一个10岁男孩的慢性多克塞毒性伪装成
James D Whitledge1,2, C James Watson3,4,5, Michele M Burns3,6
1Harvard Medical Toxicology Fellowship, Boston, MA, USA. james.whitledge@childrens.harvard.edu.
概括
慢性多克塞毒性在儿童中很罕见,但可以模仿. 这一案例强调了超治疗剂量,遗传因素 (CYP2D6) 和药物相互作用作为儿童患者不良事件的关键贡献者.
科学领域:
- 儿科药理学 儿科药理学
- 临床毒理学 临床毒理学
- 神经科学是一个神经科学.
背景情况:
- 慢性三环抗抑郁药毒性在儿童群体中很少被记录.
- 诸如困惑,和等症状可能来自于剂量错误,药物代谢的遗传变异 (CYP2C19,CYP2D6) 和同时使用药物.
- 用于失眠和抑郁症的多克西平,最大的非标签儿科剂量为3mg/kg.
研究的目的:
- 报告一个孩子的慢性多克塞毒性病例,模仿.
- 确定潜在的促成因素,包括超治疗剂量,药物基因组变异性和药物相互作用.
主要方法:
- 研究人员分析了一例10岁男孩的病例报告,该男孩表现为混乱,无氧和发作.
- 诊断评估包括心电图 (EKG) 和血清药物水平测量.
- 进行了对CYP2D6的药物遗传测试.
主要成果:
- 患者表现出与多克塞毒性一致的症状,通过血清多克塞-诺德克塞水平升高 (1419 ng/mL) 得到证实.
- 毒性与超治疗性多克西剂量 (4.41 mg/kg),同时使用CYP2D6和CYP2C19抑制剂 (克洛巴赞,托皮拉) 以及中间CYP2D6代谢器状态有关.
- 停止服用多西导致神经症状完全消失,发作没有复发.
结论:
- 处方多克塞需要仔细考虑药物基因组学,剂量,潜在的药物相互作用和患者年龄.
- 在患有持续的神经异常,包括发作的儿科患者中,即使没有急性过量服用史,也应怀疑慢性多克西毒性.
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