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锂中毒

Authors
Jeanmarie Perrone, MD, FACMT
Pia Chatterjee, MD
Section Editor
Stephen J Traub, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM
Translators
周亚雄, 主治医师

引言

19世纪后期,“锂盐”矿水第1次被用于治疗躁狂症和痛风。随着时间推移,或许是因为其锂含量较低,“锂盐”矿水最终被锂片取代了。由于片剂中的锂浓度较高,锂相关的震颤和无力变得愈发明显,于是在1898年便有了锂中毒的首次描述[1]。大约半个世纪后,有学者描述了锂治疗10例躁狂症患者的镇静作用[2];在1949年,当氯化锂作为盐的替代品用于心力衰竭患者时,人们发现了锂盐的更多毒性作用[3]。

锂的毒性效应限制了其在临床上的应用,直到后来合适的血清监测变得更加易行。20世纪70年代,碳酸锂在美国被批准用于治疗急性躁狂症和双相情感障碍,并一直沿用至今。2010年,美国毒物控制中心协会共接到了6307例锂中毒事件的报告[4,5]。

本专论将总结急性和慢性锂中毒的诊断和处理。锂的治疗应用、锂治疗的主要副作用以及急性中毒患者处理的其他方面将单独讨论。一张有助于锂中毒紧急处理的总结表提供在此(表 1)。 (参见“成人双相障碍:急性躁狂和轻躁狂的药物治疗”“成人双相障碍:维持治疗”“锂盐的肾毒性”“锂与甲状腺”“成人药物中毒的一般处理方法”)

药理学和细胞毒理学

锂的确切作用机制尚不清楚。它可影响两种细胞内信号通路,肌醇磷酸和糖原合成酶激酶-3[6]。锂可降低细胞内肌醇,这可能是其稳定情绪的机制之一。锂也可抑制糖原合成酶激酶-3,后者是能量代谢、神经保护和神经可塑性所涉及的多种信号通路的一个组成部分。

锂的治疗指标狭窄;有很大一部分长期接受锂治疗的患者都经历了至少1次治疗过程中的毒性发作[7]。脑部和肾脏细胞内的锂浓度最高。

                              

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Literature review current through: 2017-06 . | This topic last updated: 2016-09-29.
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