Non-Helicobacter pylori bacterial flora during acid-suppressive therapy: differential findings in gastric juice and gastric mucosa

Background: Intragastric growth of non-Helicobacter pylori bacteria commonl y occurs during acid-suppressive therapy. The long-term clinical consequenc es are still unclear. Aim: To investigate the luminal and mucosal bacterial growth during gastric acid inhibition, in relation to the type and duration of acid-inhibitory t reatment, as well as to concomitant H. pylori infection. Methods: A total of 145 patients on continuous acid inhibition with either proton pump inhibitors (n = 109) or histamine(2)-receptor antagonists (H2RA s, n = 36) for gastro-oesophageal reflux disease, and 75 dyspeptic patients without acid inhibition (control group) were included. At endoscopy, fasti ng gastric juice was obtained for pH measurement and bacteriological cultur e. Gastric biopsy specimens were examined for detection of H. pylori (immun ohistochemistry) and of non-H. pylori bacteria (modified Giemsa stain-posit ive and immunohistochemistry-negative at the same location). Results: Non-H. pylori flora was detected in the gastric juice of 92 (41.8% ) patients and in the gastric mucosa of 109 (49.6%) patients. In gastric ju ice, prevalence rate for non-H. pylori bacteria was higher in patients taki ng proton pump inhibitors than controls and those taking H2RAs (58.7% vs. 2 2.6% and vs. 30.6%, P < 0.0001 and P < 0.003, respectively), but did not di ffer statistically between H2RAs and controls. In gastric mucosa, prevalenc e rates for non-H. pylori bacteria were higher in patients taking proton pu mp inhibitors and H2RAs than in the controls (antrum: 46.9% and 48.6% vs. 2 5%, P < 0.05 for both; corpus: 52.2% and 56.8% vs. 23.7%, P < 0.001 for bot h), but did not differ between proton pump inhibitors and H2RAs. Both lumin al and mucosal growth of non-H. pylori bacteria were significantly greater in H. pylori-positive than -negative patients taking proton pump inhibitors (P < 0.05 for both). Luminal growth of non-H. pylori flora increased with the intragastric pH level, whilst mucosal bacterial growth increased with t he duration of acid inhibition. Conclusions: Non-H. pylori flora not only contaminates the gastric juice bu t also colonizes the gastric mucosa of a large proportion of patients treat ed long-term with acid inhibition. The relationship between H. pylori and n on-H. pylori bacteria in the pathogenesis of atrophic gastritis and gastric cancer needs further elucidation.