{'fraction_non_alphanumeric': 0.026214833759590793, 'fraction_numerical': 0.0076726342710997444, 'mean_word_length': 5.60337552742616, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Update on HDFN: new information on long-standing controversies

Abstract Hemolytic disease of the fetus and newborn (HDFN) results from maternal IgG antibodies that cross the placenta to the fetal circulation during gestation and cause RBC destruction and complications before birth (HDF), or anemia and hyperbilirubinemia after birth (HDN), or both. In its most severe form, HDF produces hydrops fetalis, which is characterized by total body edema, hepatosplenomegaly, and heart failure and can lead to intrauterine death. Before discovery of Rh immunoglobulin (RhIG), HDFN from anti-D was a significant cause of perinatal mortality or long-term disability. Routine administration of RhIG to D– women during pregnancy and shortly after the birth of D+ infants effectively reduced the incidence of HDFN caused by anti-D. Maternal alloimmunization to other RBC antigens in the Rh, Kell, and other blood group systems can not be routinely prevented and these antibodies can also cause HDFN. Advances in prenatal care, noninvasive monitoring, and intrauterine transfusion have improved the outlook for affected pregnancies to the extent that even hydrops fetalis can be reversed and effectively treated in many cases. This review will provide an update on the current issues in prevention and treatment of HDFN, emphasizing recent insights into long-standing controversies regarding maternal weak D phenotypes and D alloimmunization, noninvasive fetal diagnosis and monitoring of affected pregnancies, and recent treatment guidelines. Immunohematology2006;22:188–195.