    Volume 1, Issue 3, Fall 2011 xx             !   " # $ ! %  ! # $ ! &             ! !"  #  $    %   Address correspondence: Abeer Fathy, PhD Department of Pediatrics, Mansoura University Mansoura, Egypt E-mail: abeerfathy2000@yahoo.com  !’ The authors have nothing to disclose. ($)"*) (+,’ Kernicterus, or bilirubin encephalopathy, is a condition caused by bilirubin toxicity to the basal ganglia and various brainstem nuclei. Neither the cellular nor molecular mechanisms underlying bilirubin neurotoxicity are well understood. Insulin-like growth factor-1 (IGF-1) is a polypetide hormone that has demonstrated effects on neural cells. The aim of this study is to find out the potential role of serum IGF-1 in neonatal hyperbilirubinemia. -,’ Serum levels of IGF-1 were measured using ELISA in 40 term neonates with hyperbilirubinemia and 21 normal term neonates. "’ Serum IGF-1 level in the hyperbilirubinemia group (50.95± 12.26ng/L) was significantly lower than that in the control group (74.81±14.17 ng/L) (P<0.05). Serum IGF-1 levels were negatively correlated to the bilirubin level (r=-0.978, P: 0.000) in the hyperbilirubinemic group. *’ Serum IGF-1 levels decreased in neonates with hyperbilirubinemia and this reduction correlated with the degree of hyperbilirubinemia. IGF-1 might have a protective effect against bilirubin-induced brain damage. . /,’ hyperbilirubinemia, IGF-1, kernicterus, neonatal jaundice )"0!1*)0 Kernicterus, or bilirubin encephalopathy has been described in the medical literature for over a century. It is caused by bilirubin toxicity to the basal ganglia and various brainstem nuclei; however, neither the cellular nor molecular mechanisms underlying bilirubin neurotoxicity are well understood. 1 Evidence from in vitro studies suggests that bilirubin impairs mitochondrial function and viability of astrocytes. Higher concentrations impair mitochondrial function and cellular proliferation in neurons, and it can induce apoptosis. 2 Bilirubin also interferes with intracellular calcium homeostasis through several mechanisms and it may sensitize the cell to other injuries, and may cause neuronal hyperexcitability via excitatory amino-acid neurotoxicity. 3-6 Different factors are important determinants of bilirubin toxicity