Department of Neurology and Neuroscience, Weill Medical College of Cornell University/New York Presbyterian Hospital, 525 East 68th Street, New York, NY 10065-4885, USA.
J Neurol Sci. 2011 Aug 15;307(1-2):1-8. doi: 10.1016/j.jns.2011.05.010. Epub 2011 May 31.
Drug-induced peripheral neurotoxicity usually manifests as a length-dependent, "dying back" axonal, predominantly sensory polyneuropathy. Rarely, immune-mediated demyelinating neuropathies occur during initial or maintenance treatment with immunomodulatory, immunosuppressive or antineoplastic agents. Medication-induced immune perturbation presumably triggers a dysimmune attack directed at unidentified peripheral nerve myelin epitopes; true peripheral nerve toxicity (i.e., dependent on accumulative dose or serum level) plays no identified role. The mechanisms that underlie a paradoxical and unpredictable immune exacerbation are unclear, and may depend on patient age, drug dosage and schedule, time of treatment relative to disease course, and host genetic factors. Suspicion and recognition of a non-toxic, immune-mediated demyelinating process has management (targeted immunotherapy) and prognostic (mostly favorable) implications.
药物引起的周围神经毒性通常表现为一种长度依赖性的、“退行性”轴突为主的感觉性多发性神经病。在免疫调节、免疫抑制或抗肿瘤药物的初始或维持治疗期间，很少发生免疫介导的脱髓鞘性神经病。药物诱导的免疫失调可能引发针对未识别的周围神经髓鞘表位的自身免疫攻击；真正的周围神经毒性（即依赖于累积剂量或血清水平）没有明确的作用。导致这种矛盾和不可预测的免疫恶化的机制尚不清楚，可能取决于患者年龄、药物剂量和方案、治疗时间与疾病过程的关系以及宿主遗传因素。对非毒性、免疫介导的脱髓鞘过程的怀疑和认识具有管理（靶向免疫治疗）和预后（大多有利）意义。
