Gastric epithelial cell proliferation and cagA status in Helicobacter pylori gastritis at different gastric sites

Abstract

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≤0.002 and p≤0.009) and in the antrum in comparison to the corpus, in both H. pylori-negative (p=0.04) and positive patients (p<10⁻³). At the antral lesser curvature, PIs were higher than in all the other sites, both in H. pylori- (p≤0.002) and cagA-positive groups (p≤0.02). The PI correlated directly and significantly with inflammation in infected patients (r=0.45, p<10⁻³) and in cagA-positive patients (r=0.41, p=0.005). The PI was significantly higher in the antrum of infected patients with atrophy (p=0.03) and intestinal metaplasia (p=0.05) than in those without atrophy and intestinal metaplasia, respectively. 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.

• cagA status
• epithelial proliferation
• gastritis
• Helicobacter pylori
• topography