髓鞘少突胶质细胞糖蛋白
视神经脊髓炎
多发性硬化
医学
视神经炎
光谱紊乱
免疫学
抗体
疾病
病态的
病理
实验性自身免疫性脑脊髓炎
精神科
作者
Romain Marignier,Yael Hacohen,Álvaro Cobo‐Calvo,Anne‐Katrin Pröbstel,Orhan Aktaş,Harry Alexopoulos,Maria-Pia Amato,Nasrin Asgari,Brenda Banwell,Jeffrey L. Bennett,Fabienne Brilot,Marco Capobianco,Tanuja Chitnis,Olga Ciccarelli,Kumaran Deiva,de Sèze,Kazuo Fujihara,Anu Jacob,Ho Jin Kim,Ingo Kleiter
标识
DOI:10.1016/s1474-4422(21)00218-0
摘要
Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently identified autoimmune disorder that presents in both adults and children as CNS demyelination. Although there are clinical phenotypic overlaps between MOGAD, multiple sclerosis, and aquaporin-4 antibody-associated neuromyelitis optica spectrum disorder (NMOSD) cumulative biological, clinical, and pathological evidence discriminates between these conditions. Patients should not be diagnosed with multiple sclerosis or NMOSD if they have anti-MOG antibodies in their serum. However, many questions related to the clinical characterisation of MOGAD and pathogenetic role of MOG antibodies are still unanswered. Furthermore, therapy is mainly based on standard protocols for aquaporin-4 antibody-associated NMOSD and multiple sclerosis, and more evidence is needed regarding how and when to treat patients with MOGAD.
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