Rh disease
HDFN due to anti-D antibodies is the proper and currently used name for this disease as the Rh blood group system actually has more than 50 antigens and not only the D-antigen.
During pregnancy, there is normally a barrier between maternal and fetal blood called the placenta, a temporary organ that connects a mother’s uterus to the umbilical cord to provide nutrients and oxygen to the fetus.
The fetal spleen and liver then begin to break down those red blood cells, thinking that they are a foreign invader when in reality they are they are just mismatched.
Approximately 50% of Rh-D positive infants with circulating anti-D are either unaffected or only mildly affected requiring no treatment at all and only monitoring.
[citation needed] In the United States, it is a standard of care to test all expecting mothers for the presence or absence of the RhD protein on their RBCs.
In addition, there is more widespread use of molecular techniques to avoid missing women who appear to be Rh-D positive but are actually missing portions of the protein or have hybrid genes creating altered expression of the protein and still at risk of HDFN due to Anti-D.[8][9] Blood is generally drawn from the biological father to help determine fetal antigen status.
[13] The aim of these treatments are to prevent the mother’s immune system from becoming sensitized to the Rh antigen, which reduces the risk of hemolytic disease in future pregnancies.
[15] As medical management advances in this field, it is important that these patients be followed by high risk obstetricians/maternal-fetal medicine, and skilled neonatologists postpartum to ensure the most up to date and appropriate standard of care[citation needed] In 1939 Drs.
Philip Levine and Rufus E. Stetson published their findings about a 25-year-old mother who had a stillborn baby that died of hemolytic disease of the newborn.
This suggested for the first time that a mother could make blood group antibodies because of immune sensitization to her fetus's RBCs as her only previous exposure would be the earlier pregnancy.
In 1960, Ronald Finn, in Liverpool, England proposed that the disease might be prevented by injecting the at-risk mother with an antibody against fetal red blood cells (anti-RhD).
This was first done in the rabbit system, but subsequent human tests at the University of Manitoba conducted under Dr. Pollack's direction confirmed that anti-Rho(D) immune globulin could prevent alloimmunization during pregnancy.
[citation needed] Ms. Marianne Cummins was the first at risk woman to receive a prophylactic injection of anti-Rho(D) immune globulin (RHIG) after its regulatory approval.
In 1980, Cyril Clarke, Ronald Finn, John G. Gorman, Vincent Freda, and William Pollack each received an Albert Lasker Award for Clinical Medical Research for their work on rhesus blood types and the prevention of Rh disease.
