目的 了解高胆红素血症患儿血清谷氨酸（GLU）含量与Na+-K+-ATP酶活性的变化，为早期诊断脑损伤，判断预后提供依据。方法 91例高胆红素血症足月儿为高胆组（按照胆红素水平分为轻、中、重度3组），健康新生儿32例为对照组，比较两组血清谷氨酸含量与Na+-K+-ATP酶活性，并进行相关性分析；随访患儿有无听力损害和神经系统异常。结果 高胆红素血症患儿血清GLU含量(61.34±11.40) μmol/L，Na+-K+-ATP酶活性(0.212±0.026) μmolPi/（mg·h），中、重度组GLU含量明显升高，Na+-K+-ATP酶活性明显降低，与血清总胆红素水平存在密切相关，且与对照组比较，差异有统计学意义（P<0.01）；中、重度组TEOAE初筛，AABR初、复筛未通过例数明显增多。结论 高胆红素血症患儿血清GLU含量升高，Na+-K+-ATP酶活性降低，与胆红素神经毒性有关，可能对早期预测新生儿胆红素脑病患病风险有帮助。
Abstract
Objective To study the changes and clinical significance of serum glutamate concentrations and Na+-K+-ATPase activities in newborns with hyperbilirubinaemia. Methods Ninety-one newborns with hyperbilirubinaemia in varying severity and 32 controls were recruited in this study; their serum glutamate concentrations and Na+-K+-ATPase activities were detected using Beckman amino acid analyzer and colorimetry. At one time,they received hearing test and later interview. Results Serum glutamate concentrations and Na+-K+-ATPase activities were (61.34±11.40) μmol/L and (0.212±0.026) μmolPi/（mg·h）, respectively, in newborns with hyperbilirubinaemia, significautly different from those in controls（P<0.01）,and the changes of them were closely related to total bilirubin level. The incidence of hearing disorder also increased in high bilirubin neonates.Conclusions High glutamate level and low Na+-K+-ATPase activities in newborns with hyperbilirubinaemia are possibly closely related to toxicity of bilirubin, the changes of them are likely to predict early the risk of brain disease in newborns with hyperbilirubinaemia.
关键词
高胆红素血症 /
谷氨酸 /
Na+-K+-ATP酶 /
新生儿
Key words
hyperbilirubinaemia /
glutamate /
Na+-K+-ATPase /
newborns
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参考文献
［1］ 何俊英.血清神经元特异性烯醇化酶与S100BB蛋白在新生儿高胆红素血症中的应用［J］.中国卫生检验杂志,2009,19(6):1355-1356.
［2］ 张春雨,韩宏梅,戈清凤.缺氧缺血性脑病患儿血清谷氨酸水平动态变化及意义［J］.中国实用医药,2010,5(2):3-4.
［3］ 陈雪英, 孙碧云,邓晓凤,等. 肺性脑病患者血浆神经肽的变化及Na+-K+-ATP酶活性、血钙水平检测的临床意义［J］.中国老年学杂志,2008,28(8):783-785.
［4］ 邵肖梅,叶鸿瑁,丘小汕.实用新生儿学［M］.第4版. 北京：人民卫生出版社,2011：273-274.
［5］ Shapiro S M. Bilirubin toxicity in the developing nervous system［J］.Pediatr Neurol,2003,29(5):410-421.
［6］ Richard D, Findlay H, William T, et al. Surfactant replacement therapy for meconium aspiration syndrome ［J］.Pediatrics,1996, 97(1):48-52.
［7］ Sandra L,Silva A R,Vaz M J, et al . Neuritic growth impairment and cell death by unconjugated bilirubin is mediated by NO and glutamate, modulated by microglia, and prevented by glycoursodeoxycholic acid and interleukin-10 ［J］. Neuropharmacology, 2012,62(7):2398-2408.
［8］ 董 惠,李 彬,郭 芳,等. Na+-K+-ATP酶在大鼠皮质神经元缺氧性损伤中的作用［J］. 第二军医大学学报, 2008, 29(2):171-176.
［9］ 何斯纯, 刘文勤, 周丽丽,等. 高胆红素血症大鼠脑干听觉诱发电位与脑组织NO含量及Na+-K+-ATP酶活性的变化［J］. 中国病理生理杂志, 2008, 24(6):1101-1105.
［10］ Amit Y, Cashore W, Schiff D. Studies of bilirubin toxicity at the synaptosome and cellular levels［J］. Scm in Perinatiol, 1992, 16(2):186-190.
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