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血小板磷脂酶A2多态性与肝素诱导的血小板减少症中血栓形成的风险

Platelet PlA2 Polymorphism and the risk for thrombosis in heparin-induced thrombocytopenia.

作者信息

Harris Kenneth, Nguyen Phan, Van Cott Elizabeth M

机构信息

Coagulation Laboratory, Department of Pathology, Massachusetts General Hospital, Boston 02114, USA.

出版信息

Am J Clin Pathol. 2008 Feb;129(2):282-6. doi: 10.1309/BMW4M8NQBV0TKFRX.

Abstract

Platelet glycoprotein (GP) IIb/IIIa has an important role in platelet aggregation. A polymorphism of platelet GPIIIa (PlA2, also called HPA1b) has been associated with a higher risk of thrombosis, but its implication in heparin-induced thrombocytopenia (HIT) is unclear. To investigate the hypothesis that the PlA2 polymorphism influences the prothrombotic effects of HIT, we conducted a prospective study of 66 consecutive patients with a laboratory diagnosis of HIT. The end point of the study was the diagnosis of a thrombus within 30 days of the positive HIT test result. The Diagnostica Stago (Asnières, France) enzyme-linked immunosorbent assay was used to detect HIT antibodies, and a polymerase chain reaction assay was used to detect the PlA2 polymorphism. Of the 66 patients, thrombotic complications developed in 27 (41%). Patients with the PlA2 allele demonstrated a significantly higher thrombosis risk than did patients without (69% vs 32%; P = .0088; odds ratio, 4.68; 95% confidence interval, 1.39-15.72). The risk was stronger for arterial thrombosis and for patients 60 years or older. There was a significant association between the PlA2 polymorphism of GPIIIa and the risk of thrombosis in patients with HIT antibodies.

摘要

血小板糖蛋白(GP)IIb/IIIa在血小板聚集过程中起重要作用。血小板GPIIIa的一种多态性(PlA2,也称为HPA1b)与血栓形成风险较高有关,但其在肝素诱导的血小板减少症(HIT)中的意义尚不清楚。为了研究PlA2多态性影响HIT促血栓形成作用的假说,我们对66例经实验室诊断为HIT的连续患者进行了一项前瞻性研究。研究的终点是在HIT检测结果呈阳性后的30天内诊断出血栓。采用Diagnostica Stago(法国阿斯尼埃)酶联免疫吸附测定法检测HIT抗体,采用聚合酶链反应测定法检测PlA2多态性。66例患者中,27例(41%)发生了血栓并发症。携带PlA2等位基因的患者血栓形成风险显著高于未携带该等位基因的患者(69%对32%;P = 0.0088;比值比,4.68;95%置信区间,1.39 - 15.72)。动脉血栓形成以及60岁及以上患者的风险更高。GPIIIa的PlA2多态性与HIT抗体阳性患者的血栓形成风险之间存在显著关联。

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