Cancer is a leading cause of venous thromboembolism (VTE) and vice versa. Pulmonary embolism is the second cause of death in cancer patients. Tumor progression is associated with coagulation activation. The pathogenesis of thrombosis during cancer is particularly complex stemming from multiple connections of this disease with both systems of inflammation and hemostasis. The risk of VTE depends on cancer type and the stage of the disease, the anticancer treatments and the time since cancer diagnosis as well as on the presence of patient-related risk factors (i.e. age, obesity, previous history of VTE, underlying diseases…). The presence of other precipitating factors and the duration of the exposure to them are also key elements in the assessment of such a thrombotic risk. It is therefore important to identify all the VTE risk factors to identify patients at high vascular risk and to determine the period during which this risk is significantly increased. The integration of biomarkers of hypercoagulability in proposed risk assessment models for VTE will improve their capacity to identify patients eligible for pharmacological thromboprophylaxis. In this review, we report the current status of knowledge on the connection between cancer and hypercoagulability, the numerous risk factors for VTE must be identified in cancer patients and the best methodology to build a more accurate assessment of this vascular risk in such a complex medical context.
Keywords: Cancer; Deep vein thrombosis; Embolie pulmonaire; Génération de thrombine; Hypercoagulability; Hypercoagulabilité; Héparines de bas poids moléculaire; Low molecular weight heparin; Maladie thromboembolique veineuse; Pulmonary embolism; Thrombin generation; Thrombose veineuse profonde; Venous thromboembolic disease.
Copyright © 2016. Published by Elsevier Masson SAS.