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Utility of aquaporin-4 antibody assay in patients with neuromyelitis optica spectrum disorders
Kim, Sung-Min,Waters, Patrick,Woodhall, Mark,Kim, Jee-Young,Kim, Jee-Eun,Yang, Ji Won,Kim, Jun-Soon,Sung, Jung-Joon,Park, Kyung Seok,Lee, Kwang-Woo SAGE Publications 2013 Multiple sclerosis journal: clinical and laborator Vol.19 No.8
<P><B>Objective:</B></P><P>Our aim was to evaluate the utility of aquaporin-4 antibodies (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD).</P><P><B>Methods:</B></P><P>The clinical and radiological characteristics of 78 patients with NMOSD and 22 with multiple sclerosis (MS), who were tested for AQP4-Ab by a cell-based assay, were assessed.</P><P><B>Results:</B></P><P>The mean time interval between symptom onset and development of optic neuritis and myelitis was 39.9 months in neuromyelitis optica (NMO). About 40% of patients with limited NMO would have fulfilled the diagnostic criteria for MS in the absence of the antibody assay results. In patients with longitudinally extensive transverse myelitis, positive AQP4-Ab assay results were associated with the poor response to acute steroid treatment and asymptomatic visual evoked potential abnormality. Presence of either painful tonic spasm associated with myelitis or severe disability at onset had high specificity and relatively high sensitivity in differentiating NMOSD with AQP4-Ab from MS.</P><P><B>Conclusions:</B></P><P>The AQP4-Ab assay can facilitate the early diagnosis of NMO and prevent limited NMO from being misdiagnosed as MS. It can predict the poor response to first-line acute-phase treatment and probably detect the subclinical optic nerve involvement in subgroups of NMOSD. Lastly, it will contribute to the upcoming revision of the current diagnostic criteria for NMO.</P>
Seok Jin Myoung,Waters Patrick,Jeon Mi Young,Lee Hye Lim,Baek Seol-Hee,Park Jin-Sung,Kang Sa-Yoon,Kwon Ohyun,Oh Jeeyoung,Oh Jeeyoung,Park Kyung-Ah,Oh Sei Yeul,Kim Byoung Joon,Min Ju-Hong 대한진단검사의학회 2024 Annals of Laboratory Medicine Vol.44 No.1
Background: The clinical implications of myelin oligodendrocyte glycoprotein autoantibodies (MOG-Abs) are increasing. Establishing MOG-Ab assays is essential for effectively treating patients with MOG-Abs. We established an in-house cell-based assay (CBA) to detect MOG-Abs to identify correlations with patients’ clinical characteristics. Methods: We established the CBA using HEK 293 cells transiently overexpressing full-length human MOG, tested it against 166 samples from a multicenter registry of central nervous system (CNS) inflammatory disorders, and compared the results with those of the Oxford MOG-Ab-based CBA and a commercial MOG-Ab CBA kit. We recruited additional patients with MOG-Abs and compared the clinical characteristics of MOG-Ab-associated disease (MOGAD) with those of neuromyelitis optica spectrum disorder (NMOSD). Results: Of 166 samples tested, 10 tested positive for MOG-Abs, with optic neuritis (ON) being the most common manifestation (4/15, 26.7%). The in-house and Oxford MOG-Ab CBAs agreed for 164/166 (98.8%) samples (κ=0.883, P<0.001); two patients (2/166, 1.2%) were only positive in our in-house CBA, and the CBA scores of the two laboratories correlated well (r=0.663, P<0.001). The commercial MOG-Ab CBA kit showed one false-negative and three false-positive results. The clinical presentation at disease onset differed between MOGAD and NMOSD; ON was the most frequent manifestation in MOGAD, and transverse myelitis was most frequent in NMOSD. Conclusions: The in-house CBA for MOG-Abs demonstrated reliable results and can potentially be used to evaluate CNS inflammatory disorders. A comprehensive, long-term study with a large patient population would clarify the clinical significance of MOG-Abs.
Longitudinal analysis of myelin oligodendrocyte glycoprotein antibodies in CNS inflammatory diseases
Hyun, Jae-Won,Woodhall, Mark R,Kim, Su-Hyun,Jeong, In Hye,Kong, Byungsoo,Kim, Gayoung,Kim, Yeseul,Park, Min Su,Irani, Sarosh R,Waters, Patrick,Kim, Ho Jin BMJ Publishing Group Ltd 2017 Journal of neurology, neurosurgery, and psychiatry Vol.88 No.10
<P>Conclusions In a large adult-predominant unselected cohort of mainly relapsing CNS inflammatory diseases, we confirmed that NMOSD phenotype was most commonly observed in patients with MOG-IgG. A longitudinal analysis with 2-year follow-up suggested that persistence of MOG-IgG is associated with relapses.</P>
Hyun, Jae-Won,Huh, So-Young,Shin, Hyun-June,Woodhall, Mark,Kim, Su-Hyun,Irani, Sarosh R,Lee, Sang Hyun,Waters, Patrick,Kim, Ho Jin SAGE Publications 2019 Multiple sclerosis journal: clinical and laborator Vol.25 No.4
<P><B>Objectives:</B></P><P>We aimed to evaluate the utility of the recently described brain lesion distribution criteria to differentiate multiple sclerosis (MS) from aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein immunoglobulin G-associated encephalomyelitis (MOG-EM) at disease onset in an Asian cohort.</P><P><B>Methods:</B></P><P>A total of 214 patients who fulfilled the published criteria for MS, NMOSD, or MOG-EM and underwent brain magnetic resonance imaging (MRI) within 3 months of disease onset were enrolled. The brain lesion distribution criteria were defined as the presence of a lesion adjacent to the body of the lateral ventricle and in the inferior temporal lobe, or an S-shaped U-fiber lesion, or a Dawson’s finger-type lesion.</P><P><B>Results:</B></P><P>Brain lesions were identified in the initial MRI scans of 166/214 patients. The distribution criteria were applied to these scans (MS (<I>n</I> = 94), NMOSD (<I>n</I> = 64), and MOG-EM (<I>n</I> = 8)). The sensitivity, specificity, and positive and negative predictive values of the criteria for MS versus NMOSD were 79.8%, 87.5%, 90.4%, and 74.7%, and for MS versus MOG-EM these were 79.8%, 100%, 100%, and 29.6%, respectively.</P><P><B>Conclusion:</B></P><P>These findings suggest that the brain lesion distribution criteria are helpful in distinguishing MS from NMOSD and MOG-EM in an Asian population, even at disease onset.</P>