Semin Thromb Hemost 2008; 34(3): 251-255
DOI: 10.1055/s-0028-1082268
© Thieme Medical Publishers

Novel Considerations in the Pathogenesis of the Antiphospholipid Syndrome: Involvement of the Tissue Factor Pathway of Blood Coagulation

Murray Adams1
  • 1Senior Lecturer, School of Human Life Sciences, University of Tasmania, Tasmania, Australia
Further Information

Publication History

Publication Date:
21 August 2008 (online)

ABSTRACT

The antiphospholipid syndrome (APS) is characterized by clinical manifestations such as venous and arterial thrombosis, thrombocytopenia and/or recurrent pregnancy loss, as well as the persistent presence of laboratory markers of antiphospholipid (aPL) antibodies detected in laboratory assays. Though it is generally accepted that aPL antibodies, such as anticardiolipin (aCL), anti–β2 glycoprotein I (anti-β2GPI), and lupus anticoagulants (LA) contribute to the pathogenesis of APS, precise mechanism(s) are yet to be fully described. It is probable that aPL antibodies bind to a range of cellular targets (e.g., platelets, endothelial cells, and monocytes), leading to thrombosis and obstetric complications. There is now increasing evidence that alterations to the tissue factor (TF) pathway of blood coagulation contribute toward hypercoagulability in patients with aPL antibodies. This article reviews current evidence that suggests changes and/or interference to the major pathway of blood coagulation may represent a novel mechanism that contributes to the development of APS.

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Murray AdamsPh.D. M.A.I.M.S. 

School of Human Life Sciences, University of Tasmania

Tasmania, Australia

Email: Murray.Adams@utas.edu.au

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