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KEY POINTS
■ The hypercoagulable state induced by cancer and its treatment is likely to cause venous thromboembolism (VTE), which responds less well to standard treatment when the patient has cancer. The incidence of VTE is 4 to 6 times higher in cancer patients than in the general population, and cancer itself is considered to be an independent risk factor for VTE.
■ Traditional thrombosis management involves the administration of weight-based low molecular weight heparin (LMWH) or unfractionated heparin. Warfarin is started after the therapeutic aPTT has been achieved.
■ Several landmark trials are behind the current recommendations in various clinical practice guidelines to use LMWH in cancer patients. Strong evidence indicates that the optimal treatment for this population is LMWH for the initial thromboembolic event as well as secondary prevention for a minimal duration of 3 to 6 months.
Venous thromboembolism (VTE) is a frequent complication in patients with cancer. Its occurrence worsens quality of life and adds to the management challenges for clinicians who treat these patients. The medical literature suggests that compared to patients without cancer, those with malignancy respond less well to standard treatments for VTE and have higher rates of recurrent thromboembolism and hemorrhagic complications.1 This article describes the safety and efficacy of current therapy options for VTE in patients with cancer and investigates whether optimal treatment strategies are available.
VTE IN PATIENTS WITH CANCER
Epidemiology Since most oncology patients receive chemotherapy and/or hormonal therapies that can cause VTE, the true incidence of cancer-related VTE is difficult to identify.1 Deep vein thrombosis (DVT) and/or pulmonary embolism (PE) occur in 4% to 20% of cancer patients, and VTE constitutes the second most common cause of death in this group.2,3 Autopsy studies have demonstrated that approximately 1 of 7 hospitalized cancer patients did not die from their cancer but rather from a cause related to VTE.2 These data suggest that VTE can negatively affect prognosis in cancer patients and that anticoagulants play a vital role in treatment and prevention of recurrent VTE.2,3
The hypercoagulable state caused by both cancer and treatments for cancer is likely to cause VTE, which responds less well to standard treatment when the patient has cancer.4 Overall, the incidence of VTE is 4 to 6 times higher in cancer patients than in the general population, and
cancer itself is considered to be an independent risk factor for venous thromboembolism.3
Pathophysiology A hypercoagulable state in malignancy may result from direct activation of the clotting system by neoplastic cells; in turn, these cells lead to the production of thrombin by producing tissue factor and expressing the coagulation factor X activator known as cancer procoagulant. Tumor cells can also indirectly activate the coagulation system by eliciting tissue factor expression by monocytes, platelets, and endothelial cells.1,4