title: Expression of bcl-2 in autoimmune and Helicobacter pylori-associated atrophic gastritis.
abstract: Chronic atrophic gastritis can be induced either by H. pylori or by an autoimmune process. The protein product of bcl-2, which is a protooncogene, blocks 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 in 20 autoimmune atrophic gastritis patients to that in 20 H. pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritis but without atrophy served as controls. The bcl-2 expression was assessed by immunohistochemical staining of gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophic gastritis patients were younger, mainly females, with a significantly 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-2 expression and the presence of intestinal metaplasia (P = 0.35). Our findings confirm that H. pylori-associated atrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equal expression of bcl-2. Excessive expression of bcl-2 is found only in atrophic gastritis, but not in H. pylori antral gastritis without atrophy.
authors.affiliation: Institutes of Gastroenterology and Pathology, Meir Hospital, Sapir Medical Center, Kfar-Sava, Israel.
authors.forename: Y
authors.initials: Y
authors.lastname: Maor-Kendler
authors.forename: G
authors.initials: G
authors.lastname: Gabay
authors.forename: J
authors.initials: J
authors.lastname: Bernheim
authors.forename: T
authors.initials: T
authors.lastname: Naftali
authors.forename: I
authors.initials: I
authors.lastname: Lesin
authors.forename: G
authors.initials: G
authors.lastname: Leichtman
authors.forename: I
authors.initials: I
authors.lastname: Pomeranz
authors.forename: B
authors.initials: B
authors.lastname: Novis
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001327:Autoimmune Diseases / Q000235:genetics* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D005757:Gastritis, Atrophic / Q000235:genetics* / Q000473:pathology; D005786:Gene Expression Regulation; D019254:Genes, bcl-2 / Q000235:genetics*; D016481:Helicobacter Infections / Q000235:genetics* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged