Neonatal effects of maternal antiphospholipid syndrome

Curr Rheumatol Rep. 2009 Feb;11(1):70-6. doi: 10.1007/s11926-009-0010-8.

Abstract

Antiphospholipid antibodies (aPL) can impair the physiologic development of a fetus during pregnancy not only by causing thrombosis of the placental vessels, but also by directly binding throphoblast cells and modifying their functions. Consequently, the presence of aPL in pregnant women is linked to an increased rate of pregnancy complications. These include recurrent early miscarriages, late fetal losses, and hypertensive disorders of gestation. In this clinical setting, preeclampsia is usually early and severe and can be complicated by the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome). The close association between aPL and obstetric pathology supports the inclusion of these manifestations in the clinical classification criteria of antiphospholipid syndrome. About 30% of children born to mothers with aPL passively acquire these autoantibodies; fortunately, the occurrence of thrombosis seems extremely rare in these babies. The prospective ongoing studies of children born to antiphospholipid syndrome patients reassure us about their general good health; however, some data suggest that learning difficulties might occur, possibly related to in utero exposure to aPL.

Publication types

  • Review

MeSH terms

  • Adult
  • Animals
  • Antiphospholipid Syndrome / complications*
  • Antiphospholipid Syndrome / immunology
  • Female
  • Follow-Up Studies
  • Humans
  • Infant, Newborn
  • Infant, Newborn, Diseases / etiology*
  • Infant, Newborn, Diseases / immunology
  • Infant, Newborn, Diseases / psychology
  • Learning Disabilities / etiology
  • Learning Disabilities / immunology
  • Learning Disabilities / psychology
  • Maternal-Fetal Exchange
  • Mice
  • Pre-Eclampsia
  • Pregnancy
  • Pregnancy Complications, Hematologic* / immunology
  • Young Adult