Antiphospholipid antibodies in obstetrics: new complexities and sites of action

The antiphospholipid syndrome, the cause of which remains unknown, is chara cterized by severe pregnancy complications. Fetal losses have been attribut ed to thrombosis of the uteroplacental vasculature and placental infarction , Polyclonal and monoclonal antiphospholipid antibodies seem able to recogn ize a 'plasma cofactor' on the endothelial and trophoblast cell surfaces an d to affect cell function, inducing a procoagulant state. Although thrombos is is observed frequently in the decidua and placentas of patients with ant iphospholipid antibodies, this observation was not universal, nor present i n a sufficient degree to account for the pregnancy loss associated with thi s syndrome. Recent observations have suggested that antiphospholipid antibo dies decreased placental hormone production and trophoblast intercellular f usion and invasion, suggesting that many of the obstetric complications obs erved in the syndrome may be due to antiphospholipid antibody-induced troph oblast dysfunction, However, the complex antigens on the trophoblast surfac es 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 h eparin, together with low-dose aspirin, has replaced prednisone for treatme nt of pregnant women. Maternal treatment and careful monitoring of fetal we ll-being are mandatory in the management of these high-risk pregnancies.