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 prolif eration. Materials and methods: Gastric epithelial kinetics were revie wed and a series of studies of gastric mucosal proliferation in H. pyl ori-associated gastritis were performed in the intact and postsurgical stomach. In vitro bromodeoxyuridine labelling was performed on endosc opic antral biopsies from subjects with a normal gastric mucosa, with H. pylori-negative gastritis and with H. pylori-positive gastritis. Th e 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 increas ed in patients with H. pylori-positive gastritis and returned to norma l levels following eradication therapy. The presence of H. pylori in t he postsurgical stomach had a synergistic effect on gastric epithelial proliferation. Conclusions: H. pylori may promote gastric carcinogene sis by increasing epithelial proliferation. H. pylori and bile appear to have a synergistic effect on gastric cell proliferation.