Journal
SEMINARS IN THROMBOSIS AND HEMOSTASIS
Volume 34, Issue 3, Pages 251-255Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-0028-1082268
Keywords
tissue factor; antiphospholipid syndrome; antiphospholipid antibodies; tissue factor pathway inhibitor; thrombosis
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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-beta 2 glycoprotein I (anti-beta 2GPI), and lupus anticoagulants (LA) contribute to the pathogenesis of APS, precise mechanism(s) are vet 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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