Cancer-Associated Thrombosis~!2009-11-10~!2009-12-11~!2010-02-22~!

Abstract

Thrombosis is a common complication in patients with cancer and it is estimated that about 20% of patients with cancer experience venous thromboembolism (VTE). This complication is associated with high rate of morbidity and mortality and is sometimes the first manifestation of an occult cancer. The risk profiles and markers involved in cancerassociated thrombosis share similarities with inflammation-induced atherosclerosis and thrombosis. The type of cancer, chemotherapy, surgery, central venous catheters, pre-chemotherapy platelet and leukocyte count are associated with high risk of VTE in cancer patients. Landmark studies demonstrated that effective prophylaxis and treatment of VTE reduced morbidity and increased survival. Low-molecular-weight heparin (LMWH) is preferred as an effective and safe means for prophylaxis and treatment of VTE. It has largely replaced unfractionated heparin and vitamin K antagonists. The advantages of LMWH include increased survival and quality of life, decreased rate of VTE, low incidence of thrombocytopenia. New guidelines for prophylaxis and treatment are now available and prophylaxis is recommended in hospitalized cancer patients and patients undergoing major surgery. Treatment with LMWH should be considered as the first line of therapy for established VTE and to prevent recurrent thrombosis in patients with cancer.

Venous Thromboembolism in the Cancer Population: Pathology, Risk, and Prevention

“…Tumor cells have the capacity to express all the needed inhibitors and activators to regulate the fibrinolytic pathway (Caine et al, 2002). This Caine et al (2002), Falanga & Vignoli (2004), Gupta et al (2005), Karimi & Cohan (2010), and Kuderer et al (2009). IL-1ß = interleukin-1ß; TNF-α = tumor necrosis factor-α; VEGF = vascular endothelial growth factor; TF = tissue factor; CP = cancer procoagulant; u-PA = urokinase-type activator; t-PA = tissue-type plasminogen activator; PA-1 = plasminogen activator inhibitor-1; PAI-2 = plasminogen activator inhibitor-2.…”

“…Use your smartphone to access ASCO, ESMO, and NCCN guidelines for the management of venous thromboembolism SEE PAGE 21 of acute phase reactants, including inflammatory cytokines that activate the clotting cascade, and (4) interaction with host blood cells (Caine et al, 2002;Falanga & Vignoli, 2004;Gupta, Charan, & Kumar, 2005;Karimi & Cohan, 2010).…”

“…Cancer procoagulant, found mainly in malignant tissues, is a protease enzyme that activates factor X of the coagulation pathway directly (Varki, 2007). It is released by many different types of tumor cells, and it actively promotes thrombosis and platelet activation (Karimi & Cohan, 2010).…”

“…Tumor cells secrete a large number of different types of proinflammatory cytokines. Release of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and vascular endothelial growth factor (VEGF) inhibit the normal anticoagulant system by inducing the expression of tissue factor by vascular endothelial cells (VECs) (Caine et al, 2002;Karimi & Cohan, 2010). This downregulates the activation of the protein C system (Goldenberg, Kahn, & Solymoss, 2003), which increases the ability of the vascular wall to attach to leukocytes and platelets, promoting thrombosis formation (Caine et al, 2002;Karimi & Cohan, 2010).…”

“…Malignant cells interact with host cells such as platelets, leukocytes, and endothelial cells to promote thrombosis formation (Kuderer et al, 2009;Karimi & Cohan, 2010). When tumor cells adhere directly to the endothelial wall of the host, the tumor cells release cytokines that contribute to the adhesion of leukocytes and platelets, leading to thrombosis (Caine et al, 2002).…”