Abstract

Pregnancy complications are a frequent and unsolved condition in patients with antiphospholipid syndrome (APS). Women with antiphospholipid antibodies (aPL) are at high risk of recurrent early pregnancy loss as well as late obstetrical complications associated with impaired placental function, such as preeclampsia, intrauterine growth restriction (IUGR), and prematurity. Thrombotic events at the maternal-fetal interface were originally thought to underlie aPL-associated pregnancy complications, due to the partial beneficial effects of heparin. However, more recent clinical and experimental observations suggest instead that non-thrombotic events may play a primary role in the pathophysiology of pregnancy complications in APS patients, including complement activation, inflammation, and disruption of normal trophoblast function. This chapter will review the known pathogenic mechanisms of pregnancy complications in APS and provide a helpful instrument to all the workers in the field from both a clinical and basic view.

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