Harper C Michel, Fukodome Takayasu, Engel Andrew G
Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA.
Neurology. 2003 May 27;60(10):1710-3. doi: 10.1212/01.wnl.0000061483.11417.1b.
The authors found that fluoxetine significantly shortens at 5 microM/L and nearly normalizes at 10 microM/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 microM/L). Both patients showed marked subjective and objective improvement by quantitative muscle strength testing and electromyography.
作者发现,在5微摩尔/升时,氟西汀能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)延长的开放爆发时间,在10微摩尔/升时几乎使其恢复正常。受此观察结果的启发,他们对两名对奎尼丁过敏的SCCMS患者进行了为期3年的治疗,每天给予高达80至120毫克的氟西汀(血清氟西汀+去甲氟西汀水平为8至11微摩尔/升)。通过定量肌肉力量测试和肌电图检查,两名患者均表现出明显的主观和客观改善。