Long-term acid suppression by omeprazole in gastro-oesophageal reflux disease patients does not lead to anti-gastric autoantibody production

Background: Helicobacter pylori-associated atrophy of the gastric corpus is associated with the presence of anti-canalicular autoantibodies. Also, long-term profound acid suppression in H. pylori-infected subjects may cause atrophic corpus gastritis. Aim: To investigate whether long-term acid suppression by omeprazole leads to antigastric autoantibodies. Methods: Fifty patients, of which 34 H. pylori-positive on entry of the study, were treated with omeprazole (20-40 mg once daily) for reflux oesophagitis, and were evaluated for anti-gastric autoantibody responses by immunohistochemistry before and after treatment. H. pylori was not eradicated and patients were followed for an average of 6.6 years (range 3-14.1 years). In addition to immunohistochemistry, anti-H+, K+-ATPase reactivity was assessed by Western blot in paired sera of 41 patients (26 H. pylori-positive and 15 uninfected) and results are critically evaluated. Results: In immunohistochemistry, all patients were negative for anti-canalicular autoantibodies when omeprazole therapy started, except for two patients with corpus-predominant gastritis in the presence of H. pylori. One patient, who was H. pylori-negative, newly developed an anti-canalicular antibody response during therapy. Conclusions: Our results indicate that, as compared with non-infected patients, long-term profound acid suppression therapy in H, pylori-infected gastro-oesophageal reflux disease patients does not increase or accelerate gastric autoimmunity.

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