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首页> 外文期刊>Thrombosis Research: An International Journal on Vascular Obstruction, Hemorrhage and Hemostasis >ADP-induced platelet aggregation and thrombin generation are increased in Essential Thrombocythemia and Polycythemia Vera
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ADP-induced platelet aggregation and thrombin generation are increased in Essential Thrombocythemia and Polycythemia Vera

机译:在原发性血小板增多症和真性红细胞增多症中,ADP诱导的血小板聚集和凝血酶生成增加

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摘要

Introduction Essential Thrombocythemia (ET) and Polycythemia Vera (PV) patients are characterized by an increased rate of thrombotic complications and by several abnormalities of platelets, more pronounced in JAK2V617F positive patients. The aim of this study was to characterize the platelet aggregation as well as the platelet procoagulant potential induced by several different agonists in ET and PV patients. Materials and Methods Venous blood samples were obtained from 65 ET and 51 PV patients. Whole blood impedance aggregometry was utilized to characterize platelet aggregation induced by collagen, ADP, thrombin receptor activating peptide and arachidonic acid, while the Calibrated Automated Thrombogram (CAT) assay was used to determine the thrombin generation (TG) potential induced by ADP in platelet-rich plasma. CAT assay was also performed in the presence of annexin V to evaluate the contribution of platelet phospholipids to TG. Results and Conclusions ADP-induced platelet aggregation and TG were significantly increased in ET and PV patients compared to controls. The highest values were observed in JAK2V617F positive patients and in patients on aspirin. In these subjects, annexin V was less effective in inhibiting both basal and ADP-induced TG. This study demonstrates for first time that platelets from ET and PV patients are more responsive to the ADP stimulus, in terms of both increased platelet aggregation, and enhanced TG, particularly in the JAK2V617F positive patients. Our data support the hypothesis that the use of ADP receptor inhibitors, in addition to aspirin, might be considered in the prevention of thrombosis in these conditions, by allowing a more complete inhibition of platelet functions.
机译:简介原发性血小板增多症(ET)和真性红细胞增多症(PV)患者的特征在于血栓形成并发症的发生率增加以及血小板的几种异常,在JAK2V617F阳性患者中更为明显。这项研究的目的是表征ET和PV患者中几种不同的激动剂诱导的血小板聚集以及血小板促凝潜能。材料和方法从65名ET和51名PV患者中获得静脉血样本。全血阻抗凝集法用于表征胶原蛋白,ADP,凝血酶受体激活肽和花生四烯酸诱导的血小板凝集,而校准自动血栓图(CAT)测定法用于确定ADP诱导的血小板-血小板凝集(TG)潜力。血浆丰富。在膜联蛋白V存在下也进行CAT测定,以评估血小板磷脂对TG的贡献。结果与结论与对照组相比,ET和PV患者的ADP诱导的血小板聚集和TG显着增加。在JAK2V617F阳性患者和接受阿司匹林的患者中观察到最高值。在这些受试者中,膜联蛋白V在抑制基础和ADP诱导的TG方面效果较差。这项研究首次证明,ET和PV患者的血小板在血小板聚集增加和TG升高方面对ADP刺激反应更强,尤其是在JAK2V617F阳性患者中。我们的数据支持以下假设:通过允许更全面地抑制血小板功能,除阿司匹林外,还可考虑使用ADP受体抑制剂来预防血栓形成。

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