Gharib Miral H, AlKahlout Mohamed Awni, Garcia Canibano Beatriz, Theophiel Deleu Dirk, Malallah AlEssa Hani, AlEmadi Samar
Rheumatology, Department of Medicine, Hamad Medical Corporation, Doha, Qatar.
Neurology, Department of Medicine, Hamad General Hospital, Doha, Qatar.
Case Rep Neurol Med. 2022 Mar 7;2022:3784938. doi: 10.1155/2022/3784938. eCollection 2022.
Tumor necrosis factor antagonists (anti-TNF-) 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- in the induction of demyelination. . In this series, we present three cases of demyelination after the use of anti-TNF- 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-) 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.
Despite the small number of patients, our series adds to the growing body of evidence supporting a causal link between anti-TNF- agents and demyelination. Thus, we can conclude that on suspicion of any neurological side effects, early discontinuation of the TNF- blockers and requesting urgent MRI scan to confirm the diagnosis is of utmost importance.
肿瘤坏死因子拮抗剂(抗 TNF-)是多种自身免疫性疾病和炎性肠病的既定治疗选择。尽管它们具有临床疗效,但已有神经不良事件的报道,并且文献数据表明抗 TNF- 在脱髓鞘诱导中可能发挥作用。在本系列中,我们报告了 3 例使用抗 TNF- 药物后发生脱髓鞘的病例。第一例为一名 21 岁男性,患有 HLA-B27 阴性外周型脊柱关节炎,服用阿达木单抗 2 年。他出现头痛、尿失禁和双侧下肢麻木,并向躯干中部进展,持续 2 天。磁共振成像(MRI)显示左侧脑桥前内侧多发高信号强化病灶,符合多发性硬化症(MS)。第二例是一名 17 岁女性,因幼年特发性关节炎和慢性前葡萄膜炎接受阿达木单抗治疗 2 年,出现新发头晕和震颤。临床检查显示小脑功能障碍体征。MRI 结果符合多发性硬化症。第三例是一名 34 岁男性,因强直性脊柱炎接受英夫利昔单抗治疗 5 年,出现左手麻木和无力。脑脊液(CSF)分析和 MRI 结果符合脱髓鞘表现。停用肿瘤坏死因子拮抗剂(抗 TNF-)后,第一例患者症状缓解且未复发,但另外 2 例有复发迹象,其中 1 例用利妥昔单抗治疗,另一例经脉冲类固醇治疗后病情改善。
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- 药物与脱髓鞘之间存在因果关系。因此,我们可以得出结论,在怀疑有任何神经副作用时,尽早停用 TNF 阻滞剂并要求紧急进行 MRI 扫描以确诊至关重要。