Intestinal Protein Loss in Schistosomal Polyposis of the Colon

(;ASTHOf.:NTEHOI.OGY

Vol. fl9, No. :1 l'rintl'd in U.S.A.

Copyright © 1970 by The Williams & Wilkins Co.

INTESTINAL PROTEIN LOSS IN SCHISTOSOMAL POLYPOSIS OF THE COLON ,J.

STAUFFEI( LEHMAN, JR., M.D., ZOHEIR FAHIO, M.D., SAMIH BASS!LY ,

JoHN HAXTON,

M.

FARm ABDEL WAHAB, M.D., AND DoNALD

C.

KENT,

M.D. , M.D.

United States Naval Medical Research Unit No. 3 and Tropical Diseases Section Kasr-el-Aini Hospital, Cairo University, Cairo, Egypt

Excessive intestinal protein loss was demonstrated in 5 of 6 patients with colonic polyposis due to Schistosoma mansoni infection. The degree of protein loss was associated with the extent of polyposis and mucosal disease but not with the intensity of infection as measured by the 24-hr excretion of schistosome eggs. This previously undescribed complication of intestinal schistosomiasis may lead to serious depletion of the body albumin in patients with concomitant protein malnutrition. Polypoid lesions of the colon have been reported to occur in 17 to 20% of Egyptian patients with schistosomiasis' and have been noted less frequently in patients living in other endemic areas. 2 In Egypt, intestinal polyps may be associated with Schistosoma mansoni or Schistosoma haematobium infection, but the majority of polyps contain Schistosoma mansoni eggs. 1 The clinical significance of this complication is not yet fully defined, although symptoms of diarrhea, tenesmus, and rectal bleeding are commonly associated and intestinal blood and iron losses have been measured.:! In this study, intestinal protein loss in patients with schistosoma! colonic polyposis is evaluated. Received January 19, 1970. Accepted March 3, 1970. Address requests for reprints to: Dr. J. Stauffer Lehman, Jr. , NAMRU-3, Fleet Post Office, New York 09527. This research was supported by independent research funds provided by the Bureau of Medicine and Surgery, United States Navy Department. The opinions and assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Department of the Navy, the Naval Service at large, or the Egyptian Ministry of Public Health. The authors are grateful to A. S. Mahran for tech· nical assistance, and to Drs. V. N. Patwardhan, W. J. Darby, and J. H. Smith for advice and for review of the manuscript. 433

Materials and Methods Patients. Six Egyptian male farmers with S. mansoni infection were studied upon sigmoidoscopic and radiographic demonstration of colonic polyposis. Treatment of schistosomiasis with potassium antimony tartrate (tartar emetic) in conventional dosage was subsequently undertaken in every patient. Follow-up studies of 4 patients were performed 8 weeks following completion of treatment. Six healthy male patients, who matched the polyposis patients for age and occupation, were similarly studied as controls. Prior to study, stool examinations were negative for hookworm eggs and stool cultures were negative for Salmonella and Shigella. Quantitation of eggs of S. mansoni in 24-hr stool collections was performed by Bell's method .·' Measurement of intestinal protein loss. Human albumin (Courtland Laboratories, Los Angeles, Calif.) was labeled with Cr'" by a modification of Waldmann's technique.'' Carrierfree Cr"'-chromic chloride, 100 11c, was added to a 5-ml solution of albumin containing 50 mg per 100 ml, incubated at 37 C for 30 min, and injected intravenously. The technique described by Waldmann employs steps to remove free Cr51 following incubation. We eliminated these steps in order to simplify the method for use in tropical and developing areas. The efficiency of our labeling procedure was estimated by precipitation of albumin with phosphotungstic acid; 40 to 50% of the incubated Cl' could be precipitated. A plasma sample and a 24-hr stool collection were obtained daily for 8 days and counted re-

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LEHMAN ET AL.

spectively in a well (Nuclear Chicago, Des Plaines, lll., model C120) or bulk (Matrix large volume) counter with appropriate standards; radioactivity was expressed as disintegrations per minute. When diarrhea was present (all patients with polyposis), the plasma activity of the same day as the 24-hr stool activity was used in calculation. If formed stool was present (all controls), the previous day's plasma activity was used in the equation: milliliters of plasma cleared of protein = disintegrations per minute in 24-hr stool per disintegrations per minute in 1 ml of plasma. The amount of albumin lost in stool was calculated by multiplying the milliliters of plasma cleared per day by the serum albumin concentration.

Results All patients with polyposis had diarrhea with tenesmus, mucus, and occasional rectal bleeding; duration of symptoms ranged from 4 months to 2 years. Each patient had previously received one or more courses of antimonial treatment for intestinal schistosomiasis, but all were excreting viable eggs of S. mansoni in the stool. Physical examination in every case revealed moderTABLE

ate liver enlargement without splenomegaly. Two patients were critically ill on admission due to dehydration secondary to prolonged diarrhea and were anorexic and cachetic. Extensive supportive therapy was necessary before studies could be conducted or treatment of schistosomiasis given. The remaining 4 patients were suffering from varying degrees of dehydration, anemia, and hypoalbuminemia. The diets of all were deficient in protein prior to admission, consisting predominantly of bread and beans. The results of egg counts, sigmoidoscopies, and barium enemas and intestinal protein clearances are listed in table 1. Five of 6 patients with polyposis had increased intestinal clearance of protein. The amount of protein loss correlated well with the extent of polyposis but not with the 24-hr egg count. Patient 1 had the fewest polyps and had insignificant protein loss. Patient 6 had extensive polyposis (fig. 1), the highest intestinal clearan ce of protein, and the lowest egg count. Following antischistosomal treatment,

1. Stool egg count, sigmoidoscopy, and barium enema; Cr" albumin clearance in schistosoma/ polyposis

S. mansoni Patient

Age

egg excre· tion per 24 hr

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Barium enema and sigmoidoscopy

Intestinal plasma clearance

Before

After

ml/day

yr

1,600 Small sigmoid polyps, approximately 10; normal mucosa 9,600 Small to large rectal and sigmoid polyps, approximately 20; friable

1

15

2

31

3

28 439,000 Large polyps, rectum to transverse colon, > 100; granular mucosa 55 14,000 Large polyps, rectum to descending colon, approximately 25; friable,

9.2 55

69

Intestinal albumin loss

Before

After

g/day

Serum albumin

Before

After

g/100 ml

0.30

3.3

2.15 2.69

3.9

1.36

2.0

3. 9

mucosa, sandy patches

4

68 72

38

1.80 1.44

2.5

3.8

134

32

2 . 01 1.12

1.5

3.5

322

41

5.15 1. 27

1.6

3.1

weeping mucosa

5

28 159,000 Large rectal and sigmoid polyps, approximately 20; friable, bleeding

6

35

mucosa

800 Large polyps, rectum to transverse colon, approximately 50; pale, weeping mucosa

Controls (6) Range Mean

5-31 15.2

0. 20-1.33 0.66

3.0-5.3 4.2

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PROTEIN LOSS IN COLONIC POLYPOSIS

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FIG. 1. Patient 6, air-contrast barium enema. The barium outlines multiple large nodular filling defects, particularly in the splenic flexure and the sigmoid colon.

diarrhea and associated complaints were diminished. Intestinal plasma clearance was reduced in 3 of 4 patients restudied after treatment (table 1). Radiographic appearance of the polyps did not change following treatment. However, on sigmoidoscopy the surface of the polyps and neighboring mucosa, which had been inflamed and ulcerated prior to treatment, was improved. Discussion Protein-losing enteropathy accompanies many diseases5 but has seldom been stud-

ied in intestinal polyposis or in intestinal parasitism . It has, however, been reported in diffuse gastrointestinal polyposis with ectodermal changes (Cronkhite-Canada syndrome),'; hookworm infection, ' and hepatosplenic schistosomiasis. H The intestinal protein loss demonstrated in our patients appears to be associated with the extent of colonic polyposis and the severity of the accompanying mucosal damage. Mucosal inflammation and ulceration, similar to that noted in ulcerative colitis, most likely account for loss of plasma proteins into the gut. This is sug-

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gested by the observation that decrease in intestinal protein loss after treatment is associated with improved appearance of the mucosa rather than ·a decrease in number or size of the polyps. The sequelae of this complication of intestinal schistosomiasis may be serious; dehydration, anemia, and hypoalbuminemia have been severe in some patients. Although the magnitude of protein loss occurring in schistosoma! polyposis is not so great as that observed in certain other diseases with protein-losing enteropathy, 5 any loss must be considered important when protein malnutrition is also present. In this sense, protein depletion resulting from the combined effect of intestinal albumin loss and poor protein diet resembles the previously observed depletion of body iron stores due to chronic blood loss from schistosoma! polyposis. 3 Liver disease and intestinal malabsorption may be additional causes of hypoalbuminemia. Investigation of liver and intestinal absorptive functions, combined with albumin turnover studies, will be necessary for more complete understanding of albumin depletion in these patients. However, at present, we conclude that intestinal protein loss may lead to serious depletion of the body albumin in patients also receiving a poor protein diet. When we consider that an Egyptian farmer may suffer further blood and protein loss due

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to other helminthic and protozoal infec9 tions, the burden of parasitism on poorly nourished persons becomes more readily acknowledgeable. REFERENCES 1. Dimmette RM, Sproat AF: Rectosigmoid polyps in schistosomiasis. I. General clinical and pathologic considerations. Amer J Trop Med 4:10571067, 1955 2. Mostofi FK: The need for research in Bilharziasis, Bilharziasis, lnternatilHia l Academy of Pathology, Special Monograph. Ed ited by FK Mostofi. New York, Springer-Verlag-, 1967, p 337 3. Farid Z, Bassily S, Sch ulert AR, eta!: Blood loss in chronic Schistosoma mansoni infection in Egyptian farmers. Trans Roy Soc Trop Med Hyg 61:621-625, 1967 4. Bell DR: A new method for counting Schistosoma mansoni eggs in faece<:. Bull WHO 29:525-530, 1963 5. Waldmann TA, Wochn e r RD, Strober W: The role of the gastrointestinal t ract in plasma protein metabolism. Amer J Med 46 :275- 285, 1969 6. Jarnum S, Jensen H: Diffuse gastrointestinal polyposis with ectodermal changes. Gastroenterology 50:107-118, 1966 7. Blackman, V, Marsden PD, Banwell ,J, et al: Albumin metabolism in hookworm anemia. Trans Roy Soc Trap Med Hyg, 59:472-482, 1965 8. El Saadani AM, El Sa wy H abib M, El Gengehy MT, et al: Albumin turnover in schistosomalliver cirrhosis. Amer J Trop Med 17:844-850, 1968 9. Farid Z, Patwardhan VN, Darby WJ: Parasitism and anemia. Amer J Clin Nutr 22:498-503, 1969