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

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.