Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism

Neil Goldenberg, Susan R. Kahn, Susan Solymoss

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4194-4199
Number of pages6
JournalJournal of Clinical Oncology
Volume21
Issue number22
DOIs
StatePublished - Nov 15 2003
Externally publishedYes

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Venous Thromboembolism
Neoplasms
Control Groups
Thrombophilia
Angiogenesis Inducing Agents
von Willebrand Factor
Fibrinolysis
Tissue Plasminogen Activator
Hemostatics
Protein C
Venous Thrombosis
Anticoagulants
Prospective Studies

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism. / Goldenberg, Neil; Kahn, Susan R.; Solymoss, Susan.

In: Journal of Clinical Oncology, Vol. 21, No. 22, 15.11.2003, p. 4194-4199.

Research output: Contribution to journalArticle

Goldenberg, Neil ; Kahn, Susan R. ; Solymoss, Susan. / Markers of coagulation and angiogenesis in cancer-associated venous thromboembolism. In: Journal of Clinical Oncology. 2003 ; Vol. 21, No. 22. pp. 4194-4199.
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abstract = "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.",
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