Gastric ulcer recurrence: follow-up of a double-blind, placebo-controlled trial.

Following a multicenter, double-blind trial comparing cimetidine, antacid, and placebo for the treatment of gastric ulcer, patients whose ulcers had healed were followed prospectively to assess the frequency of ulcer relapse. Fifty-eight patients entered the follow-up study. Patients were encouraged to discontinue smoking and excessive ethanol intake, but were not maintained on antiulcer medications. Clinical evaluation was performed at monthly intervals; repeat endoscopy was performed at the time of symptom recurrence or at 6 to 9 months after ulcer healing. Gastric ulcer recurred in 20 of 58 patients (35%). While 15 (75%) with ulcer recurrence had symptoms, 5 (25%) had asymptomatic recurrences. There were no differences in the incidence of ulcer relapse or symptom recurrences between groups. We conclude that gastric ulcers recur in approximately one-third of patients within 9 months of ulcer healing.

Limitations of indirect methods of estimating small bowel transit in man.

Experiments were carried out in healthy volunteers to explore the utility of a new [14C]lactulose breath test for measuring small intestinal transit time in man and to use this procedure to test whether two antidiarrheal agents, codeine and clonidine, alter small intestinal transit time during digestion of a liquid meal. In an initial validation study performed in 12 subjects (three studies in each subject), a liquid test meal containing 10 g [14C]lactulose was administered and the colonic entry time estimated from the time course of 14CO2 excretion in breath compared with that of H2 excretion. There was a fair correlation (r = 0.77; P less than 0.001) between results obtained by the two methods; both methods gave similar results, but 14CO2 output was delayed when compared to H2 output and was incomplete. The meal also contained xylose and [13C]glycine, permitting the duodenal entry time of the meal to be estimated by the appearance of xylose in blood and 13CO2 in breath, respectively. The same liquid meal was then used to examine the effect on small intestinal transit time (colonic entry time minus duodenal entry time) of codeine or clonidine. 99Tc-sulphur colloid was also added to the meal to permit a comparison of small intestinal transit estimated by imaging with that estimated by the 14CO2-lactulose breath test. 99Tc radioactivity appeared in the cecum (as assessed using gamma scintigraphy) about 2 hr before 14CO2 radioactivity appeared in breath; the correlation between transit time estimated by the two methods was moderate (r = 0.61; P less than 0.05). Based on the [14C]lactulose data, small intestinal transit time ranged from less than 1 to 3 hr for a liquid meal containing 10 g lactulose; within-subject variation (coefficient of variation 17%) was considerably less than between-subject variation (coefficient of variation 56%). Codeine increased the small intestinal transit time significantly (from 2.7 +/- 0.3 hr to 5.0 +/- 0.9 hr; mean +/- SE), whereas clonidine did not alter small intestinal transit time, as estimated by the colonic entry time minus duodenal entry time. Neither drug influenced duodenal entry time. These results suggest that the [14C]lactulose breath test, which has only moderate accuracy, may have occasional utility as a convenient, noninvasive method for estimating small intestinal transit time in man. However, this study also suggests that indirect methods of estimating small bowel transit in man have limitations, variability, and possibly may lack the desired sensitivity.

Mesenteric venous thrombosis as sole complication of decompression sickness.

A 27-year-old male commercial diver developed massive mesenteric venous thrombosis following a dive. Symptoms at presentation included abdominal pain and diarrhea. A severe upper gastrointestinal bleed developed. Exploratory laparotomy demonstrated 130 cm of infarcted small bowel. The pathophysiologic events in decompression sickness predispose to vascular obstruction and venous infarction. This patient had a past history of possible thrombophlebitis and pulmonary embolism associated with diving but no identifiable coagulopathy.

Gastrointestinal cytomegalovirus infection in a homosexual man with severe acquired immunodeficiency syndrome.

A 44-yr-old white homosexual man with a history of Pneumocystis carinii pneumonia developed watery diarrhea and fever. Flexible sigmoidoscopy revealed yellow plaques in the sigmoid colon suggestive of pseudomembranous colitis. Stool examination for ova and parasites, Clostridium difficile toxin, and cultures for pathogens, including Clostridium difficile, were negative. Infection with multiple organisms, including Mycobacterium avium intracellulare, Toxoplasma gondii, herpes simplex, and cytomegalovirus, was demonstrated. Postmortem examination showed esophageal and colonic ulcerations with cytomegalic inclusions, and cytomegalovirus was cultured from the colonic lesions. This report describes a case of disseminated cytomegalovirus infection with esophageal and colonic involvement in a homosexual man with the acquired immunodeficiency syndrome.

Hypervitaminosis A unmasked by acute viral hepatitis.

A case of acute hypervitaminosis A complicating viral hepatitis is reported. Twenty days after presenting with hepatitis B, a 42-yr-old vegetarian developed acute hypervitaminosis A in the absence of recent, massive exposure to the vitamin. Findings included headache, confusion, skin desquamation, and hypercalcemia. Prior to developing hepatitis, he had ingested supplemental vitamin A without recognized ill effect. Liver and serum vitamin A without recognized ill effect. Liver and serum vitamin A levels were both elevated; the liver biopsy showed abundant, lipid-filled Ito cells and perisinusoidal fibrosis. This case demonstrates that patients with excessive hepatic stores of vitamin A may develop hypervitaminosis A during acute, intercurrent liver disease. Levels of retinol binding protein are reduced in hepatitis. This phenomenon may account for the findings in this case, since vitamin A is more toxic when not specifically bound to retinol binding protein. The size of the population at risk for this complication of hepatitis in unknown, but presumably it is growing with the widespread use of supplemental vitamin A.