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Rheumatology Advance Access originally published online on March 31, 2003
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Rheumatology 2003; 42: 1029-1031
© 2003 British Society for Rheumatology

Editorial

Tissue factor in antiphospholipid syndrome: shifting the focus from coagulation to endothelium

O. Amengual, T. Atsumi and M. A. Khamashta1

Department of Medicine II, Hokkaido University School of Medicine, Sapporo, Japan and
1 Lupus Research Unit, The Rayne Institute, St Thomas' Hospital, London SE1 7EH, UK

The first 10% of the full text of this article appears below.

Thrombosis, in both the arterial and the venous circulation, is one of the major manifestations of antiphospholipid syndrome (APS), a prothrombotic disorder associated with recurrent thrombotic events and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL) [1].

In the past decade, many studies have investigated the pathophysiology of thrombosis in APS and considerable interest has focused on the role of aPL as a clue to the mechanism of thrombosis. Results of intensive research have significantly advanced our understanding of the mechanisms by which these antibodies may play a direct role in clot formation. It is now recognized that many of the autoantibodies associated with APS are directed against phospholipid-binding plasma proteins, such as ß2-glycoprotein I (ß2GPI) and prothrombin, or phospholipid–protein complexes, expressed on or bound to the surface . . . [Full Text of this Article]


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