发生静脉血栓栓塞的创伤患者瓜氨酸组蛋白h3水平升高和凝血酶动力学加速。

IF 2.7 3区 医学 Q2 CRITICAL CARE MEDICINE SHOCK Pub Date : 2024-12-03 DOI:10.1097/SHK.0000000000002526
Sergio M Navarro, Riley J Thompson, Taleen A MacArthur, Grant M Spears, Kent R Bailey, Joe M Immermann, Nikoli Yudin, Jing-Fei Dong, Rosemary A Kozar, Myung S Park
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引用次数: 0

摘要

背景:中性粒细胞胞外陷阱(NETs)及其形成和释放,被称为NETosis,可能在创伤中凝血酶生成(TG)的启动中起作用。本研究的目的是评估发生症状性静脉血栓栓塞(VTE)的创伤患者是否有血浆瓜氨酸组蛋白H3 (CitH3)水平升高和TG动力学加速。方法:作为创伤激活到一级创伤中心就诊的患者与健康志愿者(HV)一起在受伤后12小时内采集样本。使用酶联免疫吸附法测定CitH3,使用凝血酶生成分析仪测定TG数据,比较损伤后90天内出现症状性静脉血栓栓塞的患者与未出现症状性静脉血栓栓塞的患者之间的结果。数据以中位数和四分位数表示[Q1, Q3],采用Wilcoxon秩和或Fisher精确检验,或单样本Spearman相关性检验,p < 0.05认为显著。结果:分析了39例创伤患者样本(10例有VTE, 29例无VTE),并与15例HV样本进行了比较。发生静脉血栓栓塞的患者的CitH3水平显著高于未发生静脉血栓栓塞的患者(12.8 ng/mL [7.1, 30.8];3.0 ng/mL [1.8,6.8], p = 0.024),两组的水平分别高于HV (1.2 [0.3, 4.1], p = 0.003, p = 0.012)。静脉血栓栓塞患者的TG谱加速,峰值高度差异(337.6 nM [304.4, 356.0];231.8 nM [180.2, 281.8], p = 0.008),内源性凝血酶电位(1718.5 nM*min [1500, 1794];1208.5 nM*min (1072, 1417), p = 0.003)和速度指数(213.2 nM/min [162.3, 260.5];124.3 nM/min [93.2, 223.1], p = 0.03)。结论:创伤患者发生静脉血栓栓塞表现出增加的NETosis,通过损伤后早期增加的CitH3水平和加速的TG来测量,概述了进一步了解创伤后静脉血栓栓塞的领域。
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INCREASED CITRULLINATED HISTONE H3 LEVELS AND ACCELERATED THROMBIN KINETICS IN TRAUMA PATIENTS WHO DEVELOP VENOUS THROMBOEMBOLISM.

Background: Neutrophil extracellular traps (NETs), and its formation and release, known as NETosis, may play a role in the initiation of thrombin generation (TG) in trauma. The objective of this study was to assess whether trauma patients, who develop symptomatic venous thromboembolism (VTE), have increased levels of plasma citrullinated histone H3 (CitH3) and accelerated TG kinetics.

Methods: Patients presenting to a Level I Trauma Center as trauma activations had samples collected within 12 hours of time of injury (TOI), alongside healthy volunteers (HV). CitH3 was measured by enzyme-linked immunosorbent assay, and TG data were measured using a thrombin generation analyzer, comparing results between patients developing symptomatic VTE vs those who did not, within 90 days of injury. Data were expressed as median and quartiles [Q1, Q3], and tested using Wilcoxon rank-sum or Fisher's exact test, or 1-sample test of Spearman's correlation, p < 0.05 considered significant.

Results: 39 trauma patient samples were analyzed (10 with and 29 without VTE), and compared to 15 HV samples. CitH3 levels in patients who developed VTE were significantly greater as compared to those who did not (12.8 ng/mL [7.1, 30.8]; 3.0 ng/mL [1.8,6.8], p = 0.024), with levels in both groups greater compared to HV (1.2 [0.3, 4.1], p = 0.003, p = 0.012), respectively. TG profiles were accelerated in patients developing VTE, with differences in peak height (337.6 nM [304.4, 356.0]; 231.8 nM [180.2, 281.8], p = 0.008), endogenous thrombin potential (1718.5 nM*min [1500, 1794]; 1208.5 nM*min (1072, 1417], p = 0.003) and velocity index (213.2 nM/min [162.3, 260.5]; 124.3 nM/min [93.2, 223.1], p = 0.03), respectively.

Conclusions: Trauma patients developing VTE exhibit increased NETosis, measured by increased CitH3 levels and accelerated TG early after injury, outlining an area for further understanding VTE after trauma.

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来源期刊
SHOCK
SHOCK 医学-外科
CiteScore
6.20
自引率
3.20%
发文量
199
审稿时长
1 months
期刊介绍: SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.
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