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抗 MOG 抗体相关的无菌性脑膜炎和软脑膜强化:综述。

Aseptic meningitis and leptomeningeal enhancement associated with anti-MOG antibodies: A review.

机构信息

Emory University, Children's Healthcare of Atlanta: Pediatrics Institute, United States of America.

Emory University School of Medicine, Department of Radiology and Imaging Sciences & Pediatrics, United States of America; Ann & Robert H. Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, United States of America.

出版信息

J Neuroimmunol. 2021 Sep 15;358:577653. doi: 10.1016/j.jneuroim.2021.577653. Epub 2021 Jul 1.

Abstract

BACKGROUND

Aseptic meningitis can be caused by autoimmune diseases, such as lupus and sarcoidosis. Aseptic meningitis with leptomeningeal enhancement can be the initial presentation of a neuroinflammatory syndrome associated with antibodies to myelin oligodendrocyte glycoprotein (MOG-abs). MOG-abs is a serum biomarker for MOG-associated disorder (MOG-AD), an acquired demyelinating syndrome that includes features of neuromyelitis optica, multiple sclerosis, optic neuritis, and acute disseminated encephalomyelitis. The purpose of this study is to review cases of aseptic meningitis and leptomeningeal enhancement associated with MOG-abs.

METHODS

Systematic review using PubMed, Embase, Ovid MEDLINE, Web of Science Core Collection, and Google Scholar up to December 2020 was performed. Cases of MOG-AD were included if they met the following criteria: 1) Initial clinical presentation of aseptic meningitis; 2) positive leptomeningeal enhancement and 3) MOG-Ab seropositivity. Descriptive statistics were used. This analysis was limited to the cases available in the literature.

RESULTS

11 total cases of aseptic meningitis and leptomeningeal enhancement in setting of MOG-ab were identified. Demyelinating type T2 lesions were also present at time of presentation in 6/11; however, 5/11 of patients had leptomeningeal enhancement alone without demyelinating lesions. All 5 patients required immunotherapy for improvement, including one patient with symptoms for 28 days, with 4/5 receiving steroids and 1/5 receiving intravenous immunoglobulin (IVIG).

CONCLUSIONS

Aseptic meningitis with leptomeningeal enhancement can be the initial presenting symptom of MOG-AD. MOG-ab testing should be considered in a patient presenting with aseptic meningitis and leptomeningeal enhancement of unknown etiology.

摘要

背景

无菌性脑膜炎可由自身免疫性疾病引起,如狼疮和结节病。伴有软脑膜增强的无菌性脑膜炎可能是与髓鞘少突胶质细胞糖蛋白(MOG-ab)抗体相关的神经炎症综合征的初始表现。MOG-ab 是髓鞘少突胶质细胞糖蛋白相关疾病(MOG-AD)的血清生物标志物,MOG-AD 是一种获得性脱髓鞘综合征,包括视神经脊髓炎、多发性硬化症、视神经炎和急性播散性脑脊髓炎的特征。本研究旨在回顾与 MOG-ab 相关的无菌性脑膜炎和软脑膜增强的病例。

方法

使用 PubMed、Embase、Ovid MEDLINE、Web of Science 核心合集和 Google Scholar 进行系统评价,检索时间截至 2020 年 12 月。如果符合以下标准,将 MOG-AD 病例纳入研究:1)初始临床表现为无菌性脑膜炎;2)软脑膜增强阳性;3)MOG-Ab 血清阳性。采用描述性统计方法。本分析仅限于文献中可用的病例。

结果

共发现 11 例 MOG-ab 相关无菌性脑膜炎和软脑膜增强的病例。6/11 例患者在发病时也存在脱髓鞘型 T2 病变;然而,5/11 例患者仅有软脑膜增强而无脱髓鞘病变。所有 5 例患者均需免疫治疗改善,包括 1 例患者症状持续 28 天,4/5 例患者接受皮质类固醇治疗,1/5 例患者接受静脉注射免疫球蛋白(IVIG)治疗。

结论

伴有软脑膜增强的无菌性脑膜炎可为 MOG-AD 的首发症状。对于病因不明的无菌性脑膜炎和软脑膜增强患者,应考虑进行 MOG-ab 检测。

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