Prevention of gastroduodenal injury induced by chronic nonsteroidal antiinflammatory drug therapy.
The fact that nonsteroidal antiinflammatory drugs (NSAIDs) damage the gastroduodenal mucosa is now accepted as NSAID use has been associated with a disproportionately high frequency of upper gastrointestinal bleeding and perforation of gastric and duodenal ulcers. More than 10% of patients receiving NSAIDs chronically will have a gastric ulcer on any given day, a point prevalence of ulcer disease 5-10 times higher than in patients who are not taking NSAIDs. Endoscopic studies comparing the effect of acute administration of NSAIDs on the gastroduodenal mucosa in normal volunteers have failed to predict which NSAIDs would be safest when administered chronically. All of the newer NSAIDs appear to be similar in their propensity to cause chronic mucosal damage, including peptic ulceration. Recent studies have suggested that in those starting NSAID therapy, prophylactic cotreatment with H2-receptor antagonists or sucralfate has minimal or no effect on preventing the development of NSAID-induced gastric ulcers, although duodenal ulcers may be reduced. Nonsteroidal antiinflammatory drug-induced gastric ulcers are also not prevented by drug formulations that prevent or markedly reduce the amount of active NSAID in the stomach. Cotreatment with the synthetic prostaglandin misoprostol was associated with a marked reduction in gastric ulcer development in patients with osteoarthritis receiving NSAIDs chronically, suggesting that prevention of prostaglandin generation in the gastric mucosa may play a pivotal role in NSAID-induced gastric ulcers.[1]References
- Prevention of gastroduodenal injury induced by chronic nonsteroidal antiinflammatory drug therapy. Graham, D.Y. Gastroenterology (1989) [Pubmed]
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