Abstract

IN 1941 Levine et al.1 proposed an etiology for erythroblastosis fetalis that required the entrance of fetal red blood cells into the maternal circulation. This requirement then led to the question of whether fetal erythrocytes enter the maternal circulation only in the disease, erythroblastosis fetalis, or do so also in many normal pregnancies. Levine considered the latter view more likely and suggested that the low incidence of erythroblastosis fetalis in relation to the frequency of the combination of Rh-negative mother and Rh-positive fetus was due to low antibody-forming ability on the part of many mothers.2 Others have held that fetomaternal . . .

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