Is There Any Effect of Tumor Burden on Hemostatic Parameters in Cancer Patients? A Case–Control Study of Hemostatic Abnormalities and Anticardiolipin Antibodies in Solid Tumors

thrombophelebitis in patients with cancer. Thrombo-sis may be a presenting feature of occult malignancy, a life-threatening component of early or advanced cancer, or a complication of anticancer therapy itself. Cancer-related thrombosis represents a complex imbalance between coagulation and fibrinolysis. The underlying pathogenetic mechanisms include hyper-coagulability due to activation of clotting by tumor cells, vessel wall injury, and stasis. The activation of coagulation factors V, VII, IX, as well as fibrinogen and fibrin degradation products occurs. Increased secretion of plasminogen activators and decrease in their inhibitors, decreased levels of protein C, pro-tein S, and antithrombin, activation of platelets, and increased platelet aggregation all assist in thrombo-sis risk. Prolongation of prothrombin time (PT) and activated partial thromboplastine time (aPTT) have also been documented. These changes are thought to be the result of ongoing low-grade disseminated intravascular coagulation (DIC).