Antiphospholipid antibodies in obstetrics: New complexities and sites of action

Abstract

The antiphospholipid syndrome, the cause of which remains unknown, is characterized by severe pregnancy complications. Fetal losses have been attributed to thrombosis of the uteroplacental vasculature and placental infarction. Polyclonal and monoclonal antiphospholipid antibodies seem able to recognize a 'plasma cofactor' on the endothelial and trophoblast cell surfaces and to affect cell function, inducing a procoagulant state. Although thrombosis is observed frequently in the decidua and placentas of patients with antiphospholipid antibodies, this observation was not universal, nor present in a sufficient degree to account for the pregnancy loss associated with this syndrome. Recent observations have suggested that antiphospholipid antibodies decreased placental hormone production and trophoblast intercellular fusion and invasion, suggesting that many of the obstetric complications observed in the syndrome may be due to antiphospholipid antibody-induced trophoblast dysfunction. However, the complex antigens on the trophoblast surfaces are still to be characterized and correlated with clinical manifestation. It is clear that successful pregnancies with the syndrome are more likely to occur after maternal treatment. Although prednisone may still be needed to treat manifestations associated with autoimmune disorders, the use of heparin, together with low-dose aspirin, has replaced prednisone for treatment of pregnant women. Maternal treatment and careful monitoring of fetal well-being are mandatory in the management of these high-risk pregnancies.