Quantification of von Willebrand factor and ADAMTS-13 after traumatic injury: a pilot study.
Quantification of von Willebrand factor and ADAMTS-13 after traumatic injury: a pilot study.
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创伤后血管性血友病因子和ADAMTS-13的定量：一项初步研究。
DOI：
10.1136/tsaco-2021-000703
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发表时间：
2021
影响因子：
2
通讯作者：
Park MS
中科院分区：
文献类型：
--
作者：
MacArthur TA;Goswami J;Moon Tasson L;Tischer A;Bailey KR;Spears GM;Dong JF;Auton M;Kozar R;Park MS
血管性血变因子（VWF）是巨核细胞和内皮细胞合成的急性期反应物。VWF形成被金属蛋白酶ADAMTS-13切割的超大型多聚体（ULVWF），阻止了VWF与血小板的自发相互作用。创伤后，ULVWF作为急性期反应的一部分被释放到循环中。我们假设创伤患者会有VWF水平升高和ADAMTS-13水平降低，这些患者会加速凝血酶的产生。我们评估了来自30名创伤患者的50个样本和来自志愿者的另外21个样本的VWF抗原和ADAMTS-13抗原的血浆浓度、VWF的自身免疫性疾病快速酶测定（REAADS）活性（测量血小板结合A1结构域的暴露）和凝血酶生成动力学。分别在损伤后0 ~ 2小时和6小时对样品进行分析。数据以中位数（IQR）表示，并在两个时间点对创伤患者和志愿者进行Kruskal-Wallis检验。创伤患者在0 - 2小时(190.0 （132.0-264.0)vs. 92.0 (71.0-114.0), p<0.002）和6小时(167.5 （108.0-312.5.0)vs. 92.0 (71.0-114.0), p<0.001）时的readads活性均高于志愿者。创伤患者的ADAMTS-13抗原水平在0 ~ 2小时（0.84（0.51-0.94）比1.00 (0.89-1.09),p=0.010）和6小时（0.653（0.531-0.821）比1.00 (0.89-1.09),p<0.001）均有所下降。创伤患者凝血酶生成动力学加速，在两个时间点均比健康志愿者具有更高的峰值高度和更短的峰值时间。与健康志愿者相比，创伤患者VWF A1结构域暴露增加，ADAMTS-13水平降低。这表明创伤后的VWF破裂可能超过ADAMTS-13的蛋白水解能力，允许循环的ULVWF多聚体结合血小板，可能导致创伤诱导的凝血病。前瞻性病例队列研究。
Von Willebrand factor (VWF) is an acute phase reactant synthesized in the megakaryocytes and endothelial cells. VWF forms ultra-large multimers (ULVWF) which are cleaved by the metalloprotease ADAMTS-13, preventing spontaneous VWF–platelet interaction. After trauma, ULVWF is released into circulation as part of the acute phase reaction. We hypothesized that trauma patients would have increased levels of VWF and decreased levels of ADAMTS-13 and that these patients would have accelerated thrombin generation. We assessed plasma concentrations of VWF antigen and ADAMTS-13 antigen, the Rapid Enzyme Assays for Autoimmune Diseases (REAADS) activity of VWF, which measure exposure of the platelet-binding A1 domain, and thrombin generation kinetics in 50 samples from 30 trauma patients and an additional 21 samples from volunteers. Samples were analyzed at 0 to 2 hours and at 6 hours from the time of injury. Data are presented as median (IQR) and Kruskal-Wallis test was performed between trauma patients and volunteers at both time points. REAADS activity was greater in trauma patients than volunteers both at 0 to 2 hours (190.0 (132.0–264.0) vs. 92.0 (71.0–114.0), p<0.002) and at 6 hours (167.5 (108.0–312.5.0) vs. 92.0 (71.0–114.0), p<0.001). ADAMTS-13 antigen levels were also decreased in trauma patients both at 0 to 2 hours (0.84 (0.51–0.94) vs. 1.00 (0.89–1.09), p=0.010) and at 6 hours (0.653 (0.531–0.821) vs. 1.00 (0.89–1.09), p<0.001). Trauma patients had accelerated thrombin generation kinetics, with greater peak height and shorter time to peak than healthy volunteers at both time points. Trauma patients have increased exposure of the VWF A1 domain and decreased levels of ADAMTS-13 compared with healthy volunteers. This suggests that the VWF burst after trauma may exceed the proteolytic capacity of ADAMTS-13, allowing circulating ULVWF multimers to bind platelets, potentially contributing to trauma-induced coagulopathy. Prospective case cohort study.
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影响因子：
2.9
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