Hemolytic disease of the newborn (anti-Rhc)
|HDN due to anti-Rhc alloimmunization|
|Classification and external resources|
|NCI||Hemolytic disease of the newborn (anti-Rhc)|
|Patient UK||Hemolytic disease of the newborn (anti-Rhc)|
Hemolytic disease of the newborn (anti-Rhc) can range from a mild to a severe disease. It is the third most common cause of severe HDN. Rh disease is the most common and hemolytic disease of the newborn (anti-Kell) is the second most common cause of severe HDN.
It occurs more commonly in women who are Rh D negative.
A Rhc negative mother can become sensitised by red blood cell (RBC) Rhc antigens by her first pregnancy with a Rhc positive fetus. The mother can make IgG anti-Rhc antibodies, which are able to pass through the placenta and enter the fetal circulation. If the fetus is Rhc positive alloimmune hemolysis can occur leading to HDN. This is similar as for Rh disease, which is usually caused when a RhD negative mother is sensitised by her first pregnancy with a RhD positive fetus.
Sensitization to Rhc antigens can also be caused by blood transfusion.
It has been suggested that women of child bearing age or young girls should not be given a transfusion with Rhc positive blood (or Kell 1 positive blood for similar reasons). This would require a lot of extra work in blood transfusion departments and it is considered not economical to do the blood group screening at the present time.
It is theoretically likely that IgG anti-Rhc antibody injections would prevent sensitization to RBC surface Rhc antigens in a similar way that IgG anti-D antibodies (Rho(D) Immune Globulin) are used to prevent Rh disease, but the methods for IgG anti-Rhc antibodies have not been developed at the present time.
It can be detected by routine antenatal antibody screening blood tests (indirect Coombs test) in a similar way to Rh disease. The treatment of hemolytic disease of the newborn (anti-Rhc) is similar to the management of Rh disease.
- Mollison PL, Engelfriet CP and Contreras M. Blood Transfusion in Clinical Medicine. 1997. 10th edition. Blackwell Science, Oxford, UK.
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