The pathogenesis of the antiphospholipid syndrome. N Engl J Med

Department of Infectious Diseases, Immunology, and Sexual Health, St. George Hospital, Kogarah, Sydney, NSW 2217, Australia.
New England Journal of Medicine (Impact Factor: 54.42). 03/2013; 368(11):1033-44. DOI: 10.1056/NEJMra1112830
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Available from: Steven Antony Krilis, Aug 28, 2015
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    • "In APS, aPL binds to endothelial cells, platelets, and monocytes , inducing a proinflammatory and prothrombotic state responsible for thrombotic complications [29]. "
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    ABSTRACT: Antiphospholipid syndrome (APS) is an acquired thrombophilia with clinical manifestations associated with the presence of antiphospholipid antibodies (aPL) in patient plasma. Obstetrical APS is a complex entity that may affect both mother and fetus throughout the entire pregnancy with high morbidity. Clinical complications are as various as recurrent fetal losses, stillbirth, intrauterine growth restriction (IUGR), and preeclampsia. Pathogenesis of aPL targets trophoblastic cells directly, mainly via proapoptotic, proinflammatory mechanisms, and uncontrolled immunomodulatory responses. Actual first-line treatment is limited to low-dose aspirin (LDA) and low-molecular weight heparin (LMWH) and still failed in 30% of the cases. APS pregnancies should be a major field in obstetrical research, and new therapeutics are still in progress.
    Clinical and Developmental Immunology 07/2013; 2013:159124. DOI:10.1155/2013/159124 · 2.93 Impact Factor
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    ABSTRACT: To identify the main causes of morbidity and mortality in patients with antiphospholipid syndrome (APS) during a 5-year period and to determine clinical and immunological parameters with prognostic significance. The clinical and immunological features of a cohort of 1000 patients with APS from 13 European countries who had been followed up from 1999 to 2004 were analysed. 200 (20%) patients developed APS-related manifestations during the 5-year study period. Recurrent thrombotic events appeared in 166 (16.6%) patients and the most common were strokes (2.4% of the total cohort), transient ischaemic attacks (2.3%), deep vein thromboses (2.1%) and pulmonary embolism (2.1%). When the thrombotic events occurred, 90 patients were receiving oral anticoagulants and 49 were using aspirin. 31/420 (7.4%) patients receiving oral anticoagulants presented with haemorrhage. 3/121 (2.5%) women with only obstetric APS manifestations at the start of the study developed a new thrombotic event. A total of 77 women (9.4% of the female patients) had one or more pregnancies and 63 (81.8% of pregnant patients) had one or more live births. The most common fetal complications were early pregnancy loss (17.1% of pregnancies) and premature birth (35% of live births). 53 (5.3% of the total cohort) patients died. The most common causes of death were bacterial infection (21% of deaths), myocardial infarction (19%) and stroke (13%). No clinical or immunological predictor of thrombotic events, pregnancy morbidity or mortality was detected. Patients with APS still develop significant morbidity and mortality despite current treatment (oral anticoagulants or antiaggregants, or both).
    Annals of the rheumatic diseases 10/2008; 68(9):1428-32. DOI:10.1136/ard.2008.093179 · 10.38 Impact Factor
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    ABSTRACT: β2-glycoprotein I (β2GPI) is the major autoantigen in the antiphospholipid syndrome. The central importance of understanding β2GPI physiology from the perspective of the rheumatologist is that it forms the foundation for understanding the pathophysiology underlying autoantibody generation, and the diverse mechanisms by which anti-β2GPI antibodies in complex with β2GPI may predispose an individual to the antiphospholipid syndrome clinical phenotype. This review examines some of the latest novel findings in this area.
    Current Rheumatology Reports 02/2011; 13(1):90-5. DOI:10.1007/s11926-010-0151-9 · 2.45 Impact Factor
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