Peptic ulcer disease, cytoprotection, and prostaglandins

Abstract

To the Editor .—The editorial in the October 1988 issue of theArchives 1 outlines the prospects of oral prostaglandin E therapy for peptic ulcer disease. In theory, the bimodal fashion of action, suppressing gastric acid secretion in addition to enhancing defensive factors (cytoprotection), makes prostaglandin E analogues ideal antiulcer drugs. In practice, however, the promise remains unfulfilled, and in light of recent controlled trials on arbaprostil, enprostil, misoprostol, rioprostil, and trimoprostil in peptic ulcer disease (reviewed elsewhere 2-4 ) the viewpoints1 appear overoptimistic. First, in doses lower than those required to decrease acid secretion, prostaglandin E analogues retain cytoprotective properties, but are no better than placebo in healing duodenal (arbaprostil and misoprostol) and gastric ulcers (misoprostol). Second, in fully antisecretory doses some prostaglandin E analogues (arbaprostil, enprostil, and misoprostol) accelerate ulcer healing compared with placebo, and some analogues (enprostil and misoprostol, but not trimoprostil) provide healing rates about as high