Department of Hematology and Transfusion Medicine, Centro Hospitalar de Trás-os-Montes e Alto Douro, Lordelo, Portugal.
Department of Medical Oncology, Centro Hospitalar Universitário do Porto, Institute of Biomedical Sciences Abel Salazar, University of Porto, Porto, Portugal.
Semin Thromb Hemost. 2021 Sep;47(6):669-676. doi: 10.1055/s-0040-1718926. Epub 2021 May 14.
Cancer-related venous thromboembolism (VTE) remains a major health problem, accounting for at least 18% of all cases of VTE. Cancer patients with VTE have worse prognosis than those without VTE. Prophylaxis reduces VTE risk, but it is not feasible for all outpatients with cancer due to an increased bleeding risk. The factors involved in the pathogenesis of cancer-related VTE are direct coagulation activation, platelet activation, induction of inflammatory responses, and inhibition of fibrinolysis. Direct coagulation activation can be due to cancer procoagulant (a cysteine protease), microvesicles, or other prothrombotic abnormalities. Risk factors for developing VTE in cancer patients can be divided into four groups: tumor-related risk factors, patient-related risk factors, treatment-related risk factors, and biomarkers. Cancers of the pancreas, kidney, ovary, lung, and stomach have the highest rates of VTE. Patient-related risk factors such as age, obesity, or the presence of medical comorbidities can contribute to VTE. Platinum-based chemotherapies and antiangiogenesis treatments have also been associated with VTE. Biomarkers identified as risk factors include high platelet count, high leukocyte count, P-selectin, prothrombin fragments, D-dimer, and C-reactive protein. Based on the known risk factors, risk assessment models were developed to stratify patients who would benefit from thromboprophylaxis. The Khorana model was the first and is still the most widely used model. Because of its low sensitivity for certain tumor types, four new models have been developed in recent years. In this review, we describe the current knowledge about the pathogenesis and risk factors for cancer-related VTE, hoping to contribute to further research on the still many obscure aspects of this topic.
癌症相关静脉血栓栓塞症（VTE）仍然是一个主要的健康问题，至少占所有 VTE 病例的 18%。患有 VTE 的癌症患者比没有 VTE 的患者预后更差。预防可降低 VTE 风险，但由于出血风险增加，并非所有癌症门诊患者都可行。与癌症相关的 VTE 发病机制涉及直接凝血激活、血小板激活、诱导炎症反应和抑制纤维蛋白溶解。直接凝血激活可能是由于癌症促凝剂（一种半胱氨酸蛋白酶）、微泡或其他促血栓形成异常引起的。癌症患者发生 VTE 的危险因素可分为四组：肿瘤相关危险因素、患者相关危险因素、治疗相关危险因素和生物标志物。胰腺、肾脏、卵巢、肺部和胃部的癌症 VTE 发生率最高。年龄、肥胖或存在合并症等患者相关危险因素也可导致 VTE。铂类化疗和抗血管生成治疗也与 VTE 相关。被确定为危险因素的生物标志物包括血小板计数高、白细胞计数高、P-选择素、凝血酶原片段、D-二聚体和 C 反应蛋白。基于已知的危险因素，开发了风险评估模型来对需要进行血栓预防的患者进行分层。Khorana 模型是第一个也是目前应用最广泛的模型。由于其对某些肿瘤类型的敏感性较低，近年来又开发了四个新模型。在这篇综述中，我们描述了癌症相关 VTE 的发病机制和危险因素的最新知识，希望有助于进一步研究这一主题中仍然存在的许多未知方面。
