The Pathophysiology of Antiphospholipid Syndrome

Pablo Ruiz Sada1, Hannah Cohen 2, David Isenberg3, *
1 Hospital Universitario de Basurto, Departamento de MedicinaInterna, Bilbao, Spain
2 University College London, London, UK
3 Centre for Rheumatology Research, Division of Medicine, University College London, London, UK

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© Sada et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Centre for Rheumatology, UCL Division of Medicine, Room 424, Rayne Building, 5 University Street, WC1E 6JF, London, UK; Tel: 0203 108 2148; Fax: 0203 108 2152; E-mail


Advances in our knowledge of the pathogenic mechanisms of antiphospholipid syndrome have been achieved in the past few years. Apart from the well-known role of anti-β2-glycoprotein I antibodies, complement, endocrine and genetic factors and a variety of other molecules are now under investigation. These new approaches should lead to novel explanations and potential new treatment options.

Keywords: Anti-β2-glycoprotein, antiphospholipid syndrome, antiphospholipid antibodies, complement.