Wong Siew L, Rajabally Yusuf A
Department of Neurology, Neuromuscular Clinic, University Hospitals of Leicester, Leicester, UK.
J Clin Neuromuscul Dis. 2010 Dec;12(2):88-90. doi: 10.1097/CND.0b013e3181fd9401.
We describe a patient on the tumor necrosis factor-α antagonist, adalimumab, for 2 years for rheumatoid arthitis, who developed a rapidly progressive inflammatory neuropathy shortly after starting oral steroids. Adalimumab was stopped at onset of neurologic symptoms. Electrophysiology showed demyelination, which persisted at 6 month follow-up, cerebrospinal fluid analysis showed persistent albuminocytologic dissociation, and magnetic resonance studies revealed enlarged and enhancing nerve roots. Treatment with intravenous immunoglobulins resulted in slow, progressive improvement. Tumor necrosis factor-α antagonists have previously been implicated in acquired demyelinating neuropathies. In this patient, we hypothesize that adalimumab may have caused an initially asymptomatic chronic inflammatory demyelinating polyneuropathy, which became symptomatic shortly after initiation of steroid therapy. This case may raise the issue of the safety of steroids in conjunction with antitumor necrosis factor-α therapy in susceptible patients.
我们描述了一名类风湿关节炎患者，使用肿瘤坏死因子-α拮抗剂阿达木单抗治疗2年，在开始口服类固醇后不久出现快速进展的炎性神经病变。在出现神经症状时停用了阿达木单抗。电生理学显示脱髓鞘，在6个月的随访中持续存在，脑脊液分析显示持续的蛋白细胞分离，磁共振研究显示神经根增粗并强化。静脉注射免疫球蛋白治疗导致缓慢、渐进性改善。肿瘤坏死因子-α拮抗剂此前曾被认为与获得性脱髓鞘性神经病变有关。在该患者中，我们推测阿达木单抗可能导致了最初无症状的慢性炎性脱髓鞘性多发性神经病变，在开始类固醇治疗后不久出现症状。该病例可能引发了在易感患者中类固醇与抗肿瘤坏死因子-α治疗联合使用的安全性问题。
