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Blood platelet inhibitors NSAIDs

Selectivity for COX-1 versus COX-2 is variable and incomplete for the older NSAIDs, but many selective COX-2 inhibitors have been synthesized. The selective COX-2 inhibitors do not affect platelet function at their usual doses. In testing using human whole blood, aspirin, ibuprofen, indomethacin, piroxicam, and sulindac are somewhat more effective in inhibiting COX-1. The efficacy of -2-selective drugs equals that of the older NSAIDs, while gastrointestinal safety may be improved. On the other hand, selective COX-2 inhibitors may increase the incidence of edema and hypertension. As of December 2008, celecoxib and the less selective meloxicam are the only COX-2 inhibitors marketed in the USA. Rofecoxib and valdecoxib, two previously marketed, selective COX-2 inhibitors, have been withdrawn from the market due to their association with increased cardiovascular thrombotic events. Celecoxib has an FDA-initiated "black box" warning concerning cardiovascular risks. It has been recommended that all NSAID product labels be revised to include cardiovascular risks. [Pg.800]

NSAIDs are associated with Gl, renal, liver, or central nervous system toxicity. Appropriate monitoring with complete blood count, serum creatinine, and hepatic transaminase levels is valuable in detecting potential toxicity. Cyclooxygenase-2 (COX-2)-specific inhibitors carry a lower risk of Gl bleeding or platelet inhibition, and may be appropriate in selected patients. [Pg.1685]


See other pages where Blood platelet inhibitors NSAIDs is mentioned: [Pg.12]    [Pg.31]    [Pg.401]    [Pg.1348]    [Pg.811]    [Pg.1526]    [Pg.68]    [Pg.71]    [Pg.9]    [Pg.294]    [Pg.1481]    [Pg.9]    [Pg.124]   
See also in sourсe #XX -- [ Pg.95 ]




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