Abstract
The etiology of ABO hemolytic disease of the newborn is complex because of the natural presence of anti-A and/or anti-B in individuals who do not possess the A and/or B antigen. Although only IgG anti-A and anti-B can cross the placenta, these antibodies are found in the circulation of most newborn infants born to blood group O mothers. The A and B antigens are much weaker on the red blood cell of newborn infants than of adults. This relatively weak reactivity constitutes a major protective factor against maternal antibodies which have crossed the placental barrier. However, much variation was found in the strength or the reactivity of the A antigen among infants born at term. This variation was large enough to account for the poor quantitative relationship between maternal antibody levels and the ensuing hemolytic process in the infant. Thus, the variation in antigen strength among newborns constitutes an unpredictable factor in the etiology of ABO hemolytic disease. Infants with a relatively weak A antigen can tolerate a moderately high level of circulatory anti-A without any untoward effects, while in the presence of the same antibody level, infants with a relatively strong A antigen, a portion of the red blood cells will be destroyed.
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