Unraveling complexity: A case report on ABO hemolytic disease of the fetus newborn in a preterm neonate and delayed hemolytic transfusion reaction in the beta thalassemic mother due to alloanti kidd a antibody

ABO hemolytic disease of the fetus and newborn (HDFN) generally occurs due to transplacental passage of maternal IgG ABO antibodies causing fetal and newborn red cell hemolysis. Preterm, premature neonates born to O blood group mothers with a high titer of anti-A and/or anti-B antibodies are more prone to developing ABO HDFN. This is a case of ABO HDFN in a preterm, premature, and low birth weight B-positive baby of an O-positive, HbE-beta thalassemic mother. The mother had a very high titer of anti-B antibodies, leading to ABO HDFN. The mother was also allo-immunized with anti-Jk (a) antibodies from past packed red blood cell (PRBC) transfusions she received for thalassemia. This anti-Jk (a) antibody was not detected in the antenatal period, probably due to the low titer of the antibody. The mother had an anamnestic response to the PRBCs provided in the antenatal period, and thus, the anti-Jk (a) became identifiable during the pretransfusion workup for the baby. Even if the baby was Jk (a) antigen positive, the baby developed HDFN mostly due to ABO incompatibility. The baby was managed with a double-volume exchange transfusion with reconstituted whole blood and phototherapy. During the postnatal period, the mother developed a delayed hemolytic transfusion reaction (DHTR) due to the anti-Jk (a) antibodies, as she had received Jk (a) antigen-positive PRBC transfusions in the antenatal period. Later, the mother responded well to the Jk (a) antigen-negative PRBC transfusions and conservative management for the DHTR.