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Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites
Mônica M D A Cabral1, Celso A Oliveira, Cláudia M C Mendes
1Faculty of Medicine, Department of Pathology, Laboratory of Research in Bacteriology, University Hospital Federal University of Minas Gerais, Brazil.
Objective:
Helicobacter pylori infection causes hyperproliferation which is believed to predispose to the development of gastric carcinoma. The aim of this study was to analyze epithelial cell proliferation topographically in H. pylori gastritis in relationship to cagA status.
Material And Methods:
The proliferative index (PI: Ki-67-labeled nuclei/total number of foveolar nuclei) was determined in gastric mucosa biopsies taken at the antrum (lesser and greater curvatures), incisura, and corpus (greater curvature) from 78 patients with H. pylori gastritis and 20 H. pylori-negative patients. H. pylori and cagA status were determined by polymerase chain reaction (PCR) and serology.
Results:
PIs were significantly higher in H. pylori- and cagA-positive patients, in comparison with H. pylori- and cagA-negative patients, at all sites (p
Conclusions:
We demonstrated that H. pylori infection and cagA-positive strains promote epithelial proliferation that was correlated with host inflammatory reaction and mostly at the antral lesser curvature, which is recognized as the area where most carcinomas arise.
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