No evidence for increased platelet activation in patients with hepatitis B- or C-related cirrhosis and hepatocellular carcinoma
No evidence for increased platelet activation in patients with hepatitis B- or C-related cirrhosis and hepatocellular carcinoma
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DOI：
10.1016/j.thromres.2014.11.016
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发表时间：
2015-02-01
影响因子：
7.5
通讯作者：
Lisman, Ton
中科院分区：
文献类型：
--
作者：
Alkozai, Edris M.;Porte, Robert J.;Lisman, Ton
简介：癌症是发生静脉血栓栓塞（VTE）的主要风险因素。血浆高凝状态是癌症相关性VTE的既定危险因素。此外，血小板增多症和血小板反应过度与VTE和癌症进展有关。肝硬化与血小板数量和功能的变化有关。肝硬化和肝细胞癌患者的血小板活化状态尚未确定。在这里，我们评估了血小板活化状态与肝炎相关的肝硬化患者在存在或不存在HCC.Materials和Methods：我们进行了一项横断面研究，包括38例连续与B肝炎或丙型肝炎相关的肝硬化患者在存在或不存在HCC。我们使用流式细胞术研究了基础和激动剂诱导的血小板活化。此外，我们研究了血浆中血管性血友病因子（VWF）和VWF裂解蛋白酶ADAMTS 13的水平。20名健康志愿者作为controls.Results：我们没有发现肝硬化患者的基础血小板活化的证据相比，对照组。然而，我们发现患者中激动剂诱导的血小板活化减少。在基础和激动剂诱导的血小板活化状态与HCC患者或非HCC患者之间没有差异。与对照组相比，患者血浆VWF水平升高，ADAMTS 13活性水平降低。VWF和ADAMTS 13的水平之间没有差异，患者有或没有hcch.Conclusions：HCC的发展或复发的患者与肝炎B-C相关的肝硬化似乎并不与血小板活化和关键蛋白在主要止血的变化。(C)2014爱思唯尔有限公司版权所有。
Introduction: Cancer is a major risk factor for developing venous thromboembolism (VTE). Plasma hypercoagulability is an established risk factor for cancer-related VTE. In addition, thrombocytosis and hyperreactive platelets have been implicated in VTE and cancer progression. Cirrhosis is associated with changes in platelet number and function. The platelet activation status of patients with cirrhosis and hepatocellular carcinoma has not yet been established. Here we assessed the platelet activation status in patients with hepatitis-related cirrhosis in presence or absence of HCC.Materials and methods: We performed a cross-sectional study including thirty-eight consecutive patients with hepatitis B- or C-related liver cirrhosis in presence or absence of HCC. We studied basal and agonist-induced platelet activation using flow cytometry. In addition, we studied the plasma levels of von Willebrand factor (VWF) and the VWF-cleaving protease ADAMTS13. Twenty healthy volunteers served as controls.Results: We found no evidence of basal platelet activation in patients with cirrhosis compared to controls. However, we found reduced agonist-induced platelet activation in patients. No differences in the basal and agonist-induced platelets activation status between patients with or without HCC were detected. Plasma levels of VWF were increased and the levels of ADAMTS13 activity were decreased in patients compared to controls. No differences between the levels of VWF and ADAMTS13 in patients with or without HCC were detected.Conclusions: HCC development or recurrence in patients with hepatitis B- C-related cirrhosis does not appear to be associated with platelet activation and changes in pivotal proteins in primary hemostasis. (C) 2014 Elsevier Ltd. All rights reserved.