塞来昔布
萘普生
环氧合酶
医学
血小板
血栓素B2
药理学
出血时间
止血
血栓素A2
安慰剂
血栓素
离体
阿司匹林
内科学
化学
血小板聚集
体外
酶
生物化学
病理
替代医学
作者
Philip T. Leese,Richard C. Hubbard,Aziz Karim,Peter C. Isakson,Shawn Yu,Gilbert Geis
标识
DOI:10.1177/00912700022008766
摘要
Conventional nonsteroidal anti‐inflammatory drugs (NSAIDs) nonspecifically inhibit cyclooxygenase‐1 (COX‐1), an enzyme critical to normal platelet function, and COX‐2, which mediates inflammatory response mechanisms. Celecoxib, an antiarthritic agent that inhibits COX‐2 but spares COX‐1 at therapeutic doses, is expected to have minimal effects on platelet function. A double‐blind, randomized, placebo‐controlled study of 10 days' duration was conducted in 24 healthy adults to compare the effects on platelet function of a supratherapeutic dose of celecoxib (600 mg bid) with a standard dose of naproxen (500 mg bid), a conventional NSAID. Ex vivo platelet aggregation in response to standard agonists (collagen, arachidonate, or U46619 [a thromboxane A 2 receptor agonist]), bleeding time, and serum thromboxane B 2 (TxB 2 level were measured. Unlike celecoxib or placebo, naproxen produced statistically significant reductions in platelet aggregation and serum TxB 2 levels and increased bleeding time. The results indicate that even at supratherapeutic doses, celecoxib will not interfere with normal mechanisms of platelet aggregation and hemostasis, supporting the premise that celecoxib is COX‐1 sparing relative to conventional NSAIDs.
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