Helicobacter pylori, gastric cancer and gastric epithelial kinetics: a review.

AIM: To review the evidence that Helicobacter pylori promotes gastric carcinogenesis, with particular reference to gastric epithelial proliferation. MATERIALS AND METHODS: Gastric epithelial kinetics were reviewed and a series of studies of gastric mucosal proliferation in H. pylori-associated gastritis were performed in the intact and postsurgical stomach. In vitro bromodeoxyuridine labelling was performed on endoscopic antral biopsies from subjects with a normal gastric mucosa, with H. pylori-negative gastritis and with H. pylori-positive gastritis. The effect of eradication therapy was assessed. Corpus biopsies from the intact stomach were also examined and compared to body-type biopsies from the postsurgical stomach. RESULTS: Cell proliferation was increased in patients with H. pylori-positive gastritis and returned to normal levels following eradication therapy. The presence of H. pylori in the postsurgical stomach had a synergistic effect on gastric epithelial proliferation. CONCLUSIONS: H. pylori may promote gastric carcinogenesis by increasing epithelial proliferation. H. pylori and bile appear to have a synergistic effect on gastric cell proliferation.