STUDIES ON PHYSIOLOGIC HYPERBILIRUBINEMIA OF NEGRO AND WHITE PREMATURE INFANTS

Abstract

Serial determinations of the concentration of bilirubin in the plasma were obtained with 39 premature infants commencing with cord blood in 18 cases. The group consisted of 25 Negro infants and 14 white infants. Concentrations in the plasma were followed until the level fell below 2 mg/100 ml. The hyperbilirubinemia exhibited by these prematures appeared to be due to so-called "physiologic processes" as all procedures to establish other causes were uniformly negative. A definite inverse relationship between the degree of bilirubinemia and the maturity of the infant was shown in both white and Negro infants. Statistical significance was demonstrated when the mean peak concentrations of bilirubin in the plasma of the least mature infants were compared with those of the most mature infants, within each racial group. There was a statistically significant difference between the concentrations of bilirubin in the plasma reached in the two racial groups in the most immature infants. The concentrations were lower in the Negro group. A similar trend was present in the more mature infants, but this was not statistically significant. These findings agree with the fact that the Negro infant is a more mature baby than a white child of the same weight. They also lend support to the thesis that the degree of bilirubinemia is a reflection of the functional maturity of the infant. The possible causes of physiologic hyperbilirubinemia in full-term and premature infants were discussed. Several fields for experimental research are still unexplored. The role of the excretory capacity of the liver, particularly the functional activity of glucuronyl transferase, appears to be preeminent in the etiology of neonatal bilirubinemia. The sudden changes in the dynamics of hepatic blood flow which occur at birth may account, in part at least, for the hepatic immaturity. That the premature infant can develop kernicterus in the presence of hyperbilirubinemia without evidence of isoimmunization is becoming more generally accepted. The incidence of kernicterus in this hospital and in this study is quite low. The possible role of racial groups and administration of vitamin K in this regard was discussed. The bulk of the evidence indicates that premature infants exhibit jaundice and hyperbilirubinemia more frequently and to a greater degree than is reported in full-term infants. The duration of this hyperbilirubinemia is related to fetal maturity, persisting longer in the most immature infants. Because of the variability of concentrations of bilirubin in the plasma of premature infants, and because of the multitude of factors that play a possible role in determining the ultimate concentration of bilirubin, routine exchange transfusion for elevated concentrations of bilirubin does not seem warranted. The critical level over which exchange transfusion should be done cannot be stated on the basis of any available data.