ABSTRACT
Table 10.3. The risk of thromboembolism varies according to the type of thrombophilia, as shown in Table 10.4.
The relationship between cancer and thrombosis has been known since 1865, when Trousseau first described ‘a particular condition of the blood which predisposed it to spontaneous coagulation’.1 Multiple prothrombotic pathogenic processes are involved in malignancy, including activation of the coagulation cascade and fibrinolytic system, procoagulant activation of tumor cells, and tumor-cell interaction with blood cells and endothelium, as well as clinical situations with increased risk of thrombosis (for example, chemotherapy, immobilization, surgery, and infection).2 While the role of acquired thrombophilia as one of the possible pathogenic mechanisms in venous thromboembolism (VTE) in cancer, has been thoroughly explored (see Chapter 2), the issue of thrombophilia as a cause or additional contributor to the hypercoagulable state in cancer patients has not been fully investigated. This chapter
Table 10.2
Surgery Oral contraceptives and hormone-replacement treatment Cancer and its treatment (chemo-or hormonal therapy) Myeloproliferative disorders Trauma Immobility Antiphospholipid syndrome Pregnancy and puerperium Long travel Heart failure Stroke Nephrotic syndrome Inflammatory bowel disease Behçet’s disease
Type of thrombophilia Healthy subjects Unselected patients (%) (%)
Antithrombin deficiency 0.02 1-2 Protein C deficiency 0.2-0.4 3-4 Protein S deficiency ? 2 Factor V Leiden 5 20 Prothrombin G20210A 2-3 7 Elevated factor VIII levels 11 25 Hyperhomocysteinemia 5 10
