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Complement activation as a mediator of antiphospholipid antibody induced pregnancy loss and thrombosis

J E Salmon¹, G Girardi¹, V M Holers²

¹ Department of Medicine, Hospital for Special Surgery-Weill Medical College, Cornell University, New York, USA
² Departments of Medicine and Immunology, University of Colorado Health Sciences Center, Denver, USA

Correspondence to:
Correspondence to:
Dr J E Salmon, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA;
salmonj@hss.edu

Keywords: pregnancy; thrombosis; complement activation; antiphoshpolipid antibody syndrome

Abbreviations: aPL, antiphospholipid; APS, antiphospholipid antibody syndrome; SLE, systemic lupus erythematosus

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

The antiphospholipid antibody syndrome (APS) is characterised by increased risk of vascular thrombosis involving venous, arterial, and placental circulations. The last of these is associated with poor obstetrical outcomes, including fetal death and growth retardation. Pregnancy loss is a defining criterion for APS and occurs with particularly high frequency in systemic lupus erythematosus (SLE) patients bearing this antibody. Patients meet the criteria for APS if they have three otherwise unexplained embryonic losses (before 10 weeks gestation) or one otherwise unexplained fetal loss after 10 weeks, with or without placental infarction or fetal growth restriction.^1–3

Over the past two decades, APS has emerged as a leading cause of pregnancy loss and pregnancy related morbidity. It is now recognised that recurrent miscarriage occurs in 1% of couples,^4–7 that up to 20% of women with recurrent miscarriage have antiphospholipid (aPL) antibodies, and that in about 15% of otherwise apparently normal women aPL is . . . [Full text of this article]

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