Original Contribution | Published:

Gastric acid control with esomeprazole, lansoprazole, omeprazole, pantoprazole, and rabeprazole: a five-way crossover study

American Journal of Gastroenterology volume 98, pages 26162620 (2003) | Download Citation

Subjects

Abstract

OBJECTIVES:

Proton pump inhibitors owe their clinical efficacy to their ability to suppress gastric acid production. The objective of this study was to evaluate and compare intragastric pH following standard doses of esomeprazole, lansoprazole, omeprazole, pantoprazole and rabeprazole.

METHODS:

This randomized, open-label, comparative five-way crossover study evaluated the 24-h intragastric pH profile of oral esomeprazole 40 mg, lansoprazole 30 mg, omeprazole 20 mg, pantoprazole 40 mg, and rabeprazole 20 mg once daily in 34 Helicobacter pylori–negative patients aged 18–60 yr with symptoms of gastroesophageal reflux disease. Patients were randomly assigned to one of five treatment sequences and study drug was taken on 5 consecutive mornings 30 minutes prior to a standardized breakfast. A washout period of at least 10 days separated each treatment phase.

RESULTS:

Thirty-four patients provided evaluable data for all five comparators. The mean number of hours of evaluable pH data was ≥23.75 hours. On day 5, intragastric pH was maintained above 4.0 for a mean of 14.0 h with esomeprazole, 12.1 h with rabeprazole, 11.8 h with omeprazole, 11.5 h with lansoprazole, and 10.1 h with pantoprazole (p ≤ 0.001 for differences between esomeprazole and all other comparators). Esomeprazole also provided a significantly higher percentage of patients with an intragastric pH greater than 4.0 for more than 12 h relative to the other proton pump inhibitors (p < 0.05). The frequency of adverse events was similar between treatment groups.

CONCLUSIONS:

Esomeprazole at the standard dose of 40 mg once daily provided more effective control of gastric acid at steady state than standard doses of lansoprazole, omeprazole, pantoprazole, and rabeprazole in patients with symptoms of gastroesophageal reflux disease.

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Acknowledgements

The authors would like to acknowledge Christopher Rains, Karen van Hoeven, and Caroline Spencer for their assistance with manuscript preparation.

Author information

Affiliations

  1. Oklahoma Foundation for Digestive Research, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA

    • Philip Miner Jr.
  2. Department of Medicine, Graduate Hospital, Philadelphia, USA

    • Philip O Katz
  3. Division of Biostatistics, AstraZeneca, LP, Wilmington, Delaware, USA

    • Yusong Chen
  4. Division of Clinical Research, AstraZeneca, LP, Wilmington, Delaware, USA

    • Mark Sostek

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Correspondence to Philip Miner Jr.

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DOI

https://doi.org/10.1111/j.1572-0241.2003.08783.x