Demyelinating Neurological Adverse Events following the Use of Anti-TNF-α Agents: A Double-Edged Sword

IF 0.9 Q4 CLINICAL NEUROLOGY
Miral H Gharib, M. AlKahlout, Beatriz Garcia Canibano, Dirk Theophiel Deleu, Hani Malallah AlEssa, S. AlEmadi
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引用次数: 5

Abstract

Background Tumor necrosis factor antagonists (anti-TNF-α) are an established therapeutic option for several autoimmune and inflammatory bowel diseases. Despite their clinical effectiveness, neurological adverse events have been reported, and literature data suggest a potential role of anti-TNF-α in the induction of demyelination. Case Presentation. In this series, we present three cases of demyelination after the use of anti-TNF-α agents. The first case involved a 21-year-old man with HLA-B27 negative peripheral spondylarthritis who had been taking adalimumab for 2 years. He developed headache, urinary incontinence, and bilateral lower extremity numbness that progressed to the middle of the trunk for 2 days. Magnetic resonance imaging (MRI) showed multiple hyperintense enhancement lesions in the left paramedian anterior pons consistent with multiple sclerosis (MS). The second case included a 17-year-old woman who was on 2 years of adalimumab treatment for juvenile idiopathic arthritis and chronic anterior uveitis and developed new-onset dizziness and tremors. The clinical examination showed signs of cerebellar dysfunction. MRI findings were consistent with multiple sclerosis. The third case was a 34-year-old male who was on 5 years of infliximab treatment for ankylosing spondylitis when he developed left hand numbness and weakness. Cerebrospinal fluid (CSF) analysis and MRI findings were consistent with demyelination. Discontinuation of tumor necrosis factor antagonists (anti-TNF-α) resulted in resolution of the symptoms with no recurrence in the first case, but there was evidence of recurrence in the other 2 cases, where one was managed with rituximab and the second one improved with pulse steroid therapy. Conclusion Despite the small number of patients, our series adds to the growing body of evidence supporting a causal link between anti-TNF-α agents and demyelination. Thus, we can conclude that on suspicion of any neurological side effects, early discontinuation of the TNF-α blockers and requesting urgent MRI scan to confirm the diagnosis is of utmost importance.
使用抗tnf -α药物后脱髓鞘神经系统不良事件:一把双刃剑
肿瘤坏死因子拮抗剂(抗tnf -α)是几种自身免疫性和炎症性肠病的既定治疗选择。尽管它们的临床有效性,神经系统不良事件已被报道,文献数据表明抗tnf -α在诱导脱髓鞘中的潜在作用。案例演示。在这个系列中,我们提出了使用抗tnf -α药物后脱髓鞘的三个病例。第一个病例涉及一名患有HLA-B27阴性周围性脊柱炎的21岁男性,他已经服用阿达木单抗2年。患者出现头痛、尿失禁和双侧下肢麻木,并进展至躯干中部,持续2天。磁共振成像(MRI)显示左侧桥前旁位多发高强度强化病灶,符合多发性硬化症(MS)。第二个病例包括一名17岁的女性,她因青少年特发性关节炎和慢性前葡萄膜炎接受了2年的阿达木单抗治疗,并出现了新发头晕和震颤。临床检查显示有小脑功能障碍的迹象。MRI表现符合多发性硬化症。第三例为34岁男性,因强直性脊柱炎接受英夫利昔单抗治疗5年后出现左手麻木和无力。脑脊液(CSF)分析和MRI结果与脱髓鞘一致。停止使用肿瘤坏死因子拮抗剂(抗tnf -α)导致第一例症状缓解,无复发,但其他2例有复发迹象,其中1例使用利妥昔单抗治疗,另1例使用脉冲类固醇治疗改善。结论:尽管患者数量较少,但我们的系列研究增加了越来越多的证据,支持抗tnf -α药物与脱髓鞘之间的因果关系。因此,我们可以得出结论,在怀疑任何神经系统副作用时,早期停用TNF-α阻滞剂并要求紧急MRI扫描以确认诊断是至关重要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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