{'fraction_non_alphanumeric': 0.04468802698145025, 'fraction_numerical': 0.03372681281618887, 'mean_word_length': 5.118556701030927, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Assessment of Insulin-Like Growth Factor-1 Level in Neonates with Hyperbilirubinemia

Background: 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. Methods: Serum levels of IGF-1 were measured using ELISA in 40 term neonates with hyperbilirubinemia and 21 normal term neonates. Results: 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. Conclusions: 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.