Changing patterns of Helicobacter pylori gastritis in long-standing acid suppression
- PMID: 11179985
- DOI: 10.1046/j.1523-5378.2000.00032.x
Changing patterns of Helicobacter pylori gastritis in long-standing acid suppression
Abstract
Background: Helicobacter pylori colonization and associated inflammation are influenced by local acid output. Infected subjects with acid-related diseases, such as gastroesophageal reflux disease (GERD) are likely to have an antral-predominant gastritis. We hypothesized that long-term acid suppression would result in relatively greater bacterial colonization in the corpus leading to diffuse or corpus-predominant gastritis and that this would be prevented by prior H. pylori eradication.
Materials and methods: To investigate this, we conducted a prospective, double-blind trial of the effect on gastric histology of 12-month maintenance treatment with omeprazole in H. pylori-positive GERD patients randomly assigned to either an eradication or omeprazole-alone regime. A control group of 20 H. pylori-negative GERD patients also received omeprazole throughout the study period. Biopsies taken at baseline and at 12 months were graded "blind" by a single observer according to the updated Sydney System. The 41 H. pylori-positive subjects with grade B or C esophagitis were randomly assigned (20 to omeprazole alone, 21 to eradication) and 33 subjects completed the 12-month study.
Results: There was a significant decline in antral chronic inflammation in initially positive patients between baseline and end in both the eradication group (p =.035) and the omeprazole-alone group (p =.008). However, corpus chronic inflammation increased in the omeprazole-alone group (p =.0156) but decreased in the eradication group. The change toward corpus predominance between baseline and end for the omeprazole-alone group is highly significant (p =.0078). Furthermore, 5 of 11 in the omeprazole-alone group developed mild corpus atrophy, compared to 0 of 8 who had undergone H. pylori eradication. The change in frequency of corpus atrophy between the two groups is significant (p =.02).
Conclusion: In H. pylori-positive subjects with GERD, long-term acid suppression leads to a shift from antral- to corpus-predominant gastritis that can be prevented by prior eradication. The shift is accompanied by an increase in corpus atrophy. H. pylori infection should be eradicated prior to long-term acid suppression with proton pump inhibitors.
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