Isoagglutinins Associated With Abo Erythroblastosis*

The occurrence and severity of erythroblasto-sis fetalis, due to maternal Rh isoimmunization, can be predicted through simple prenatal sero-logical tests (1, 2). If Rh isoagglutinins are pres-ent in maternal serum, and if the incompatible Rh antigen is transmitted from the father, the new-born will have hemolytic disease, the severity of which is often proportional to the titer of the mother's serum Rh isoagglutinins (1, 2). In the event that the isoimmunized Rh negative mother delivers an Rh negative infant, the titer of Rh antibodies in the cord serum, except for saline agglutinins, is generally equal to the titer obtained in the maternal serum (3). For practical pur-poses, almost all maternal Rh isoagglutinins seem to cross the placental barrier freely, and their titration value affords guidance toward the ef-fective management of hemolytic disease of the newborn. This has not been the case for erythro-blastosis fetalis due to ABO incompatibility (1, 2). ABO erythroblastosis of sufficient severity to warrant exchange transfusion therapy for the con-trol of hyperbilirubinemia, has a frequency equal to that of erythroblastosis due to Rh incompati-bility (2, 4), and yet prenatal tests have been of little value thus far in identifying those mothers who may deliver affected infants (4). Since ABO erythroblastosis occurs often in the first incom-patible pregnancy (5, 6), a reliable prenatal test would be of extreme importance in anticipating the occurrence of this disease for intelligent management. A varying proportion of maternal anti-A (a) and anti-B (,/) isoagglutinins can be demonstrated in the serum of the newborn (7, 8). Most ABO isoagglutinins cannot cross the placenta and there-fore play no role in the pathogenesis of erythro-