Expression of bcl-2 in autoimmune and Helicobacter pylori-associated atrophic gastritis

Chronic atrophic gastritis can be induced either by H. pylori or by an auto immune process. The protein product of bcl-2, which is a protooncogene, blo cks apoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aim of this study was to compare bcl-2 expression i n 20 autoimmune atrophic gastritis patients to that in 20 H. pylori-associa ted atrophic gastritis patients. Twenty patients with H. pylori antral gast ritis but without atrophy served as controls. The bcl-2 expression was asse ssed by immunohistochemical staining of gastric biopsies, using mouse anti- human bcl-2 monoclonal antibodies. Autoimmune atrophic gastritis patients w ere younger. mainly females, with a significantly higher serum gastrin leve l than the H. pylori-associated atrophic gastritis group (P < 0.001). The b cl-2 was expressed in 10/20 (50%) of autoimmune atrophic gastritis patients , in 9/20 (45%) of H. pylori-associated atrophic gastritis patients (P = 0. 73), and in 2/20 (10%)of controls. There was no correlation between bcl-2 e xpression and the presence of intestinal metaplasia (P = 0.35). Our finding s confirm that H. pylori-associated atrophic gastritis and autoimmune atrop hic gastritis are two different conditions, but with equal expression of bc l-2. Excessive expression of bcl-2 is found only in atrophic gastritis, but not in H. pylori antral gastritis without atrophy.