Ectopic gastric mucosa—rare but not forgotten

Candida invasion of the stomach and duodenum has been described by Toshi Shobha et a1. 3 in a patient with renal transplant. Minoli et a1. 4 described two patients with gastroduodenal candidiasis, which appeared to be among nonimmunosuppressed individuals. In one of their patients, there was Candida invasion of antral and bulbar ulcers, while the other patient had nodular antral and bulbar lesions without concomitant illness. Candida invasion of gastric and duodenal ulcers has been described by Ochtert and Preuss5 who found an increased incidence with benign and malignant ulcers. Neeman et a1. 6 found Candida in seven of 128 gastric ulcers at endoscopy, and five of these seven failed to heal on antacids and cimetidine but healed when cimetidine was replaced with mycostatin. This suggests the possibility that Candida may be more than a benign resident of these ulcers. The major reason for paucity of Candida infections in the stomach and intestine is attributed to gastric acidity. Interference with gastric acid production is known to increase the frequency of Candida albicans in gastric aspirate cultures. Thirty-one of 50 patients had Candida species in their gastric content after vagotomy, compared to a preoperative incidence of three of 63,7 and the recognition of Candida in the stomach increased after partial gastrectomy.8 The role of cimetidine in increasing gastroduodenal candidiasis has been examined less critically, but it is only logical to think that the relationship may be a valid one. Webster et a1. 9 described a patient who had erosive gastritis and duodenitis after a 3-month treatment with cimetidine. The incidence of Candida in gastric ulcers was only 10% in 1950 to 1953; it increased to 37% in 1972 to 1977 (the cimetidine era in England). Recently, Minoli l l reported a case of duodenal candidiasis after 4 weeks of cimetidine therapy. If it were not for the reduction of gastric acid production, cimetidine per se should not result in increased incidence of candidiasis. Immunity against candida is aT-cell mediated delayed hypersensitivity type reaction. Cimetidine, by its anti-H 2 receptor effect, interfaces with suppressor T -cells which are supposed to have H 2 receptorsP Clinically, cimetidine has been found to augment T-cell mediated delayed hypersensitivity reaction measured by skin test1 3 as well as leukocyte migration inhibitory factor. l4 With endoscopic and laboratory evidence of symptomatic duodenal candidiasis in the clinical setting of prolonged cimetidine-induced gastric acid suppression, there is a need for vigilence during chronic cimetidine therapy. A. Roy, MD Richard W. McCallum, MD Department of Internal Medicine Yale University School of Medicine New Haven, Connecticut

REFERENCES 1. Rifkind D, Marchioro TL, Schneck SA, et al. Systemic fungal infections complicating renal transplantation and immunosuppressive therapy. Clinical, microbiologic, neurologic and pathologic features. Am J Med 1967;43:28. 2. Eras P, Goldshine MJ, Shirlock P. Candida infection of gastrointestinal tract. Medicine 1972;51:367. 3. Toshi Shobha N, Garvin PJ, Sunwoo Young C. Candidiasis of duodenum and jejunum. Gastroenterology 1980;81:828. 4. Minoli G, Tirruzi V, Rossini A. Gastroduodenal candidiasis

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occurring without underlying disease. Endoscopy 1976;11:18. 5. Ochtert W, Preuss B. Incidence and significance of candidiasis in biopsy material of gastric ulcers. Dtsch Med Wschr 1980;105:1733. 6. Neeman A, Avidor I, Kedish U. Candidal infection of benign gastric ulcers in aged patients. Am J GastroenterolI981;75:211. 7. Brooks RJ, Smith HF, Pease FB. Bacteriology of stomach immediately following vagotomy. Ann Surg 1974;179:859. 8. Borg I, Hukkenskjold B, Wehlin L. Massive growth of yeasts in resected stomach. Gut 1966;7:244. 9. Webster J, Petrie JC, Mowat NAG. Erosive gastritis and duodenitis during continuous cimetidine treatment. Br Med J 1978;1:20. 10. Nicholas PE, Henry K. Gastritis and cimetidine, a possible explanation. Lancet 1978;1:1095. 11. Minoli G. Candidiasis of duodenum and jejunum. Gastroenterology 1981;81:825. 12. Askenase PW. Histamine-2 antagonist inhibition of delayed hypersensitivity (DH). Clin Res 1977;25:481A. 13. Avella J, Madsen JE, Binder HJ, Askenase PW. Effect of histamine H 2 receptor antagonist on delayed hypersensitivity. Lancet 1978;1:624. 14. Jorizzo JL, Sams WM Jr, Jegasothy BV, Olansky AJ. Cimetidine as an immunomodulator: chronic mucocutaneous candidiasis as a model. Ann Intern Med 1980;92:192.

Ectopic gastric mucosa-rare but not forgotten To the Editor: Isolated gastric mucosa may be found throughout the gastrointestinal tract. Documentation of the presence of ectopic gastric mucosa has previously been rare, but the increasingly sophisticated and refined diagnostic modalities of endoscopy and scintigraphy make it possible to identify more cases.! In the past year, we have encountered two such cases. An 81-year-old white woman was admitted with the chief complaint of recurrent midepigastric pain. She had a 30year history of peptic ulcer disease treated successfully by antacids. Physical findings included a nontender, soft abdomen and normal bowel sounds. Stool guaiac was negative. Esophagogastroduodenoscopy revealed antral gastritis and a 2 by 6 mm duodenal polyp which was biopsied. Microscopic examination of the polyp revealed that it was composed of ectopic gastric mucosa. A 50-year-old black man with a history of recurren,; abdominal pain was admitted for evaluation. On physical examination, he exhibited mild epigastric tenderness. His stool guaiac was negative. An upper gastrointestinal series revealed a deformed duodenal bulb with a questionable submucosal filling defect in the apex of the bulb. At esophagogastroduodenoscopy a biopsy was taken from thickened mucosa in the apex of the bulb. Microscopic examination revealed multiple foci of heterotopic gastric mucosa. The association of ectopic gastric mucosa with Meckel's diverticulum and Barrett's esophagus is well known. Congenital intestinal duplications often contain gastric mucosa 2 ; however, isolated ectopic gastric mucosa is rare. According to Lee et al.,3 as of 1970 only 16 cases have been reported and most of these were in the jejunum. Ten patients presented with symptoms of intermittent obstruction thought to be secondary to intermittent intussusception related to the ectopic gastric mucosa. Since 1970, several more cases have appeared in the GASTROINTESTINAL ENDOSCOPY

literature.4-l; In 1976, Doberneck et al! reported a case in which an 8-year-old boy presented with an ileocolic intussusception, the leading edge of which was a 2-cm area of ectopic gastric mucosa. In 1979, Briggs and MooreS reported a 15-year-old boy who had perforated an ileal ulcer which had formed secondary to gastric secretions from a 17 cm length of gastric mucosa in the ileum. Recently, Blundell et al. 6 reported an 83-year-old man with obstructive jaundice secondary to biliary obstruction at the ampulla of Vater from heterotopic gastric mucosa. Chartes A. Jungreis, MD Matthew McKinley, MD North Shore University Hospital Manhasset. New York

REFERENCES 1. Spakianakis GN, Conway JJ. Detection of ectopic gastric mu-

2. 3. 4. 5. 6.

cosa in Meckel's diverticulum and in other aberrations by scintigraphy: Part 1, Pathophysiology and ten year clinical experience. J Nuclear Moo 1981;22(7):647-54. Newmark H III, Ching G, Halls J, Levy IJ. Bleeding peptic ulcer caused by ectopic gastric mucosa in a duplicated segment of jejunum. Am J Gastroenterol 1981;158-62. Lee SM, Mosenthal WT, Weismann RE. Tumorous heterotopic gastric mucosa in the small intestine. Arch Surg 1970;100:61922. Doberneck RC, Deane WM, Antoine JE. Ectopic gastric mucosa in the ileum: a cause of intussusception. J Pediatr Surg 1976;11(1):99-100. Briggs FL, Moore JP. Heterotopic gastric mucosa of the small bowel with perforated ulcer. Am Surg 1979;45(6):413-7. Blundell CR, Kanun CS, Earnest DL. Biliary obstruction by heterotopic gastric mucoSll at the ampulla of Vater. Am J GastroenteroI1982;77(2).

Duodenal ulcerations after monooctanoin therapy To the Editor: Monooctanoin is a solvent of cholesterol stones that is clinically effective and safe. 1- 4 Side effects of perfusion with monooctanoin are common and include mild anorexia, nausea, emesis, and abdominal discomfort. We report a patient with secondary biliary cirrhosis whose epigastric pain and gastrointestinal bleeding during monooctanoin therapy were shown to have occurred from intestinal ulcerations. A 57-year-old man who had a cholecystectomy 16 years previously was admitted to the hospital with an 8-day history of vomiting, fever, and progressive jaundice. He was cachectic, icteric, and febrile. The liver was markedly enlarged and the spleen tip was palpable. An upper gastrointestinal x-ray series demonstrated the presence of esophageal varices. A percutaneous transhepatic cholangiogram revealed a dilated common bile duct with several large stones and multiple small intrahepatic stones involving both lobes of the liver (Fig. 1). He improved following placement of catheters into the left hepatic and common bile duct and a course of antibiotics. An infusion with monooctanoin (Capmul 8210) was begun at 5 ml/hour and subsequently increased to 10 ml/hour. Because of vomiting, epigastric pain, and diarrhea, the infusion was stopped on the sixth day. A cholangiogram revealed no significant reduction in stone size, and the infusion was restarted several days after his VOLUME 30. NO.1, 1984

Figure 1. Percutaneous transhepatic cholangiogram demonstrating several large stones in dilated common bile duct and multiple, small stones in dilated intrahepatic ducts.

symptoms abated. The patient again experienced abdominal pain and diarrhea, and on the 11th day of monooctanoin infusion at 10 ml/hour he developed hematemesis accompanied by increasing abdominal pain. Vasopressin successfully controlled the bleeding which was thought to be variceal in origin. Because of the marked side effects from perfusion therapy, the decision was made to remove the stones by surgical laparotomy, and several large black stones were removed from the common bile duct and the intrahepatic radicles. AT-tube was left in place and a sphincteroplasty was performed. In the postoperative period, intestinal bleeding recurred and endoscopy demonstrated duodenal ulcerations in the descending duodenum. The distal limb of the T-tube was visualized, extending into the duodenum (Fig. 2). The patient's course was complicated by hepatic encephalopathy and biliary sepsis, and he expired 4 weeks following surgery. Duodenal ulceration following monooctanoin therapy has not been previously reported, although Hofmann et al.,2 in 49