Falanga A, Rickles F R
Department of Hematology-Oncology, Ospedali Riuniti, Bergamo, Italy.
Semin Thromb Hemost. 1999;25(2):173-82. doi: 10.1055/s-2007-994919.
The "hypercoagulable state" of malignancy is due to a complex interaction of tumor cells and their products with host cells, leading to various degrees of impairment of the normal defense mechanisms that ordinarily protect the host against thrombogenesis. Tumor cells can activate directly the blood clotting cascade and cause thrombosis or can induce procoagulant properties and inhibit anticoagulant properties of vascular endothelial cells, platelets, and monocytes and macrophages. In the setting of the local and systemic effects of cancer (e.g., stasis induced by prolonged bed rest and/or vascular invasion by tumor), together with iatrogenic complications of the treatment of cancer (e.g., the use of central vein catheters and angiopathic chemotherapy), this basic pathophysiology conspires to make cancer perhaps the best example of "acquired thrombophilia." In this brief review, we have attempted to describe what is currently known about the mechanisms for the hypercoagulable state of cancer and provide a summary of the evidence that indicates the many levels of defects in patients with malignancies that predispose them to thrombosis. A better understanding of the pathophysiology of thrombophilia in cancer should provide clinicians with an improved rationale for more aggressive and specific anticoagulant strategies in selected patients.
恶性肿瘤的“高凝状态”是肿瘤细胞及其产物与宿主细胞复杂相互作用的结果，导致通常保护宿主免受血栓形成的正常防御机制出现不同程度的损害。肿瘤细胞可直接激活血液凝固级联反应并导致血栓形成，或可诱导血管内皮细胞、血小板、单核细胞和巨噬细胞产生促凝特性并抑制其抗凝特性。在癌症的局部和全身影响（如长期卧床休息引起的血流淤滞和/或肿瘤对血管的侵犯）的背景下，再加上癌症治疗的医源性并发症（如中心静脉导管的使用和血管病变化疗），这种基本病理生理学共同作用，使癌症可能成为“获得性易栓症”的最佳例证。在这篇简短的综述中，我们试图描述目前已知的癌症高凝状态的机制，并总结证据，这些证据表明恶性肿瘤患者存在多层次缺陷，使他们易患血栓形成。更好地理解癌症中易栓症的病理生理学，应为临床医生在特定患者中采取更积极、更具特异性的抗凝策略提供更好的理论依据。
