CELL-PROLIFERATION IN HELICOBACTER-PYLORI-ASSOCIATED GASTRITIS AND THE EFFECT OF ERADICATION THERAPY

Helicobacter pylori causes chronic (type B) gastritis. The ''intestina l'' form of gastric cancer arises against a background of chronic gast ritis, and prospective epidemiological studies have shown that H pylor i is a major risk factor for this. An increase in mucosal cell prolife ration increases the likelihood of a neoplastic clone of epithelial ce lls emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endos copic antral biopsy specimens was used to measure mucosal cell prolife ration in H pylori associated gastritis before and after therapy for H pylori triple infection. Cell proliferation was increased in H pylori associated gastritis patients compared with normal controls and patie nts with H pylori negative chronic gastritis (p=0.0001; Tukey's Studen tised range). There was no difference in antral epithelial cell prolif eration between duodenal ulcer and non-ulcer subjects infected with H pylori (p=0.62; Student's t test). Antral mucosal cell proliferation f ell four weeks after completing triple therapy, irrespective of whethe r or not H pylori had been eradicated (p=0.0001). At retesting six to 18 months later (mean=12 months), however, those in whom H pylori had not been successfully eradicated showed increased mucosal proliferatio n compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four w eeks after completion of triple therapy (p=0.024). These findings sugg est that H pylori infection causes increased gastric cell proliferatio n and in this way may play a part in gastric carcinogenesis.