Abstract OBJECTIVE: Insulin-like grouth factor-1 (IGF-1) is polypetide hormone that has demonstrated effects on neural cells. Up to now, there is few reports about the relation between serum IGF-1 and brain damage in neonates with hyperbilirubinemia. This study explored the potential role of serum IGF-1 in neonatal hyperbilirubinemia. METHODS: Serum levels of IGF-1 were measured using ECLIA in 57 term neonates with hyperbilirubinemia and 25 normal term neonates. Meanwhile, total serum bilirubin (TSB), unconjugated bilirubin (USB) and serum albumin (ALB) contents were measured by the automatic biochemistry analyzer and the ratio of USB/ALB (B/A) was calculated. The hyperbilirubinemia group was classified into three subgroups based on serum TSB levels: mild (221-256 μmol/L), moderate (257-342 μmol/L) and severe (>342 μmol/L). Serum TSB levels in the 25 normal neonates were less than 85 μmol/L (control group). NBNA was performed on the day of serum sample collection. RESULTS: Serum IGF-1 levels in the mild, moderate and severe hyperbilirubinemia groups (39.38±8.42, 30.77±4.65 and 26.34±2.05 ng/L, respectively) were obviously lower than those in the control group (50.16±15.73 ng/L) (P<0.01). There were significant differences among the three hyperbilirubinemia subgroups in serum IGF-1 levels (P<0.01). Mean NBNA scores in the mild, moderate and severe hyperbilirubinemia groups (35.01±2.26, 32.45±2.74 and 26.77±5.02, respectively) were significantly lower than those in the control group (38.24±0.78) (P<0.01). Significant differences in the NBNA scores were noted among the three hyperbilirubinemia subgroups (P<0.01). Serum IGF-1 levels were positively correlated to NBNA scores (r=0.603, P<0.01) and negatively correlated to the ratio of B/A (r=-0.483, P<0.01). CONCLUSIONS: Serum IGF-1 levels decreased obviously in neonates with hyperbilirubinemia and correlated to the severity of disease. IGF-1 might be associated with bilirubin-induced brain damage.[Chin J Contemp Pediatr, 2009, 11 (5):357-360]
LIU Fang,TU Wei-Qi,SONG Xia et al. Serum levels of insulin-like growth factor-1 in neonates with hyperbilirubinemia[J]. 中国当代儿科杂志, 2009, 11(05): 357-360.
LIU Fang,TU Wei-Qi,SONG Xia et al. Serum levels of insulin-like growth factor-1 in neonates with hyperbilirubinemia[J]. CJCP, 2009, 11(05): 357-360.
[5]Guan J, Skinner SJ, Beilharz EJ. The movement of IGF-1 into the brain parenchyma after hypoxic-ischaemic injury[J]. Neuroreport, 1996, 7(2):632-636.
[6]Lesort M, Johnson GV. Insulin-like growth factor-1 and insulin mediate transient site-selective increases in tau phosphorylation in primary cortical neurons[J]. Neuroscience, 2000, 99(2):305-316.
[7]Guan J, Beilharz EJ, Skinner SJ, Williams CE, Gluckman PD. Intracerebral transportation and cellular localisation of insulin-like growth factor-1 following central administration to rats with hypoxic-ischemic brain injury[J]. Brain Res, 2000, 853(2):163-173.
[8]Brywe KG, Mallard C, Gustavsson M, Hedtjarn M, Leverin AL, Wang X, et al. IGF-I neuroprotection in the immature brain after hypoxia-ischemia, involvement of Akt and GSK3beta?[J]. Eur J Neurosci, 2005, 21(6):1489-1502.
[9]Wood TL, Loladze V, Altieri S, Gangoli N, Levison SW, Brywe KG, et al. Delayed IGF-1 administration rescues oligodendrocyte progenitors from glutamate-induced cell death and hypoxic-ischemic brain damage[J]. Dev Neurosci, 2007, 29(4-5):302310.
[11]Wennberg RP, Ahlfors CE, Bhutani VK, Johnson LH, Shapiro SM.Toward understanding kernicterus:a challenge to improve the management of jaundiced newborns[J].Pediatrics, 2006, 117(2): 474-485.