Pathogenesis of Erythroblastosis Fetalis

Abstract

The pathogenesis of erythroblastosis fetalis has been ascribed to the isoimmunization of the mother by the Rh, or, more rarely, by other factors in the blood of the fetus. 1 , 2 According to this concept maternal agglutinins produced in response to this stimulus after passing the placenta, act on the susceptible blood of the fetus, and thus produce the various syndromes known as erythroblastosis fetalis. This theory does not differ in principle from the older concept of “heterospecific pregnancy” 3 based on the 4 blood groups. Thus, if the property A or B in the fetus is not present in the mother, the maternal agglutinin by its action on the fetal blood was thought to induce icturus gravis, (one of the manifestations of erythroblastosis fetalis). 4 Recently it was shown by Jonsson, 5 and confirmed by Levine, 6 that in the example cited the mother's normal agglutinins may be specifically increased in titer as a result of isoimmunization.

Nevertheless, the theory of heterospecific pregnancy was abandoned because of lack of evidence. 7 Furthermore, the demonstration that the factors A and B are present, also, in tissue cells and body fluids indicate that maternal isoantibodies are specifically inactivated after passing the placenta. However, this wide distribution of the A and B blood factors applies only to about 80% of individuals (secretors) and in the remainder (non-secretors) the A and B substances are presumably limited to red blood cells. 8 , 9 , 10

These facts suggested experiments to determine whether the Rh factor is also present in tissue cells or in body fluids. The tests were carried out with saliva because of its high concentration of the A and B substances.