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Involvement of Inflammation in Venous Thromboembolic Disease: An Update in the Age of COVID-19
Seminars in Thrombosis and Hemostasis ( IF 5.7 ) Pub Date : 2021-08-13 , DOI: 10.1055/s-0041-1732372
Peter Poredos 1 , Pavel Poredos 2
Affiliation  

The inflammatory process is strongly involved in the pathophysiology of venous thromboembolism (VTE) and has a significant role in disease prediction. Inflammation most probably represents a common denominator through which classical and nonclassical risk factors stimulate thrombotic process. Inflammation of the venous wall promotes the release of tissue factor, inhibits the release of anticoagulant factors, and hampers endogenous fibrinolysis. Systemic inflammatory response also inhibits restoration of blood flow in the occluded vessel. Recent studies indicate that increased inflammatory response (“cytokine storm”) is related to prothrombotic state and thromboembolic events in patients with coronavirus disease 2019 (COVID-19). The growing evidence of involvement of inflammation in the pathogenesis of VTE indicates the importance of anti-inflammatory treatment and prevention of VTE. While aspirin was shown to be effective in prevention of recurrent venous thrombosis after treatment with anticoagulant drugs, some other anti-inflammatory drugs like nonsteroidal anti-inflammatory agents may have prothrombotic effect, thus potentially increasing the risk of VTE. Recently, new specific anti-inflammatory drug inhibitors of inflammatory markers that have been shown to be involved in the pathogenesis of VTE are being searched. As thrombogenesis is based on activation of coagulation provoked by inflammation, then prevention and treatment of VTE should include both anticoagulant and anti-inflammatory agents. Combined treatment is related to increased risk of bleeding complications, therefore subtherapeutic doses of both drugs should be used to improve the efficacy of management of VTE without increasing the risk of bleeding.



中文翻译:

炎症参与静脉血栓栓塞性疾病:COVID-19 时代的最新进展

炎症过程与静脉血栓栓塞 (VTE) 的病理生理学密切相关,并且在疾病预测中具有重要作用。炎症很可能代表了经典和非经典危险因素刺激血栓形成过程的共同特征。静脉壁炎症促进组织因子释放,抑制抗凝因子释放,阻碍内源性纤溶。全身炎症反应也抑制闭塞血管中血流的恢复。最近的研究表明,炎症反应增加(“细胞因子风暴”)与 2019 年冠状病毒病 (COVID-19) 患者的血栓前状态和血栓栓塞事件有关。越来越多的证据表明炎症参与 VTE 的发病机制表明抗炎治疗和预防 VTE 的重要性。虽然阿司匹林被证明可有效预防抗凝药物治疗后复发性静脉血栓形成,但其他一些抗炎药如非甾体类抗炎药可能具有促血栓作用,因此可能增加 VTE 的风险。最近,正在寻找已被证明与 VTE 发病机制有关的炎症标志物的新的特异性抗炎药物抑制剂。由于血栓形成是基于炎症引起的凝血激活,因此 VTE 的预防和治疗应包括抗凝剂和抗炎剂。

更新日期:2021-08-15
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