Hematology-Hemotherapy Center, State University of Campinas, Campinas, SP, Brazil.
Platelets. 2009 Sep;20(6):367-75. doi: 10.1080/09537100903096676.
Microparticles (MPs) are blebs released from cellular surfaces during activation/apoptosis. They are procoagulant, pro-inflammatory and could contribute to pathogenesis of deep venous thrombosis (DVT). This study compared the number, cellular origin and procoagulant activity of MPs on DVT patients in different clinical situations: at diagnosis (n = 9, 5F/4M; mean age = 41.11), 1-3 years after warfarin withdrawal (n = 10, 7F/3M; mean age = 32.90), associated to antiphospholipid syndrome (APS; n = 11, 9F/2M; mean age = 33.82), or asymptomatic carriers of Factor V Leiden (FVL; n = 7, 7F/0M; mean age = 34.00) vs healthy controls (CTR). The quantification and characterization were performed by flow cytometry using CD235, CD61, CD45, CD31, CD14, CD45, anti-TF and Annexin V. The plasmatic procoagulant activity was investigated by prothrombin fragment 1 + 2 (F1 + 2) determination. The MPs procoagulant activity was analyzed by D-dimer (DD2) and Thrombin Generation Test (TGT) on a healthy pool of plasmas adjusted or not by their number (10,000 MPs). The MPs percentages were not different between the groups, but absolute number was increased in patients 1-3 years after warfarin withdrawal vs CTR (P = 0.02). There was no difference of the MPs cellular origin comparing patients to controls. TGT using 10,000 MPs was lower on these patients (P = 0.01). APS patients showed a reduction of plasmatic procoagulant activity (P = 0.004), but they were under warfarin therapy. DD2 in the presence of MPs, independently of its number, was higher in patients with DVT at diagnosis (P < 0.0001). MPs of patients with spontaneous DVT at diagnosis can promote coagulation activation demonstrated by increased DD2. Even the increased MPs from patients 1-3 years after thrombotic episode generated lower amount of thrombin, they can have a protective effect by activation of Protein C anticoagulant pathway.
微粒（MPs）是细胞表面在激活/凋亡过程中释放的泡状结构。它们具有促凝、促炎作用，可能导致深静脉血栓形成（DVT）的发病机制。本研究比较了不同临床情况下 DVT 患者 MPs 的数量、细胞来源和促凝活性：诊断时（n=9，5 女/4 男；平均年龄=41.11）、华法林停药 1-3 年后（n=10，7 女/3 男；平均年龄=32.90）、合并抗磷脂综合征（APS；n=11，9 女/2 男；平均年龄=33.82）或无症状因子 V Leiden 携带者（FVL；n=7，7 女/0 男；平均年龄=34.00）与健康对照组（CTR）。通过流式细胞术使用 CD235、CD61、CD45、CD31、CD14、CD45、抗 TF 和 Annexin V 进行定量和特征分析。通过测定凝血酶原片段 1+2（F1+2）来研究血浆的促凝活性。通过 D-二聚体（DD2）和血栓生成试验（TGT）分析 MPs 的促凝活性，方法是调整或不调整健康血浆的数量（10,000 MPs）。各组 MPs 百分比无差异，但与对照组相比，华法林停药 1-3 年后的患者 MPs 绝对数增加（P=0.02）。与对照组相比，患者 MPs 的细胞来源无差异。使用 10,000 MPs 的 TGT 在这些患者中较低（P=0.01）。APS 患者表现出血浆促凝活性降低（P=0.004），但他们正在接受华法林治疗。存在 MPs 时的 DD2，与其数量无关，在诊断时患有 DVT 的患者中更高（P<0.0001）。诊断时自发性 DVT 患者的 MPs 可通过增加 DD2 促进凝血激活。即使来自血栓形成事件后 1-3 年的患者的 MPs 产生的凝血酶量较少，它们也可以通过激活蛋白 C 抗凝途径产生保护作用。
