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

Autor: Bergman, M. P., Klinkenberg‐Knol, E. C., Faller, G., Aar, A., Lakhai, W., Vandenbroucke‐Grauls, C. M. J. E., Kuipers, E. J., Appelmelk, B. J.
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Zdroj: Alimentary Pharmacology & Therapeutics; Apr2005, Vol. 21 Issue 8, p977-983, 7p
Abstrakt: : Helicobacter pylori-associated atrophy of the gastric corpus is associated with the presence of anti-canalicular autoantibodies. Also, long-term profound acid suppression inH. pylori-infected subjects may cause atrophic corpus gastritis.: To investigate whether long-term acid suppression by omeprazole leads to antigastric autoantibodies.: Fifty patients, of which 34H. 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. pyloriwas 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 (26H. pylori-positive and 15 uninfected) and results are critically evaluated.: 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 ofH. pylori. One patient, who wasH. pylori-negative, newly developed an anti-canalicular antibody response during therapy.: Our results indicate that, as compared with non-infected patients, long-term profound acid suppression therapy inH. pylori-infected gastro-oesophageal reflux disease patients does not increase or accelerate gastric autoimmunity. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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