Abstract
Gastric ulceration associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) affects approximately 15-20% of patients using these agents on a chronic basis and has a significant financial impact on health care systems. The pathogenesis of NSAID gastropathy is not fully understood, although it is generally believed that these agents produce ulcers through a combination of direct topical irritant actions and systemic inhibition of prostaglandin synthesis. A number of recent studies have focused on the early events in the pathogenesis of NSAID gastropathy, and suggest that a principal site of action of these agents is the mucosal vasculature. In this review, some of these recent advances are outlined
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More From: European Journal of Gastroenterology & Hepatology
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