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Partial D Phenotype and Hemolytic Disease in Babies
Alloimmune hemolytic disease of the fetus and newborn (HDFN) may occur when a pregnant woman has an antibody against an antigen on the fetal red cells inherited from the father. Many antibodies to red blood cell antigens can cause HDFN, including those from the ABO, Rh, and other blood group systems. Women can develop antibodies either through previous pregnancy or transfusion.
Fatal consequences from this disorder have become rare with the appropriate use of immunoprophylaxis. However, to avoid the fatal consequences of this disorder, prompt recognition and treatment are vital. The risk for HDFN can be identified by testing the mother with an ABO group/Rh and antibody screen during the pregnancy. RhD HDFN can be prevented through passive anti-D administration to suppress the mother’s immune response against the fetal RhD antigen.
Some women may exhibit weak or discrepant results on RhD typing, or current results may differ from historical results. A common type of RhD variant is the weak D phenotype. Women with this phenotype have a weak expression of the RhD antigen and may present with variable RhD typing depending on the antisera or testing method used in the laboratory. Another type of RhD variant is the partial D phenotype where the RhD antigen is altered, potentially allowing an individual to form alloantibodies to the epitopes on RhD-positive red blood cells that are different than their own.
In this podcast episode, we will discuss the types of HDFN, the role that partial D groups, and the presence of anti-D as it relates to its prevalence, prognosis, and management.
About our Speaker:
Dr. Genghis Lopez is a Senior Scientist at the Australian Red Cross Lifeblood in Brisbane, Australia. Genghis received his Ph.D. degree from Griffith University, Australia. At Lifeblood, he worked at the Platelet and Granulocyte Reference Laboratory and Red Cell Reference Laboratory and is now part of the Transfusion Science research team that investigates complex red cell blood group variants. He has published several papers in Vox Sanguinis and Transfusion journals reporting novel red cell antigens, novel blood types, and red cell antibodies including several associated with hemolytic transfusion reactions or hemolytic disease of the fetus and the newborn.
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Alloimmune hemolytic disease of the fetus and newborn (HDFN) may occur when a pregnant woman has an antibody against an antigen on the fetal red cells inherited from the father. Many antibodies to red blood cell antigens can cause HDFN, including those from the ABO, Rh, and other blood group systems. Women can develop antibodies either through previous pregnancy or transfusion.
Fatal consequences from this disorder have become rare with the appropriate use of immunoprophylaxis. However, to avoid the fatal consequences of this disorder, prompt recognition and treatment are vital. The risk for HDFN can be identified by testing the mother with an ABO group/Rh and antibody screen during the pregnancy. RhD HDFN can be prevented through passive anti-D administration to suppress the mother’s immune response against the fetal RhD antigen.
Some women may exhibit weak or discrepant results on RhD typing, or current results may differ from historical results. A common type of RhD variant is the weak D phenotype. Women with this phenotype have a weak expression of the RhD antigen and may present with variable RhD typing depending on the antisera or testing method used in the laboratory. Another type of RhD variant is the partial D phenotype where the RhD antigen is altered, potentially allowing an individual to form alloantibodies to the epitopes on RhD-positive red blood cells that are different than their own.
In this podcast episode, we will discuss the types of HDFN, the role that partial D groups, and the presence of anti-D as it relates to its prevalence, prognosis, and management.
About our Speaker:
Dr. Genghis Lopez is a Senior Scientist at the Australian Red Cross Lifeblood in Brisbane, Australia. Genghis received his Ph.D. degree from Griffith University, Australia. At Lifeblood, he worked at the Platelet and Granulocyte Reference Laboratory and Red Cell Reference Laboratory and is now part of the Transfusion Science research team that investigates complex red cell blood group variants. He has published several papers in Vox Sanguinis and Transfusion journals reporting novel red cell antigens, novel blood types, and red cell antibodies including several associated with hemolytic transfusion reactions or hemolytic disease of the fetus and the newborn.