Department of Surgery, Division of Acute Care Surgery, The University of Texas Health Science Center and the McGovern School of Medicine, and the Center for Translational Injury Research, Houston, TX.
Department of Surgery, Division of Acute Care Surgery, The University of Texas Health Science Center and the McGovern School of Medicine, and the Center for Translational Injury Research, Houston, TX.
Surgery. 2023 Aug;174(2):376-381. doi: 10.1016/j.surg.2023.04.049. Epub 2023 Jun 2.
Venous thromboembolism is a leading cause of morbidity after trauma. Endothelial cells are essential regulators of coagulation. Although endothelial cell dysregulation is widely reported after trauma, the link between endothelial injury and venous thromboembolism has not been reported.
We conducted a secondary analysis of the Pragmatic Randomized Optimal Platelets and Plasma Ratios study. Deaths from hemorrhage or within 24 hours were excluded. Venous thromboembolism was diagnosed by duplex ultrasound or chest computed tomography. Endothelial markers soluble endothelial protein c receptor, thrombomodulin, and syndecan-1 were measured in plasma by enzyme-linked immunosorbent assay and compared over the first 72 hours from admission using the Mann-Whitney test. Multivariable logistic regression assessed the adjusted effects of endothelial markers on venous thromboembolism risk.
Of 575 patients enrolled, 86 developed venous thromboembolism (15%). The median time to venous thromboembolism was 6 days ([Q1, Q3], [4, 13]). No differences were identified in demographics or injury severity. Soluble endothelial protein c receptor, thrombomodulin, and syndecan-1 showed significant increases over time among patients who developed venous thromboembolism compared to those who did not. Using the last available values, patients were stratified into high and low-soluble endothelial protein c receptor, thrombomodulin, and syndecan-1 groups. Multivariable analyses revealed an independent association between elevated soluble endothelial protein c receptor and venous thromboembolism risk (odds ratio 1.63; 95% confidence interval 1.01, 2.63; P = .04). Cox proportional hazards modeling demonstrated a strong yet nonsignificant trend between elevated soluble endothelial protein c receptor and time to venous thromboembolism.
Plasma markers of endothelial injury, particularly soluble endothelial protein c receptor, are strongly associated with trauma-related venous thromboembolism. Therapeutics targeting endothelial function could mitigate the incidence of venous thromboembolism after trauma.
静脉血栓栓塞症是创伤后发病率较高的主要原因。内皮细胞是凝血的重要调节剂。尽管创伤后内皮细胞失调广泛报道，但内皮损伤与静脉血栓栓塞症之间的联系尚未报道。
我们对 Pragmatic Randomized Optimal Platelets and Plasma Ratios 研究进行了二次分析。排除因出血或 24 小时内死亡的患者。通过双功能超声或胸部计算机断层扫描诊断静脉血栓栓塞症。通过酶联免疫吸附试验测量血浆中可溶性内皮蛋白 C 受体、血栓调节蛋白和 syndecan-1 等内皮标志物，并使用 Mann-Whitney 检验比较入院后 72 小时内的变化。多变量逻辑回归评估内皮标志物对静脉血栓栓塞症风险的调整影响。
在纳入的 575 名患者中，86 名发生静脉血栓栓塞症（15%）。静脉血栓栓塞症的中位时间为 6 天（[Q1，Q3]，[4，13]）。两组患者在人口统计学和损伤严重程度方面无差异。与未发生静脉血栓栓塞症的患者相比，发生静脉血栓栓塞症的患者可溶性内皮蛋白 C 受体、血栓调节蛋白和 syndecan-1 的水平随时间显著升高。使用最后一次可用值，将患者分为高和低可溶性内皮蛋白 C 受体、血栓调节蛋白和 syndecan-1 组。多变量分析显示，高可溶性内皮蛋白 C 受体与静脉血栓栓塞症风险独立相关（比值比 1.63；95%置信区间 1.01，2.63；P=0.04）。Cox 比例风险模型显示，高可溶性内皮蛋白 C 受体与静脉血栓栓塞症时间之间存在强烈但无统计学意义的趋势。
内皮损伤的血浆标志物，特别是可溶性内皮蛋白 C 受体，与创伤相关的静脉血栓栓塞症密切相关。针对内皮功能的治疗方法可能会降低创伤后静脉血栓栓塞症的发生率。
