Once these cells attach the baby to the uterus, they form a new cell called the syncytiotrophoblast, which is like a filter cell between the mother's blood and the baby's blood. This cell transports all the nourishment to the baby and removes the waste from the baby's blood so that the mother can eliminate it for her baby. These antibodies also cause the embryo to attach too weakly to the uterus. Women with APAs belong to category 2 of immune disorders. This abnormality can be seen by doing immune pathology of the placental tissue paraffin blocks of the baby that died and miscarried.
Phospholipids are essential for trophoblast growth and development.
Their incidence and titers increase with each successive pregnancy loss when compared to controls. In addition to pregnancy loss, several obstetrical complications are associated with APAs, such as preeclampsia, fetal growth retardation in the second or early third trimester, abnormal fetal heart-rate tracing, abruption of the placenta, bleeding during pregnancy, subchorionic hemorrhages and preterm delivery. We have also found that women who are HLA DQ A1 4.1, and who gestate a fetus of the same phenotype, are at the risk to develop APAs to phospholipid molecules and lose their pregnancy despite of optimal therapy. Each pregnancy that is lost makes the problem worse. A woman effectively vaccinates herself against a successful pregnancy.