Treatment of Campylobacter pylori does not alter gastric acid secretion.

The effect of treatment of Campylobacter pylori-associated gastritis on acid secretion was studied to examine further the strong association between C. pylori and peptic diseases. Twelve symptomatic patients with non-ulcer dyspepsia and C. pylori-associated histologic gastritis had basal and pentagastrin-stimulated gastric acid analysis before and after a 14-day course of amoxicillin 250 mg qid and bismuth subsalicylate 524 mg qid. Endoscopy, antral biopsies, and symptom questionnaires were obtained at entry and at the conclusion of the study. C. pylori was identified by Warthin-Starry stain. Biopsy specimens were also graded for the severity of chronic inflammation and the presence of neutrophils in the epithelium. The treatment regimen cleared C. pylori in 10 of 12 patients. Dyspeptic symptoms improved in 10 of 12 patients, two of whom did not clear the organism, and were unchanged in the remaining two patients, both of whom cleared the bacteria. Neutrophil infiltration in the antral biopsies resolved in 10 patients, including nine with C. pylori clearance and one with persistence of the organism. The severity of the underlying chronic inflammation improved in only one of the 10 organism-free patients and one of the two persistently infected individuals. Pretreatment gastric acid analysis demonstrated hypochlorhydria in three of 12 patients, mild hyperchlorhydria in three of 12 patients, mild hyperchlorhydria in two of 12, and normal acid secretion in the remaining seven patients. Posttreatment acid studies revealed that four of 12 patients were hypochlorhydric, one of 12 had hyperchlorhydria, and seven of 12 were normochlorhydric. After treatment, there was no significant change in basal or maximal acid secretion in the 10 patients who cleared the organism. The two patients who failed to clear C. pylori had insignificant increases in acid secretion after treatment. Our data show no consistent pretreatment pattern of acid secretion in patients with C. pylori-associated gastritis. In addition, gastric acid output did not show a consistent change after treatment for C. pylori. This suggests that the association between C. pylori infection and peptic diseases does not occur via altered acid secretion.