Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy

• Published in: Gut 1995-03, Vol.36 (3), p.346-350
• Main Authors: Lynch, D A, Mapstone, N P, Clarke, A M, Sobala, G M, Jackson, P, Morrison, L, Dixon, M F, Quirke, P, Axon, A T
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Cell Division; Chronic Disease; Drug Therapy, Combination; Gastric Mucosa - pathology; Gastritis - drug therapy; Gastritis - microbiology; Gastritis - pathology; Gastroenterology. Liver. Pancreas. Abdomen; Helicobacter Infections - drug therapy; Helicobacter Infections - pathology; Helicobacter pylori; Humans; Immunohistochemistry; Malformations; Medical sciences; Metronidazole - therapeutic use; Organometallic Compounds - therapeutic use; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tetracycline - therapeutic use
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.36.3.346

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.