探讨足月新生儿高未结合胆红素血症血清神经元特异性烯醇化酶(neuron specific enolase, NSE)与γ-谷氨酰转移酶(γ-glutamyl transferase, γ-GT)含量变化及其关系。

选取2009年1月至2010年12月在本院确诊的高未结合胆红素血症足月新生儿60例为研究对象，纳入UCB组。将其按照血清未结合胆红素(unconjugated bilirubin，UCB)水平分为轻度UCB组[(220.6~256.5) μmol/L, n= 22]，中度UCB组[(256.6~342.0) μmol/L，n=30]及重度UCB组(>342.0 μmol/L，n=8)。随机选取同期在本院分娩的正常足月新生儿(血清未结合胆红素<85.5 μmol/L) 30例，纳入对照组(本研究遵循的程序符合本院人体试验委员会所制定的伦理学标准，得到该委员会批准，分组征得受试对象监护人的知情同意，并与之签署临床研究知情同意书)。UCB组及对照组均排除先天畸形、感染、窒息等新生儿。UCB组与对照组，轻度、中度和重度UCB组新生儿性别、孕龄、分娩方式、Apgar评分、出生体重及日龄等比较，差异无显著意义(P>0.05)。采用化学发光免疫分析法测定UCB组和对照组新生儿神经元特异性烯醇化酶含量，采用全自动生化仪测定γ-谷氨酰转移酶含量。

UCB组新生儿血清神经元特异性烯醇化酶平均值为(17.54±4.57)μg/L，γ-谷氨酰转移酶平均值为(108.19±21.53) U/L，均较对照组明显升高[(7.23±1.64) μg/L, (62.02±14.78) U/L]，两组比较，差异有显著意义(P<0.01)。神经元特异性烯醇化酶与γ-谷氨酰转移酶呈正相关(r=0.7832，P<0.001)；γ-谷氨酰转移酶与未结合胆红素水平呈较弱正相关(r=0.2923，P<0.05);神经元特异性烯醇化酶与未结合胆红素水平呈较弱正相关(r=0.3145,P< 0.01)。

神经元特异性烯醇化酶与γ-谷氨酰转移酶可早期敏感判断新生儿高未结合胆红素血症导致的脑损害，可作为对新生儿高未结合胆红素血症临床干预的合理指标。若未开展神经元特异性烯醇化酶检测，γ-谷氨酰转移酶亦不失为其重要参考指标。

To investigate changes of serum neuron specific enolase (NSE) and γ-glutamyl transferase (γ-GT) in full-term neonates with unconjugated hyperbilirubinemia, and explore correlation between neuron specific enolase and γ-glutamyl transferase in full-term neonates with unconjugated hyperbilirubinemia.

From January 2009 to December 2010, 60 full-term neonates with unconjugated hyperbilirubinemia (UCB group) were divided into three groups according to the level of unconjugated bilirubin (UCB), mild UCB group [(220.6~256.5) μmol/L, n=22], moderate UCB group [(256.6~342.0) μmol/L, n = 30] and severe UCB group (>342.0 μmol/L, n=8). Meanwhile, 30 healthy full-term neonates with unconjugated bilirubin level less than 85.5 μmol/L were recruited into control group. Informed consent was obtained from all participates. There were no significant difference between UCB group and control group, also among mild, moderate and severe UCB group in gender, gestational age, mode of delivery, Apgar score, birth weight and day ages of neonate (P>0.05). Serum neuron specific enolase level was determined by chemiluminescence immunoassay (CLIA), and γ-glutamyl transferase were determined by processing biology and chemistry.

Neuron specific enolase level [(17.54 ± 4.57) μg/L] and γ-glutamyl transferase [(108.19 ± 21.53) U/L] in UCB group were obviously higher than those in control group [(7.23 ± 1.64) μg/L, (62.02 ± 14.78) U/L] (P<0.01). By linear correlation analysis, levels of γ-glutamyl transferase were inversely associated with levels of serum neuron specific enolase (r=0.7832, P<0. 001), the correlation between levels of γ-glutamyl transferase, serum neuron specific enolase and unconjugated hyperbilirubinemia were poor (r=0.2923, P<0.05 ; r=0.3145, P<0.05).

Levels of neuron specific enolase and γ-glutamyl transferase may have potential value of estimating bilirubin related brain damage. If neuron specific enolase can not be determined, γ-glutamyl transferase may be as a significant reference index.