Evaluation of diagnostic criteria and red flags of myelin oligodendrocyte glycoprotein encephalomyelitis in a clinical routine cohort

Veselaj, Krenar; Kamber, Nicole; Briner, Myriam; Friedli, Christoph; Diem, Lara; Guse, Kirsten; Miclea, Andrei; Wiest, Roland; Wagner, Franca; Grabe, Hilary; Abegg, Mathias; Horn, Michael P.; Bigi, Sandra; Chan, Andrew; Hoepner, Robert; Salmen, Anke

doi:10.1111/cns.13461

Cited by 7 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…International comparative studies of different MOG-IgG1 assays have shown that live cell–based assays yield the highest specificity for MOGAD . However, MOGAD is rare, and indiscriminate testing for MOG-IgG1 may lead to false-positive results despite high specificity . The positive predictive value (PPV), which provides the likelihood that a positive test result is truly positive for the disease of interest, is arguably of greater clinical utility.…”

Section: Introductionmentioning

confidence: 99%

Positive Predictive Value of Myelin Oligodendrocyte Glycoprotein Autoantibody Testing

et al. 2021

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Positive Predictive Value of Myelin Oligodendrocyte Glycoprotein Autoantibody Testing

et al. 2021

View full text Add to dashboard Cite

show abstract

“… 68 , 75 Given the overall rarity of double positive cases based on the results of the larger studies, and considering the superior specificity of the AQP4-IgG test compared to the MOG-IgG test, and that a reliable cell-based-assay (CBA) for detecting MOG-IgG has been available just recently (2017), there is a high possibility that most of the double positive cases may likely be AQP4-IgG + NMOSD with false positive MOG-IgG test results, especially in reports made before this time with using enzyme-linked immunosorbent assay (ELISA). 68 , 75 …”

Section: Discussionmentioning

confidence: 99%

Autoimmune diseases and cancers overlapping with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): A systematic review

Molazadeh

Bose

Lotan

et al. 2022

Multiple Sclerosis Journal - Experimental, Translational and Cl

View full text Add to dashboard Cite

Background Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has various similarities with AQP4-IgG-seropositive Neuromyelitis Optica Spectrum Disorder (AQP4-IgG + NMOSD) in terms of clinical presentations, magnetic resonance imaging (MRI) findings, and response to treatment. But unlike AQP4-IgG + NMOSD, which is known to coexist with various autoimmune diseases and cancers, an association of MOGAD with these conditions is less clear. Methods We conducted a systematic search in PubMed, Scopus, Web of Science, and Embase based on the preferred reporting items for systematic reviews and meta-analysis (PRISMA). Duplicates were removed using Mendeley 1.19.8 (USA production) and the citations were uploaded into Covidence systematic review platform for screening. Results The most common autoimmune disease overlapping with MOGAD was anti-N-Methyl-D-Aspartate receptor encephalitis (anti-NMDAR-EN), followed by autoimmune thyroid disorders, and the most common autoantibody was antinuclear antibody (ANA), followed by AQP4-IgG (double-positive MOG-IgG and AQP4-IgG). A few sporadic cases of cancers and MOG-IgG-associated paraneoplastic encephalomyelitis were found. Conclusion Unlike AQP4-IgG + NMOSD, MOGAD lacks clustering of autoimmune diseases and autoantibodies associated with systemic and organ-specific autoimmunity. Other than anti-NMDAR-EN and perhaps AQP4-IgG + NMOSD, the evidence thus far does not support the need for routine screening of overlapping autoimmunity and neoplasms in patients with MOGAD.

show abstract

“…2,3 Although typical criteria for multiple sclerosis (MS) are usually not met, 1 clinical differentiation of MOGAD and MS may still be difficult. 4 MOGAD cannot be considered as equivalent to aquaporin 4 (AQP4)-IgG-seronegative neuromyelitis optica spectrum disorder (NMOSD) 5 due to different epidemiologic, clinical, radiographic features and outcome 6 and most interestingly remarkable immunologic differences. [7][8][9] Retrospective studies suggest that treatment strategies that work well in MS and NMOSD, e.g., targeting CD20 + B cells, are not similarly effective in MOGAD.…”

Section: Discussionmentioning

confidence: 99%

“… 2 , 3 Although typical criteria for multiple sclerosis (MS) are usually not met, 1 clinical differentiation of MOGAD and MS may still be difficult. 4 …”

mentioning

confidence: 99%

Antineonatal Fc Receptor Antibody Treatment Ameliorates MOG-IgG–Associated Experimental Autoimmune Encephalomyelitis

Remlinger

Madarasz

Guse

et al. 2022

Neurol Neuroimmunol Neuroinflamm

Self Cite

View full text Add to dashboard Cite

Background and ObjectivesMyelin oligodendrocyte glycoprotein antibody–associated disorder (MOGAD) is a rare, autoimmune demyelinating CNS disorder, distinct from multiple sclerosis and neuromyelitis optica spectrum disorder. Characterized by pathogenic immunoglobulin G (IgG) antibodies against MOG, a potential treatment strategy for MOGAD is to reduce circulating IgG levels, e.g., by interference with the IgG recycling pathway mediated by the neonatal Fc receptor (FcRn). Although the optic nerve is often detrimentally involved in MOGAD, the effect of FcRn blockade on the visual pathway has not been assessed. Our objective was to investigate effects of a monoclonal anti-FcRn antibody in murine MOG-IgG–associated experimental autoimmune encephalomyelitis (EAE).MethodsWe induced active MOG35-55 EAE in C57Bl/6 mice followed by the application of a monoclonal MOG-IgG (8-18C5) 10 days postimmunization (dpi). Animals were treated with either a specific monoclonal antibody against FcRn (α-FcRn, 4470) or an isotype-matched control IgG on 7, 10, and 13 dpi. Neurologic disability was scored daily on a 10-point scale. Visual acuity was assessed by optomotor reflex. Histopathologic hallmarks of disease were assessed in the spinal cord, optic nerve, and retina. Immune cell infiltration was visualized by immunohistochemistry, demyelination by Luxol fast blue staining and complement deposition and number of retinal ganglion cells by immunofluorescence.ResultsIn MOG-IgG–augmented MOG35-55 EAE, anti-FcRn treatment significantly attenuated neurologic disability over the course of disease (mean area under the curve and 95% confidence intervals (CIs): α-FcRn [n = 27], 46.02 [37.89–54.15]; isotype IgG [n = 24], 66.75 [59.54–73.96], 3 independent experiments), correlating with reduced amounts of demyelination and macrophage infiltration into the spinal cord. T- and B-cell infiltration and complement deposition remained unchanged. Compared with isotype, anti-FcRn treatment prevented reduction of visual acuity over the course of disease (median cycles/degree and interquartile range: α-FcRn [n = 16], 0.50 [0.48–0.55] to 0.50 [0.48–0.58]; isotype IgG [n = 17], 0.50 [0.49–0.54] to 0.45 [0.39–0.51]).DiscussionWe show preserved optomotor response and ameliorated course of disease after anti-FcRn treatment in an experimental model using a monoclonal MOG-IgG to mimic MOGAD. Selectively targeting FcRn might represent a promising therapeutic approach in MOGAD.

show abstract

Evaluation of diagnostic criteria and red flags of myelin oligodendrocyte glycoprotein encephalomyelitis in a clinical routine cohort

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 7 publications

References 33 publications

Positive Predictive Value of Myelin Oligodendrocyte Glycoprotein Autoantibody Testing

Positive Predictive Value of Myelin Oligodendrocyte Glycoprotein Autoantibody Testing

Autoimmune diseases and cancers overlapping with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD): A systematic review

Antineonatal Fc Receptor Antibody Treatment Ameliorates MOG-IgG–Associated Experimental Autoimmune Encephalomyelitis

Contact Info

Product

Resources

About