Soliven B, Dhand U K, Kobayashi K, Arora R, Martin B, Petersen M V, Janisch L, Vogelzang N J, Vokes E E, Ratain M J
Department of Neurology, Brain Research Institute, The University of Chicago, Illinois 60637, USA.
Muscle Nerve. 1997 Jan;20(1):83-91. doi: 10.1002/(sici)1097-4598(199701)20:1<83::aid-mus11>3.0.co;2-2.
Suramin, a promising chemotherapeutic agent, causes a dose-limiting sensorimotor polyneuropathy. We undertook a phase 1 study of suramin that included serial neurologic and electrophysiologic examinations as part of the safety evaluation. We found that 6 of 41 (15%) patients developed suramin-induced demyelinating neuropathy which resembled Guillain-Barre syndrome clinically. There was 1 asymptomatic patient with electrophysiologic abnormalities suggestive of a demyelinating neuropathy. In addition, 1 patient with mild axonal neuropathy at baseline had deterioration of his symptoms during suramin treatment. Four asymptomatic patients developed electrophysiologic findings suggestive of a mild axonal neuropathy. We conclude that: (1) serial electrophysiologic monitoring is helpful for early detection of suramin-induced neuropathy; and (2) fixed dosing schedule of suramin without adaptive control does not lead to an increased incidence of demyelinating neuropathy when compared to adaptively controlled dosing schedules.
苏拉明是一种很有前景的化疗药物，会引起剂量限制性感觉运动性多发性神经病。我们开展了一项苏拉明的1期研究，其中包括进行系列神经学和电生理学检查作为安全性评估的一部分。我们发现，41名患者中有6名（15%）发生了苏拉明诱导的脱髓鞘性神经病，临床上类似于吉兰-巴雷综合征。有1例无症状患者出现提示脱髓鞘性神经病的电生理异常。此外，1例基线时患有轻度轴索性神经病的患者在苏拉明治疗期间症状恶化。4例无症状患者出现提示轻度轴索性神经病的电生理表现。我们得出结论：（1）系列电生理监测有助于早期发现苏拉明诱导的神经病；（2）与适应性控制给药方案相比，固定给药方案且无适应性控制的苏拉明不会导致脱髓鞘性神经病发病率增加。
