A CRITICAL ANALYSIS, WITH APPROPRIATE CONTROLS, OF GASTRIC-ACID AND PEPSIN-SECRETION IN CLINICAL ESOPHAGITIS

Because esophagitis is a presumed "acid-peptic" disease, fasting gastric contents (volume and acid and pepsin concentrations) and basal and pentagastrin-stimulated acid and pepsin outputs were studied in 155 patients with endoscopically defined (and graded 1-4) esophagitis and 508 control patients without esophagitis. Basal pepsin and maximal acid and pepsin outputs were lower in the patients with esophagitis than in those without esophagitis. In further analysis, the patients were subdivided into three categories, duodenal ulcer, nonulcer with no disease other than esophagitis, and postgastric surgery, because these categories affect gastric secretion independently of esophageal disease and in the rank order given. Each category was subdivided by sex, because men secreted more than women. Within each category there was no systematic difference in fasting, basal, or maximal gastric acid or pepsin secretion between patients with and patients without esophagitis. Severity of esophagitis was not related to any secretion parameters. Hiatal hernia was present in 50% of patients with esophagitis vs. 15% of controls without the condition (P < 0.01); however, this did not independently influence the gastric secretion findings. Lower esophageal sphincter pressure was also measured in 62 of the patients, 31 with and 31 without esophagitis. Below 10 mm Hg (incompetent sphincter), 9 of 10 patients had esophagitis but accounted for only <30% of the patients with esophagitis, whereas none of 11 patients with basal acid output of <0.1 mEq/h and lower esophageal sphincter pressure of >10 mm Hg had esophagitis. Because neither the composition of gastric juice nor basal or stimulated gastric acid or pepsin output could be correlated to the presence or severity of esophagitis, factors other than amount or composition of gastric juice per se must be responsible for susceptibility to esophagitis. © 1991.