Abstract

Nimesulide is a selective cyclooxygenase type 2 (COX2) inhibitor that, although having the characteristic antiinflammatory effects of nonsteroidal anti-inflammatory drugs (NSAIDs), has better gastrointestinal tolerability (with less gastric and duodenal injury) than conventional nonselective cyclooxygenase inhibitors) (1). It is well known that toxicity in chronic NSAIDs users is not specific to the gastroduodenal tract. Over the past few years several reports have focused on the prevalence, clinical aspects, and pathogenesis of NSAIDs-induced adverse side effects (ASEs) on the small and large intestine, including diaphragm-like strictures, ulcerations, and perforations, associated with blood and protein loss (2‐5). The prevalence of NSAID-associated enteropathy in the upper gastroenteric tract (UGT) is approximately 20%, and among patients chronically taking NSAIDs the incidence of severe bleeding or perforation complications is 1t o2 %per year of use (6). Nevertheless, the assumption that enteropathy is mainly located in the UGT may be considered a bias, as demonstrated by retrospective, hospital-based, systemic studies showing that ASEs may sometimes have a higher prevalence in the lower gastroenteric tract (LGT) than in the UGT (7). Furthermore, a threeto-one ratio of large-versus-small bowel injuries (ulcers or perforations) was found (8). However, these intestinal complications were not reported in patients on nimesulide. A clinical survey carried out on a large population taking nimesulide gave no ev

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