title: Basal and pentagastrin stimulated acid secretion in duodenal ulcer subjects before and after Helicobacter pylori eradication: a 12-month follow-up study.
abstract: BACKGROUND
  The effect of infection by Helicobacter pylori on gastric physiology in duodenal ulcer subjects is controversial. There is evidence that the infection is associated with abnormalities in gastrin homeostasis. Consistent changes in pentagastrin-stimulated acid secretory status have proved difficult to establish. This may be because patients have been studied too soon after Helicobacter pylori eradication.
  
  
  OBJECTIVE
  To study the immediate and longer term effect of Helicobacter pylori eradication on basal and pentagastrin-stimulated acid secretion in duodenal ulcer subjects.
  
  
  METHODS
  Patients with active duodenal ulcer disease were studied. Ulcers were healed with sucralfate 2 g bd or ranitidine 300 mg nocte. Helicobacter pylori eradication was attempted with bismuth-based "Triple Therapy", and the nine patients in whom the organism was successfully eradicated were followed and studied over the 12-month period. Acid secretion was studied at entry (prior to the initiation of therapy), following healing, following eradication and 12 months later. Basal, low dose (0.1 microgram/kg) and high dose (6 micrograms/kg) pentagastrin-stimulated acid secretion was determined.
  
  
  RESULTS
  Whilst there was a tendency for basal and low dose-stimulated acid secretion to fall following eradication, in this study only the reduction in high dose-stimulated acid secretion achieved significance following eradication (entry mean = 59.6, post eradication mean = 49.6, p < 0.03). This effect of eradication on high dose pentagastrin-stimulated acid secretion was also seen at the 12-month study (mean = 48.9, p < 0.02 versus entry).
  
  
  CONCLUSIONS
  The findings of this study suggests that maximally stimulated acid secretion is modestly, albeit significantly, reduced following Helicobacter pylori eradication and that this effect persists.
authors.affiliation: Gastrointestinal Clinic, University of Cape Town, South Africa. japie@uctgsh2.uct.ac.za
authors.forename: J A
authors.initials: JA
authors.lastname: Louw
authors.forename: G O
authors.initials: GO
authors.lastname: Young
authors.forename: W
authors.initials: W
authors.lastname: Lucke
authors.forename: S
authors.initials: S
authors.lastname: Bridger
authors.forename: T A
authors.initials: TA
authors.lastname: Winter
authors.forename: I N
authors.initials: IN
authors.lastname: Marks
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D005260:Female; D005500:Follow-Up Studies; D005744:Gastric Acid / Q000378:metabolism*; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D010418:Pentagastrin / Q000494:pharmacology*
chemical_list: D000897:Anti-Ulcer Agents; D010418:Pentagastrin