erythroblastosis fetalis ərĭth˝rəblăstō´sĭs [key], hemolytic disease of a newborn infant caused by blood group incompatibility between mother and child. Although the Rh factor is responsible for the most severe cases of erythroblastosis fetalis, the disease may be produced by any of the other blood group antigens, such as those of the AOB system. With an Rh-negative mother and an Rh-positive father, the possibility exists that the fetus will be Rh positive. Microhemorrhages during gestation permit fetal red blood cells to enter the maternal circulation, causing an immunologic reaction that leads to sensitization of the mother against the Rh factor. Maternal antibodies against fetal red blood cell antigens pass through the placenta into the fetus, where an excessive destruction of fetal red blood cells occurs. When such hemolysis begins during pregnancy, stillbirth may result. While there is little danger of damage to the fetus during the first pregnancy, by the second pregnancy sufficient antibodies will have accumulated in the mother's bloodstream to cause increasing danger of hemolytic disease. The formation of maternal anti-Rh antibodies has been largely prevented in the United States by the injection of human immune globulin into the mother within 72 hours after delivery. This globulin contains antibodies against the Rh-positive fetal red blood cells, destroying them before the maternal bloodstream reacts by producing its own anti-Rh antibodies. Thus during the next pregnancy there will be few, if any, antibodies in the maternal bloodstream to destroy the fetal Rh-positive blood cells.
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