Abstract
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.
Keywords:
Cancer - thrombophilia - hypercoagulability - chemotherapy - tumor cells - procoagulants
