title: Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease.
abstract: OBJECTIVE
  The mechanism by which Helicobacter pylori predisposes to duodenal ulcers (DUs) remains unclear. The aim of this study was to investigate the effect of the infection on acid secretion.
  
  
  METHODS
  Acid output was examined basally and in response to gastrin-releasing peptide (GRP) and gastrin in healthy volunteers with and without H. pylori infection and in patients with DUs before and after eradication of the infection.
  
  
  RESULTS
  Compared with H. pylori-negative healthy volunteers, patients with DUs with H. pylori had the following abnormalities of acid secretion: (1) threefold increase in basal acid output, (2) sixfold increase in acid response to GRP, (3) increased maximal acid response to exogenous gastrin, (4) increased ratio of basal acid output to maximal gastrin-stimulated output, and (5) increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output. All of these abnormalities resolved fully after H. pylori eradication except for increased maximal acid output to gastrin, which was unchanged. Infected healthy volunteers showed a threefold increase in acid response to GRP that resolved after eradication of H. pylori infection.
  
  
  CONCLUSIONS
  These disturbances in acid secretion caused by H. pylori infection are consistent with impaired inhibitory control and are likely to be relevant to the mechanism by which the infection predisposes to DU.
authors.affiliation: University Department of Medicine and Therapeutics Western Infirmary, Glasgow, Scotland.
authors.forename: E M
authors.initials: EM
authors.lastname: el-Omar
authors.forename: I D
authors.initials: ID
authors.lastname: Penman
authors.forename: J E
authors.initials: JE
authors.lastname: Ardill
authors.forename: R S
authors.initials: RS
authors.lastname: Chittajallu
authors.forename: C
authors.initials: C
authors.lastname: Howie
authors.forename: K E
authors.initials: KE
authors.lastname: McColl
mesh_terms: D000658:Amoxicillin / Q000627:therapeutic use; D000863:Antacids / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000209:etiology* / Q000382:microbiology; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism; D019886:Gastrin-Releasing Peptide; D005755:Gastrins; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D016014:Linear Models; D008297:Male; D008795:Metronidazole / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000627:therapeutic use; D010455:Peptides; D015203:Reproducibility of Results
chemical_list: D000863:Antacids; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D005755:Gastrins; D009942:Organometallic Compounds; D010455:Peptides; D008795:Metronidazole; D019886:Gastrin-Releasing Peptide; D000658:Amoxicillin; C002791:bismuth tripotassium dicitrate