What is the reason for blood incompatibility between me and my daughter?
Q: At the beginning of my second pregnancy, I was told that I have anti-Ce antibodies. I have never had a blood transfusion, so the doctors believe that during my first pregnancy some how my daughter's blood came in contact with mine due to which I have these antibodies. During my 2nd pregnancy my titres were tested and the highest were 4:1 at 38 weeks. Since they were fairly low, why did my second daughter get jaundice and now has slight anaemia? How will this affect her later? What is the reason for blood incompatibility when both of us are O positive?
A:There are about 20 known blood group systems that consist of over 200 antigens. Only two of these, however, (the ABO and the Rh) can commonly cause haemolytic transfusion reaction (HTR) as well as haemolytic disease of the newborn (HDN). Several other systems (Kell, Duffy, Kidd) can occasionally lead to HTR and HDN while two other systems (P and MN) very rarely cause HTR and HDN. The Lutheran and Lewis systems rarely cause HTR but not HDN. The Rh system is the second most important blood group system after the ABO and the Rh antigens are highly immunogenic (i.e. induce antibody production) and thus are frequently associated with HTR and HDN. Two closely linked genes on the short arm of chromosome 1 - the RHD gene that encodes the D antigen and the RHCE gene encoding the Cc and Ee antigens are involved. HDN results from the passage of Ig (antibodies) from the mother’s circulation across the placenta into the circulation of the developing baby where they react with red cells and mediate their destruction. Anti-D antibodies used to be responsible for majority of cases of HDN leading either to intrauterine death or to the birth of severely affected child. This has dramatically declined following successful prophylaxis of the HDN due to anti-D antibodies. Most cases are now due to immune anti-A antibodies produced in a group O mother, to anti-c and anti-E antibodies and to antibodies to other blood group systems (e.g. anti-Kell). Sensitisation of a D mother with D fetal red blood cells occurs typically at birth when fetal D cells cross into the maternal circulation. Sensitisation can also occur as a result of a previous miscarriage, amniocentesis and blood transfusion and is more likely if mother and foetus are ABO compatible. In a subsequent pregnancy, entry of even a few fetal red blood cells into the maternal circulation induces a secondary anti-D response and such antibodies can cross the placenta and bind red blood cells. The clinical features of HDN depend on the titre (levels) and affinity of maternal anti-D antibodies. In severe cases intrauterine death occurs from hydrops fetalis; in milder cases the foetus is born live with severe anaemia, jaundice, oedema and hepatosplenomegaly. Diagnosis is by the presence of erythroblasts, high reticulocyte count and a positive direct antiglobulin test (DAT) in cord blood and a positive indirect antiglobulin test (IAT) in maternal blood. Pregnant d mothers should have regular indirect antiglobulin tests. As a guide anti-D antibody levels < 0.2 mg/ml require no action while higher levels require action; levels > 2.0 mg/ml typically are associated with severe disease. Prevention of HDN is now carried out with anti-D Ig (intramuscular within 72 hours of delivery) in all d mothers giving birth to a D child. A Kleihauer test for fetal haemoglobin can be used as a guide for the dose of anti-D Ig to be administered.