Misoprostol and gastroduodenal mucosal protection (cytoprotection)

Misoprostol, a synthetic methyl analogue of prostaglandin E1 (PGE1), accelerates significantly the healing of duodenal and gastric ulcers in man. In addition to its acid antisecretory actions, misoprostol exhibits gastroduodenal mucosal protective (cytoprotective) effects in animals and in man against diverse damaging agents such as ethanol and non-steroidal anti-inflammatory drugs (NSAIDs). There are preliminary data indicating that misoprostol is superior to placebo and cimetidine in reducing mucosal damage secondary to the chronic administration of NSAIDs in man. Several studies indicate that patients with peptic ulcer disease secrete and/or produce less gastroduodenal prostaglandins that non-ulcer patients and thus may have a relative deficiency of mucosal prostaglandin synthesis. Ulcers are known to heal more slowly in cigarette smokers than non-smokers and have a higher rate of recurrence. There is also evidence that cigarette smoking inhibits gastric mucosal prostaglandin synthesis. Therefore smokers may also represent a group of individuals with depressed gastric mucosal prostaglandin synthesis, in addition to patients who consume NSAIDs. A preliminary study indicates that misoprostol may reverse the deleterious effect of smoking on duodenal ulcer healing.