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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-beta2 glycoprotein I (anti-beta2GPI), 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.

Item Type:	Refereed Article
Research Division:	Medical and Health Sciences
Research Group:	Cardiorespiratory Medicine and Haematology
Research Field:	Haematology
Objective Division:	Health
Objective Group:	Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:	Blood Disorders
UTAS Author:	Adams, MJ (Dr Murray Adams)
ID Code:	52371
Year Published:	2008
Web of Science® Times Cited:	8
Deposited By:	Health Sciences A
Deposited On:	2008-08-01
Last Modified:	2009-07-21
Downloads:	554 View Download Statistics