Helicobacter pylori, gastric cancer and gastric epithelial kinetics: a review.
OBJECTIVE
To review the evidence that Helicobacter pylori promotes gastric carcinogenesis, with particular reference to gastric epithelial proliferation.


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.
Lynch
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Centre for Digestive Diseases, General Infirmary, Leeds, UK.
Axon
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D000818:Animals; D002455:Cell Division; D004848:Epithelium / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D013274:Stomach Neoplasms / Q000382:microbiology* / Q000473:pathology*