Venous Thrombo-Embolism (VTE) In Cancer Patients

Abstract

Venous thromboembolism (VTE), includes both deep vein thrombosis (DVT) and pulmonary embolism (PE), is the second-leading causes of death in hospitalized and ambulatory cancer patients. The risk of VTE in cancer patients is increased three- to five fold for those who are undergoing surgery and 5-6 folds for those who are receiving chemotherapy. In the 19th century, the association between thrombosis and malignancy was described in 1823 by Bouillaud and then in 1865 by Armand Trousseau and is now often referred to as Trousseau syndrome. A few years later, in 1878, histological evidence for tumor cells within a thrombus was founded by Theodor Billroth. This rate of venous thromboembolism (VTE) in patients with cancer is greater than that in patients without cancer and chemotherapy increases the risk to a greater fold. The mechanism of the so-called “Trousseau’s syndrome” probably includes all aspects of Virchow's triad: stasis of blood, trauma or pathology of the endothelium and hypercoagulability of the blood itself. The pathogenesis of VTE in cancer patients is complex and involves the interplay of multiple factors – related to the tumor itself, patient and anticancer therapies. Several biomarkers were identified as potential predictors of VTE events. These include elevated platelet and leukocyte counts, decreased hemoglobin, elevated D-dimer, elevated prothrombin activation products, elevated soluble P-selectin, peak thrombin generation and elevated levels of TF bearing microparticles.