The Neurological Institute, University Hospitals Case Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, Ohio 44106-5040, USA.
Muscle Nerve. 2010 May;41(5):723-7. doi: 10.1002/mus.21584.
Biologic therapy with tumor necrosis factor (TNF)-alpha antagonists for rheumatoid arthritis has been well established. We describe two patients with rheumatoid arthritis who developed chronic inflammatory demyelinating polyneuropathy (CIDP) during their course of therapy with TNF-alpha antagonists. A 45-year-old woman and a 49-year-old man, both with a history of rheumatoid arthritis, were treated with etanercept and infliximab, respectively. Clinical signs of peripheral neuropathy developed 2 weeks and 12 months after the initiation of TNF-alpha antagonists. Electrodiagnostic studies at variable points during the disease course showed signs of acquired demyelination consistent with CIDP. Cerebrospinal fluid examination showed albuminocytologic dissociation (total protein concentration 118 mg/dl and 152 mg/dl, respectively). Both patients failed to improve after discontinuation of the offending agent, and they responded poorly to corticosteroids. However, there was clinical and electrophysiologic recovery after initiation of intravenous immunoglobulin (IVIg) therapy. CIDP may occur early or late during the treatment course with TNF-alpha antagonists. IVIg may reverse and stabilize the inflammatory process.
肿瘤坏死因子 (TNF)-α拮抗剂的生物疗法已被广泛应用于类风湿关节炎的治疗。我们描述了两名在接受 TNF-α拮抗剂治疗过程中发生慢性炎症性脱髓鞘性多发性神经病 (CIDP)的类风湿关节炎患者。一名 45 岁女性和一名 49 岁男性，均有类风湿关节炎病史，分别接受了依那西普和英夫利昔单抗治疗。在开始使用 TNF-α拮抗剂后 2 周和 12 个月，出现了周围神经病的临床体征。疾病过程中不同时间点的电诊断研究显示出与 CIDP 一致的获得性脱髓鞘迹象。脑脊液检查显示白蛋白细胞分离（总蛋白浓度分别为 118mg/dl 和 152mg/dl）。两名患者在停用致病药物后均未改善，且对皮质类固醇反应不佳。然而，在开始静脉注射免疫球蛋白 (IVIg) 治疗后，他们的临床和电生理状况得到了恢复。CIDP 可能在 TNF-α拮抗剂治疗过程中的早期或晚期发生。IVIg 可能逆转和稳定炎症过程。
