Psarelis Savvas, Hajineocli Andreas P D, Hadjicosta Eleni, Elliott Hugh St A, Johnson Paul
St George's, University of London Medical Programme, Delivered in Cyprus by the University of Nicosia Medical School, Nicosia, Cyprus.
Rheumatology Department, Nicosia General Hospital, Nicosia-Limassol Old Road No. 215, 2029, Strovolos, Nicosia, Cyprus.
Clin Rheumatol. 2017 May;36(5):1197-1199. doi: 10.1007/s10067-017-3573-1. Epub 2017 Feb 23.
In this report, we aim to add to the existing body of evidence regarding a link between anti- tumor necrosis factor alpha (anti-TNF-α) treatment and demyelination leading to neurological disorders, specifically Guillain Barré syndrome (GBS), and treatment with an interleukin-17A (IL17A) antagonist as a safe alternative for ankylosing spondylitis (AS). A literature review was carried out of current research concerning anti-TNF-α and induced GBS. Only papers published in English were reviewed and only peer-reviewed journals searched. Papers published up to September 2016 were included. Animal studies were excluded. Data bases searched for publications online included: Pub Med, Google Scholar, The Cochrane Library, and Web of Science. Searched terms include "anti-TNF" and "Guillain Barré", "IL17 Ankylosing Spondylitis", "Secukinumab" and "TNF-α", "adalimumab", "infliximab", and "etanercept". All combinations and outcomes were used, and from these searches, a provisional reference list was constructed. The short-listed articles were read and their reference lists were reviewed. The electromyogram done for the patient showed demyelination, the MRI of the brain showed no pathologies, and the MRI of the spine was consistent with ankylosing spondylitis without myelopathy. The lumbar puncture results showed albuminocytological dissociation that was consistent with GBS. TNF has a proinflammatory action, and various immunoregulatory actions that, together, seem to promote the development of peripheral neuropathies syndromes in the organism. However, there is no clear mechanism of why or how anti-TNF-α treatment can induce a demyelinating event in a patient. In the case presented, it was found that the patient developed GBS due to treatment with etanercept, an anti-TNF agent. The treatment was stopped immediately. Two years later, he was switched to secukinumab and has been well controlled for the last 8 months with no neurological findings.
在本报告中，我们旨在补充现有证据，以证明抗肿瘤坏死因子α（抗TNF-α）治疗与导致神经系统疾病（特别是吉兰-巴雷综合征，GBS）的脱髓鞘之间存在关联，并证明白细胞介素-17A（IL17A）拮抗剂作为强直性脊柱炎（AS）的一种安全替代治疗方法的有效性。我们对当前有关抗TNF-α与诱发GBS的研究进行了文献综述。仅查阅了英文发表的论文，且仅检索了同行评审期刊。纳入了截至2016年9月发表的论文。排除了动物研究。在线检索出版物的数据库包括：PubMed、谷歌学术、考克兰图书馆和科学网。检索词包括“抗TNF”和“吉兰-巴雷”、“IL17强直性脊柱炎”、“司库奇尤单抗”和“TNF-α”、“阿达木单抗”、“英夫利昔单抗”和“依那西普”。使用了所有组合及结果，并据此构建了一个临时参考文献列表。对入围文章进行了阅读，并对其参考文献列表进行了审查。为该患者进行的肌电图显示有脱髓鞘表现，脑部MRI未显示病变，脊柱MRI与无脊髓病的强直性脊柱炎相符。腰椎穿刺结果显示蛋白细胞分离，与GBS相符。TNF具有促炎作用以及多种免疫调节作用，这些作用共同似乎促进了机体周围神经病变综合征的发展。然而，目前尚不清楚抗TNF-α治疗为何或如何能在患者中诱发脱髓鞘事件。在本病例中，发现患者因使用抗TNF药物依那西普而患上GBS。治疗立即停止。两年后，他改用司库奇尤单抗，在过去8个月里病情得到良好控制，未出现神经系统症状。
