The Pathogenesis of NSAID-induced Gastrointestinal Lesions Ichiro Hirata 1 1Department of Gastroenterology, Fujita Health University, Toyoake, Japan Keyword: NSAID , aspirin , 消化管病変 , H. pylori , PGE2 pp.1685-1689
Published Date 2007/11/25
DOI https://doi.org/10.11477/mf.1403101221
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 NSAID restrains the composition of prostaglandin and thromboxane by obstructing the action of cyclooxygenase in arachidonate cascade and shows anti-inflammatory activity, analgesia and antipyretic effect.

 Most side effects of NSAID are gastrointestinal mucosal damage. The first stages of gastrointestinal lesions brought on by NSAID are, (1) chemical damage to the epithelium, (2) mucosal defence factor degradation due to a prostaglandin composition obstruction in the gastrointestinal mucosa, (3) immunologic inhibition aberration of the gastrointestinal mucosa.

 Eradication of H. pylori infection in patients who have experienced long-term use of NSAID retards the ulcer healing. The antagonism for a NSAID ulcer of this H. pylori is due to upregulation of COX-2 expression by H. pylori infection resulting in promoting PGE2 production which enhances gastric mucosal defence factors. On the other hand, a H. pylori infection patient undergoing NSAID treatment for the first time can decrease the risk of ulcer outbreak if H. pylori is eradicate.

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