PT  - JOURNAL ARTICLE
AU  - D A Lynch
AU  - N P Mapstone
AU  - A M Clarke
AU  - G M Sobala
AU  - P Jackson
AU  - L Morrison
AU  - M F Dixon
AU  - P Quirke
AU  - A T Axon
TI  - Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy.
AID  - 10.1136/gut.36.3.346
DP  - 1995 Mar 01
TA  - Gut
PG  - 346--350
VI  - 36
IP  - 3
4099  - http://gut.bmj.com/content/36/3/346.short
4100  - http://gut.bmj.com/content/36/3/346.full
SO  - Gut1995 Mar 01; 36
AB  - Helicobacter pylori causes chronic (type B) gastritis. The 'intestinal' form of gastric cancer arises against a background of chronic gastritis, and prospective epidemiological studies have shown that H pylori is a major risk factor for this. An increase in mucosal cell proliferation increases the likelihood of a neoplastic clone of epithelial cells emerging where there is chronic epithelial cell injury associated with H pylori gastritis. In vitro bromodeoxyuridine labelling of endoscopic antral biopsy specimens was used to measure mucosal cell proliferation 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 patients with H pylori negative chronic gastritis (p = 0.0001; Tukey's Studentised range). There was no difference in antral epithelial cell proliferation between duodenal ulcer and non-ulcer subjects infected with H pylori (p = 0.62; Student's t test). Antral mucosal cell proliferation fell four weeks after completing triple therapy, irrespective of whether 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 proliferation compared with both H pylori negative subjects at a similar follow up interval and all cases (whether H pylori positive or negative) four weeks after completion of triple therapy (p = 0.024). These findings suggest that H pylori infection causes increased gastric cell proliferation and in this way may play a part in gastric carcinogenesis.