The pharmacology, pharmacokinetics, clinical efficacy,
contraindications and precautions, adverse effects, dosage, and cost of
misoprostol are reviewed.
Misoprostol is a synthetic analogue of natural
prostaglandin E1. It produces a dose-related inhibition of gastric acid and
pepsin secretion and enhances mucosal resistance to injury.
Misoprostol is extensively absorbed from the stomach and undergoes rapid de-esterification to its biologically active metabolite,
misoprostol acid. The average absorption after an oral dose is 88%; peak plasma concentrations of
misoprostol acid are achieved in less than 30 minutes. Clinical trials have demonstrated
ulcer healing rates of approximately 60-80% in patients with
duodenal ulcers who received
misoprostol 800 micrograms daily for four weeks.
Misoprostol was generally no more efficacious than conventional
therapy with the H2-receptor antagonists
cimetidine and
ranitidine. The healing rate observed for
gastric ulcers was less than that observed for
duodenal ulcers. In trials involving healthy volunteers and patients with
arthritis receiving
aspirin,
naproxen,
tolmetin,
ibuprofen, or
piroxicam,
misoprostol was consistently superior to placebo,
cimetidine, and
sucralfate in the prevention of nonsteroidal anti-inflammatory
drug (
NSAID)-induced gastropathy. The majority of these studies have been of short duration; however, long-term studies (up to three months) have corroborated superiority over placebo.
Misoprostol is an abortifacient and is contraindicated in pregnant women and women of childbearing potential not using effective
contraception. The most common adverse effect of
misoprostol therapy is
diarrhea, which is often mild and self-limiting and can be minimized by administration of
misoprostol after meals and at bedtime. The cost (based on retail price) of four weeks of
therapy with
misoprostol is comparable to that of other antiulcer agents.
Misoprostol has been shown to be an effective agent for the prevention of
NSAID-induced
gastric ulcers. However, there is no evidence that it offers any clinical advantage over H2-receptor antagonists for the treatment of gastric or
duodenal ulcer disease.