradictory. A logical discussion of these influences requires brief mention of the more important and best understood phases wherein the contradictory factors become evident. 1. T h e cephalic phase of activity, excited through the vagus by hypoglycemia and emotional reactions, results in gastric hypersecretion and vigorous contraction. 2. T h e gastric phase (antrum-gastrin), stimulated by the presence

Physiologic Considerations

31

in Management

of food, excites parietal cell hypersecretion and gastric contractions, which have significant influence on evacuation. 3. Antral distention or alkalinization, alone or in combination, probably not entirely separable from the gastric phase, is a strong stimulus to gastric secretion. T h e fact that antral acidification, despite continued distention, however, does not have such an influence suggests the possibility of a questionable separate mechanism. 4. The intestinal phase, hormonal in character, is responsible for less than 10% of the secretory stimulation and may therefore not be of great significance. 5. Mucus, the alkaline barrier, provides physical protection by its coating action, chemically binds acid, inactivates pepsin, and is a parietal cell inhibitor. An acid pH seriously hampers its influence. 6. Gastric "layering," overlooked in most physiologic discussions, is probably a motor phenomenon whereby the weak contractions of the fundus hold solid foods for acid-pepsin digestion, while liquids, especially if they are cold and hypotonic, move around and beyond the fundus into the antrum. Radiologically, endoscopically, by aspiration, and by pH electrodes, layering is demonstrable in the human patient and probably has greater significance than heretofore recognized. The food in the fundus is in the parietal cell area, i.e., at the site of maximal secretion of hydrochloric acid; here digestion, with its concomitant use of acid, takes place. The antral (gastrin) mechanism, on the other hand, continues to be stimulated by alkaline exposure until the digestive process is completed and acid and distention inactive the mechanism. PHYSIOLOGIC CONTROL O F GASTRIC SECRETION AND MOTOR

ACTIVITY

The acceptable approaches to the control of gastric secretory and motor activity again involve contradictory data and an overlapping mechanism that are probably compensatory. Food Whereas all foods are gastric stimulants, they are also neutralizers. Since the usual diet comprises three principal components, carbohydrate, protein, and fat, and since fat has the greatest influence on delaying gastric emptying indirectly by enterogastrone stimulation of suppressing secretion, clinical management should logically include a reasonably high fat content. Ironically, carbohydrates and fats, which are the least stimulating, are also the least neutralizing, and proteins, which are stimulating, are the most neutralizing. Monotony of diet (as in the case of the usual ulcer diet) in animal and

o GÛ

Physiologie

Considerations

in Management

37

human experimentation results in suppression of the cephalic phase of gastric secretion, and adherence to the unattractive bland diet is therefore justified on this physiologic basis (Figures 1 and 2). Whereas gastric emptying is generally regarded as a rapid action wherein the bulk food empties early, bulky food actually "layers" and awaits digestion, hypertonic solutions leave slowly, warm liquids are retained longer than are cold liquids, and fats inhibit gastric emptying. Anticholinergics T h e optimum effective individualized dosage, although inconsistent in controlling gastric secretion, is an adjunct in altering appreciably, although not entirely, the cephalic phase, the gastric phase, and nocturnal secretion. These agents are consistently effective when administered parenterally, are more efficient orally when given on an empty stomach, and are least beneficial when administered immediately postprandially. Regardless of the mode of administration, definite gastric and duodenal atonicity for periods varying from three to twelve hours delays gastric emptying (Figures 3 and 4). T h e duration of action is more consistent for inherently long-acting preparation than for those modified to decelerate release of the drug, but variations occur in the same and in different individuals. In delaying gastric emptying, in vitro effectiveness of antacids is achieved in vivo only if the antacid remains in the stomach for a long enough time. T h e question arises as to whether or not delayed gastric emptying by distention cause antrum stimulation to gastric secretion of hydrochloric acid, and if antacid is present to alkalinize the antrum whether this is not further stimulation. Further value of anticholinergics lies in the relief of the deep pain of distention or tension in the gastric wall. Antacids Alkalinization of the gastric content protects the mucus, irreversibly inactivates pepsin, and relieves pain produced by nerve endings exposed to hydrochloric acid in the base of the ulcer. Most antacids are admittedly effective in vitro. T h e problem has been posed, however, that since gastric emptying is considered a relatively rapid action, most antacids are evacuated from the stomach before exhaustion of the agent's action, i.e., within 40 minutes. Secondly, it is contended that whereas an antacid is ideally administered about 60 to 90 minutes after ingestion of a meal, when hydrochloric acid secretion is at its height, this is also the time when, theoretically,

38

Gordon

McHardy

acidification of the a n t r u m is m a x m u m parietal cell therefore ceases.

and stimulation

of

the

Tranquilizers T h e action of these agents on the central nervous system is known. T h r o u g h control of hostility and anxiety, two principal components of cephalic phase stimulation, these agents can conceivably alter gastric secretion. If administration of tranquilizers, tailored to the patient s specific needs, achieves normalization, then they suppress nocturnal secretion, for the normal individual is not a noctural hypersecretor. Yet secretory studies have demonstrated little, if any, influence of these agents on histamine, hypoglycemic, or basal secretory levels.

DISCUSSION

On the basis of this analysis, the therapeutic situation is extremely confusing. T e n patients with hypersecretory duodenal ulcers were studied for secretory activity (indwelling p H electrodes and aspiration) over 24-hour periods for 14 consecutive days first by using each of several procedures individually in succession; when thus used alone, each proved ineffective in uniformly controlling gastric p H through a greater part of any daily period. Next, combinations of the procedures were tried and, finally, all of them were employed together. T h e procedures included the following items given for 24-hour periods: blended food at hourly intervals, antacids hourly, anticholinergics at ideal period, and tranquilizers with appreciable sedative action. O n alternate 24-hour periods the patient was placed at rest for control. Anticholinergics and antacids in combination were more effective than dual combinations of food and anticholinergics, food and antacids, or food and tranquilizers. However, in all patients the continuation of all these therapeutic aids was uniformly efficient. Clinically substantial evidence exists that food, when taken in solids, "layers" in the gastric fundus, where it remains until the digestive process is completed. Liquids continue, meanwhile, to move a r o u n d and beyond the solid food bolus to enter the a n t r u m , where effective, vigorous peristaltic contractions evacuate the material into the d u o d e n u m in a partially reversible procedure in which backflow from the d u o d e n u m occurs (Figure 5). An illustrative film study, based on 20 surveys, shows the result of ingested h a m b u r g e r accompanied by a barium-milk drink. " C h u n k s " of the solid food occupy the fundus, and the liquid barium milk

Physiologie

Considerations

in Management

39

"layers" below in the a n t r u m . T h e c o m b i n a t i o n of food a n d b a r i u m leaves the stomach slowly over a period of four hours, in contrast to gastric emptying of b a r i u m alone in 60 to 90 minutes. Premedciation of the patient with an effective anticholinergic before adm i n i s t r a t i o n of b a r i u m retards evacuation f r o m the stomach for the d u r a t i o n of action of the drug, as is illustrated by the average film study f r o m twenty surveys of b a r i u m motility (not available at present. Antacid stained with green dve was endoscopically seen to rem a i n in the fasting stomach in excess of two hours. W h e n an anticholinergic is given with the antacid, retention may be prolonged beyond six hours. O u r experience confirms the fact that control of gastric emptying by food and anticholinergic "layering" action of the stomach cause variation in p H in different gastric segments at the same interval. Gastric retention can be aided by administering an anticholinergic concomitantly with an antacid. Since gastric secretion a n d motility are susceptible to such control and since cooperation a n d receptiveness of the patient can be enhanced t h r o u g h the use of tranquilizers, the prevalent use of all four of these a d j u n c t s in m a n a g e m e n t of ulcer represents practical, physiologically directed therapy. Such comb i n e d therapy probably accounts for the favorable prognosis achieved in the majority of patients with d u o d e n a l ulcer, despite o u r inability to improve mucosal resistance except t h r o u g h sustained protection of mucus and avoidance of ulcerogenics, a n d such sources of gastric atrophy as irradiation.

T H E PROBLEM OF INTRACTABLE DUODENAL ULCER Stephen

J. Stempien*

and Angelo E.

Dagradi*

INTRODUCTION

O f recent years emphasis has been placed on the rare association of pancreatic tumors and other endocrinopathies with intractable duodenal ulcer. 1 T h i s has tended to de-emphasize the larger and more urgent problem of the common "garden" variety of intractable duodenal ulcer. It is our intention to report an independent and objective study of this problem, with special emphasis on the evaluation of selection of the surgical patient and the therapeutic efficacy of vagotomy in intractable duodenal ulcer.

METHOD

OF

STUDY

Between 1956 and 1959, a group of 54 patients admitted solely with the diagnosis of intractable duodenal ulcer was studied with the primary purpose of determining what objective data could best serve surgical selection. T h e plan of study included a complete history and physical examination, an upper gastrointestinal X-ray series, a 2-hour basal secretion, and gastroscopy where such procedure was indicated. Insulin gastric analyses were also performed preoperatively in some of these patients and postoperatively whenever suspicion of ulcer recurrence was entertained. An evaluation of the effectiveness of vagotomy-pyloroplastv in these patients was also undertaken by follow-up in clinic and rehospitalization for repeat study at the end of the postoperative year. An up-to-date follow-up survey of the entire group was made by clinic visits in late 1961. • F r o m the Gastroenterology Beach, C a l i f o r n i a .

Section, Veterans Administration

40

Hospital,

Long

The Problem

of Intractable RESULTS O F

Duodenal

Ulcer

41

STUDY

I. Objective Evaluation for Surgical Selection A. Clinical Data on 54 Patients T h e ages ranged from 20 to 69, with a majority (36) between 30 and 49; the duration of disease encompassed a wide range, from 9 months to 27 years, with the largest g r o u p of patients (29) having disease longer than 10 years. Another characteristic of the g r o u p was the frequency of regular a n n u a l recurrences (27) a n d the onset of constancy of pain when intractability was manifest. Symptomatology comprised epigastric pain (51) , back pain (8) , nausea a n d vomiting without organic obstruction (11), and diarrhea (1). Past histories revealed that 22 patients had previously bled one or more times, 8 had preforated, and 1 had obstructed. Although most patients gave an erratic history with respect to adherence to an adequate medical regimen over a long period, yet conventional therapy was deemed adequate in the i m m e d i a t e period preceding hospitalization in 47 of the 54 patients. B. Secretory Data Two-hour basal acid secretion was obtained in 39 patients. Eighteen (46%) showed basal acid secretion within the n o r m a l range (less t h a n 1.5 milliequivalents per hour), 2 whereas 21 (54%) showed basal hypersecretion. In addition, extraordinary basal hypersecretion of acid (5 to 12 milliequivalents per hour) was f o u n d in 10 patients. Uropepsin data 3 in 37 patients showed h y p e r u r o p e p s i n u r i a of more t h a n 50 units per hour in 29 patients ( 8 0 % ) . Insulin gastric analyses performed in some of these patients revealed a p a t t e r n of sustained high secretion over a period of 4 hours. T h i s pattern contrasts sharply with the usual n o r m a l type where secretory response to insulin lasts about 2 hours. 4 Although some of the secretory data were within range of the Zollinger-Ellison syndrome, the subsequent surgical e x p l o r a t i o n or postoperative course did not support this diagnosis in any patient. C. Roentgenographs Data A second thorough look at all u p p e r gastrointestinal X-ray series was made with the purpose of grading organic changes of the pylorod u o d e n a l segment, evaluating the character of the gastric mucosal pattern, and confirming the diagnosis of d u o d e n a l ulcer disease. Organic changes of the pyloroduodenal segment were graded one to four-plus. One-plus was d u o d e n a l ulcer crater w i t h o u t cicatricial change, two-plus was m i n i m a l cicatricial deformity with d u o d e n a l

42

Stephen J. S tempieri, Angelo E. Dagradi

bulb contours well maintained, three-plus was a cloverleaf of either the symmetrical or asymetrical variety, four-plus was complete obliteration of the contours of the duodenal bulb, with or without stenosis, and with or without penetration of ulcer. Stenosis and deep penetration without retention were also considered to be advanced organic change and so listed. A survey of these 54 patients' films revealed changes assessed as "advanced organic" in 39 patients. Of these, 33 had 3+ to 4+ deformity of pyloroduodenal segment, 9 had pvloroduodenal stenosis, and 9 had deep penetration. Nineteen patients had an unusually striking prominence of the gastric mucosal pattern, compatible with mucosal hypertrophy. D. Gastroscopie Data Gastroscopy was performed in 23 patients, yielding a diagnosis of diffuse mucosal hypertrophy (hypertrophic gastritis of Schindler) 5 in 9 patients. T h e remainder were normal or showed only minor grades of gastritis. T h e significance of these gastrscopic findings is reinforced by the fact that all 9 subjects had corroborating X-rav findings of gastric mucosal prominence and 7 had secretory data in the high hypersecretory range. In summary, objective data reasonably supporting intractability were found in 43 of 54 patients. In 39, the principal factor was advanced organic change, although the association of extraordinary hypersecretion (6) and gastric mucosal hypertrophy (17) was also present. In 4 patients, extraordinary basal hypersecretion was found to be the most prominent factor, in 2 of whom associated gastric mucosal hypertrophy was also present. These observations are not new or original with us, as they have been previously alluded to in various reports by Bockus,® Kirsner, 7 Palmer, 8 Cox,® and others. A composite clinical picture of the "intractable" duodenal ulcer group of patients is given in Table 1. TABLE 1 COMPOSITE

P I C T U R E OF

"INTRACTABLE"

DUODENAL

ULCER

Sex Age Duration of disease Recurrences Epigastric pain Complications Medical response .

Male 30 to 50 yean 5 to 20+ years Annual Frequently constant Usually bleeding and perforation Poor

X-ray findings

Advanced organic change (marked deformity, stenosis, penetration) Hypertrophic gastric mucosa. Hypersecretion

The Problem

of Intractable

Duodenal

Ulcer

43

Laboratory findings

Hypersecretion of gastric acid and pepsin and extraordinary hypersecretion

Gastroscopy

Hypertrophic gastric mucosa (frequently of extraordinary degree) II Effectiveness of Vagotomy-Pyloroplasty

Of this group of 54 patients, 41 were subjected to vagotomy, with pyloroplasty (40) and gastroenterostomy (1) after a joint medicalsurgical conference appraisal. It is of interest to state that 24 of the group had an adequate response to the hospital regimen, but it was deemed inappropriate to equate this response with that of the patients' environment in view of the objective findings. Twenty-six patients did not respond adequately to the hospital program. In 4 patients, response was not rated. T h e 13 patients who were not operated upon either had symptoms out of all proportion to the objective findings or if surgery was recommended, they refused it, or for other reasons surgery was inadvisable. An adequate follow-up on this small group of patients was not obtained. Postoperative follow-up observation were obtained over a period of 3 to 5 years in 30 of the operated patients (75%), and over a period of 1 to 3 years in 11 patients (25%). However, in 3 of the later group, adequate follow-up information to judge results properly was not rendered, and they are considered as lost to follow-up. T h e appraisal is therefore given for 38 operated patients. Satisfactory clinical results after the initial vagotomy procedure were obtained in 24 patients (63%), and unsatisfactory results in 14 patients 37%). T h e unsatisfactory group was characterized by the early recurrence of duodenal ulcer in the face of incomplete vagotomy (lOpatients— 24%). T h e remainder were unsatisfactory because of dumping syndrome (2), peptic esophagitis and stricture (1), or recurrent ulcer symptoms with status of vagotomy unknown (1). It is also of interest that during the 1-year post-operative hospitalization study, all gastric insulin tests done at random in the satisfactory group showed adequate or complete vagotomy (11 patients). T h e conclusion is reached that vagotomy is effective in controlling intractable duodenal ulcer disease providing it is adequate or complete. On the other hand, when vagotomy is incomplete in this group, there is a prompt recurrence of duodenal ulcer at a higher incidence (24%) than is found for all duodenal ulcer patients treated by vagotomy (5 to 12%). 10

44

Stephen

J. Stempien,

Angelo E. Dagradi

E F F I C A C Y O F ADDITIONAL

PROCEDURES

I N T H E UNSATISFACTORY

GROUP

In an a t t e m p t to improve results in the unsatisfactory group, Rillroth 1 gastrectomy was performed in 4, and radiation therapy was given to 3. In the gastrectomy group, two were satisfactorily improved, but two remained unsatisfactory because of development of d u m p i n g syndrome not present pre-operativelv. T w o patients were strikingly improved by radiation therapy. I n the remainding one, although X-ray therapy produced satisfactory suppression of acid, the symptoms of esophagitis and stricture persisted. W e are very much encouraged by the results of X-ray therapy in these few cases. T h e over-all end results are given in T a b l e 2. TABLE

2

OVER-ALL END RESULTS AFTER VAGOTOMY-PYLOROPLASTY

(38),

ADDED GASTRECTOMY ( 4 ) , AND ADDED RADIATION T H E R A P Y

Satisfactory clinical result Unsatisfactory clinical result Recurrence of duodenal ulcer Peptic esophagitis and stricture Dumping syndrome

(3) 28

(74%)

10 (26%) 5

1 4

III. T h e Role of Vagotomy and Antrectomy in Control of Gastric Secretion in Intractable Duodenal Ulcer In view of the evidence that vagal activity is responsible for gastrin release from the gastric antrum, which in turn stimulates gastric acid secretion, there has been a trend toward advocacy of vagotomy combined with antrectomy, especially in the high secretor group. 1 1 · 1 2 · 1 3 In an effort to evaluate the respective roles of vagal and antral influence, we reviewed our gastric insulin test date before and after vagotomy-pyloroplasty and after vagotomy-gastrectomy (Billroth 1). T h e data show that if the vagotomy is adequate or complete, even enormous pre-operative gastric acid hypersecretion is adequately suppressed ( T a b l e 3). If the vagotomy is incomplete, the gastric acid secretory response to insulin may be as great as it was prior to surgical intervention (Table 3). Furthermore, if the vagotomy is incomplete, the addition of antrectomy (Billroth 1) may not satisfactorily suppress acid in all instances, and the insulin gastric analyses may still be positive (Table 4). T h e argument may be raised that an insufficient a m o u n t of a n t r u m was removed. T h i s may be true, but it would be difficult to j u d g e how much is enough for each patient since this would range from n o antral removal needed if vagotomy is complete

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The Value of

Pancreozymin

103

was paid to the presence of typical cholesterol crystals and/or calcium bilirubinate pigments in the sediment. The combination of these two findings in the biliary sediment is pathognomonic of the presence of stones in the biliary tract. 1 · 13 Cholesterol crystal alone in the bile has been representative of stones in about 90% of the cases, and in the remaining 10% cholesterosis of the gall bladder was found. T h e finding of calcium bilirubinate pigment in the bile in the absence of jaundice, or jaundice of recent date, has been reported to be invariably associated with stones. On the other hand, the finding of calcium bilirubinate pigment in the bile in a jaundice patient may or may not be associated with stones in the biliary tract and is thus not included in the present analysis. Of the 4 patients who had a normal gall bladder and absence of calculi on roentgen examination (Table 1), 2 had positive microscopic findings after routine biliary drainage, but all 4 had positive microscopic findings in the bile after pancreozymin stimulation. All these eases had typical calcium bilirubinate pigments on microscopic examination of the post-pancreozymin bile sediments. One patient each, of those who had a faint visualization and a nonvisualization of the gall bladder and no calculi on roentgen examination, had negative findings on routine biliary drainage. However, both had typical cholesterol crystals and calcium bilirubinate pigments in the postpancreozymin bile sediments. Two patients with postcholecystectomy syndrome, who had negative findings on intravenous cholangiography study, had positive microscopic findings in the postpancreozymin bile sediment. These results indicate a superiority of the pancreozymin as the stimulant in the nonsurgical biliary drainage, possibly due to its potent stimulation on the contraction of the gall bladder and consequently an almost complete emptying. On the other hand, of the 3 patients who had findings of calculi on cholecystogram, 2 had positive microscopic findings on pancreozymin stimulation. Thus, a negative finding on nonsurgical biliary drainage does not rule out the presence of stones. All thse cases were explored surgically and cholelithiasis and/or choledocholithiasis were found at operation.

DISCUSSION

Variations in the bilirubin concentration of the duodenal aspirates collected before and during the pancreozymin-secretin stimulation provide reliable information: on the concentrating function of the gall bladder and the possible presence of a cystic duct stump in a postcholecystectomy patient. T h e physiological interpretation of these responses is as follows: in the normal patient bile from the liver enters the gall bladder and is discharged into the duodenum inter-

104

Sun, Tattory,

Chen

mittently, whereas in patients with no gall-bladder function, bile enters the duodenum continuously. As a result, in the presence of a functioning gall bladder, there is marked dilution of bile in the duodenal specimens during the period of maximum pancreatic flow after secretin stimulation, whereas in the absence of the gall bladder, there is only a very slight dilution. A functioning gall bladder concentrates and stores the bile and its bile has a much higher bilirubin concentration. This is reflected by a significant increase in the bilirubin concentration after pancreozymin stimulation. T h e use of pancreozymin in the nonsurgical biliary drainage gives us the best method for the detection of stones in the biliary tract in this group of patients, as compared with roentgen study and routine duodenobiliary drainage. Pancreozymin facilitates the biliary drainage procedure by shortening the time required, 30 minutes as opposed to 120 minutes in the routine biliary drainage using magnesium sulfate as the stimulant. Positive microscopic findings of cholesterol crystals and calcium bilirubinate pigments in the bile sediments have been found with pancreozymin in 8 patients with cholelithiasis and/or choledocholithiasis when routine biliary drainage has failed and when oral or intravenous cholecystography is normal. However, this study was not designed to compare the relative yield of the effectiveness of roentgen examination and pancreozymin nonsurgical biliary drainage on the diagnosis of calculi in the biliary tract. T h e patients in this series were consecutive cases subjected to pancreozymin-secretin test. Cholecystography and biliary drainage are not competitive, but when sensibly employed, complement each other. Nonsurgical duodenobiliary drainage procedure has been shown to be the most important diagnostic examination in a small number of patients having symptoms suggestive of cholelithiasis but showing, by cholecystography, normal gall bladder shadow without stone. However a negative finding on nonsurgical biliary drainage does not rule out the presence of stones.

SUMMARY

A comparative study of three diagnostic tests for biliary tract disease was done in 59 patients. T h e bile sediments following pancreozymin stimulation were examined for cholesterol crystals and calcium bilirubinate pigments. This was compared with the result of routine biliary drainage and roentgen studies of the biliary tract. T h e use of pancreozymin as the stimulant in the biliary drainage gives us the best methods for the detection of stones in this group of patients. In addition, pancreozymin facilitates the biliary drainage procedure by shortening the time required. Variations in the bilirubn concentraton of the duodenal aspirates collected before and during the

The

Value

of

Pancreozymin

105

pancreozymin-secretin s t i m u l a t i o n provides r e l i a b l e i n f o r m a t i o n o n t h e c o n c e n t r a t i n g f u n c t i o n of t h e gall b l a d d e r a n d t h e possible presence of a cystic d u c t s t u m p in a postcholecystectomy p a t i e n t .

REFERENCES

1. BOCKUS, H. L. Gastroenterology, Vol. 3. W. B. Saunders, Philadelphia, 1946. 2. ACREN, G., and LAGERLOF, H. Biliary response in secretin test. Acta Med. Scand. 99:359 (1937). 3. DIAMOND, J . S., SIEGEL, S. Α . , a n d

MYERSON, S. B i l i a r y p i g m e n t

curve

during test secretin test: its diagnostic significance in non-functioning gall bladder. Am. J. Digest. Dis. 7:133 (1940). 4. DREILING, D. Α., and HOLLANDER, F. Studies in pancreatic function; preliminary series of clinical studies with secretin test. Gastroent. 22:714 (1948). 5. AELERCRTNTZ, E., JORPES, E., MUTT, V . , a n d WECELIUS, C . L ' e m p l o i d e l a

cholecystokinine dans la cholecystographie. Arch. Mal. App. Digest. 46:414 (1957). 6. HARPER, Α . Α . ,

7. 8. 9.

10. 11. 12.

and

RÂPER, H .

S. P a n c r e o z y m i n ,

a stimulant

of

the

secretion of pancreatic enzymes in extracts of small intestine. J. Physiol. 202:115 (1943). IVY, A. C., and OLDBERG, E. Hormone mechanism for gall bladder contraction and evacuation. Am. J. Physiol. 86:599 (1928). MARKS, I. N. Changes in the icteric index of the duodenal aspirate after the injection of secretin and pancreozymin. Gastroent. 37:73 (1959). SUN, D. C. H., and SHAY, H. Pancreozymin-secretin test: T h e combined study of serum enzymes and duodenal contents in the diagnosis of pancreatic disease. Gastroent. 55:570 (1960). SOMOGYI, M. Micromethods for the estimation of diastase. J. Biol. Chem. 225:399 (1938). MALLOY, H. T., and EVELYN, K. A. T h e determination of bilirubin with the photoelectric colormeter. J. Biol. Chem. 229:481 (1937). LYON, Β. Β. V. Non-surgical Drainage of the Gall Tract. Lea 8c Febiger, Philadelphia, 1923.

13. BOCKUS, H . L . , SHAY, H . , WILLARD, J . H . , a n d PESSEL, J . F . C o m p a r i s o n

of biliary drainage and cholecystography in gallstone diagnosis with special reference to bile microscopy. J . A. M. A. 96:311 (1931).

CHRONIC PANCREATITIS Plinio Bove*

Chronic pancreatitis may be produced by the action of the etiologic agents on the pancreatic ducts (cholelithiasis, cholangitis, papillitis, inflammatory stenosis of the Wirsung duct) or on the pancreatic parenchyma (alcoholism, chronic protein depletion). In both cases, when the disease has deeply damaged the gland, we found obstruction of the pancreatic ducts accompanied by stasis and hypertension above stenosis. We believe that the intrapancreatic hypertension is the cause of the most important symptoms presented by the patient. This point of view comes from the fact that we obtained the immediate relief of the pain and also of nausea and vomiting by the surgical removal of the stasis. In our opinion, the suppression of the pancreatic stasis must be the purpose of any kind of surgical procedure employed in the treatment of this disease. This can be achieved either by the surgical correction of the stenosis or by the anastomosis of the duct of Wirsung to the digestive tube. SYMPTOMATOLOGY

The character and intensity of the symptoms and signs of the chronic pancreatitis may vary within large limits. The same can happen with its evolution. In this way, we may have a multitude of clinical features which renders difficult the diagnosis of chronic pancreatitis. The symptoms and signs presented by the 107 patients studied in this paper during the acute period of the disease are given in Table 1 : Per cent

Symptom

100 92 85

Pain .... Nausea Vomiting Jaundice * Sao Paulo, Brazil.

60

106

Chronic

Pancreatitis

Symptom Abdominal distention Constipation

107 Per cent 55 44

Diarrhea

14

Palpable mass Fever Diabets Steatorrhea

17 38 13 75

Pain was the most important symptom, and it presented great variations according to its initiation, location, radiation, and character (Figure 1). In certain cases the pain suggested that the pancreas was the organ involved, which could be established by laboratory and roentgenologic examiations. In the great majority of our cases the course was in waves of varying intensity followed by parital or total remission of the symptoms. In 88 cases of this series, the number of attacks are given in Table 2: Attacks 1 2 3 4

Cases 0 3 8 4

5

19

More than 5

53

T h e diagnosis of the disease is generally difficult and the clinical features may be obscure if we do not have the pancreas in mind. When the diagnosis of pancreatitis is clinically made, we may confirm by laboratory examinations and roentgen studies. In our opinion, it is very important to emphasize the radiological examination both in the preoperative period and during the operation. T h e preoperative radiological study is helpful for the diagnosis. T h e radiological examination during the operation permits the choice of the best surgical procedure for each particular case. ROENTGEN EXAMINATION

Preoperative Period In our cases, we found very useful for the diagnosis the following

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radiological studies: simple roentgenography of the abdomen, RX examination of the stomach and duodenum, and splenoportography. When the patient was not jaundiced, we also performed oral cholecystography and intravenous cholangiography. T h e importance of these examinations is unanimously accepted. During Operation Operative cholangiography was performed in all cases of this series. This examination permitted us to choose the correct surgical procedure to treat the biliary lesions when they were present. Figures 2, 3, and 4 show some examples of the biliary alterations more frequently found. T h e pancreatography was taken in 40 cases of this series by catheterism or by punction of the Wirsung's duct. In our experience, pancreatography is the best way to choose the exact procedure for each particular case, cystic dilation of the pancreatic duct in combination with stenosis of the ampullary and cephalic portion of the duct of Wirsung indicates pancreatojejunostomy; obstruction of the ampullary region indicates papillotomy with intubation of the pancreatic duct; multiple obstructions with or without pancreatic lithiasis leads to pancreatic resection or even to the reconstruction of the main pancreatic duct. We think that the diagnosis of the conditions of the pancreatic ducts may be done only by means of the pancreatography. Figures 5 through 12 show particular pancreatographic aspects found in some of our cases. MANAGEMENT

There are many therapeutic measures employed in the management of chronic pancreatitis. T h e medical care that is used mainly during the acute attack is similar to that which is indicated in acute pancreatitis. However, this treatment is unable to cure the patient or prevent recurrence of new attacks, because it cannot remove the etiologic agent of the disease. This can only be accomplished by surgical means; it is wrong to suppose that surgical treatment must be employed when the medical measures have failed. T h e surgical treatment must attain three main purposes: removal of the etiologic agent, correction of the pancreatic ductal stenosis, and partial or total resection of the pancreatic tissue, when it is replaced by extensive fibrosis. T h e operations indicated for the treatment of chronic pancreatitis, which do not aim to attain these purposes, have not given good

Chronic CHRONIC

Pancreatitis

109

PANCREATITIS

Surgical -trtalment tm^lotjid in 107 costs Numb»»· "Results of Patients Good Poor Death

Procidur«

0

BilûUrol Spiane finie «ctomy 1

0

1

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1

r

Al

15

i r

26

2A

ζ

0

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Al

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. ν W M M —• ν o fe* m o m «r> — to o> io o S ' ».«·

x-s PQ < ^—· OO o; m cm etj o «o CMm

m CMm t^ CMoo CM m

^-v ûû — , _ •c s S 3 '-'to o m io σ; t> Oí o — ci m cm ori« l i oints when treating his patients. T h e health authorities will have to control the environmental hygiene, particularly the consumption of potable water, by means of a good water supply system, and the correct control of the excreta, mainly in rural zones. THERAPEUTIC ASPECTS

In the following chart we summarize all the aspects concerning drugs used in each case of intestinal parasites. This chart, based on the data obtained from McHardy, 1 3 · 1 4 · 2 1 Jones, 11 Heilmayer, 12

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Agustine, 18 Alesandri, 1 · Armas Cruz, 17 Frye,18 Martín, 19 Sappenfield, 20 and thoe from our own experience with patients suffering intestinal parasites.®· M · 28 1. Ascaris lumbricoides Selective drug Piperazine Dithiazanine Hexylresorcinol Dithiazanine 2. Trichuris trichiura Selective drug Hexlresorcinol by enema 3. Hookworm Selective drug Tetrachloroethylene Dithiazanine 4. Enterobious vermicularis Selective drug Piperazine Dithiazanine Dithiazanine 5. Strongyloides stercolaris Selective drug Atabrine 6. Giardia lamblia Selective drug Oxytetracycline 7. Balantidium coli Selective drug (Terramycin) 8. Endamoeba histolytica Combination of drugs: Emetine and OxyAcute: tetracyline (Terramycin) and Oxyquinoline Chronic and carrier: Combination cycle of Carbarsone, Oxyquinoline, Chioroquine, and Bismuth Blycolylarsan ilate 9. Teniasis Duodenal drainage Atabrine and castor oil. The dithiazanine iodite must be administered with a double enteric coat in order to avoid gastric irritation. Since this drug is useful in cases of multiple parasitic infestation (Ascaris lumbricoides, Trichuris trichiura, Strongyloides stercolaris, Enterobius vermicularis, Necator americanus), its use is advisable in such cases. SUMMARY AND CONCLUSIONS

1. The intestinal parasitism in Colombia is a serious social and medical problem. It can be said that more than 50% of the population suffers from parasites and very frequently has three or more parasites at the same time.

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2. According to the survey made in hot, mild, and cold areas, in which we checked 138,193 stool examinations, the predominant parasites in Colombia are as follows: 1. Ascaris lumbricoides 38.15% 2. Trfichuris trichiura 31.05% 3. Endamoeba histolytica 23.67% 4. Giardia lamblia 11.31% 3. Health education and public health measures must be simultaneously applied with the therapeutic ones. The authorities must try to supply useful drugs at a low price in order to obtain a good treatment for the mass of sufferers. During the sanitary campaigns, mainly in the rural zones, the authorities must help in the construction of privies at a low price, as well as other engineering and public works of a sanitary nature. Also the authorities should provide the economic facilities and tax deductions to the owners of farms on which these constructions are made. 4. In the schools of medicine it is important that the students be confronted with this kind of social and medical problem from a right point of view. They must have good training both in technical laboratory procedures and in preventive medicine. The authorities should sponsor specialized studies about nutrition in relation to intestinal parasites.

1.

H A B I B , A . Report on Parasitism in Barranquilla. File of the Colombian Society of Gastroenterology (1960). 2. R O J A S , W. Report on Parasitism in Antioquia. File of the Colombian Society of Gastroenterology (1960). S. BORRERO, J . Report on Parasitism in Antioquia. File of the Colombian Society of Gastroenterology (1960). 4 . MEJLA-RUIZ, £. Report on Parasitism in Manizales. File of the Colombian Society of Gastroenterology (1960). 5 . GOMEZ-VESGA, H . Report on Parasitism in Bogota. File of the Colombian Society of Gastroenterology (1960). 6. HERRNSTADT, Β . Report on Parasitism in Bogota. File of the Colombian Society of Gastroenterology (1960). 7. RAMIREZ, J. Report on Parasitism in the I. C. S. S. (Colombian Institute of Social Security) of Bogota. File of the Colombian Society of Gastroenterology (I960). 8. ALBORNOZPLATA, A . Report on Parasitism in Bogota. File of the Colombia Society of Gastroenterology (1960). 9. ALBORNOZ-PLATA, A . Medicina Preventiva. Pág. 162-201. Editorial Omnia. Bogota. 10. ALBORNOZ-PLATA, A. Ascaridiasis en Bogotá. VI Pan American Congress of Gastroenterology, Caracas-Venezuela. Memorias pa. 4 3 5 - 4 4 9 Editoria

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Borrero,

Rojas, Mej'ia-Ruiz

and.

Habib

Grafos (1958). S. Modern Trends in Gastroenterology. Second Series ( 1 9 5 8 ) . Butterworth Co., London. 1 2 . H E I L M A Y E R , W . Manual de Antibióticos y Quimioterápicos en la Terapéutica Moderna. Editorial Praxis ( 1 9 5 8 ) . 1 3 . M C H A R D Y , G. Amebiasis in the United States. VI Pan American Congress of Gastroenterology, Caracas-Venezuela. Memorias pg. 459. Editora Grafos ( 1 9 5 8 ) . 1 4 . M C H A R D Y , G. et al.. Clinical Aspect of Amebiasis, Gastroenteroolgy 286 (1958). 15. ACUSTINE, D., and NEVA, F. T h e Diagnosis and Treatment of Intestinal Parasitism. Medical Clinics of North America (Sept., 1958). 1 6 . ALESANDRI, H . , et al. Advance in the Therapeutics of Intestinal Amebiasis in Adults. World Congress of Gastroenterology, Washington, 1958. The Williams and Wilkins Co. Baltimore ( 1 9 5 9 ) . 1 7 . ARMAS-CRUZ, R . , et al. A Clinical Evaluation of Intestinal Amebiasis. World Congress of Gastroenterology, Washington, 1958. The Williams and Wilkins Co. Baltimore. ( 1 9 5 9 ) . 18. FRYE, W., et al. Ann Ν. Y. Academ. Sc. 55:1106 (1952). 1 1 . JONES,

1 9 . MARTIN,

G.

A.

GARFINKEL,

B.

T.,

BROOKE,

M.

M.,

P.

F.

and

FRYE,

W. Comparative Efficacy of amebicides and antiobiatics in Acute Amebic Dysentery. J. A. M. A. 757:1055 (1953). 2 0 . SAPPENFIEL, R . W . , CARTER, F . R . N . , CULBERSTON, C „

BROOKE, M .

M.,

M. and FRYE, W. W. Therapeutic Aspects of a Water-Born Outbreak of Amebiasis in South Bend, Indiana. J. A. M. A. 159:1009 (1955). 2 1 . M C H A R D Y , G . , and FRYE, W . W . Antibiotics in the Management of Amebiasis. J. A. M. A. 154:646 (1954) 22. ALBORNOZ-PLATA, A. Eritromicina-Carbarsone en el Tratamiento de la Amibiasis. Review: Facultad de Medicina, Bogotá. Vol. 27 No. 10-12 (Oct.-Dec. 1959). 2 3 . ALBORNOZ-PLATA, A . Clinical experiment with Dithiazanine Iodide in Bogota. Amer. J. Gastroenterology. 32:729 (1959) . PAYNE, F .

DISCUSSION OPENED BY FIGUEIREDO MENDES Dr. Mendes: I want to congratulate Dr. Nemir for his execellent presentation on surgical treatment of achalasia. I wonder if h e could give us some more information regarding two points concerning the cause of achalasia in his cases. As you know, there are two groups of patients, the ones with Chagas' disease we see in o u r country a n d the other g r o u p you see in your country. T h e second p o i n t refers to the size of dilatation of the esophagus. Of course, as you might expect, we are concerned about the regurgitation. Dr. Berk: I w o u l d n o w like to call o n Dr. H a f t e r . H e has some-

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thing he would like to tells us. Dr. Hafter: Will you give we two and half minutes? I hardly remember a congress of gastroenerologists in which Heller's operation has not been emphasized as the best method for treatment of achalasia. I don't quite agree with this statement. It is certainly better than dilatations with a balloon or with a mercury dilator. However there is another method which I think, is not as well known as it deserves to be: the method with the metallic dialtor of Starck. This instrument has been constructed some years ago and is used nearly everywhere in Germany, in the German part of Switzerland, and in Spain, but is rejected in other countries. They say that it is a brutal German method, not to be applied to citizens of the United States, Britain, or of France. I have been using it for more than 10 years, on 42 Swiss and on 6 French citizens who came over the frontier to have it done. I think it is German but it is far less brutal than a Heller's operation. May I show you how it works: I do it on private patients in my office. T h e patient sits on a chair and Is given some local anesthesia of the pharynx. T h e n the flexible instrument is introduced into the stomach. There is opened (like an umbrella) and withdrawn until it stops at the cardia. It is closed now and withdrawn 3 more cm. to reach the level of the cardia. In this position it is opened abruptly, closed and taken out. T h e patient feels a rather severe pain for 1 or 2 minutes, which disappears after an intravenous injection of petidine. After lying down for two hours, he returns home by taxi. He is advised to take liquid food all day, to call in the afternoon about his condition, and to call again the next morning. You will hear that he had a wonderful breakfast which passed the cardia without difficulty and which he enjoyed as never before. It is advisable to introduce a soft tube once a week for a duration of 1 month. T h a t is all. I think this is a very simple method, somewhat simpler than Heller's operation. It is inexpensive and without danger. Among 48 cases I had one hemorrhage which was not severe and twice fever a few days following the management, which could be controlled by antibiotic therapy. I was not able to pass the cardia in two cases, and these had to be patients there was one who had had Heller's operation without operated by Heller's procedure. Among the successfully treated benefit two years previously by the most competent man in esophageal surgery in Paris. All 46 treated patients are content with the results; 37 are very well, 9 are well. I think this mthod should be known and applied, even by surgeons, as they do in Zürich. Dr. Berk: T h a n k you very much, Dr. Hafter. I don't know haw it is in Switzerland, but I am going to assume that it is pretty much as it is in the United States and so, if I were you, I would sit at the back of the room close to the door and not let anyone out before

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Albornoz-Plata, Borrero, Rojas, Mejia-Ruiz and. Habib

you ge that instrument back. I shall now recognize Dr. Haubrich and Dr. Sifre and then I am going to ask Dr. McHardy and Dr. Bove to close the discussion on this subject. Dr. Haubrich·. Does Dr. Nemir still supplement the Heller operation with pyloroplasty? Dr. Sifre: We certainly don't have in Puerto Rico the enormous experience of Dr. Mendes and other Brazilians with this condition. Within the last 2 years, we have had 4 cases of achalasia which we had to refer to surgery because they failed to respond to the procedures we employed. One of these patients was sent to Dr. Nemir's group in Philadelphia and was operated upon. He is doing very nicely. Another patient was operated upon by one of our local surgeons with the same procedure and is again doing very nicely. We have a third patient, however, who had a Heller procedure done. The patient developed a stricture following the operation, and was again operated upon. Now she again is having difficulties and has to have dilatations. So here is one result which is not so good. I would like to ask Dr. Nemir how often does a stricture result after this procedure. Dr. McHardy: Dr. Hafter's inference that the Starck dilator has been discarded in the United States is incorrect. It is still in wide usage, but in my opinion it has not proven more satisfactory than the mercury pneumatic diator. It serves exactly the same purpose. It is however, my impression that the extensiveness of the dilatation of the Browne-McHardy mercury pneumatic dilator is greater, less traumatic, and dilatation is practiced with less risk than is encountered with the rigidity of the Starck dilator. We have no objection to the Starck dilator. We, however, advocate the pneumatic dilator. Dr. Bove: We have in Brazil extensive experience with achalasia. We use, generally, dilatation kith hydrostatic balloons. The results are very good; generali one or two dilatations are sufficient. Operation is done only in special cases—about less than 1% of patients —and we believe that dilatation in achalasia is the best procedure. Dr. Berk: What operation do you do in Brazil? Dr. Bove: Heller's operation. Dr. Berk: Dr. Nemir, do you want to answer some of the questions? Dr. Nemir: In answer to Dr. Mendes' question, these esophagi are in many cases very large in size. In answer to your second question, certainly not all of these patients have gone along well. We calculate that about 80% of them have had excellent results and that about 20% of them have had subsequent difficulties requiring further operations or dilatation. I think only 2 patients are still having dilatation. Around 4 have been re-operated upon and have had a repair of a hiatal henia or have had a jejunal interposition because

Intestinal Parasitism in Colombia

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of irreversible stenosis. In answer to Dr. Hafter's comments, we certainly believe that dilatation should be done first, and most of our patients have had a course of dilatation before they have been operated upon. Approximately 15% of patients with achalasia come to surgery. I want to say, however, that this is a simple procedure and if it is carried out properly the results in most cases will be good. Dr. Berk: I think Dr. Haubrich asked you abut complementary pyloroplasty. Dr. Nemir: Yes, it is being done routinely. Dr. Berk: And now we move on to the next papers. Dr. Mendes: I wan to congratulate Dr. Antia for his brilliant presentation about the relative incidence of diverticulosis in his country. I got the impression that his findings coincide with the statistics of other countries. I would like to make some points before starting the discussing. Among the 543 barium enema studies, how many cases of cancer of the colon did you find? Secondly, how many of your cases of diverticulosis went on to diverticulitis- And the third question: is the average life standard in India going u p Dr. Berk: I would now like to ask Dr. Bockus for his comment. Dr. Bockus: On a brief little trip through the Orient not too long ago, I was impressed with the fact that I encountered a number of surgeons in the Far East who had never operated on a patient with diverticulosis. Dr. Barborka and I became very much impressed with the fact that diverticulosis either didn't occur, or was exceedingly rare. This was particularly true in India. And for this reason we thought it would be a fine thing if someone would make a statiscal survey. We sensed that diverticulosis did occur but that X-ray studies were less frequent than in Western countries. I wish merely to speak to this point for one reason. One of the surgeons in the Women's Medical College of New Delhi told me that he felt the reason why diverticulosis didn't occur was that the average Indian didn't allow himself to become constipated, that they took laxatives every night if their bowels didn't move. I never thought that constipation has very much to do with the development of diverticulosis. Dr. Barborka came up with a much more sensible explanation. He said: "Harry, have you noticed in looking around that Indians never sit, they squat." And so Dr. Barborka hit on the notion that the reason why Indians didn't get diverticulosis is because of certain pressure changes or the basence of them in the person who spends so much time squatting rather than sitting. Dr. Berk: Despite this interesting observation by Dr. Barborka, it would appear from Dr. Antia's report that his countrymen do have diverticulosis after all. Are there any other comments? Dr. de la Vega: I would like to comment on this topic because

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it has some interesting points. I do agree with Dr. Antia on the incidence of diverticulosis of the colon, which is more or less the same in the different areas of the world. However, there is no doubt in my mind that the incidence and particularly the severity of complications varies from country to country. This brings up, for further discussion, the possible influence of the milieu and the environmental factors in the evolutive aspects of some pathological conditions which might afflict the human being. Dr. Antia: Carcinoma of the colon was detected in only 4 cases of this series. With roentgenograms alone it was not easy to decide whether there was only diverticulosis or associated diverticulitis. Diverticulitis also requires clinical assessment, and we have not touched that aspect. I was also asked about the incidence of diaphragmatic hiatal hernia in cases of diverticulosis. Unless a careful study is made they are missed. Also, not all the patients studied for the colon had the barium study of the upper gastrointestinal tract, and I therefore cannot answer thaat question. Some gastroenterologists have postulated about the possible causes of lower incidence of diverticulosis in my country. This reminded me of my initial chemistry lecture, where I was told by my professor that there was a heated controversy amongst the ancient Greeks as to why the dead body weighed more than the live one. Plenty of theories were put forward until one wise guy weighed bodies and found that the dead did not weigh more. The same holds good for the theories of vegetarian diet, and squatting posture assumed by some Indians during defecation, as the probable causes for the low incidence of diverticulosis in Indians. Actually, as already shown from the data, within the higher age group, the incidence of diverticulosis amongst Indians is as high as in the Western countries. Dr. Berk: It was interesting to attend two important papers: one dealing with the high incidence and widespread distribution of intestinal parasitism and the other, of Dr .Beker, showing the histologic changes in intestinal parasitism. The Colombian Group stressed the extraordinary importance of these parasites and I think that the same applies to most of the countries of South America. A recent survey made in Rio de Janeiro generali agrees with the finding of the Colombian group. I have one question for the Colombian group—how many stool examinations were made to reach these conclusions? It is well known that the number of parasits increases considerably with the number of stool-examinations. Dr. Berk: Dr. Job has requested the opportunity to make some comments. Dr. Job: I have noticed that several patients who came to me for cardiovascular symptoms (tachycardia, chest pain, etc.) with ob-

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vious intestinal symptoms were found to have intestinal parasites. After treatment with antiparasitic durgs their cardiovascular symptoms disappeared. I should like to hear from our Colombian colleagues whether they have observed the same type of what I have called extra-intestinal symptoms of amebiasis and lambliasis. Dr. Raghavan: I would like to ask Dr. Beker whether the biopsies were taken from cases which showed a malabsorption syndrome. Dr. Berk·. Dr. Dapena, what do you think of these biopsies? Dr. Dapena: I really don't have a very firm opinion after seeing just one slide. I would like to see the biopsy specimen. I didn't think that they showed a frank malabsorption pattern. I detected one, stained with trichrome stain, which showed definite fibrosis I wonder whether that has been checked out in allthese cases. Dr. Hawkins: In a small percentage of children with coeliac disease at the Children's Hospital, Birmingham, giardia lamblia organisms have been seen, often in great numbers, in the jejunal biopsy specimens. T h e mucosa of these does not show the typical flat appearance of coeliac disease but rather the partial villous "atrophy" with increased round cells suggestive of jejunitis (Cameron et al., 1962). Mepacrine (quinacrine) often cures the steatorrhea, and further studies may show improvement in the changes seen on biopsy. [References Cameron, A. H., Astley, R., Hallowell, M., Rawson, A. B„ Miller, C. G., French, J. M., and Hubble, D. V. Duodenojejunal biopsy in the investigation of children with coeliac disease. Quart. J. Med. N. S. 31:125 (1962).] Dr. Berk: I want to ask a question of Dr. Orellana as a representative of Chile One of your countrymen told us at the last World Congress that finding amebae in the stool in patients with vague symptoms was not of much significance and does not necessarily rerequire energetic antiamebic treatment. What about this? And what about all the parasites they find in Colombia? Ahe they responsible for such disturbances as De. Beker showed in the intestine? Dr. Orellana: Even though I do not have much experience concerning parasitic diseases, I can say that we find amebae in the stools very frequently but we do not consider it necessarily a pathogenic entity. Dr. Berk: My recollection was that a group controls were treated with placebos. They apparently did just as well symptomatically and the amebae disappeared from their stools. Now, Dr. Beker, you have about 25 questions to answer in one minute. Dr. Beker: All our cases with strongyloidiasis had a malabsorption syndrom. The patients had a thorough study from the clinical point of view and a radiological study with the spruelike pattern; in addition, they were given a biochemical investigation with abnormal

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1-1131-trioleine study and the D-xylose test. In the cases infested with Necator Americanus we found only an abnormal folic acid test, with normal I-131-trioleine and D-xylose tests. As I stated at the end of my paper, these changes are not specific but they should be known when cases with parasitism are studied. Dr. Jàcome-Valderrama: Symptomatology of intestinal parasitism is quite different from one case to another. Sometimes there are no direct digestive symptoms but rather extra-intestinal symptoms, and this is very frequent in our experience. Dr. Orellana states that it is possible to find patients suffering from amebiasis always produces some kind of symptoms and very frequently they are extra-intestinal. Histolytic amebae are some of the most dangerous parasites. Dr. Berk: Dr. Jacome, do you see extra-intestinal symptoms, cardiovascular and others, in patients with these parasites? And do they clear up when you treat the parasite? Dr. Jacome: Yes, that's right. Dr. Berk: I should like now to close the scientific session by expressing my personal deep thanks to all of the participants. I think they have brought us much of great value and we are very grateful.

CHAPTER VI NOTICES

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T H E SOCIAL ACTIVITIES OF T H E FOURTH MEETING OF THE BOCKUS INTERNATIONAL SOCIETY OF GASTROENTEROLOGY

Most of the participants to our meeting arrived on Sunday, May 6, and saw Geneva on a beautiful and sunny day. The famous fountain in the middle of the lawn was reaching its 300 feet (it is the highest in the world, although it is not in the U. S. A.) and the snow-capped mountains were making a lovely circle around the city with Mount Blanc in the background (it is the highest in Europe although it is not in Switzerland). After a walk along the lake or in the old city, everybody was back in time to the Hotel Richemond for the cocktail party offered by the chairman of the local committee, Dr. Bernard Wissmer, and his wife. T h i s was a good start, because even before the official opening, the typical friendly atmosphere of this Fourth Meeting was created. T h e next day, after a morning of very stimulating presentations and discussions, the whole group was taken in buses to visit Geneva and the surroundings. T h e sky was as blue as ever and everybody enjoyed the many interesting monuments, churches, magnificent parks, and the numerous international organizations (U.N., W.H.O., International Labor Office, Red Cross, etc.) which make Geneva the h u b of the world. At six, the Geneva municipal government gave a lavish reception at the famous Palais Eynard, where the Big Four met once during the Summit Conference. After eating, drinking, and admiring the splendid rooms of the purest Empire style, our people spread throughout the city for a "free evening" which, for some of them (no names, because of medical ethics), was extremely freel Tuesday, the blue of the sky was a mixture of California and Riviera blue when the magic roof of the Hotel Richemond opened at the end of the brilliant Symposium. Taking a huge picnic basket, everyone found a seat on one of the busses which took the road for Lausanne along the lake. After eating lunch on the terrace of the 288

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Château de Chillón, the cars left the lake and started to climb the terrifying Col des Mosses. For Swiss people, this is a kind of highway, but for Americans (including daredevil driver Da Pena) it was like a mule path. Scared, but happy, the group reached the pass still covered with snow, and a snowball fight relaxed tense nerves. Finally the busses arrived in the old medieval city of Gruyères and, after sightseeing and shopping, the congressiste met for cocktails on the terrace of the beautiful castle where Dr. Wissmer introduced Mr. and Mrs. Maurice Guigoz, who were offering this party and the following banquet. After another short drive, the admiring group saw the impressive castle of Oron, brilliantly illuminated, where they were received by clarion players and guards in uniforms of the thirteenth century. After a tour of the castle, an explosive cocktail party was given in the armor room. Then a magnificentn candlelight dinner was served and many good speeches were given. Dr. Wissmer thanked Mr. and Mrs. Guigoz and offered them a gift, and our Presidentn Dr. Wiebenga thanked Dr. Wissmer and presented him with a beautiful antique Chinese plate. After hearing Dr. Bockus, Dr. Valencia-Parparcen, and many others thanking each other, local folk singers in Swiss costumes sang lovely old songs. Very cute dolls were offered to the lonely guys to keep them company. Only in the early hours of the morning everyone joined this bed for a short rest. Wednesday, May 9, Dr. Hunt, President of the British Society, was supposed to participate to the meeting. For that reason problably, the weather became extremely Londonian, and the cruise on the lake started under heavy rain. Some were afraid and stayed home, but the others certainly did not regret their effort. T h e sky cleared u p very soon and for three hours the boat sailed along the shores of Lake Geneva while a very gay jazz band was keeping everybody on their feet. Dr. Bockus did not miss one dance. At the end, the orchestra had been practically replaced by members of the Society and a group of South American singers was giving excellent vocal accompaniment. Officers President Adolf H. Wiebenga Eindhoven, Netherlands President-Elect José Maria de la Vega Mexico City, Mexico Vice-President Bernard Wissmer Geneva, Switzerland Secretary-General James L. A. Roth Philadelphia, Pa., U.S.A.

Entry of the Castle of Oron. An old Swiss Guard and the curator of the castle greet the gnests with B. Wissmer.

Boat Cruise on the Lake of Geneva. Dr. H. L. Bockas dancing with Mrs. B. Wissmer and Dr. B. Wissmer with Mrs. H. L. Bockas.

Candlelight banquet at the Castle of Oron.

Boat Cruise on the Lake of Geneva. From left to right: Dr. E. Deutsch, Dr. J. M. de la Vega, Mrs. B. Wissmer, Dr. H. L. Bockas, Mrs. F. Vilardell, Dr. A. Wiebenga, Dr. B. Wissmer, Mrs. A. Wiebenga, Mrs. H. L. Bockus, and Dr. F. Vilardell.

Cocktail party in the Court of the Castle of Gruyeres.

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Recording Secretary Ramon Sifre, Jr. San Juan, Puerto Rico, U.S.A. Treasurer J. Edward Berk Detroit, Mich., U.S.A. Counsel T . Figueiredo Mendes Rio de Janeiro, Brazil Honorary

President

Henry L. Bockus, 250 S. 18th Street, Philadelphia 3, Pa. Members Faculty Members Cohn, Edwin M., 4652 No. Warnock Street, Philadelphia, Pa. Hodes, Philip J., Jefferson Medical College Hospital, 11th and Walnut, Philadelphia 4, Pa. Hundley, J. Wàrren, 3818 Chesnut Street, Philadelphia, Pa. Katz, Albert B„ 5581 No. Park Ave., Philadelphia 41, Pa. Metzger, Harry M., 1815 Pine Street, Philadelphia, Pa. Pessel, Johannes F., 224 W. State Street, Trenton, N.J. Pincus, Irwin J., 4833 Fountain Ave., Los Angeles, Calif. Rothman, Maurice M., 1727 Spruce Street, Philadelphia, Pa. Rush, Alexander, 330 S. 9th Street, Philadelphia, Pa. Shay, Harry, Fels Research Institute, 3400 N. Broad St., Philadelphia, Pa. Tumen, Harry J., 1830 Rittenhouse Square, Philadelphia 3, Pa. Willard, John H„ Ivy Hill. Harlan, Ky. Associate

Members

Atkins, Joseph, 1201 Knox Road, Wynnewood, Pa. Breslow, Irving, Graduate Med. Bldg., Suite #205, Philadelphia, Pa. Burros, Harry M„ 903 Hagys Ford Rd„ Penn Valley, Narberth, Pa. Cohn, Isidore, Jr., 510 Iona Street, Metaria, La. Cooper, Donald R., 1237 Arwyn Lane, Gladwynne, Pa. Dapena, Antonio, M. Valdes, 3006 Midvale Ave., Philadelphia, Pa. Ferguson, L. K„ 419 S. 19th Street, Philadelphia 46, Pa. Finkelstein, Arthur, 480 Latch's Lane, Merion, Pa. Frobese, Alfred S., 1425 Scrope Road, Rydal, Pa. Hawthorne, H. R., 1016 Yardley Rd., Morrisville, Pa. Hincapié, Jorge Ivan, Facultad de Med., Univ. de Antioquia, Medellin, Colombia, S.A.

Social Activities of the Fourth

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Nemir Jr., Paul, Grad. Med. Building, 419 S. 19th Street, Philadelphia, 46, Pa. Poinsard, Paul J., 407 Wynmere Rd., Wynnewood, Pa.. Ritter, Joseph Α., 2031 Locust St., Philadelphia, Pa. Rome, Howard, 622-5th Street, S.W. Rochester, Minn. Samitz, Μ. H„ 1715 Pine Street, Philadelphia 3, Pa. Schulz, Norbert J., Rittenhouse Plaza, Philadelphia, Pa. Stahlgren, Leroy, Grad. Med. Building (Suite 304), Philadelphia 46, Pa. Stein, George N., 544 Howe Rd., Merion Station, Pa. Tulsky, Emanuel, 8331 High School Road, Elkins Park 17, Pa. Widmann, Bernard, 2031 Locust St., Philadelphia, Pa. Active

Members

ARGENTINA

Kohan, Samuel, 51 Monies de Oca Ave., 1-B Buenos Aires. Schor, Isaias, Zavalia 2136, Buenos Aires. BRAZIL

Almeida, Paulo E., R. Francisco Sa., 61 Apt. 802, Rio de Janeiro. Capparelli, Vittorio, Rua Santos Dumont 431, Uberlandia, Minas Gérais. Friozzi, Gustavo, Rua Xavier de Toledo, 44, Sao Paulo. Moraes, Julio S. De, Guulhermina Guinle 210, Rio de Janeiro. Mendes, Figueiredo, Av. Rio Branco, 257-18, Rio de Janeiro. Pacheco-Cervalho, Hypolito, Gaixa Postal 1596 Porto Alegre, R. G. Sisl. Passarelli, Nelson, Rua General Artigas 222, Lebion, Rio de Janeiro. Miranda, Mario Pinto de. Rua Prof. Alfredo Goma 15, Rio de Janeiro. Pontes, J. Fernandes, Rua Japura 42, Sao Paulo. Siffert, Geralda, Avenida Graca Aranha 81, Rio de Janeiro. Toledo, Jorge de, Av. Paulo de Frontin 198, Αρ. 101., Rio de Janeiro. Job, Jose Martins, Rua Augusto Pestana 25, Porto Alegre, Rio Grande do Sul. Mello, Flavio Migues de, Caixa, Postal 1039, Rio de Janeiro. Reis, Francisco Alves dos, Instituto de Gastroenterologia de Minas Gérais, Avenida Amazonas, 314-9, andar, Belo Horizonte. CENTRAL AMERICA

Cordillo, Rosendo, 2a, Calle No. 4-41, Guatemala 1, Guatemala. Martinez, Guillermo., la La Calle Oriente # 6 , Santa Ana, El Salvador.

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of the Fourth

Meeting

CANADA

Ballem, Charles Miller, 1374 Sherbrooke St., West, Suite 8a, Montreal, Quebec. Bogoch, Abraham, 3195, Granville St., Vancouver, 9, B. C. Bourne, Robert H. 5584 Queen Mary Rd., Montreal .Quebec. Langis, Camille, 2570 Lajoie Street, Trois Rivières, Quebec. McKenna, Richard D., 1390 Sherbrooke St., West, Suite 25, Montreal, Quebec. Moros, George, 23 St. Joseph Blvd. West, Montreal 14, Quebec. Solway, Samuel D., 158 St. George St. #101, Toronto 10, Ontario. Sutherland, L. J., 854-lst Avenue West, Owensound, Ontario. Taube, Η. Ν., 732 Spadina Ave., Toronto 4, Ontario. Thibert, Florent, Hospital Masonneuve, Montreal, Quebec. Tremblay, J. Jacques, 78 Quest Baul, St. Joseph, Montreal, Quebec. CHILE

Orellana-Alcalde, Jose, Hosp. Clinico Univ. de Chile, Santois Dumont 999, Santiago. Klinger, Jaime, Hospital del Salvador, Ave. Salvador 562, Casilla 70 D, Santiago. COLOMBIA

Alban, Vincente, Calle 34 #22-08, Bogota. Albornoz-Plata, Α., Calle 17, #8-50, Bogota. Aljure, Farid, Apdo. Aereo 540, Armenia. Alvarado, Silvano Α., Calle 38 #15-42, Bogota. Burbano, Luis Carlos G., Carrero 28 No. 18-31, Pasto. Habib, Antonio, Calle 42 No. 41-118, Apt. Aereo 1700, Barranquilla. Lega-Siccar, Jorge, Apartado Aereo #4628, Cali. Martinez, Abelardo P., Carrera 18 No. 58-59, Bogota. Moreno, Bernardo, Carerra 5a #81-26, Bogota. Osorio, Carlos Α., Calle 22 No. 12-40, Bogota. Pelaez, Jorge, Calle 54 No. 49-93, Medellin. Rodriguez, Miguel M., Calle 59, No. 53-33, Barranguilla. Velez Escobar, Ignacio, Aptd. Aereo 705, Medellin. CUBA

Heros, Orlando de los, Calle 1, No. 506 Entre 23 y 25. Vedado, Havana.

Social Activities of the Fourth Meeting

295

DENMARK

Barfred, Arne, Viborg. DOMINICAN REPUBLIC

Brea, Aulio R., Ave. Independencia 18, Cuidad Trujillo. Brozza Jordi, Clinica Abreu, Sano Domingo. EGYPT

Mouhran, Y. Z., 49 Giza Street, Cairo. ENGLAND

Cooper, C. Foster, 149 Harley Street, London W l . Hawkins, C. F., 89 Harborne Rd., Edgbaston, Birmingham 15. Leveau, Vivian M„ Dunvegan, Stoke D'Abernon, Cobham, Surrey. GREECE

Archimandritis, Achileus, 11 Tsoptous Street, Volos. Bellonias, Evangelos, 17 Roverton Galli St., Athens. Dambassis, John Nicholas, 14 Sina Street, Athens. HAWAII

Chang, Richard C., 1481 South King St., Honolulu. Okazaki, Kyuro, 1448 Liliha St., Honolulu. INDIA

Antia, Framroz Perojahaw, 534 Sandhurst Bridge, Bombay 7. Raghavan, P., Seth Cordhandas Sunder das Med. Coll., Parel, Bombay 12. IRAN

Ghavami Abolghassen, Shiraz Medical Center, The Nemazee Hospital, Shiraz. IRELAND

Logan, John S., 24 Malone Rd., Belfast, No. Ireland.

296

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KOREA

Lee, Po Young, Dept. of Medicine, Severance Hosp., Seoul. Mexico Brucilovsky, David, Paseo de la Reforma 510-202, Mexico 6, D.F. (Debrian) Manuel Pelaez, Presa Palmito 23-4, Mexico 10, D.F. Fregoso, Joaquin Α., Durango 145, Mexico 7, D.F. Naves-Gonzales, Jose, Monterrey 132-101, Mexico, D.F. Pena y de lo Pena, Enrique, Durango 296 Ler Pis, Mexico 11, D.F. Pena-Garza, Febronio, Lic. Virgilio Garza, # 1 3 5 Col. Chepe Vera, Monterrey, N. L. Ponce de Leon, Alfredo L., Cerrada de Pachuca 12, Mexico 11, D.F. Ramirez, Adolfo Hernandez, Nextengo # 1 8 4 Sta. Lucia Atzco, Mexico 16, D.F. Silva-Contreras, Richardo, Vermount #11, Co. Ñapóles, Mexico 1. D.F. Tovia, Francisco, Arriaja, 13 sur 301, Puebla Pue. Vega, Jose Maria de la., 1265 Paracaima, Mexico 10, D.F. Villalobos, Jose de Jesus, Estocolmo No. 22 Mexico 6, D.F. NETHERLANDS

Wiebenga, Adolf, 89 Parklaan, Eindhoven. PERU

Biber, Max, Casilla No. 2204 Lima. Klinge, G. Garrido, Belen 1081-212, Lima. Ugarte, Carlos R. Merino, Trinidad, Moran 905, Lince, Lima. PHILLIPPINES

Liboro, Oscar Lopez, 1552 Espana, Manila, Phillippines. Roman, Francisco J., Suite 212 Alcopar Bldg. Manila, Phillippines. PORTUGAL

Monteiro, Jose G., R. Augusta 13, Coimbra. PUERTO RICO

Berio-Suarez, Jose M. Professional Bldg. 207, Ave. de Diego 310, Santurce.

Social Activities of the Fourth

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297

Borras-Rivera, Bartolome, 1054 Ponce de Leon Ave., Parado 16, Apartado 9123, San Juan. Hernandez-Morales, Frederico, Wilson Med. Building, 1475 Wilson St., Santurce. Nigaglioni, Adan, 1302 Ponce de Leon, Santurce. Robert, Jose L., 1653 Ponce de Leon Ave., Santurce. Sifre, Ramon., Ave. de Diego 322, Santurce. SPAIN

Vilardell-Vinas, Francisco, Calle Bruch 125, Barcelona 9. SWITZERLAND

Affooer, Heinz P., Berchenstrasse 12, Olten. Ammann, Rudolf W., Pestalozzistrasse, Zurich 32. Wissmer, Bernard, 7 Bd. Jacques-Dalcroze, Geneva. THAILAND

Bodhidatta, Pranot, 440 Boholyotin Rd., Ampur Dusit. Bangkok. Settachan, Sammeans, Provincial Hospital, Korat. TAIWAN

Li, Cheng-Bih, # 2 0 , Lane 119, Section 1, Hain-'Scheng So. Road, Taipei. TURKEY

Cokdegerli, Muzeyyen, Denizciler Cad. Saka Han, Ankara. User, Tevfik E„ 78 Sokak St, 12/3 Bagcelievler, Ankara. VENEZUELA

Beker, Simon G., San Bernardino, Av. Los Procereres No. 12 Caracas. Oliver-Luengo, Walter E., Avenida 5, No. 21-52, Merida. Osualdo, Garcia Arenas, Av. 34-No. 69-05, Maracaibo, Venezuela. Rosa, de la Pedro Emilio Ramos, Manzana Β. Qta, "Gla-Zora" URB, Las Fuentes, Caracas. Ruiz-Velutini, Ramon, Instituto Diagnostico, Ave. Anauco, San Berdino, Caracas. Stolk-Mendez, Gustavo, Centro Medico, Consultori 5, Caracas. Szotlender, Natalio, Av. San Gabriel, No. 43 La Florida, Caracas.

298

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U.SA. Active Members Aaron, Oris, 606 Hill St., Columbia, Ky. Arhens, Lawrence B., 300 Main Street, New Britain. Conn. Albacete, Rene Andres, 2250 Washington Ave., Silver Spring, Maryland. Aucremann, Charles Emile, 330 Beach Drive N., St. Petersberg, Fla. Ayulo, Julio Α., 27 No. London St., Mt. Sterling, Ohio. Banks, Benjamin, 416 Marlborough St., Boston 15, Mass. Banks, Roland, Palmetto Medical Clinic, Wauchula, Fla. Becker, Irvin M., 2040 Wisconsin Ave., West, Milwaukee 3, Wis. Beman, Floyd, Ohio State Univ. Hospital, Columbus, Ohio. Berk, J. Edward, California College of Medicine, 1721 Griffin Avenue, Los Angeles, 31, Cal. Billingsley Jr., William K., 660 W. Broadway, Glendale, Calif. Bippus, William E., 1939 No. Flagler D„ West Pam Beach, Fla. Bressler, Victor, 5607 Ventnor Avenue, Ventnor, N.J. Bruns, Hans, East Genesee Med. Bldg., 1200 E. Genesee Street, Syracuse 10, N.Y. Buchman, E., 325 College Court, Iowa City, Iowa. Cantor, Jack L., 960 Arthur Godfrey Road, Miami Beach, Fla. Cash, Isadore I., 945 N. 12th Street, Milwaukee 3, Wis. Chamovitz, Robert, 3515 Fifth Ave., Pittsburgh 17, Pa. Chipman Jr., I. Lewis, 607 W. 18th St., Wilmington 2, Del. Choi, Heung Jai, Graduate Hosp., Univ. of Pa., Phila., Pa. Coleman, Blair, Wichita Falls Clinic, Wichita, Tex. Commanduras, Peter, 4512-Slst Street, Arlington, Va. Connelly, Richard C., 1360 Three Mile Drive, Grosse Pointe 30, Mich. Crismon, Lester C., 347 St. Johns Way, Lewiston, Idaho. Curb, Dolph L , 6448 Fannin, Houston 25, Tex. Davidson, Jay H., 1002 Spruce Street, Phila. Pa. Davis, Thos. G., 12 No. State St., Ephrata, Pa. Dietchman, Morris, 207 West Valencia, San Clements, California. Falla-Alvarez, Laureano, 1550 Ancona Avenue, Coral Gables, Fla. Fernandez, Adolfo, Field Clinic, 1800 W. Wilson Ave., Chicago 40, 111. Firestone, Bertram I., 318 5th Avenue, Youngstown 2, Ohio. Forester, Virgil R„ Pasteur Med. Bldg., 1111 N. Lee St., Oklahoma City, Okla. Freeman Jr., Arthur M., 614 Medical Arts Bldg. Birmingham, Ala. Garner, Jay M., 723 Elm Street, Winnetka, 111. Gelber, Isaac, 712 N. Broad Street, Elizabeth 3, N.J. Goldstein, Edward W., 561 E. 28th Street, Patterson, N.J. Goldstein, Franz, 1012 Walnut Street, Philadelphia 7, Pa. Gordon, Arnold Milton, 4406 Greenwood Drive, Des Moines 12, Iowa. Gould, James Patrick, 6202 S. Campbell St., Chicago, 111.

Social Activities of the Fourth

Meeting

299

Gracyzk, Stephen Α., 1105 Broadway, Buffalo 12, N.Y. Greenfield, Herbert Z., 1096 Munn St., East Orange, N.J. Grunow, Albert C„ 763 Broad Street, Newark 2, N.J. Hamley, John J., 573 Irvington Ave., Elizabeth, N.J. Haubrich, William S. Henry Ford Hospital, Detroit 2, Mich. Holiey, Atmor, 512 Douglas Ave., Brewton, Alabama. Hoyt, Ralph C., 328 N. 5th Street, Reading, Pa. Hutchinson, W. James, 814 E. Market Street, York, Pa. Hyatt, Irvin, 11 East Chase Street, Baltimore 2, Md. Jobb, Emil 5,59 Med. Dental Bldg., Seattle, Wash. Jones, Charles Α., Box 1365, Williamson, W. Va. Kaiser, Martin H., 7445 S.W. 135th St. Miami, Florida. Kaminsky, Aaron L., 121 Second Terrace, Di Lido Island, Miami Beach, Fla. Kaplan, Allan Α., 1674 Meridian Avenue, Suite 207, Miami Beach 39, Fla. Kaplan, Eliah, 223 No. Mercer Street, New Castle, Pa. Kasich, Anthony M„ 242 E. 72nd Street, New York, N.Y. Koolpe, Louis, 7400 Georgian Road N„ Philadelphia 38, Pa. Koziol, Edward S., 2010 Wilshire Blvd., Los Angeles 57, Calif. Krohn, Stuart E., 18 Hopper Street, Utica 2, N.Y. Leiter, Samuel S., 1301 Westbury Drive, Philadelphia 31, Pa. Lerner, Jacobo, V. A. Hospital, Temple, Tex. Leteer, Clarence Ralph, 414 Navarro Street, San Antonio, Tex. Lilley, George Wood, 316 W. 9th Street, Chester, Pa. Ling, William, 34 East Seventy-Second Street, New York 21, N.Y. Lipman, Max Peter, 6317 Wilshire Blvd., Los Angeles, Calif. Logan, Victor W., 115 Stonybrook Drive, Rochester 18, N.Y. Lopusniak, Mieczyslow S., Lankenau Medical Bldg. Philadelphia 31, Pa. Magnes, Max, 646 Broadway, Paterson, N.J. Manier, James W., IV, 313 3rd Street, Marshfield, Wis. Manson, T i m J., 103 Interstate Bldg., 540 McCallie Ave., Chattanooga 2, Tenn. Mantell, Cecil, 86 Hamilton Avenue, Staten Island, N.Y. Mensh, Maurice, 1732 Eye Street, N.W., Washington, D.C. Miller, Joseph C., 3701 N. Broad St., Suite 1205, Philadelphia, Pa. Mitchell, Jr., Robert E„ Med. Arts Bldg., 2nd 8c Franklin Sts., Suite 311, Richmond 19, Va. Monroe, Colin Α., The Hollywood Clinic, P. O. Box 2308, Hollywood, Fla. Monroe, Lee S., Scripps Clinic, 476 Prospect St., La Jolla, Calif. Morgan, Allan V., # 4 Colonial Place, Pittsburgh 4, Pa. Nast, Philip R., Bryn Mawr Med. Bldg, Bryn Mawr, Pa. Nielson, Orville F., 2101 Chestnut St., Philadelphia, Pa.

300

Social Activities of the Fourth

Meeting

Paustian, Frederick F., 301 Doctors Bldg. Omaha, Nebr. Peraltos, George P., 32 Grove Hill, New Britain, Conn. Pises, Pracha, Geisinger Medical Center, Danville, Pa. Pope, L. J., 502 State Office Bldg., # 1 , Sacramento 14, Calif. Posado, Jaime, 238 Pinebrook Blvd., New Rochelle, N.Y. Priest, Robert J., 9312 Faust Avenue, Detroit 28, Mich. Puschak, Theodore, York Rd. & Maplewood Ave., Abington, Pa. Raffensperger, E. C., 2039 North Second Street, Harrisburg, Pa. Raimondi, Phillip J., 519 Magnolia Ave., Piedmont 11, Calif. Ramos, Pedro Emilio, 2104 No. Scott St., Apt. 30, Arlington 9, Va. Resnick, Solomon, 2672 Hudson Blvd., Jersey City 6, N.J. Robinson, Samuel W., 363 E. Town Street, Columbus 15, Ohio. Rodriquez, Felix, Lahey Clinic, Boston, Mass. Rosenstein, Gladys, Park Drive Manor, Apt. A-205, Philadelphia 44, Pa. Rosenthal, Sydney, 742 Clinton Avenue, Newark 8, N.J. Rosenthal, L. Theodore, 6317 Wilshire Blvd., Los Angeles 48, Calif. Roth, James L. Α., Suite 302, G. Μ. B„ 419 S. 19th Street, Philadelphia, Pa. Rubio, Carlos E., 950 E. 59th St., Chicago 37, 111. Rudner, Henry Gordon, 1108 Madison Avenue, Memphis 4, Tenn. Sanchez, Gustavo, 132-45 Maple Ave., Apt. 180, Flushing 35, N.Y. Sappington, Thomas, 1025 Connecticut Ave., N.W., Washington 6, D.C. Schoen, Arthur M., 606 Heyburn Bldg. 4th 8c Broadway, Louisville 2, Ky. Selesnick, Sydney, Veterans Administration Hospital, Boston, Mass. Shafer, Floyd, 731 Sarah Street, Stroudsburg, Pa. Shaiken, Joseph, 836 N. 12th Street, Milwaukee, Wis. Shlansky, Elliott, 1905 Spruce St., Phila., Pa. Sharp, Reuben Lore, 719 Cooper Street, Camden, N.J. Sherman, Henry Thomas, 10114 W. Brook wood, Valdosta, Ga. Silberner, Herbert, 2130 Millburn Ave., Maplewood, N.J. Staub, Wilbert R., 124 W. Broadway, Salem, N.J. Stempien, Stephen J., 15372 Shasta Lane, Huntington Beach, Cal. Stitcher, Joseph E., Lt. Cdr. (M.C.) U.S.A., U.S Naval Hospital, Navy # 1 1 5 , Box 36, F.P.O., New York, N.Y. Strelinger, Alexander, 650 N. Broad Street, Elizabeth 3, N.J. Sullivan, Benjamin H., Jr Cleveland Clinic, Cleveland, Ohio. Sun, David C. H., Mount Alto, V. A. Hospital, 2650 Wisconsin Ave., N.W., Washington, D.C. Tachjian, Vahaken O., 1147 Morris Road, Wynnewood, Pa Tesler, James, 489 E. 18th Street, Brooklyn 26, N.Y. Thomen, Francisco J., Graduate Hosp. Phila. 46, Pa. Thompson Lloyd LeGland, Jr., Mattie Williams Hospital, Richlands, Va.

Social Activities of the Fourth

Meeting

301

Traitz, James J., 1674 Meridian Ave., Miami Beach 39, Fla. Tucker, W. Homer, 1507 Springhill Avenue, Mobile, Ala. Uyeyoma, Kahn, Univ. of Calif. Med. Center, 3rd & Parnosser Ave., San Francisco 22, Calif. Voegtlin, Walter L., 819 Boylston Ave., Seattle 4, Wash. Walter, Henry, Jr., 37 E. Orange, Lancaster, Pa. Weaver, David H„ 4200-9th Street N.W., Washington, D.C. Weber, Frederick L„ 1506 State Tower Bldg., Syracuse 2. N.Y. Wechsler, Richard, 3500-5th Ave., Pittsburgh, Pa. Weese, William J., 195 S.W. 3rd Avenue, Ontario, Ore. Weiner, Leon, 11040 Kelvin Ave., Philadelphia, Pa. Williams, L. D., 726 Watchung Ave., Plainfield, N.J. Young, James F., 46 E. Clay Street Lancaster, Pa. Yuvachitti, Anek. Albert Einstein Med. Center, York and Tabor, Phila., Pa. Zubritsky, Desiderius I., 212 Sixth Ave., McKeesport, Pa.

ACKNOWLEDGMENTS The fourth meeting of the Bockus International Society of Gastroenterology in Geneva and the edition of these Proceedings have been supported by the following firms: American Cyanamid Co., Lederle Laboratories Division Ciba, S.A. Continental Pharma J. J. Darboven, Idee Kaffee J . R. Geigy, S.A. Guigoz Infant Food and Dietetic Products F. Hoffmann-La Roche 8c Cie, S.A. Laevosan, S.A. Medial, S.A. Nestlé, S.A. Ν. V. Organon Parke-Davis & Co. Philips Duphar Recordati Laboratorio Farmacologico S.p.A. Robapharm, S.A. Roter, Pharmaceutische Fabriek Sandoz, S.A. Dr. A. Wander, S.A. Wyeth International Zyma, S.A. We wish to express our appreciation an gratitude to these firms for their interest and very kind generosity.

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