Background. Randomized controlled trials (RCTs) have been conducted comparing the efficacy of rabeprazole 20?mg or omeprazole 20?mg once daily for patients with erosive gastroesophageal reflux disease (GERD). Until now, no study has synthesized all available data examining this issue. Method. Medline, Embase, and the Cochrane central register of controlled trials were searched (through December 2012). Eligible RCTs recruited adults with erosive GERD and reported endoscopic and symptomatic relief rates at the last point of follow-up. The effect of rabeprazole versus omeprazole was reported as relative risk (RR) of relief with a 95% confidence interval (CI). Results. The search identified 605 citations, and six RCTs containing 1,895 patients were eligible. Endoscopic relief rates were not significantly different between rabeprazole 20?mg and omeprazole 20?mg in treatment trials of up to 8 weeks. Heartburn relief rates were significantly different between the two groups for 8-week treatment trials. Adverse events were not significantly different between the two groups for 8-week treatment trials. Conclusion. These data suggest that rabeprazole demonstrates a clinical advantage over omeprazole in symptomatic relief but no significant difference in endoscopic relief of erosive GERD for up to 8 weeks of treatment. Rabeprazole and omeprazole were both tolerated by GERD patients. 1. Introduction Gastroesophageal reflux disease (GERD) is a recurrent chronic disorder characterized by increased reflux of gastric contents into the lower esophagus that affects approximately 20%–30% of the population worldwide, particularly in western countries [1–3]. Severe reflux esophagitis may develop complications such as esophageal stricture or Barrett’s esophagus [4]. Previous clinical studies have shown that proton pump inhibitors (PPIs) are safer and more effective than H2 receptor antagonists at healing esophageal lesions, relieving heartburn symptoms, and preventing symptomatic and endoscopic relapse [5, 6]. Omeprazole and rabeprazole are both potent inhibitors of H+K+-ATPase, which is responsible for the terminal step in gastric acid secretion [7]. Rabeprazole is a second-generation proton pump inhibitor that has 2- to 10-fold greater antisecretory activity in vitro than omeprazole, the prototypical PPI [8–11]. A rapid pharmacodynamic response may translate to faster onset of symptom relief [9]. However, meta-analysis by Caro et al. showed that rabeprazole was of similar efficacy to omeprazole in terms of heartburn control, healing rates, and relapse rates [5]. Other
References
[1]
S. Nasseri-Moghaddam, A. Mofid, M.-H. Ghotbi et al., “Epidemiological study of gastro-oesophageal reflux disease: reflux in spouse as a risk factor,” Alimentary Pharmacology and Therapeutics, vol. 28, no. 1, pp. 144–153, 2008.
[2]
P. Bytzer, A. Blum, D. De Herdt, and D. Dubois, “Six-month trial of on-demand rabeprazole 10?mg maintains symptom relief in patients with non-erosive reflux disease,” Alimentary Pharmacology and Therapeutics, vol. 20, no. 2, pp. 181–188, 2004.
[3]
T. Kennedy and R. Jones, “The prevalence of gastro-oesophageal reflux symptoms in a UK population and the consultation behaviour of patients with these symptoms,” Alimentary Pharmacology and Therapeutics, vol. 14, no. 12, pp. 1589–1594, 2000.
[4]
A. Soni, R. E. Sampliner, and A. Sonnenberg, “Health-related quality of life and severity of symptoms in patients with Barrett's esophagus and gastroesophageal reflux disease patients without Barrett's esophagus,” American Journal of Gastroenterology, vol. 95, no. 8, pp. 1881–1887, 2000.
[5]
J. J. Caro, M. Salas, and A. Ward, “Healing and relapse rates in gastroesophageal reflux disease treated with the newer proton-pump inhibitors lansoprazole, rabeprazole, and pantoprazole compared with omeprazole, ranitidine, and placebo: evidence from randomized clinical trials,” Clinical Therapeutics, vol. 23, no. 7, pp. 998–1017, 2001.
[6]
E. C. Klinkenberg-Knol, F. Nelis, J. Dent et al., “Long-term omeprazole treatment in resistant gastroesophageal reflux disease: efficacy, safety, and influence on gastric mucosa,” Gastroenterology, vol. 118, no. 4, pp. 661–669, 2000.
[7]
C. P. M. Dekkers, J. A. Beker, B. Thjodleifsson, A. Gabryelewicz, N. E. Bell, and T. J. Humphries, “Double-blind, placebo-controlled comparison of rabeprazole 20?mg vs. omeprazole 20?mg in the treatment of erosive or ulcerative gastro-oesophageal reflux disease,” Alimentary Pharmacology and Therapeutics, vol. 13, no. 1, pp. 49–57, 1999.
[8]
S. Pallotta, F. Pace, and S. Marelli, “Rabeprazole: A second-generation proton pump inhibitor in the treatment of acid-related disease,” Expert Review of Gastroenterology and Hepatology, vol. 2, no. 4, pp. 509–522, 2008.
[9]
M. Robinson, P. N. Maton, S. Rodriguez, B. Greenwood, and T. J. Humphries, “Effects of oral rabeprazole on oesophageal and gastric pH in patients with gastro-oesophageal reflux disease,” Alimentary Pharmacology and Therapeutics, vol. 11, no. 5, pp. 973–980, 1997.
[10]
M. P. Williams, J. Sercombe, M. I. Hamilton, and R. E. Pounder, “A placebo-controlled trial to assess the effects of 8 days of dosing with rabeprazole versus omeprazole on 24-h intragastric acidity and plasma gastrin concentrations in young healthy male subjects,” Alimentary Pharmacology and Therapeutics, vol. 12, no. 11, pp. 1079–1089, 1998.
[11]
A. Prakash and D. Faulds, “Rabeprazole,” Drugs, vol. 55, no. 2, pp. 261–268, 1998.
[12]
J.-C. Delchier, G. Cohen, and T. J. Humphries, “Rabeprazole, 20?mg once daily or 10?mg twice daily, is equivalent to omeprazole, 20?mg once daily, in the healing of erosive gastro-oesophageal reflux disease,” Scandinavian Journal of Gastroenterology, vol. 35, no. 12, pp. 1245–1250, 2000.
[13]
K. Adachi, T. Hashimoto, N. Hamamoto et al., “Symptom relief in patients with reflux esophagitis: comparative study of omeprazole, lansoprazole, and rabeprazole,” Journal of Gastroenterology and Hepatology, vol. 18, no. 12, pp. 1392–1398, 2003.
[14]
F. Pace, V. Annese, A. Prada et al., “Rabeprazole is equivalent to omeprazole in the treatment of erosive gastro-oesophageal reflux disease. A randomised, double-blind, comparative study of rabeprazole and omeprazole 20?mg in acute treatment of reflux oesophagitis, followed by a maintenance open-label, low-dose therapy with rabeprazole,” Digestive and Liver Disease, vol. 37, no. 10, pp. 741–750, 2005.
[15]
P. Bytzer, A. Morocutti, P. Kennerly, M. Ravic, and N. Miller, “Effect of rabeprazole and omeprazole on the onset of gastro-oesophageal reflux disease symptom relief during the first seven days of treatment,” Scandinavian Journal of Gastroenterology, vol. 41, no. 10, pp. 1132–1140, 2006.
[16]
A. Pilotto, M. Franceschi, G. Leandro et al., “Comparison of four proton pump inhibitors for the short-term treatment of esophagitis in elderly patients,” World Journal of Gastroenterology, vol. 13, no. 33, pp. 4467–4472, 2007.
[17]
I. M. Gralnek, G. S. Dulai, M. B. Fennerty, and B. M. R. Spiegel, “Esomeprazole versus other proton pump inhibitors in erosive esophagitis: a meta-analysis of randomized clinical trials,” Clinical Gastroenterology and Hepatology, vol. 4, no. 12, pp. 1452–1458, 2006.
[18]
M. L. Cloud, N. Enas, T. J. Humphries, and S. Bassion, “Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD),” Digestive Diseases and Sciences, vol. 43, no. 5, pp. 993–1000, 1998.
[19]
C. Schmitt, C. J. Lightdale, C. Hwang, and B. Hamelin, “A multicenter, randomized, double-blind, 8-week comparative trial of standard doses of esomeprazole (40?mg) and omeprazole (20?mg) for the treatment of erosive esophagitis,” Digestive Diseases and Sciences, vol. 51, no. 5, pp. 844–850, 2006.
[20]
C. J. Lightdale, C. Schmitt, C. Hwang, and B. Hamelin, “A multicenter, randomized, double-blind, 8-week comparative trial of low-dose esomeprazole (20?mg) and standard-dose omeprazole (20?mg) in patients with erosive esophagitis,” Digestive Diseases and Sciences, vol. 51, no. 5, pp. 852–857, 2006.
[21]
P. J. Easterbrook, J. A. Berlin, R. Gopalan, and D. R. Matthews, “Publication bias in clinical research,” The Lancet, vol. 337, no. 8746, pp. 867–876, 1991.
[22]
J. P. A. Ioannidis, “Why most published research findings are false,” PLoS Medicine, vol. 2, no. 8, pp. 0696–0701, 2005.