Amiodarone neurotoxicity: the other side of the medal

G. Galassi, E. Georgoulopoulou, A. Ariatti
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引用次数: 4

Abstract

The efficacy of amiodarone is tempered by its toxicity, with 50% of long-term users discontinuing the drug. The non-cardiac side effects of amiodarone may involve central and peripheral nervous system. We studied two patients treated with amiodarone for 46 and 15 months respectively. Both patients exhibited progressive distal extremity weakness, impaired perception, loss of deep reflexes. Electrophysiology identified a widespread, sensorimotor polyneuropathy with features of axonal loss and demyelination. Visual evoked potentials (VEPs) showed prolonged P100 latency bilaterally in absence of visual symptoms or brain magnetic resonance imaging (MRI) abnormalities. Extensive laboratory examinations excluded known causes of peripheral neuropathies. At 21 months after amiodarone withdrawal, P100 latency of case 1 VEPs returned to normal, whereas polyneuropathy continued to progress. In the second patient neuropathy has worsened similarly over 2 years whereas P100 latency of VEPs recovered to normal within 7 months after withdrawal of amiodarone. These findings may suggest different mechanisms of toxicity, which could be due to amiodarone pharmacokinetic and its metabolite effects on the peripheral nerves, as opposed to the optic nerve. We emphasize that use of amiodarone needs monitoring of patients at risk of development side effects.
胺碘酮神经毒性:奖牌的另一面
胺碘酮的疗效因其毒性而减弱,50%的长期服用者停药。胺碘酮的非心脏副作用可能涉及中枢和周围神经系统。我们研究了两例分别用胺碘酮治疗46个月和15个月的患者。两例患者均表现出进行性远端肢体无力,知觉受损,深反射丧失。电生理学鉴定了一种广泛的感觉运动多发性神经病,其特征是轴突丧失和脱髓鞘。在没有视觉症状或脑磁共振成像(MRI)异常的情况下,视觉诱发电位(vep)显示双侧P100潜伏期延长。广泛的实验室检查排除了周围神经病变的已知原因。在胺碘酮停药21个月后,病例1 vep的P100潜伏期恢复正常,而多发性神经病变继续进展。在第二例患者中,神经病变在2年内同样恶化,而vep的P100潜伏期在停用胺碘酮后7个月内恢复正常。这些发现可能提示不同的毒性机制,这可能是由于胺碘酮药代动力学及其代谢物对周围神经的影响,而不是视神经。我们强调,使用胺碘酮需要监测有发展副作用风险的患者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Central European Journal of Medicine
Central European Journal of Medicine 医学-医学:内科
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审稿时长
4-8 weeks
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