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

Chronic atrophic gastritis can be induced eitherby H. pylori or by an autoimmune process. The proteinproduct of bcl-2, which is a protooncogene, blocksapoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aimof this study was to compare bcl-2 expression in 20autoimmune atrophic gastritis patients to that in 20 H.pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritisbut without atrophy served as controls. The bcl-2expression was assessed by immunohistochemical stainingof gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophicgastritis patients were younger, mainly females, with asignificantly higher serum gastrin level than the H.pylori-associated atrophic gastritis group (P < 0.001). The bcl-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-2expression and the presence of intestinal metaplasia (P= 0.35). Our findings confirm that H. pylori-associatedatrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equalexpression of bcl-2. Excessive expression of bcl-2 isfound only in atrophic gastritis, but not in H. pyloriantral gastritis without atrophy.