title: Pathogenesis of gastric metaplasia of the human duodenum: role of Helicobacter pylori, gastric acid, and ulceration.
abstract: OBJECTIVE
  The pathogenesis of gastric metaplasia (GM) in the duodenum is unclear. The aim of this investigation was to study the effect on the extent of GM of ulcer healing, Helicobacter pylori eradication, and acid suppression singly and in combination. The relationship between GM and gastroduodenal inflammation and H. pylori infection density was also studied.
  
  
  METHODS
  Duodenal and gastric antral biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer and from H. pylori-positive nonulcer subjects. Biopsy procedures from patients with duodenal ulcer were repeated after 6 months of treatment. Nonulcer subjects were treated symptomatically and did not undergo re-endoscopy.
  
  
  RESULTS
  Ulcer healing alone produced no change in GM or in gastroduodenal inflammation. H. pylori eradication produced a 42% reduction in GM and improvement in inflammation. Acid suppression produced a 43% reduction in GM but without a significant change in inflammation. A combination of H. pylori eradication and acid suppression produced an additive effect with a 66% reduction in GM. A positive relationship was detected between the extent of GM and antral H. pylori density, duodenitis score, and antral gastritis score.
  
  
  CONCLUSIONS
  This study shows that the extent of duodenal GM is unrelated to the presence or absence of ulceration but is partly due to H. pylori and partly due to acid.
authors.affiliation: Department of Medicine, St. George's Hospital Medical School, London, England.
authors.forename: S
authors.initials: S
authors.lastname: Khulusi
authors.forename: S
authors.initials: S
authors.lastname: Badve
authors.forename: P
authors.initials: P
authors.lastname: Patel
authors.forename: R
authors.initials: R
authors.lastname: Lloyd
authors.forename: J M
authors.initials: JM
authors.lastname: Marrero
authors.forename: C
authors.initials: C
authors.lastname: Finlayson
authors.forename: M A
authors.initials: MA
authors.lastname: Mendall
authors.forename: T C
authors.initials: TC
authors.lastname: Northfield
mesh_terms: D000328:Adult; D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use; D000863:Antacids / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000150:complications* / Q000188:drug therapy; D004382:Duodenitis / Q000150:complications / Q000473:pathology; D004386:Duodenum / Q000473:pathology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D005756:Gastritis / Q000150:complications / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008679:Metaplasia; D008795:Metronidazole / Q000627:therapeutic use; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000627:therapeutic use; D010406:Penicillins / Q000627:therapeutic use
chemical_list: D000863:Antacids; D000897:Anti-Ulcer Agents; D009942:Organometallic Compounds; D010406:Penicillins; D008795:Metronidazole; D000658:Amoxicillin; C002791:bismuth tripotassium dicitrate; D009853:Omeprazole