The presence of aPL has been clearly shown to have an adverse effect on pregnancy outcome. These effects may be apparent in the first trimester, presenting as recurrent pregnancy loss, or may be associated with the later development of PET, IUGR, placental abruption, pre-term delivery, and intrauterine death. What appear to be most important in the aetiology, initially, are factors that disturb the vital interaction between the embryonic trophoblastic tissue and the host (maternal) endometrial tissue. It seems that the presence of aPL may impair trophoblastic invasion, thus interfering with implantation and subsequent placental development. As the pregnancy advances, women are more prone to thrombosis in the uteroplacental vasculature. Indeed, women with PAPS suffer from a live birth rate as low as 10% in the absence of pharmacological intervention.
Dramatic improvements in pregnancy outcome can be achieved by a combination of aspirin and heparin. However, although the live birth rate is increased sevenfold, it should be acknowledged that these births are associated with an increased rate of prematurity and possible neonatal complications. The increased incidence of pregnancy-related complications necessitates the need for careful antenatal surveillance, and for delivery to be conducted in a unit with facilities for operative delivery and neonatal intensive care. For the women themselves, the significance of aPL outside pregnancy is far from clear, and the ideal management for optimising long-term health is yet to be determined.
