R La Corte, M Caselli, M Ruina, G Bajocchi, V Alvisi, F Trotta
{"title":"Therapy of NSAIDs-induced gastropathy.","authors":"R La Corte, M Caselli, M Ruina, G Bajocchi, V Alvisi, F Trotta","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>NSAID-induced gastropathy is the most frequent side effect due to NSAID use. The resulting clinical event is usually of little significance and only in a small percentage of cases results in serious side effects. Nevertheless, the large worldwide use of NSAIDs makes, even a rare side effect, numerically consistent. The pathogenesis of NSAID-induced gastropathy is related to two main mechanisms: an initial topical effect which is pH dependent and a systemic effect which is, more slowly developing, and mainly correlated to the inhibition of prostaglandin synthesis. The therapy of NSAID-gastropathy is almost completely identified with the therapy of NSAID ulceration because of its frequent relation to the development of potentially serious complications. In the case of symptomatic ulcer development the first therapeutic step is NSAID suspension and, in such a case all \"antiulcer\" drugs are efficient. When the NSAID can not be discontinued, omeprazole seems to be the most efficient drug; H2 blockers can promote ulcer healing but at a slower rate; sucralfate shows an efficacy similar to H2 blockers; misoprostol is useful in the prevention of NSAID-gastropathy. However, it is not so efficient in the treatment of established lesions and shows poor efficacy in the reduction of dyspeptic symptoms. For each one of these drugs it is necessary to obtain further data.</p>","PeriodicalId":22546,"journal":{"name":"The Italian journal of gastroenterology","volume":"28 Suppl 4 ","pages":"37-41"},"PeriodicalIF":0.0000,"publicationDate":"1996-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Italian journal of gastroenterology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
NSAID-induced gastropathy is the most frequent side effect due to NSAID use. The resulting clinical event is usually of little significance and only in a small percentage of cases results in serious side effects. Nevertheless, the large worldwide use of NSAIDs makes, even a rare side effect, numerically consistent. The pathogenesis of NSAID-induced gastropathy is related to two main mechanisms: an initial topical effect which is pH dependent and a systemic effect which is, more slowly developing, and mainly correlated to the inhibition of prostaglandin synthesis. The therapy of NSAID-gastropathy is almost completely identified with the therapy of NSAID ulceration because of its frequent relation to the development of potentially serious complications. In the case of symptomatic ulcer development the first therapeutic step is NSAID suspension and, in such a case all "antiulcer" drugs are efficient. When the NSAID can not be discontinued, omeprazole seems to be the most efficient drug; H2 blockers can promote ulcer healing but at a slower rate; sucralfate shows an efficacy similar to H2 blockers; misoprostol is useful in the prevention of NSAID-gastropathy. However, it is not so efficient in the treatment of established lesions and shows poor efficacy in the reduction of dyspeptic symptoms. For each one of these drugs it is necessary to obtain further data.