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化疗及其他癌症治疗带来的血栓形成风险。

Thrombotic Risk from Chemotherapy and Other Cancer Therapies.

作者信息

Debbie Jiang M D, Alfred Ian Lee M D

机构信息

Department of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.

Yale School of Medicine, New Haven, CT, USA.

出版信息

Cancer Treat Res. 2019;179:87-101. doi: 10.1007/978-3-030-20315-3_6.

DOI:10.1007/978-3-030-20315-3_6
PMID:31317482
Abstract

Cancer patients have an increased risk of thrombosis. The development of cancer thrombosis is dependent on a number of factors including cancer type, stage, various biologic markers, and the use of central venous catheters. In addition, cancer treatment itself may increase thrombotic risk. Tamoxifen increases the risk of venous thromboembolism (VTE) by two- to sevenfold, while an impact on risk of arterial thrombosis is uncertain. Immunomodulatory imide drugs (IMiDs) such as thalidomide and lenalidomide increase the risk of VTE in patients with multiple myeloma (MM) by about 10-40% when given in combination with glucocorticoids or other chemotherapy agents; the risk of VTE in MM patients treated with IMiD-containing regimens necessitates that such patients receive thromboprophylaxis with aspirin, low-molecular-weight heparin, or warfarin. Among cytotoxic chemotherapy agents, cisplatin, and to a lesser extent fluorouracil, has been described in association with thrombosis. L-asparaginase in treatment of acute lymphoblastic leukemia is significantly associated with increased thrombosis particularly affecting the CNS, which may be due to acquired antithrombin deficiency; at some centers, plasma infusions or antithrombin replacement is used to mitigate this. Bevacizumab, an inhibitor of vascular endothelial growth factor, increases arterial and possibly venous thrombotic risk, although the literature is conflicting about the latter. Supportive care agents in cancer care, such as erythropoiesis-stimulating agents, granulocyte colony stimulating factor, and steroids, also have some impact on thrombosis. This review summarizes the mechanisms by which these and other therapies modulate thrombotic risks and how such risks may be managed.

摘要

癌症患者发生血栓形成的风险增加。癌症血栓形成的发展取决于多种因素,包括癌症类型、分期、各种生物标志物以及中心静脉导管的使用。此外,癌症治疗本身可能会增加血栓形成风险。他莫昔芬使静脉血栓栓塞(VTE)风险增加2至7倍,而对动脉血栓形成风险的影响尚不确定。免疫调节性酰亚胺药物(IMiDs),如沙利度胺和来那度胺,与糖皮质激素或其他化疗药物联合使用时,会使多发性骨髓瘤(MM)患者的VTE风险增加约10%-40%;接受含IMiD方案治疗的MM患者发生VTE的风险使得此类患者需要接受阿司匹林、低分子肝素或华法林的血栓预防。在细胞毒性化疗药物中,顺铂以及程度较轻的氟尿嘧啶,已被描述与血栓形成有关。急性淋巴细胞白血病治疗中使用的L-天冬酰胺酶与血栓形成增加显著相关,尤其影响中枢神经系统,这可能是由于获得性抗凝血酶缺乏所致;在一些中心,使用血浆输注或抗凝血酶替代疗法来减轻这种情况。贝伐单抗是一种血管内皮生长因子抑制剂,会增加动脉血栓形成风险,可能也会增加静脉血栓形成风险,尽管关于后者的文献存在矛盾之处。癌症护理中的支持性护理药物,如促红细胞生成素、粒细胞集落刺激因子和类固醇,也对血栓形成有一定影响。本综述总结了这些及其他疗法调节血栓形成风险的机制以及如何管理此类风险。

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