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Rabeprazole

A Review of its Use in Acid-Related Gastrointestinal Disorders

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Abstract

Rabeprazole is an inhibitor of the gastric proton pump. It causes dose-dependent inhibition of acid secretion and has a more rapid onset of action than omeprazole.

Duodenal ulcers healed faster after treatment with rabeprazole 20 or 40 mg/day than placebo or ranitidine 150mg 4 times daily and at a generally similar rate to omeprazole 20 mg/day in patients with duodenal ulcers; rabeprazole was similar or superior to these agents in relieving symptoms. Rabeprazole 20 and 40 mg/day healed gastric ulcers faster than placebo, and rabeprazole 20 mg/day healed ulcers at a similar healing rate, to omeprazole 20 mg/day in well controlled 6-week studies. Gastric ulcer symptom relief with rabeprazole was similar or superior to that provided by omeprazole or placebo. In 8-week studies in patients with gastro-oesophageal reflux disease (GERD), rabeprazole 10,20 and 40 mg/day were more effective than placebo, rabeprazole 20 mg/day was more effective than ranitidine 150mg twice daily, and rabeprazole 20 mg/day was similar in efficacy to omeprazole 20 mg/day. Symptom relief with rabeprazole in 8-week trials in patients with GERD was superior to that provided by placebo, and similar to ranitidine or omeprazole. Rabeprazole was similar to omeprazole and superior to placebo in both maintenance of healing and prevention of symptoms in patients with healed GERD in 1-year studies. One-week triple therapy with rabeprazole 20mg twice daily plus 2 antibacterial agents achieved ≥90% Helicobacter pylori eradication, but, as would be expected, a regimen of rabeprazole 20mg twice daily plus 1 antibacterial agent was less successful. The drug was as effective as omeprazole and lansoprazole as part of triple therapy for H. pylori eradication.

Rabeprazole successfully reduced acid output to target levels and prevented further pathological changes in 10 patients with Zollinger-Ellison syndrome.

Usual dosages of rabeprazole are 20 mg/day for 4 weeks to treat duodenal ulcers, 6 weeks for gastric ulcers and 8 weeks for GERD, although some patients with duodenal ulcer may respond to a 10 mg/day dosage. For long term maintenance of GERD healing, 10 or 20mg daily doses are adequate. Patients with hypersecretory states may need individualised dosages starting at 60 mg/day. The drug was well tolerated in clinical trials, with headache, rash, infection, diarrhoea and flu syndrome as the most common adverse events.

In conclusion, rabeprazole appears to be a well tolerated proton pump inhibitor with a rapid onset of action and a low potential for drug interactions. The drug may be used to achieve healing and the relief of symptoms of duodenal ulcer, gastric ulcer and GERD, maintain GERD healing, and can form part of effective regimens to eradicate H. pylori.

Pharmacodynamic Effects

Rabeprazole interacts at the same site on the proton pump as omeprazole, but did not produce conformational changes in the protein in an in vitro study. The effects of rabeprazole on acid secretion are dose dependent over dosages from 5 to 40 mg/day in volunteers. Importantly, an increase in gastric pH, coupled with a reduction in oesophageal acid exposure, was seen in patients with GERD who received rabeprazole 20 or 40mg once daily for 7 days.

In volunteers, 24-hour acidity on day 1 was significantly lower with rabeprazole 20mg/day than omeprazole 20mg/day (p < 0.001).

Increases in gastrin after rabeprazole administration were dose dependent and directly related to increases in gastric pH. In clinical trials, rabeprazole appeared to produce greater increases in fasting serum gastrin levels than omeprazole in patients with duodenal ulcers, but had similar effects to omeprazole in patients with gastric ulcers or GERD. In these trials serum gastrin levels at endpoint did not exceed 3 times the upper limit of normal in patients with normal levels at baseline.

Rabeprazole and amoxicillin had at most additive effects on H. pylori isolates in vitro; however, synergistic anti-H. pylori effects were seen when the thioether metabolite of rabeprazole was combined with amoxicillin. H. pylori urease protects the micro-organism from gastric acid, but is inhibited in vitro at lower concentrations of rabeprazole than of lansoprazole or omeprazole. Rabeprazole does not appear to differ from other proton pump inhibitors in its ability to affect gastric cells. Long term rodent carcinogenicity studies have shown the potential for rabeprazole to cause enterochromaffin-like cell hyperplasia without causing more severe proliferative changes. Unlike omeprazole (which reduced gastric mucin) and lansoprazole (which had no effect), rabeprazole was reported to significantly increase the production of gastric mucin (a defensive factor) in rats. Like omeprazole, rabeprazole prevented or reduced the size of gastric ulcers caused by water immersion in rats, and prevented stress-induced increases in gastric mucosal peptide-leukotriene content without altering mucosal prostaglandin levels. Rabeprazole, unlike omeprazole, had no effect on steroido-genesis or other aspects of endocrine function.

Pharmacokinetic Properties

Pharmacokinetic studies of rabeprazole 1 to 80mg in single and multiple doses have been conducted in volunteers. Both the peak plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) for rabeprazole were roughly proportional to the dose after single oral doses of 10 to 80mg. The time to reach the rabeprazole Cmax(tmax) was 2.9 to 3.8 hours after administration of single doses of 10 to 80mg and was independent of the dose. Rabeprazole absorption pharmacokinetic s were generally similar after single and multiple daily 20 and 40mg doses. The drug was 96.3% bound to plasma proteins.

Rabeprazole is rapidly cleared by hepatic metabolism and renal excretion. The drug has an elimination half-life of ≈1 hour and an apparent oral clearance ranging from 0.26 to 0.50 L/h/kg (4.3 to 8.4 ml/min/kg) which was not dependent on the dose from 10 to 80mg. Rabeprazole is metabolised by human cytochrome P450 enzymes CYP2C19 and CYP3A to demethyl and sulfone metabolites. The major metabolite is a thioether carboxylic acid compound. The interaction of rabeprazole with CYP2C19 was less than that of omeprazole and interaction with CYP3A was similar to or lower than the low level of interaction seen with omeprazole. There were no clinically significant changes in pharmacokinetic parameters when rabeprazole was administered to patients with renal or hepatic dysfunction or elderly individuals.

Absorption of rabeprazole was unaffected by concomitant or prior administration of an aluminum hydroxide/magnesium hydroxide antacid preparation, whereas administration of rabeprazole with food delayed the tmax by 1.7 hours. In interaction studies in volunteers, rabeprazole had no significant effects on most cytochrome P450 enzyme systems, although predictable interactions occurred with ketoconazole and digoxin as a result of rabeprazole-induced changes in gastric pH.

Clinical Efficacy

The efficacy of rabeprazole has been studied in patients with duodenal or gastric ulcers, GERD, Zollinger-Ellison syndrome and H. pylori infection.

In 3 well controlled 4-week studies in patients with duodenal ulcers, rabeprazole 20 and 40 mg/day were compared with placebo, and rabeprazole 20 mg/ day was compared with omeprazole 20 mg/day or ranitidine 150mg twice daily. Rabeprazole healed duodenal ulcers faster than placebo or ranitidine and at a generally similar healing rate to omeprazole in patients with duodenal ulcers. The relief of overall and day or night-time symptoms with rabeprazole in 4-week trials in patients with duodenal ulcers was similar or superior to that provided by placebo, ranitidine or omeprazole.

In 2 well controlled 6-week studies in patients with benign gastric ulcers, rabeprazole 20 and 40 mg/day dosages were compared with placebo and rabeprazole 20 mg/day was compared with omeprazole 20 mg/day. Rabeprazole healed ulcers faster than placebo and at a similar healing rate to omeprazole in patients with gastric ulcers. The relief of symptoms provided by rabeprazole in 6-week trials in patients with gastric ulcers was similar or superior to that provided by placebo or omeprazole. Day pain at 3 weeks, pain frequency at 6 weeks and night pain at 6 weeks were all significantly less common or severe with rabeprazole than omeprazole in a trial in 127 patients.

The efficacy of rabeprazole in achieving healing and the relief of symptoms of erosive or ulcerative GERD has been tested in 4 well controlled 8-week clinical trials comparing it with placebo, omeprazole or ranitidine. Rabeprazole 10, 20 and 40 mg/day doses (8-week healing rates 93, 84 and 85%) were more effective than placebo (12%, p < 0.001) and rabeprazole 20 mg/day (4- and 8-week healing rates 58 and 88%) was more effective than ranitidine 150mg 4 times daily (36 and 65%, p < 0.001). Eight-week healing rates were similar after rabeprazole 20mg once daily (92 or 97%) or 10mg twice daily (98%) and omeprazole 20 mg/day (94 or 100%) in 2 studies. Symptom relief with rabeprazole in 8-week trials in patients with GERD was similar or superior to that provided by placebo, ranitidine or omeprazole.

Two 1-year trials examined the efficacy of rabeprazole 10 and 20 mg/day compared with placebo or omeprazole in maintaining healing and symptom relief in patients following healing of grades 2 to 4 GERD. Rabeprazole was similar to omeprazole and superior to placebo in both maintenance of healing and prevention of symptoms in patients with healed GERD.

In two 1-week pilot studies, rabeprazole 20mg twice daily significantly improved H. pylori eradication when added to a regimen of amoxicillin 500mg 4 times daily. In a larger study, 1-week triple therapy with rabeprazole 20mg twice daily plus 2 of clarithromycin 500mg twice daily, metronidazole 400mg twice daily or amoxicillin 1g twice daily achieved ≥90% H. pylori eradication, but rabeprazole 20mg twice daily plus clarithromycin 500mg once daily was less successful (63% eradication). Rabeprazole 20mg twice daily was as effective as omeprazole 20mg twice daily and lansoprazole 30mg twice daily as part of 1-week triple therapy for H. pylori infection, in a randomised study. Each antisecretory drug was combined with amoxicillin 1500 mg/day and clarithromcyin 400 mg/day. Intention to treat cure rates were 87.5% in the rabeprazole group versus 85.3 and 83.8% in the omeprazole and lansoprazole groups, respectively.

In a nonblind comparative 12-month study in 10 patients with hypersecretory conditions (age 41 to 75 years), rabeprazole successfully reduced acid output to target levels and prevented further pathological changes. Patients with Zollinger-Ellison syndrome and idiopathic gastric hypersecretion received rabeprazole 60 mg/day, with 1 patient requiring rabeprazole, 60mg twice, daily.

Tolerability

Rabeprazole was well tolerated in comparative trials of up to 1 year in duration enroling a total of >2500 patients, with tolerability that was not significantly different from that seen with in patients receiving placebo, omeprazole or ranitidine. The most common adverse events in clinical trials were headache, rash, infection, diarrhoea and flu syndrome, each of which was present in <5% of patients.

Dosage and Administration

The usual oral dosage of rabeprazole is 20 mg/day, although some patients with Administration duodenal ulcer may respond to 10 mg/day. Usual durations of rabeprazole therapy are 4 weeks for duodenal ulcer healing, 6 weeks for gastric ulcer healing, 8 weeks for healing and symptom relief for erosive or ulcerative GERD and long term (>1 year) for maintenance of GERD healing or for hypersecretory conditions such as Zollinger-Ellison Syndrome. In patients with H. pylori infection, rabeprazole 20 mg/day is usually administered with 2 antibacterial agents for 1 week. Patients with Zollinger-Ellison syndrome usually require rabeprazole 60 mg/day, although larger dosages (e.g. 60mg twice daily) have been used in clinical practice. Rabeprazole can alter concentrations of ketoconazole and digoxin because of the dependency of these drugs on gastric pH for absorption.

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Correspondence to Anthony Markham.

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Various sections of the manuscript reviewed by: S. Bank, Long Island Jewish Medical Center, Division of Gastroenterology, New York, New York, USA; N. Chiba, Division of Gastroenterology, Department of Medicine, McMaster University, Hamilton, Ontario, Canada; C. Florent, Hôpital Saint Antoine, Paris, France; A.W. Harris, Kent and Sussex Hospital, Tunbridge Wells, England; R.T. Jensen, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, USA; K. Kobashi, Toyama Medical and Pharmaceutical University, Toyama, Japan; J. Labenz, Jung-Stilling Hospital, Siegen, Germany; M. Robinson, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, USA; W.A. Stack, Bon Secours Hospital, Cork, Ireland; N. Takeguchi, Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Toyama, Japan; J.H. Walsh, CURE: Digestive Diseases Research Center, West Los Angeles VA Medical Center, Los Angeles, California, USA.

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Langtry, H.D., Markham, A. Rabeprazole. Drugs 58, 725–742 (1999). https://doi.org/10.2165/00003495-199958040-00014

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