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

Yaakov Maor-Kendler*, G. Gabay, J. Bernheim, T. Naftali, I. Lesin, G. Leichtman, I. Pomeranz, B. Novis

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)680-685
Number of pages6
JournalDigestive Diseases and Sciences
Issue number4
StatePublished - 1999


  • Atrophic gastritis
  • Autoimmune gastritis
  • Helicobacter pylori
  • bcl-2


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