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Why does the Rh factor react with the fetus and cause hydrops fetalis?

Q: Why do other blood group antigens like A, O, AB and B from the mother side not react with the fetus and why does only the Rh factor react with fetus and cause hydrops fetalis? Is it concerned with their permeability through the placenta?

A:The ABO blood group antibodies are naturally occurrring i.e. persons who have blood group A have anti-B antibodies, group B anti-A antibodies, group O both anti-A and anti-B antibodies and group AB individuals no antibodies. As the mother's serum contains antibodies against the ABO blood group red cells of the fetus, fetal red cells are destroyed in the maternal circulation before Rh sensitization can proceed to a significant extent. Thus feto-maternal ABO incompatibility is rarer, though by no means absent. Hemolysis associated with ABO incompatibility is limited to type O mothers with fetuses who have type A or B blood. In mothers with type A and B blood, naturally occurring antibodies are of IgM class, which do not cross the placenta, whereas in type O mothers, the antibodies are predominantly IgG in nature. Because A and B antigens are widely expressed in a variety of tissues besides RBCs, only small portion of antibodies crossing the placenta is available to bind to fetal RBCs. In addition, fetal RBCs appear to have less surface expression of A or B antigen, resulting in few reactive sites—hence the low incidence of significant hemolysis in affected neonates. Unlike ABO system, the Rh system antibodies are not naturally occurring and an Rh negative individual when exposed to the Rh antigen forms these antibodies. Rh incompatibility is a condition that occurs when a woman of Rh-negative blood type is exposed to Rh-positive red blood cells and subsequently develops Rh antibodies. Although the Rh blood group system consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic and hence is most commonly involved in Rh incompatibility. This can occur by 2 main mechanisms - a) when an Rh-negative mother is exposed to Rh-positive fetal red cells secondary to fetomaternal hemorrhage during the course of pregnancy (spontaneous or induced abortion, trauma, invasive obstetrical procedures, delivery etc.) and b) when an Rh-negative individual receives a blood transfusion that contains Rh antigens. Procedures such as amniocentesis, chorionic villus sampling, and cordocentesis also increase the risk of alloimmunization. Because in most pregnancies the transplacental hemorrhage is less than 0.1 mL, most women are sensitized as a result of small undetectable fetomaternal hemorrhage. Once produced, maternal Rh immunoglobulin G (IgG) antibodies can freely cross the placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-positive fetal red cells. These are eventually destroyed, resulting in a fetal hemolytic anemia (anemia due to destruction of red cells). The infant born to an alloimmunized mother shows clinical signs based on severity of the disease. The typical diagnostic findings are jaundice, pallor, hepatosplenomegaly, and hydrops fetalis in severe cases.


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