Abstract

Jaundice in newborns provides a different response from the parents whencompared to jaundice in older children and adults. 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.In Neonatal hyperbilirubinemia (NHB) the total bilirubin level is greater than 15mg/dL in 15 day or less old neonates and 2mg/dL in neonates above 15 days of age. Estimation of total bilirubin is preferred in the routine analyses for NHB compared to measurement of direct bilirubin. If certain conditions like sepsis, hepatic infections and other liver diseasesare present it may be prudent to use direct bilirubin measurement. Yet 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 toscavenge 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. Therefore bilirubin metabolism and its understanding may help improve its diagnosis and prognosis.

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