title: Cell proliferation in Helicobacter pylori associated gastritis and the effect of eradication therapy.
abstract: 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.
authors.affiliation: Centre for Digestive Diseases, General Infirmary at Leeds.
authors.forename: D A
authors.initials: DA
authors.lastname: Lynch
authors.forename: N P
authors.initials: NP
authors.lastname: Mapstone
authors.forename: A M
authors.initials: AM
authors.lastname: Clarke
authors.forename: G M
authors.initials: GM
authors.lastname: Sobala
authors.forename: P
authors.initials: P
authors.lastname: Jackson
authors.forename: L
authors.initials: L
authors.lastname: Morrison
authors.forename: M F
authors.initials: MF
authors.lastname: Dixon
authors.forename: P
authors.initials: P
authors.lastname: Quirke
authors.forename: A T
authors.initials: AT
authors.lastname: Axon
mesh_terms: D000328:Adult; D002455:Cell Division; D002908:Chronic Disease; D004359:Drug Therapy, Combination; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D008795:Metronidazole / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000627:therapeutic use; D013752:Tetracycline / Q000627:therapeutic use
chemical_list: D009942:Organometallic Compounds; D008795:Metronidazole; D013752:Tetracycline; C002791:bismuth tripotassium dicitrate