A patient with acute leukemia who typed as AintB received 10 packs of platelets of group 0. Subsequent transfusion of A1B blood resulted in a hemolytic transfusion reaction. Anti-A1 was detected in the serum and on the red blood cells of a post-transfusion sample. This anti-A1 reacted with the transfused A1B red blood cells and other A1 cells, but not with the patient's pretransfusion red blood cells. The plasma of the transfused platelet concentrates had a high titer of immune anti-A.
A serologically typical group A2B mother with no unusual anti-A or anti-B agglutinins delivered a normal group O infant with no demonstrable A or B antigens. By the age of 1 year the child had developed anti-A and anti-B agglutinins. He had H antigen and secreted H substance in his saliva. A second group O child has since been born. Although family studies were inconclusive, the most likely explanation is that the mother is a cis-AB. If this is the case, she differs from other reported cis-ABs in her apparently normal B antigen and the lack of anti-B antibodies in her serum.
An anti‐Lub antibody with a titer of 128 to 256 was found in a pregnant woman. The antibody was IgG of the IgG1 subclass. Two newborns of successive pregnancies were free of clinical hemolytic disease of the newborn. The failure of this antibody to cause clinical hemolytic disease is ascribed to the weak expression of the Lub antigen on cord red blood cells.
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