INCREASE OF HELICOBACTER-PYLORI-ASSOCIATED CORPUS GASTRITIS DURING ACID SUPPRESSIVE THERAPY - IMPLICATIONS FOR LONG-TERM SAFETY

Objectives: Helicobacter pylori causes chronic active gastritis with p redominant localization in the gastric antrum. This predisposes to dev elopment of mucosal atrophy, intestinal metaplasia, and eventually, ga stric cancer. The effects of acid suppression on H. pylori infection a nd associated gastritis are unclear. However, rapid development of atr ophic gastritis has been consistently observed in a number of studies during low acid output. We therefore studied the histological features of antrum and corpus of the stomach before and during acid suppressiv e therapy. Methods: Fifty patients with either reflux esophagitis (n = 21), benign gastric ulcer (six patients), gastric erosions (three pat ients), or duodenal ulcer (20 patients) were treated for 8 wk with ome prazole 40 mg o.d. Esophagogastroduodenoscopy was performed pre-entry and at 8 wk. Biopsy specimens were sampled from the antrum and corpus for histology and cultures. Results: Seventeen H. pylori-negative pati ents had no histological signs of active gastritis, before or after th erapy. Thirty-three H. pylori-positive patients showed predominant col onization and associated inflammation in the antrum before therapy. Af ter therapy, however, the infection predominantly affected the corpus. The inflammation and bacterial colonization in the antrum significant ly decreased, leading to negative antral cultures in 61% (20 of 33 pat ients). In contrast, the inflammation of the corpus mucosa significant ly increased despite stable bacterial counts. Conclusions: We conclude I) that H. pylori testing in patients on profound acid suppressive th erapy should be performed on combined corpus and antral specimens, and 2) that omeprazole therapy leads to a strong increase in corpus gastr itis, which may explain the observed development of corpus atrophy in a substantial number of patients after several years of continuous aci d suppressive treatment. Therefore, we suggest that patients in need o f long-term acid suppressive therapy should receive bacterial eradicat ion therapy if they are H. pylori positive.