title: Rabeprazole is superior to omeprazole for the inhibition of peptone meal-stimulated gastric acid secretion in Helicobacter pylori-negative subjects.
abstract: BACKGROUND
  Peptone meal-stimulated gastric acid output is considered to be a reliable means to evaluate drug-mediated inhibition of stimulated gastric acid output, an important measure of the efficacy of the agents--such as proton pump inhibitors--used to treat acid-related disorders.
  
  
  OBJECTIVE
  To compare the initial and overall inhibitory effects on peptone meal-stimulated gastric acid secretion of rabeprazole and omeprazole, 20 mg, in Helicobacter pylori-negative subjects on the first and eighth days of treatment.
  
  
  METHODS
  Healthy volunteers (n = 27) were randomized in a single-centre, double-blind, double-dummy, 2 x 2 cross-over study. Subjects received an oral dose of rabeprazole or omeprazole, 20 mg once daily, for 8 days. After a 2-4-week washout period, subjects were crossed over to receive the other medication for 8 days. Peptone meal-stimulated gastric acid secretion was measured at hours 11 and 23 at baseline and on days 1 and 8 of treatment.
  
  
  RESULTS
  On days 1 and 8, rabeprazole demonstrated a significantly greater inhibition of peptone meal-stimulated gastric acid secretion compared with omeprazole at all time points (P < 0.03). Median values of steady-state inhibition on day 1 were statistically significant at hour 23 (rabeprazole 100% vs. omeprazole 74%, P < 0.02).
  
  
  CONCLUSIONS
  Rabeprazole, 20 mg, demonstrated superior control of peptone meal-stimulated gastric acid secretion compared with omeprazole, 20 mg, after the first dose and after the eighth daily dose. Rabeprazole achieved a more rapid onset of acid inhibition and a greater steady-state reduction in peptone meal-stimulated gastric acid secretion.
authors.affiliation: Research and Medical Services, Department of Veteran Affairs, VA GLAHS-West Los Angeles Healthcare Center, and the Department of Medicine, School of Medicine, University of California, Los Angeles, CA 90073, USA. gohning@ucla.edu
authors.forename: G V
authors.initials: GV
authors.lastname: Ohning
authors.forename: J H
authors.initials: JH
authors.lastname: Walsh
authors.forename: J R
authors.initials: JR
authors.lastname: Pisegna
authors.forename: A
authors.initials: A
authors.lastname: Murthy
authors.forename: J
authors.initials: J
authors.lastname: Barth
authors.forename: T O G
authors.initials: TO
authors.lastname: Kovacs
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000328:Adult; D000897:Anti-Ulcer Agents / Q000494:pharmacology*; D001562:Benzimidazoles / Q000494:pharmacology*; D018592:Cross-Over Studies; D004305:Dose-Response Relationship, Drug; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005745:Gastric Acidity Determination; D006801:Humans; D008297:Male; D009853:Omeprazole / Q000494:pharmacology*; D019518:Postprandial Period / Q000502:physiology; D064750:Rabeprazole; D016896:Treatment Outcome
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D001562:Benzimidazoles; D064750:Rabeprazole; D009853:Omeprazole