EDITORIALS

Antiphospholipid syndrome dilemmas still to be solved: 2008 status

Yehuda Shoenfeld¹, Pier Luigi Meroni², Ricard Cervera³

¹ Department of Medicine "B" and Centre for Autoimmune Diseases, Sheba Medical Centre, Sackler Faculty of Medicine, Tel-Aviv University, Israel
² Department of Internal Medicine, University of Milan Allergy, Clinical Immunology and Rheumatology Unit, IRCCS, Istituto Auxologico Italiano, Italy
³ Department of Autoimmune Diseases, Hospital Clínic, Barcelona, Spain

Correspondence to:
Yehuda Shoenfeld, Sheba Medical Center, 52621 Tel-Hashomer, Israel; shoenfel@post.tau.ac.il

Accepted 3 January 2008

The first 150 words of the full text of this article appear below.

Extensive investigation of antiphospholipid syndrome (APS) has improved our knowledge of the disease, but raised new questions. Although the pathogenic role of antiphospholipid antibodies (aPL) is widely accepted, the fact that aPL induces thrombotic events only occasionally suggests the need for a "second hit" to display the thrombogenic effect. Infectious agents are thought to trigger autoantibody production through a molecular mimicry mechanism, but may also induce an inflammatory process that eventually favours clotting. The involvement of complement and cytokines in the pathogenesis further supports the role of inflammation in APS as well as the possibility for new therapeutic approaches. The question of whether other environmental triggers or a genetic individual susceptibility can behave as a second hit is still open. The clinical involvement of different organs and systems poses the question of whether the syndrome should be considered a true systemic autoimmune disease, rather than an acquired autoimmune coagulopathy. A . . . [Full text of this article]

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