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.
KEYWORDS
Tissue factor - antiphospholipid syndrome - antiphospholipid antibodies - tissue factor
pathway inhibitor - thrombosis
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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