Cancer and venous thromboembolism.
Clinical examples of coagulation abnormalities may occur from single or multiple abnormailties and include both inherited and acquired defects. Risk factors that further increase clotting include obesity, recent surgery, pregnancy and cancer. Venous thrombosis is a common complication in patients with malignant diseases. The estimates of the prevalence of cancer among patients with venous thrombosis vary from 3 to 18%. Since cancer is a common disorder in the aging population, it may be responsible for a considerable proportion of all cases of thrombosis. The pathogenic mechanisms of thrombosis in the cancer patient involve a complex interaction between the tumor cell, the patient, and the hemostatic system. These include activation of the coagulation system, platelet activation, endothelial damage, indwelling venous access devices, direct effects of chemotherapy/hormonal therapy, and host inflammatory responses. Furthermore, local peritumoral activation of coagulation may have important effects on the biology of cancer. In recent years there have been many new developments in understanding basic mechanisms and optimizing clinical care of thrombosis in cancer patients. Subcutaneous low-molecular weight heparin LMWH) has replaced intravenous unfractionated heparin (UFH) for the initial treatment of thrombosis. In the search for new agents matching the "ideal" anticoagulant profile, a number of different steps in the coagulation cascade have been targeted, including direct thrombin inhibition, and inhibition of factor Xa, factor IXa, the factor VIIa-tissue factor complex and the factor Va-factor VIIIa complex. Such agents could potentially improve thrombosis magement in cancer patients.
Grudeva-Popova
J
J
Department of Hematology, University Hospital - Plovdid, Bulgaria.