Neonatal Jaundice: A Disorder of Transition or an Adaptive Process?

Abstract

Physiologic hyperbilirubinemia occurs commonly in term newborn infants in the absence of any underlying pathologic cause. Yet, the jaundice itself is commonly regarded as a problem in the transition to extrauterine life. Contrary to the usual assumption of pathology, there are several lines of evidence supporting an adaptive role for neonatal hyperbilirubinemia. First, experimental and clinical evidence indicate that neonatal enzyme systems are not yet mature at birth; bilirubin has been demonstrated to scavenge potentially toxic oxygen free radicals that in later life are removed by the mature antioxidant enzyme system. Second, presence of bilirubin in mammals, similar patterns of expression of neonatal hyperbilirubinemia in nonhuman primates, and significant interpopulation variation in newborn serum bilirubin levels among humans all suggest that bilirubin production, metabolism, and excretion are under genetic control. Thus, subject to selective pressure, this condition would not be maintained if deleterious.