Bilirubin toxicity in the developing nervous system

Bilirubin toxicity in the developing nervous system
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DOI:
10.1016/j.pediatrneurol.2003.09.011
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发表时间:
2003-11-01
影响因子:
3.8
通讯作者:
Shapiro, SM
Shapiro, SM
中科院分区:
医学3区
文献类型:
--
作者:
Shapiro, SM

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尽管最近在黄疸(高胆红素血症)新生儿的护理方面取得了进展,胆红素毒性仍然是一个重大问题。最近报告的经典核黄疸病例激增,部分原因是住院时间提前和高胆红素血症治疗标准的放宽,以及使用基于诱发电位的婴儿测试和听力筛查的高胆红素血症诱导听觉功能障碍的新报告,强调需要更好地了解高胆红素血症如何导致一些婴儿脑损伤,特别是因为这种损伤是可以预防的。在了解胆红素结合和未结合或“游离”未结合胆红素引起的神经毒性方面的最新进展,胆红素如何影响体内和体外中枢神经系统,以及在新生儿中使用新的临床工具,例如磁共振成像显示双侧白球和丘脑下病变,以及内耳功能正常的脑干听觉诱发电位异常。可能导致改善检测和预防胆红素引起的神经功能障碍和损害。最后,人们担心部分或孤立的神经系统后遗症,例如听神经病变和其他中枢听觉处理障碍,可能是由于在神经发育的不同阶段过量和持续暴露于游离、非偶联胆红素所致。(C) 2003年Elsevier Inc.版权所有。
Bilirubin toxicity remains a significant problem despite recent advances in the care of jaundiced (hyperbilirubinemic) neonates. A recent surge in reported cases of classical kernicterus, due in part to earlier hospital discharge and relaxation of treatment criteria for hyperbilirubinemia, and new reports of hyperbilirubinemia-induced auditory dysfunction using evoked potential based infant testing and hearing screening, underscore the need to better understand how hyperbilirubinemia causes brain damage in some infants, especially because the damage is preventable. Recent progress in understanding bilirubin binding and neurotoxicity resulting from unbound or "free" unconjugated bilirubin, how bilirubin affects the central nervous system in vivo and in vitro, and the use of new clinical tools in neonates, for example magnetic resonance imaging revealing bilateral lesions in globus pallidus and subthalamus, and abnormal brainstem auditory evoked potentials with normal inner ear function, may lead to improved detection and prevention of neurologic dysfunction and damage from bilirubin. Finally, the concern is raised that partial or isolated neurologic sequelae, for example auditory neuropathy and other central auditory processing disorders, may result from excessive amount and duration of exposure to free, unconjugated bilirubin at different stages of neurodevelopment. (C) 2003 by Elsevier Inc. All rights reserved.