The Link Between Cancer and Venous Thromboembolism

A Review

Abstract

Cancer is the most important acquired but often overlooked risk factor for the development of venous thromboembolism (VTE). Tumors can express procoagulant proteins, for example, and tumor masses may compromise venous blood flow by extrinsic compression of adjacent vessels. Cancers can also induce the production of inflammatory cytokines that indirectly contribute to the development of hypercoagulability and the risk of thromboembolism. Additional risk factors for VTE experienced by patients with cancer include immobilization, because of cancer or its treatment, and the potential presence of thrombophilic genetic factors. Many common therapeutic modalities also increase VTE risk, including surgery, chemotherapy agents, adjuvant hormonal manipulation, the use of angiogenesis inhibitors, and the presence of central venous access devices. The risk of VTE seems to be greater with certain tumor types, such as cancers of the pancreas, kidney, or brain. The value of extensive screening of patients with the first episode of idiopathic thromboembolism for the presence of an occult malignancy remains debatable at this time. VTE continues to pose a substantial risk to patients with cancer because of a variety of tumor-, host-, and therapy-related factors.