Treatment of slow-channel congenital myasthenic syndrome with fluoxetine
Treatment of slow-channel congenital myasthenic syndrome with fluoxetine
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DOI：
10.1212/01.wnl.0000061483.11417.1b
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发表时间：
2003-05-27
期刊：
影响因子：
9.9
通讯作者：
Engel, AG
中科院分区：
文献类型：
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作者：
Harper, CM;Fukodome, T;Engel, AG
作者发现，氟西汀在5 μ M/L时显著缩短成纤维细胞中表达的慢通道先天性肌无力综合征（SCCMS）乙酰胆碱受体（AChR）的延长开放爆发，在10 μ M/L时几乎恢复正常。根据这一观察结果，他们治疗了两名对奎尼丁过敏的SCCMS患者，每天给予高达80至120 mg氟西汀，持续3年（血清氟西汀+去甲氟西汀水平为8至11 μ M/L）。通过定量肌力测试和肌电图，两例患者均显示出明显的主观和客观改善。
The authors found that fluoxetine significantly shortens at 5 muM/L and nearly normalizes at 10 muM/L the prolonged opening bursts of slow-channel congenital myasthenic syndrome (SCCMS) acetylcholine receptors (AChR) expressed in fibroblasts. Prompted by this observation, they treated two SCCMS patients allergic to quinidine with up to 80 to 120 mg of fluoxetine per day over 3 years (serum fluoxetine + norfluoxetine levels 8 to 11 muM/L). Both patients showed marked subjective and objective improvement by quantitative muscle strength testing and electromyography.