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

Bergman MP, Klinkenberg-Knol EC, Faller G, Aar A, Lakhai W, Vandenbroucke-Grauls CM, Kuipers EJ, Appelmelk BJ

Departments of Medical Microbiology and Infection Control, Vrije Universiteit Medical Center, Amsterdam, The Netherlands. m.bergman@erasmusmc.nl

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.

Published 7 April 2005 in Aliment Pharmacol Ther, 21(8): 977-83.
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