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Cystic changes of gastric mucosal glands have been described mainly after gastric operations, and like intestinal metaplasia and dysplasia, they may represent a premalignant condition. Their association with gastritis raises the possibility of their being secondary to the inflammatory process. Enterogastric reflux of duodenal contents, local chronic ischemia, and inflammatory reaction as a result of gastric surgery and suture at gastroenterostomy have been considered responsible for this lesion. In 18 of 157 consecutive patients (11.5%) who underwent endoscopic gastric biopsy within a year we found cystic changes of gastric mucosal glands. Cystic changes were present in 43% of 30 patients after gastric operation for duodenal ulcer disease, within an average of 8.4 years in contrast to only 4% of patients with an intact stomach. This change is statistically significant (Z = 1.97, (p less than 0.05) and suggests that there is a cause-and-effect link between the operation and the development of cystic lesions. In three patients we traced the original operative specimen, and in none did we find cystic changes. All the cases were associated with chronic gastritis; mild dysplasia was found in four (22%). The cystic glands were shown (by alcian blue-periodic acid-schiff staining) to secrete neutral mucin like normal gastric glands, and unlike dysplastic glands or intestinal metaplasia where acid mucin is characteristic. Thus, our findings suggest an inflammatory cause for the cystic glandular change (reactive, hyperplastic change of glands), and suggest that it is probably not a preneoplastic state.

We evaluated the significance of bile seen in the stomach at the time of endoscopy. Twenty-three percent of 110 consecutive patients undergoing elective panendoscopy were found to have bile in their stomachs. Gastric biopsies were obtained from these patients. To assess the significance of bile reflux, the patients underwent a quantitative gastric bile analysis on two separate days. On day 1, gastric juice was aspirated by nasogastric suction, and bile acid concentrations were measured. On day 2, bile reflux into the stomach was quantitated by scintiscan measurement of gastric nucleotide after intravenous administration of 99mTc-DISIDA. Approximately half the patients with bile reflux showed histologic evidence of mucosal injury. However, fewer than half with histologic injury had significant bile reflux when measured by quantitative methods. There was no correlation among the gastric bile acid concentration, degree of histologic injury, or severity of endoscopic changes. We conclude that finding bile reflux at endoscopy is probably of no clinical significance.

We have studied the accuracy of diagnostic methods in achieving a diagnosis in 75 patients with 81 proven episodes of recurrent ulceration. When the endoscopic findings did not permit an accurate diagnosis, radiology usually provided no additional information. The sensitivity of a combined diagnostic approach was not different from that of endoscopy alone, and so the routine use of upper GI radiographs in addition to endoscopy should, therefore, be abandoned. We also assessed observer variation among endoscopists prospectively in 38 patients investigated for dyspepsia after operation for peptic ulcer. Major observer variation in diagnosing suspected recurrent ulceration occurred in 11% of patients, with a sensitivity and specificity higher than 77 and 94%, respectively. As not all the postoperative gastroduodenojejunal mucosal breaches are peptic, we suggest that acid output and enterogastric reflux assessments are useful diagnostic adjuncts to endoscopy.