title: Helicobacter pylori and gastric acid secretion: the ulcer link?
abstract: Helicobacter pylori is a recognized cause of chronic active gastritis and is frequently associated with peptic ulcer disease, but its effect on acid secretion is unclear. Transient hypochlorhydria occurs with acute infections. Despite the theoretical possibility of an increase in parietal cell mass or a response to stimulation occurring secondary to the associated hypergastrinaemia observed with H. pylori, no consistent increase in basal, pentagastrin-stimulated acid secretion or 24-h intragastric acidity has been reported. Although H. pylori is accepted as one of the many factors involved in peptic ulcer disease, and eradication results in decreased ulcer recurrence, its pathogenic role is still poorly understood. The progression of chronic active gastritis to atrophic gastritis and hypochlorhydria may in part explain the natural tendency for duodenal ulcer disease to resolve.
authors.affiliation: Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, Canada.
authors.forename: J W
authors.initials: JW
authors.lastname: Rademaker
authors.forename: R H
authors.initials: RH
authors.lastname: Hunt
mesh_terms: D000818:Animals; D005744:Gastric Acid / Q000378:metabolism*; D005745:Gastric Acidity Determination; D005756:Gastritis / Q000382:microbiology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D010434:Pepsin A / Q000378:metabolism; D010435:Pepsinogens / Q000378:metabolism; D010437:Peptic Ulcer / Q000382:microbiology* / Q000503:physiopathology
chemical_list: D010435:Pepsinogens; D010434:Pepsin A