Noroian Gary, Clive David
Department of Medicine, Division of Renal Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Drug Saf. 2002;25(3):165-72. doi: 10.2165/00002018-200225030-00003.
Cyclo-oxygenase (COX) is one of the key enzymes in the biosynthesis of prostaglandins. Two isoforms of this enzyme COX-1 and COX-2 are known to exist. Among other functions, prostaglandins play an important role in the protection of the gastric mucosa and maintenance of renal function in pathophysiological conditions which would otherwise threaten it. Conventional nonsteroidal anti-inflammatory drugs (NSAIDs) block prostaglandin synthesis, resulting in gastric mucosal injury and renal dysfunction in susceptible individuals. The recent introduction of selective COX-2 inhibitors, celecoxib and rofecoxib, appear to induce less gastrointestinal morbidity. Although conclusive data are still lacking, there is evidence to suggest that COX-2 antagonists may be capable of causing some of the same renal syndromes seen in association with the older, less selective NSAIDs.
环氧化酶(COX)是前列腺素生物合成中的关键酶之一。已知该酶存在两种同工型,即COX-1和COX-2。在其他功能中,前列腺素在保护胃黏膜以及在病理生理状况下维持肾功能方面发挥着重要作用,否则这些状况会对肾功能构成威胁。传统的非甾体抗炎药(NSAIDs)会阻断前列腺素的合成,从而在易感个体中导致胃黏膜损伤和肾功能障碍。最近引入的选择性COX-2抑制剂塞来昔布和罗非昔布,似乎引起的胃肠道发病率较低。尽管仍缺乏确凿数据,但有证据表明,COX-2拮抗剂可能会引发一些与较老的、选择性较低的NSAIDs相关的相同肾脏综合征。