title: A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer.
abstract: OBJECTIVE
  Helicobacter pylori infection and duodenal ulcer disease are firmly correlated. However, the bacteria do mainly colonize the antrum, indicating an indirect pathogenic mechanism. The aim of this study was to test a concept claiming that H. pylori infection of the antrum selectively blocks normal inhibitory reflex pathways to gastrin and parietal cells.
  
  
  METHODS
  The effect of antral distention was studied on gastric acid secretion stimulated by pentagastrin and on gastrin release stimulated by gastrin-releasing peptide in H. pylori-infected and noninfected patients with and without duodenal ulcer disease, as well as after eradication of the bacteria.
  
  
  RESULTS
  The inhibitory effect on gastric acid secretion induced by antral distention was absent in H. pylori-infected patients irrespective of whether or not they had duodenal ulcer disease. The inhibitory mechanism was restituted in 8 of 10 patients within 9 months after successful eradication of H. pylori infection. Similar results were obtained in studies on gastrin release.
  
  
  CONCLUSIONS
  H. pylori infection blocks normal, physiological inhibitory mechanisms from the antrum to both the gastrin cells and to the parietal cell region, resulting in increased gastrin release and impaired inhibition of gastric acid secretion, which will probably lead to an increased duodenal acid load as a general prerequisite for the development of duodenal ulcer disease.
authors.affiliation: Department of Surgery, Sahlgrenska Hospital, Göteborg, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Olbe
authors.forename: A
authors.initials: A
authors.lastname: Hamlet
authors.forename: J
authors.initials: J
authors.lastname: Dalenbäck
authors.forename: L
authors.initials: L
authors.lastname: Fändriks
mesh_terms: D000328:Adult; D000368:Aged; D004381:Duodenal Ulcer / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D013271:Gastric Dilatation / Q000503:physiopathology; D019886:Gastrin-Releasing Peptide; D005755:Gastrins / Q000378:metabolism; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D010295:Parietal Cells, Gastric / Q000187:drug effects / Q000378:metabolism; D010418:Pentagastrin / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology; D011706:Pyloric Antrum / Q000187:drug effects / Q000378:metabolism; D013272:Stomach Diseases / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D005755:Gastrins; D010455:Peptides; D019886:Gastrin-Releasing Peptide; D010418:Pentagastrin