PEDIATRICS Vol. 10 No. 3 September 1952, pp. 337-347
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Round Table Discussion

ERYTHROBLASTOSIS FETALIS

LOUIS K. DIAMOND M.D., FRED H. ALLEN JR. M.D., DOROTHEA D. VANN M.D., and JOHN RAY POWERS M.D.

Chairman Diamond: Erythroblastosis fetalis is a variable disease, ranging in severity from fetal death in utero to a disturbance so mild as to be unrecognizable except by delicate laboratory tests. Intrauterine death is the greatest source of fetal loss. The development of kernicterus is the most important cause of unfavorable result in untreated liveborn babies. The use of exchange transfusion has resulted in the recovery of most liveborn babies, and has nearly eliminated kernicterus in a clinic where it has been used liberally.

Etiology

Erythroblastosis fetalis occurs as a result of fetal-maternal blood group incompatibility. Table 1 shows the most important blood group factors known at present. In Column I are the common names of the various genetically and serologically independent families or "systems" of blood group [See Table 1 in source pdf] factors. In Column II are shown those factors which may cause transfusion reactions or, presumably, erythroblastosis fetalis (although e, N, and Fya have not yet been reported as causes of erythroblastosis). The blood group factors in Column III seem not to cause clinical difficulties. At least 80% of cases of erythroblastosis fetalis are caused by "Rh" (D) incompatibility. Although D is an effective antigen, as judged by the fact that at least 75% of D-negative ("Rh-negative") individuals are sensitized by transfusion of D-positive blood, only 5% of families in which the mother is D-negative and the father D-positive ever have erythroblastotic babies. A and B, which are presumably even more effective antigens than D. cause less than 20% of the cases of erythroblastosis, although 35% of matings are incompatible for A or B.


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