Epidemiology of myelin oligodendrocyte glycoprotein antibody-associated disease: a review of prevalence and incidence worldwide

被引:32
作者
Hor, Jyh Yung [1 ]
Fujihara, Kazuo [2 ,3 ]
机构
[1] Penang Gen Hosp, Dept Neurol, George Town, Malaysia
[2] Fukushima Med Univ, Dept Multiple Sclerosis Therapeut, Sch Med, Koriyama, Japan
[3] Southern TOHOKU Res Inst Neurosci, Multiple Sclerosis & Neuromyelitis Opt Ctr, Koriyama, Japan
关键词
myelin oligodendrocyte glycoprotein; MOG antibody-associated disease; neuromyelitis optica spectrum disorder; population study; prevalence; incidence; epidemiology; SPECTRUM; ADULTS;
D O I
10.3389/fneur.2023.1260358
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an inflammatory demyelinating disease of the central nervous system (CNS) with the presence of conformation-sensitive antibodies against MOG. The spectrum of MOGAD includes monophasic/relapsing optic neuritis, myelitis, neuromyelitis optica spectrum disorder (NMOSD) phenotype without aquaporin 4 (AQP4) antibodies, acute/multiphasic demyelinating encephalomyelitis (ADEM/MDEM)-like presentation, and brainstem and cerebral cortical encephalitis. There is no apparent female preponderance in MOGAD, and MOGAD can onset in all age groups (age at onset is approximately 30 years on average, and approximately 30% of cases are in the pediatric age group). While prevalence and incidence data have been available for AQP4+ NMOSD globally, such data are only beginning to accumulate for MOGAD. We reviewed the currently available data from population-based MOGAD studies conducted around the world: three studies in Europe, three in Asia, and one joint study in the Americas. The prevalence of MOGAD is approximately 1.3-2.5/100,000, and the annual incidence is approximately 3.4-4.8 per million. Among White people, the prevalence of MOGAD appears to be slightly higher than that of AQP4+ NMOSD. No obvious latitude gradient was observed in the Japanese nationwide survey. The data available so far showed no obvious racial preponderance or strong HLA associations in MOGAD. However, precedent infection was reported in approximately 20-40% of MOGAD cases, and this is worthy of further investigation. Co-existing autoimmune disorders are less common in MOGAD than in AQP4+ NMOSD, but NMDAR antibodies may occasionally be positive in patients with MOGAD. More population-based studies in different populations and regions are useful to further inform the epidemiology of this disease.
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