title: Pathophysiology of the antiphospholipid antibody syndrome.
abstract: Antiphospholipid antibodies (aPL) are associated with the recurrent pregnancy loss and thrombosis that characterizes the antiphospholipid antibody syndrome (APS). Although the ontogeny of these pathogenic antibodies has not been fully elucidated, there is evidence that indicates the involvement of both genetic and environmental factors. The ability of aPL to induce a procoagulant phenotype in APS patients plays a central role in the development of arterial and venous thrombotic manifestations typical of the disease. Inflammation serves as a necessary link between this procoagulant phenotype and actual thrombus development and is an important mediator of the placental injury seen in APS patients with obstetric complications. Recent evidence has indicated a role for abnormal cellular proliferation and differentiation in the pathophysiology of APS, especially in those patients with pregnancy morbidity and other more atypical manifestations that have no identifiable thrombotic cause. The interplay of genetic and environmental factors responsible for aPL development and the mechanisms by which these antibodies produce disease in APS patients is the focus of this review.
authors.affiliation: Department of Microbiology, University of the West Indies, Mona Campus, Kingston, Jamaica, West Indies.
authors.forename: Rohan
authors.initials: R
authors.lastname: Willis
authors.affiliation: Division of Rheumatology/Internal Medicine, University of Texas Medical Branch, Brackenridge Hall 2.108 301 University Boulevard, Galveston, TX 77555-0883 USA.
authors.forename: Silvia S
authors.initials: SS
authors.lastname: Pierangeli
keywords: Anti-β2 glycoprotein I antibodies; Antiphospholipid antibodies; Endothelial cells; Lupus anticoagulant