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Evaluation of ADAMTS13 activity in Venous Thromboembolism

Grant number: 12/03841-3
Support Opportunities:Regular Research Grants
Start date: October 01, 2012
End date: September 30, 2014
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Joyce Maria Annichino-Bizzacchi
Grantee:Joyce Maria Annichino-Bizzacchi
Host Institution: Centro de Hematologia e Hemoterapia (HEMOCENTRO). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated researchers:Fernanda Loureiro de Andrade Orsi

Abstract

Venous Thromboembolism (VTE) is a complex disease that affects 1:1000 individuals worldwide and whose etiology lays on the interaction of genetic and acquired factors. Although many risk factors for VTE are well defined, at least 30% of cases are still idiopathic, raising suspicions of the existence of other etiologic factors yet unknown. Furthermore, individuals with hereditary or acquired thrombophilia have different clinical presentation, which suggests the presence of other risk factors undefined and that can interfere with the phenotypic expression. High levels of inflammatory markers and coagulation factors, mainly factor VIII (FVIII) and von Willebrand factor (VWF) have recently risen as possible risk factors for VTE. The reasons for this association is still to be evaluated and apparently is not related to genetic mutation in the factors gene. ADAMTS13 (A Disintegrin And Metalloprotease with Thrombospondin type 1 repeats) is the enzyme responsible for VWF proteolysis. In different clinical situations, as pregnancy, inflammatory diseases and arteriosclerosis, there is a clear relation between high levels of VWF and decrease ADAMTS13 activity. Apparently, the ADAMTS13 activity may be impaired by inflammatory cytokines. It is possible that the decreased activity of ADAMTS13 is the cause of elevated levels of VWF observed in some cases of VTE and thus functioning as an independent risk factor for its occurrence. In this project we intend to develop a case-control study in a population of patients with VTE without hereditary or acdquired thrombophilia in order to explore the role of ADAMTS13 activity as a risk factor for VTE. (AU)

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