Myelin-oligodendrocyte glycoprotein antibody-associated disease

Marignier, Romain; Hacohen, Yael; Cobo‐Calvo, Álvaro; Pröbstel, Anne Katrin; Aktaş, Orhan; Alexopoulos, Harry; Amato, Maria Pia; Asgari, Nasrin; Banwell, Brenda; Bennett, Jeffrey L.; Brilot, Fabienne; Capobianco, Marco; Chitnis, Tanuja; Ciccarelli, Olga; Deiva, Kumaran; Sèze, Jérôme De; Fujihara, Kazuo; Jacob, Anu; Kim, Ho Jin; Kleiter, Ingo; Lassmann, Hans; Leite, Maria Isabel; Linington, Christopher; Meinl, Edgar; Palace, Jacqueline; Paul, Friedemann; Petzold, Axel; Pittock, Sean J.; Reindl, Markus; Sato, Douglas Kazutoshi; Selmaj, Krzysztof; Síva, Aksel; Stankoff, Bruno; Tintoré, Mar; Traboulsee, Anthony; Waters, Patrick; Waubant, Emmanuelle; Weinshenker, Brian G.; Derfuss, Tobias; Vukusic, Sandra; Hemmer, Bernhard

doi:10.1016/s1474-4422(21)00218-0

Cited by 359 publications

(323 citation statements)

References 100 publications

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“…Antibody titers may decrease over months from presentation and become negative after the attack 40 . Secondly, assay-specific factors such as those that affect conformation of the MOG protein, type of secondary antibodies, and whether the tests are conducted in the research or clinical setting may affect the assay sensitivities and specificities 41 …”

Section: Discussionmentioning

confidence: 99%

“…40 Secondly, assay-specific factors such as those that affect conformation of the MOG protein, type of secondary antibodies, and whether the tests are conducted in the research or clinical setting may affect the assay sensitivities and specificities. 41 A recent study by Sechi et al 42 showed that although the MOG antibody test was highly specific (97.8%), its positive predictive value was titer dependent. The overall positive predictive value was 72%, and at low titers (using a cutoff of 1:20), it was even lower at 51%.…”

Section: Anti-mog Antibody Testingmentioning

confidence: 98%

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Optic Neuritis in the Era of NMOSD and MOGAD: A Survey of Practice Patterns in Singapore

Foo

Yau

Singhal

et al. 2022

Asia-Pacific Journal of Ophthalmology

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Purpose: The Optic Neuritis Treatment Trial was a landmark study with implications worldwide. In the advent of antibody testing for neuromyelitis optica spectrum disease (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), emerging concepts, such as routine antibody testing and management, remain controversial, resulting mostly from studies in White populations. We evaluate the practice patterns of optic neuritis investigation and management by neuro-ophthalmologists and neurologists in Singapore. Design: 21-question online survey consisting of 4 clinical vignettes. Methods: The survey was sent to all Singapore Medical Council– registered ophthalmologists and neurologists who regularly manage patients with optic neuritis. Results: Forty-two recipients (17 formally trained neuro-ophthalmol-ogists [100% response rate] and 25 neurologists) responded. Participants opted for routine testing of anti–aquaporin-4 antibodies (88.1% in mild optic neuritis and 97.6% in severe optic neuritis). Anti-MOG antibodies were frequently obtained (76.2% in mild and 88.1% in severe optic neuritis). Plasmapheresis was rapidly initiated (85.7%) in cases of nonresponse to intravenous steroids, even before obtaining anti–aquaporin-4 or anti-MOG serology results. In both NMOSD and MOGAD, oral mycophenolate mofetil was the preferred option if chronic immunosuppression was necessary. Steroids were given for a longer duration and tapered more gradually than in idiopathic optic neuritis cases. Conclusions: Serological testing for NMOSD and MOGAD is considered as a routine procedure in cases of optic neuritis in Singapore, possibly due to local epidemiological features of these conditions. Chronic oral immunosuppression is preferred for the long term, but further research is necessary to establish the efficacy and cost-effectiveness of these practices.

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Section: Discussionmentioning

confidence: 99%

Section: Anti-mog Antibody Testingmentioning

confidence: 98%

Optic Neuritis in the Era of NMOSD and MOGAD: A Survey of Practice Patterns in Singapore

Foo

Yau

Singhal

et al. 2022

Asia-Pacific Journal of Ophthalmology

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“…The accumulating evidence of differences in clinical-MRI features, relapse risk, treatment, and outcome led to the concept that patients with MOG antibodies are affected by a distinct syndrome that differs from MS and AQP4-IgG-seropositive NMOSD. The term MOG antibody-associated disease (MOGAD) was thus coined to characterize these patients with autoimmune oligodendrocytopathy ( 16 ).…”

Section: Introductionmentioning

confidence: 99%

Serum and Cerebrospinal Fluid Biomarkers in Neuromyelitis Optica Spectrum Disorder and Myelin Oligodendrocyte Glycoprotein Associated Disease

et al. 2022

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The term neuromyelitis optica spectrum disorder (NMOSD) describes a group of clinical-MRI syndromes characterized by longitudinally extensive transverse myelitis, optic neuritis, brainstem dysfunction and/or, less commonly, encephalopathy. About 80% of patients harbor antibodies directed against the water channel aquaporin-4 (AQP4-IgG), expressed on astrocytes, which was found to be both a biomarker and a pathogenic cause of NMOSD. More recently, antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG), have been found to be a biomarker of a different entity, termed MOG antibody-associated disease (MOGAD), which has overlapping, but different pathogenesis, clinical features, treatment response, and prognosis when compared to AQP4-IgG-positive NMOSD. Despite important refinements in the accuracy of AQP4-IgG and MOG-IgG testing assays, a small proportion of patients with NMOSD still remain negative for both antibodies and are called “seronegative” NMOSD. Whilst major advances have been made in the diagnosis and treatment of these conditions, biomarkers that could help predict the risk of relapses, disease activity, and prognosis are still lacking. In this context, a number of serum and/or cerebrospinal fluid biomarkers are emerging as potentially useful in clinical practice for diagnostic and treatment purposes. These include antibody titers, cytokine profiles, complement factors, and markers of neuronal (e.g., neurofilament light chain) or astroglial (e.g., glial fibrillary acidic protein) damage. The aim of this review is to summarize current evidence regarding the role of emerging diagnostic and prognostic biomarkers in patients with NMOSD and MOGAD.

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“…Since anti-MOG antibody testing has become clinically available, 18–35% of children who present with acute demyelinating syndromes are reported to be seropositive for anti-MOG antibodies. 1 – 3 A relapsing or multiphasic course is reported in around 30–50% of seropositive patients, and most patients do not require long term immunomodulatory treatment or can achieve disease control with one immunomodulatory agent. 3 , 4 Here, however, we present a case of MOGAD with rapidly relapsing ADEM requiring escalation of immunotherapy beyond the current treatment algorithms.…”

Section: Introductionmentioning

confidence: 99%

Refractory MOG-Associated Demyelinating Disease in a Pediatric Patient

Kroenke

Ankar

Shukla

2022

Child Neurology Open

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Background: MOG antibody associated demyelinating disease (MOGAD) is a newly described autoimmune disorder that presents with monophasic or multiphasic demyelination in children. Case: We report a case of MOGAD that was refractory to current treatment algorithms and required rapid escalation of immunotherapy to achieve disease control. Conclusion: This case helps to further expand the phenotype of MOGAD and emphasizes the need to consider MOGAD in patients presenting with focal neurologic deficits, altered mental status, and/or seizures.

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Myelin-oligodendrocyte glycoprotein antibody-associated disease

Cited by 359 publications

References 100 publications

Optic Neuritis in the Era of NMOSD and MOGAD: A Survey of Practice Patterns in Singapore

Optic Neuritis in the Era of NMOSD and MOGAD: A Survey of Practice Patterns in Singapore

Serum and Cerebrospinal Fluid Biomarkers in Neuromyelitis Optica Spectrum Disorder and Myelin Oligodendrocyte Glycoprotein Associated Disease

Refractory MOG-Associated Demyelinating Disease in a Pediatric Patient

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