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沙利度胺诱发的神经病变

Thalidomide-induced neuropathy.

作者信息

Chaudhry V, Cornblath D R, Corse A, Freimer M, Simmons-O'Brien E, Vogelsang G

机构信息

Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

出版信息

Neurology. 2002 Dec 24;59(12):1872-5. doi: 10.1212/01.wnl.0000037480.59194.85.

DOI:10.1212/01.wnl.0000037480.59194.85
PMID:12499476
Abstract

BACKGROUND

Thalidomide is effective for the treatment of some refractory dermatologic and oncologic diseases. Toxic neuropathy limits its use, as embryopathy can be avoided by contraceptive measures.

OBJECTIVE

To describe the clinical, electrophysiologic, and pathologic features of thalidomide-induced peripheral neuropathy.

METHODS

Clinical and electrophysiologic examinations were performed in seven patients with thalidomide-induced peripheral neuropathy. Thalidomide was used for graft-vs-host disease, pyoderma gangrenosum, and discoid lupus with dosages ranging from 100 to 1,200 mg/day for 5 to 16 months (cumulative dosages of 24 to 384 g).

RESULTS

All seven patients had clinical and electrophysiologic evidence of a sensory more than motor, axonal, length-dependent polyneuropathy that presented as painful paresthesias or numbness. Sural nerve biopsies, done in three patients, showed evidence of Wallerian degeneration and loss of myelinated fibers. The symptoms, signs, and electrophysiologic data correlated with total cumulative dose of thalidomide.

CONCLUSIONS

Thalidomide induces a dose-dependent sensorimotor length-dependent axonal neuropathy; it should be judiciously used with close neurologic monitoring.

摘要

背景

沙利度胺对某些难治性皮肤病和肿瘤性疾病有效。毒性神经病变限制了其使用,因为避孕措施可避免胚胎病。

目的

描述沙利度胺所致周围神经病变的临床、电生理和病理特征。

方法

对7例沙利度胺所致周围神经病变患者进行了临床和电生理检查。沙利度胺用于移植物抗宿主病、坏疽性脓皮病和盘状红斑狼疮,剂量为100至1200毫克/天,持续5至16个月(累积剂量为24至384克)。

结果

所有7例患者均有感觉神经受累超过运动神经、轴索性、长度依赖性多发性神经病变的临床和电生理证据,表现为疼痛性感觉异常或麻木。3例患者进行了腓肠神经活检,显示有华勒变性和有髓纤维丢失的证据。症状、体征和电生理数据与沙利度胺的总累积剂量相关。

结论

沙利度胺可诱发剂量依赖性感觉运动性长度依赖性轴索性神经病变;使用时应谨慎并密切进行神经学监测。

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