Effect of Hp infection on gastric epithelial cell kinetics in stomach diseases

AIM To investigate the effect of Helicobacter pylori (Hp) infection on the gastric epithelial cell kinetics in the progression from normal mucosa to gastric carcinoma and the mechanisms of Hp causing gastric maligancy. METHODS By using immunohistochemical technique, the Ki 67 labelling index (LI%) was used to assess the gastric antral epithelial cell proliferation in bioptic gastric mucosa specimens of normal gastric mucosa dyspeptic subjects (NS, n =14 ) and five groups of patients (chronic superficial gastritis, CSG, n =56 ; chronic atrophic gastritis, CAG, n =20 ; chronic atrophic gastritis with intestinal metaplasia, CAGIM, n =16 ; dysplasia, Dys, n =18 ; gastric cancer, GC, n =17 ). Each was comprised of Hp positive and negative patients. RESULTS Ki 67 labelling index (LI%) was 17±5 in seventy five Hp positive patients, significantly higher than 13±6 in fifty two Hp negative patients ( P 0 05). CSG with Hp infection showed higher LI% than NS or CSG without Hp infection. There was no significant difference between the patients with or without Hp infection of CAG, CAGIM, Dys and GC. Five groups of patients had increased LI% compared with normal control, regardless of Hp infection. There was no correlation between LI% and the severity of gastritis. CONCLUSION Hp infection plays a role in the hyperproliferation of gastric epithelial cell predominantly in the early stage of gastric mucosa lesion, but not influcences the increased cell proliferation seen in precancerous lesion or GC. This provides further evidences that Hp infection may be an initiating step in the progression from normal mucosa to gastric carcinoma.