Abstract
ERYTHROBLASTOSIS fetalis has long been recognized as a hemolytic disease of unknown origin with varying degrees of anemia and hepatic damage. The historical aspect of the problem has been thoroughly covered by Javert,1 Potter2 and others. The forms manifested by the illness were individually described by many writers, and a relationship between fetal hydrops, icterus gravis and congenital hemolytic anemia of the newborn was assumed in 1932.3 Other unclassified varieties of the syndrome are known to exist.4 Therapy, even before the recent elucidation of the pathogenesis, was directed at correction of the anemia by repeated transfusions. This treatment proved effective in some instances, but in the majority of cases there were severe reactions, with increased hemolysis, fever and death. These reactions are now known to have been caused by the use of Rh-positive blood from random donors, and from the fathers, whose erythrocytes always carried the