Abstract
THE plasma of the human infant at birth contains a concentration of bilirubin that on the average considerably exceeds the figures for normal adults; the concentration increases rapidly after birth to reach a peak at two to five days and thereafter slowly decreases.1 2 3 4 It is believed that the hyperbilirubinemia occurs because of a relative lack of glucuronyl transferase activity in the liver5 6 7 or inhibition of this enzyme.8 In many premature infants and some full-term infants this hyperbilirubinemia can reach levels comparable to those in cases of blood incompatibility.3 , 4 Exchange transfusion in the treatment of hemolytic disease due to Rh or . . .
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