Kocer B, Sucak G, Kuruoglu R, Aki Z, Haznedar R, Erdogmus N Ince
Department of Neurology, Gazi University School of Medicine, Ankara, Turkey.
Acta Neurol Belg. 2009 Jun;109(2):120-6.
Whether thalidomide induces a sensory ganglionopathy or a length-dependent axonal neuropathy is disputed. Moreover no agreement exists concerning the effects of thalidomide dosage on the clinical and electrophysiological findings.
We examined the effect of age, gender disease duration, total cumulative dose on the clinical and electrophysiologic parameters.
Fifteen patients who had previously received 100 mg/day of thalidomide for the treatment of multiple myeloma were evaluated retrospectively. Clinical findings and nerve conductions studies were evaluated using a modified total neuropathy scoring system.
Sensory symptoms (p = 0.033, r = 0.552) and objective sensory findings (p = 0.002, r = 0.730) worsened with higher thalidomide doses. There was no effect of age, gender and disease duration, neither on clinical symptoms and objective findings, nor on electrophysiologic data. Twelve patients (80%) developed the electrophysiological findings of neuropathy. Six (40%) had pure sensory and 4 (26.6%) had sensori-motor peripheral neuropathy, while 4 (26.6%) had carpal tunnel syndrome. Sural sensory nerve action potential (SNAP) amplitudes were more prominently reduced compared to SNAPs obtained from the upper extremities. Sural SNAP amplitude showed a tendency toward reduction as the total cumulative dose, although it is not statistically significant (respectively; p = 0.187). Significantly reduced ulnar peroneal and tibial compound muscle action potential amplitudes, slow motor nerve conduction velocities of the ulnar and peroneal nerves were found in the study group compared to reference norms (p < 0.05).
Our results suggest that thalidomide produces a dose dependent peripheral neuropathy, mainly localized to the peripheral nerves in a length dependent manner. The patient must be monitored closely to prevent irreversible consequences.
沙利度胺引发的是感觉神经节病还是长度依赖性轴索性神经病存在争议。此外，关于沙利度胺剂量对临床及电生理结果的影响尚无定论。
我们研究了年龄、性别、病程及总累积剂量对临床和电生理参数的影响。
对15例曾接受每日100毫克沙利度胺治疗多发性骨髓瘤的患者进行回顾性评估。使用改良的全神经病评分系统评估临床结果和神经传导研究。
沙利度胺剂量越高，感觉症状（p = 0.033，r = 0.552）和客观感觉结果（p = 0.002，r = 0.730）越严重。年龄、性别和病程对临床症状、客观结果及电生理数据均无影响。12例患者（80%）出现了神经病的电生理表现。6例（40%）为纯感觉性，4例（26.6%）为感觉运动性周围神经病，4例（26.6%）患有腕管综合征。与上肢获得的感觉神经动作电位（SNAP）相比，腓肠神经SNAP波幅降低更为明显。腓肠神经SNAP波幅随总累积剂量增加有降低趋势，尽管无统计学意义（分别为p = 0.187）。与参考标准相比，研究组尺神经、腓总神经和胫神经复合肌肉动作电位波幅明显降低，尺神经和腓总神经运动神经传导速度减慢（p < 0.05）。
我们的结果表明，沙利度胺可产生剂量依赖性周围神经病，主要以长度依赖性方式累及周围神经。必须密切监测患者以防止不可逆转的后果。
