Cancer patients show an increased susceptibility to develop thromboembolic diseases, suggesting that disorders of coagulation are very common in this pathology.
Tumor cells possess the capacity to interact with the
hemostatic system, activating the coagulation cascade and stimulating the prothrombotic properties of other blood cell components; the same events while inducing a hypercoagulable state, also contribute to the processes of
tumor growth, neoangiogenesis and metastatic formation. Multiple risk factors associated with malignant disease contribute to the
hypercoagulability state: stasis induced by prolonged
bed rest, vascular invasion by the
tumor and iatrogenic complications including the use of central vein
catheters and
chemotherapy. Several tests have been developed to assess the hypercoagulable state, however their clinical significance still needs to be defined, especially in terms of their predictive value for
thrombosis. Clinical manifestations vary from localized
deep venous thrombosis (DVT) or
pulmonary embolism, more generally associated with solid
tumors, to
disseminated intravascular coagulation, frequent in
hematologic malignancies and metastatic
cancer. Diagnosis of idiopathic DVT, in the absence of other risk factors, could indicate the presence of occult
cancer, but the usefulness of an extensive work-up to detect
malignancy in terms of cost to benefit ratio still has to be demonstrated. Patients with
cancer and
thromboembolism must be treated with
anticoagulant therapy; a large number of studies have shown that either low molecular weight heparins or standard
unfractionated heparin for the treatment of acute
deep vein thrombosis in hospitalized patients are equally safe and effective; however, the first treatment has been reported to be associated with a lower mortality. After an episode of
thrombosis the patients should be protected by a long term course of oral anticoagulation, remaining high the risk of recurrence for as long as the
cancer is active.