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.
Dr Bergman and colleagues investigated whether long-term acid suppression by omeprazole leads to antigastric autoantibodies.
|1 patient developed an anti-canalicular antibody response during therapy|
|Alimentary Pharmacology and Therapeutics|
The researchers treated 50 patients, of which 34 were H. pylori-positive on entry of the study, with 20 to 40 mg omeprazole once daily for reflux esophagitis.
The research team evaluated the patients for anti-gastric autoantibody responses by immunohistochemistry before and after treatment.
The team did not eradicate H. pylori and patients were followed for an average of 7 years.
In addition to immunohistochemistry, anti-H+, K+-ATPase reactivity was assessed by Western blot in paired sera of 41 patients, of which 26 were H. pylori-positive and 15 uninfected.
Results were critically evaluated by the team.
The investigators reported that in immunohistochemistry, most patients were negative for anti-canalicular autoantibodies when omeprazole therapy started.
Only 2 patients with corpus-predominant gastritis in the presence of H. pylori were not negative for anti-canalicular autoantibodies when omeprazole therapy started.
The research team also observed that 1 patient, who was H. pylori-negative, had newly developed an anti-canalicular antibody response during therapy.
Dr Bergman’s team concluded, “Our results indicate that, as compared with non-infected patients, long-term profound acid suppression therapy in H. pylori-infected gastro-esophageal reflux disease patients does not increase or accelerate gastric autoimmunity.”