A HUMAN LIPOPROTEIN POLYMORPHISM

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Abstract
Further studies on the Ag(a) human serum polymorphism, which involves low-density S-lipoprotein components, are presented. Population, family, and twin studies with the hypothesis that the presence of this component, which is identified by a precipitation reaction with the serum of a patient who had received numerous transfusions, is determined by an autosomal, dominantly-transmitted gene designated AgA. Examination of the paired sera of mothers and newborn children leads to the conclusion that the Ag(a) phenotype may not be expressed at birth. Mothers may transmit the lipoprotein across the placenta in some cases, rendering the newborn a phenocopy. From the evidence at hand, the Ag(a+) phenotype can be expressed as early as 57 days after birth. In one of the antibody-forming patients, the slight temperature rise in response to transfusion was independent of the Ag(a) phenotype of the transfused blood. After the discovery of antibody, four of the five antibody-formers continued to receive transfusions with no apparent severe reaction. Study of other transfused individuals has detected four subjects who form precipitins with normal sera. All of these patients received approximately 40 or more transfusions.