Sloos Pieter H, Dujardin Romein W G, Meijers Joost C M, Gaarder Christine, Davenport Ross, Stanworth Simon, Johansson Pär I, Stensballe Jakob, Maegele Marc, Juffermans Nicole P, Kleinveld Derek J B
Department of Intensive Care Medicine, Amsterdam University Medical Center location University of Amsterdam, Amsterdam, the Netherlands.
Amsterdam Institute for Infection and Immunity, Laboratory of Experimental Intensive Care and Anesthesiology, Amsterdam University Medical Center location University of Amsterdam, Amsterdam, the Netherlands.
Res Pract Thromb Haemost. 2025 Apr 17;9(4):102857. doi: 10.1016/j.rpth.2025.102857. eCollection 2025 May.
In bleeding patients with trauma-induced coagulopathy (TIC), factor (F)V becomes depleted, which may not be corrected with existing treatment strategies. It is currently unknown whether supplementing FV or FVa improves TIC.
To explore the relationship between FV activity and mortality in trauma patients, and to investigate the effect of FV(a) supplementation in addition to other treatment strategies in an model of TIC.
The association between FV activity and mortality was studied using an international prospective cohort study of trauma patients. In an whole blood and plasma model of TIC, the effect of FV(a) on rotational thromboelastometry and fibrin formation was studied. Effects of FV(a) were evaluated either as a standalone therapy or as adjunctive therapy in combination with tranexamic acid, fibrinogen concentrate, and/or prothrombin complex concentrate.
A total of 1285 patients were included, with a median injury severity score of 16 (interquartile range: 8-26). Decreased FV activity was associated with increased mortality. In the whole blood TIC model, FVa increased maximum clot firmness and reduced fibrinolysis, both as a single and combination therapy. In the plasma TIC model, with lower tissue factor concentrations than in the whole blood model, FV(a) prolonged clotting times, both as a single treatment and in combination with other treatments.
FV depletion after trauma is associated with increased mortality. In an model of TIC, FV(a) results in procoagulant, antifibrinolytic, and anticoagulant effects. Further research is highly warranted.
在创伤性凝血病（TIC）出血患者中，因子（F）V会耗竭，现有治疗策略可能无法纠正这一情况。目前尚不清楚补充FV或FVa是否能改善TIC。
探讨创伤患者FV活性与死亡率之间的关系，并研究在TIC模型中除其他治疗策略外补充FV（a）的效果。
通过一项针对创伤患者的国际前瞻性队列研究，研究FV活性与死亡率之间的关联。在TIC的全血和血浆模型中，研究FV（a）对旋转血栓弹力图和纤维蛋白形成的影响。评估FV（a）作为单一疗法或与氨甲环酸、纤维蛋白原浓缩物和/或凝血酶原复合物浓缩物联合作为辅助疗法的效果。
共纳入1285例患者，中位损伤严重程度评分为16（四分位间距：8 - 26）。FV活性降低与死亡率增加相关。在全血TIC模型中，FV（a）作为单一疗法和联合疗法均能增加最大血凝块硬度并减少纤维蛋白溶解。在血浆TIC模型中，由于组织因子浓度低于全血模型，FV（a）作为单一治疗和与其他治疗联合使用时均延长凝血时间。
创伤后FV耗竭与死亡率增加相关。在TIC模型中，FV（a）具有促凝、抗纤溶和抗凝作用。非常有必要进行进一步研究。
