Pathophysiology of the thrombophilic state in the cancer patient

The "hypercoagulable state" of malignancy is due to a complex interaction o f tumor cells and their products with host cells, leading to various degree s of impairment of the normal defense mechanisms that ordinarily protect th e 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, platel ets, and monocytes and macrophages, In the setting of the local and systemi c effects of cancer (e.g., stasis induced by prolonged bed rest and/or vasc ular invasion by tumor), together with iatrogenic complications of the trea tment of cancer (e.g., the use of central vein catheters and angiopathic ch emotherapy), this basic pathophysiology conspires to make cancer perhaps th e 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 patie nts with malignancies that predispose them to thrombosis. A better understa nding of the pathophysiology of thrombophilia in cancer should provide clin icians with an improved rationale for more aggressive and specific anticoag ulant strategies in selected patients.