Fetal anemia due to non-Rhesus-D red-cell alloimmunization

Abstract

Although anti-RhD was once the major etiology of hemolytic disease of the fetus/newborn (HDFN), the widespread adoption of antenatal and postpartum Rhesus immune globulin has resulted in a marked decrease in the prevalence of alloimmunization to the RhD antigen in pregnancy. Maternal alloimmunization to other red cell antigens continues to play a role as the cause of fetal disease since no prophylactic immune globulins are available to prevent the formation of these antibodies. An increasing incidence of the Kell (anti-K1) antibody has been noted in the United States. Guidelines for intervention in cases of irregular red cell antibodies are limited by the bias of anecdotal reports in the literature in favor of severe cases of HFDN. Although most diagnostic protocols used in the management of the RhD-alloimmunized pregnancy can be applied in cases of non-RhD sensitization, Kell (K1 and K2) alloimmunization should be managed more conservatively.