Diabetic Neuropathy Project, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Adv Exp Med Biol. 2019;1190:357-369. doi: 10.1007/978-981-32-9636-7_23.
A large variety of drugs have been reported to cause peripheral neuropathies as dose-limiting adverse effects; however, most of them primarily affect axons and/or neuronal cell bodies rather than Schwann cells and/or myelin sheaths. In this chapter, we focus on the drugs that seem to elicit the neuropathies with schwannopathy and/or myelinopathy-predominant phenotypes, such as amiodarone, dichloroacetate, and tumor necrosis factor-α antagonists. Although the pathogenesis of demyelination induced by these drugs remain largely obscure, the recent in vivo and in vitro studies have implicated the involvement of metabolic abnormalities and impaired autophagy in Schwann cells and immune system disorders in the disruption of neuron-Schwann cell contact and interactions.
已有大量报道称，多种药物可引起以周围神经病变为剂量限制的不良反应；然而，它们大多数主要影响轴突和/或神经元细胞体，而非施万细胞和/或髓鞘。在本章中，我们重点关注那些似乎引起以雪旺病和/或髓鞘病为主的神经病变的药物，如胺碘酮、二氯醋酸和肿瘤坏死因子-α拮抗剂。尽管这些药物引起脱髓鞘的发病机制在很大程度上仍不清楚，但最近的体内和体外研究表明，施万细胞代谢异常和自噬受损以及免疫系统紊乱导致神经元-施万细胞接触和相互作用中断，与脱髓鞘的发生有关。
