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Management of Pregnancy with ABO Incompatibility

Sep 2011 – by M. Mennuti, MD

ABO incompatibility is the most common maternal-fetal blood group incompatibility and the most common cause of hemolytic disease of the newborn (HDN). ABO incompatibility is more often seen in newborns who have type A blood because of the higher frequency of type A compared to type B in most populations. ABO incompatibility in the newborn generally presents as neonatal jaundice due to a Coombs positive hemolytic anemia and occurs in 0.5-1% of newborns. In contrast to the severe intrauterine or neonatal hemolytic anemia that is associated with Rh sensitization, clinically important neonatal anemia due to ABO incompatibility occurs infrequently. The major clinical issue with HDN due to ABO incompatibility is jaundice.

Several reasons have been proposed to account for lack of intrauterine hemolysis due to ABO incompatibility. These include less well developed A and B antigens on fetal red blood cells to stimulate maternal antibody production, and the ubiquitous distribution of A and B antigens in other tissues resulting in fewer antibodies that cross the placenta binding to antigens on fetal red cells. However, the most important reason that ABO incompatibility does not cause hydrops fetalis is that naturally occurring anti-A and anti-B antibodies are IgM and thus do not cross the placenta.

It is estimated that <1% of type-O mothers have clinically significant anti-A or anti-B antibody which is IgG. ABO incompatibility with transplacental transfer of IgG anti-A antibody, or more commonly, anti-B antibody has rarely been reported to cause intrauterine hemolysis leading to hydrops fetalis. It should be noted that other causes of nonimmune hydrops fetalis have not been systematically excluded in these case reports. The most likely explanation for these rare cases is that exposure to antigens similar to the A or B antigen may occur from sources other than the fetus and stimulates IgG production in the mother. For example, an antigen similar to the B antigen is found in E.coli, and exposure to this organism may stimulate production of IgG anti-B antibody in type O individuals.

In contrast to Rh incompatibility which tends to become more severe with each subsequent Rh positive pregnancy, ABO incompatibility does not demonstrate any consistent pattern. Thus, the patient's first offspring may have clinically important hemolytic disease of the newborn due to ABO incompatibility, while subsequent newborns may be unaffected or very mildly affected. Because of the rarity of severe intrauterine hemolysis due to ABO incompatibility, assessment for intrauterine fetal anemia is not recommended based on the mother having type O blood. Measurement of IgG anti-A and anti-B antibody may be considered part of the evaluation of unexplained signs of fetal anemia such as ascites or hydrops when the mother is type O. Collecting a cord blood sample at birth for blood type and direct antibody testing should be considered when the mother is type O, when and a previous child had hemolytic disease of the newborn due to ABO incompatibility.

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