The Pathophysiology of Antiphospholipid Syndrome

Sada, Pablo Ruiz; Cohen , Hannah; Isenberg, David

The Pathophysiology of Antiphospholipid Syndrome

Pablo Ruiz Sada¹, Hannah Cohen ², David Isenberg^{3, *}

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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Identifiers and Pagination:

Year: 2015
Volume: 8
Issue: 2
First Page: 2
Last Page: 9
Publisher ID: TOUNJ-8-2
DOI: 10.2174/1874303X01508010002

Article History:

Received Date: 2/7/2014
Revision Received Date: 1/9/2014
Acceptance Date: 2/9/2014
Electronic publication date: 20/2/2015
Collection year: 2015

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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 (http://creativecommons.org/licenses/by-nc/3.0/) 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 d.isenberg@ucl.ac.uk

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.

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RESEARCH ARTICLE

The Pathophysiology of Antiphospholipid Syndrome

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