Bang N U, Dwyer A M, Marks C A, Mattler L E, Heidenreich R O, Campbell S S, Ridolfo A S
J Rheumatol Suppl. 1980;6:27-35.
Benoxaprofen did not impair platelet function or platelet prostaglandin synthesis in vivo or in vitro in contrast to indomethacin, a known prostaglandin synthesis inhibitor. Platelet cyclic AMP levels were not changed by either drug in vivo or in vitro. The results of routine tests for hemostatic function (template bleeding time and blood clotting assays) were not changed by either drug. A trend towards inhibition of cAMP-dependent protein kinase by benoxaprofen was observed. The significance of this observation, if valid, remains obscure. These studies suggest that benoxaprofen, which does not appreciably suppress hemostatic function, may be used safely in patients with acquired or congenital coagulation defects (e.g. patients receiving oral anticoagulant, hemophiliacs with arthropathy).
与已知的前列腺素合成抑制剂吲哚美辛不同,苯恶洛芬在体内或体外均未损害血小板功能或血小板前列腺素合成。体内或体外,两种药物均未改变血小板环磷酸腺苷(cAMP)水平。两种药物均未改变止血功能常规检测结果(模板出血时间和凝血检测)。观察到苯恶洛芬有抑制cAMP依赖性蛋白激酶的趋势。这一观察结果(如果成立)的意义仍不明确。这些研究表明,苯恶洛芬不会明显抑制止血功能,可安全用于获得性或先天性凝血缺陷患者(如接受口服抗凝剂治疗的患者、患有关节病的血友病患者)。