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 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 i...

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Bibliographic Details
Published in:Digestive diseases and sciences 1999-04, Vol.44 (4), p.680-685
Main Authors: MAOR-KENDLER, Y, GABAY, G, BERNHEIM, J, NAFTALI, T, LESIN, I, LEICHTMAN, G, POMERANZ, I, NOVIS, B
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Autoimmune Diseases - genetics
Autoimmune Diseases - pathology
Biological and medical sciences
Case-Control Studies
Female
Gastritis, Atrophic - genetics
Gastritis, Atrophic - pathology
Gastroenterology. Liver. Pancreas. Abdomen
Gene Expression Regulation
Genes, bcl-2 - genetics
Helicobacter Infections - genetics
Helicobacter Infections - pathology
Helicobacter pylori
Humans
Immunohistochemistry
Male
Medical sciences
Middle Aged
Other diseases. Semiology
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
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Summary: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.
ISSN:0163-2116
1573-2568
DOI:10.1023/A:1026641204860