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Markers of Coagulation and Angiogenesis in Cancer-Associated Venous Thromboembolism

Neil Goldenberg, Susan R. Kahn, Susan Solymoss

From the Departments of Internal Medicine and Pediatrics, University of South Florida, Tampa, FL; and the Department of Medicine and Center for Clinical Epidemiology and Community Studies, SMBD-Jewish General Hospital, and the Department of Hematology, Montreal General Hospital and St Mary’s Hospital, McGill University, Montreal, Quebec, Canada.

Address reprint requests to Neil Goldenberg, MD, Department of Hematology, Oncology, and Bone Marrow Transplantation, The Children’s Hospital, 1056 E 19th Ave, B-115, Denver, CO 80218; e-mail: goldenberg.neil{at}tchden.org.

Purpose: We sought to determine whether venous thromboembolism in cancer patients is associated with aberrant plasma levels of hemostatic and angiogenic factors.

Patients and Methods: Peripheral blood was collected before anticoagulant therapy from cancer patients with acute deep venous thrombosis (DVT; DVT + cancer group, n = 32), those without DVT (cancer control group, n = 36), and patients with acute DVT but no cancer (DVT control group, n = 58). Plasma assays of activation and inhibition of coagulation and fibrinolysis, as well as angiogenesis activation, were then performed.

Results: Median levels of thrombin-antithrombin complex, prothrombin fragments 1 + 2, and von Willebrand factor antigen were significantly greater in the DVT + cancer group than in the cancer control and DVT control groups (17.8 ng/mL v 4.6 ng/mL and 9.8 ng/mL, P = .0001 and P = .003, respectively; 3.65 nmol/L v 1.60 nmol/L and 2.71 nmol/L, P < .0001 and P = .011, respectively; and 4.04 U/mL v 2.26 U/mL and 2.06 U/mL, P < .0001, respectively). Median levels of tissue-type plasminogen activator were also significantly higher, while protein C activity was lower in the DVT + cancer group than in the DVT control group (14.6 ng/mL v 9.50 ng/mL, respectively, P = .0005; 0.89 U/mL v 1.11 U/mL, respectively, P = .0008).

Conclusion: These data not only support prior observations of coagulation activation in patients with malignancy, but also provide new evidence for enhanced coagulation activation in the setting of acute venous thromboembolism in cancer. Future prospective studies are warranted to determine whether these and other potential markers of hypercoagulability may help to identify cancer patients at highest risk for venous thromboembolism.

Supported in part by an unrestricted research grant from Pharmacia and Upjohn.

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