MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome.

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Abstract

A subset of patients with neuromyelitis optica spectrum disorders (NMOSD) has been shown to be seropositive for myelin oligodendrocyte glycoprotein antibodies (MOG-IgG).

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Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients

Sven Jarius, Klemens Ruprecht, Brigitte Wildemann … (2012)

Background The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results Seropositive patients were found to be predominantly female (p 1 myelitis attacks in the first year were identified as possible predictors of a worse outcome. Conclusion This study provides an overview of the clinical and paraclinical features of NMOSD in Caucasians and demonstrates a number of distinct disease characteristics in seropositive and seronegative patients.

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Overlapping demyelinating syndromes and anti–N-methyl-D-aspartate receptor encephalitis.

Maarten J. Titulaer, Romana Höftberger, Takahiro Iizuka … (2014)

To report the clinical, radiological, and immunological association of demyelinating disorders with anti–Nmethyl- D-aspartate receptor (NMDAR) encephalitis. Clinical and radiological analysis was done of a cohort of 691 patients with anti-NMDAR encephalitis. Determination of antibodies to NMDAR, aquaporin-4 (AQP4), and myelin oligodendrocyte glycoprotein (MOG) was performed using brain immunohistochemistry and cell-based assays. Twenty-three of 691 patients with anti-NMDAR encephalitis had prominent magnetic resonance imaging (MRI) and/or clinical features of demyelination. Group 1 included 12 patients in whom anti-NMDAR encephalitis was preceded or followed by independent episodes of neuromyelitis optica (NMO) spectrum disorder (5 cases, 4 anti-AQP4 positive) or brainstem or multifocal demyelinating syndromes (7 cases, all anti-MOG positive). Group 2 included 11 patients in whom anti-NMDAR encephalitis occurred simultaneously with MRI and symptoms compatible with demyelination (5 AQ4 positive, 2 MOG positive). Group 3 (136 controls) included 50 randomly selected patients with typical anti-NMDAR encephalitis, 56 with NMO, and 30 with multiple sclerosis; NMDAR antibodies were detected only in the 50 anti-NMDAR patients, MOG antibodies in 3 of 50 anti-NMDAR and 1 of 56 NMO patients, and AQP4 antibodies in 48 of 56 NMO and 1 of 50 anti-NMDAR patients (p<0.0001 for all comparisons with Groups 1 and 2). Most patients improved with immunotherapy, but compared with anti-NMDAR encephalitis the demyelinating episodes required more intensive therapy and resulted in more residual deficits. Only 1 of 23 NMDAR patients with signs of demyelination had ovarian teratoma compared with 18 of 50 anti-NMDAR controls (p50.011). Patients with anti-NMDAR encephalitis may develop concurrent or separate episodes of demyelinating disorders, and conversely patients with NMO or demyelinating disorders with atypical symptoms (eg, dyskinesias, psychosis) may have anti-NMDAR encephalitis.

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MOG cell-based assay detects non-MS patients with inflammatory neurologic disease

Patrick Waters, Mark Woodhall, Kevin O'Connor … (2015)

Objective: To optimize sensitivity and disease specificity of a myelin oligodendrocyte glycoprotein (MOG) antibody assay. Methods: Consecutive sera (n = 1,109) sent for aquaporin-4 (AQP4) antibody testing were screened for MOG antibodies (Abs) by cell-based assays using either full-length human MOG (FL-MOG) or the short-length form (SL-MOG). The Abs were initially detected by Alexa Fluor goat anti-human IgG (H + L) and subsequently by Alexa Fluor mouse antibodies to human IgG1. Results: When tested at 1:20 dilution, 40/1,109 sera were positive for AQP4-Abs, 21 for SL-MOG, and 180 for FL-MOG. Only one of the 40 AQP4-Ab–positive sera was positive for SL-MOG-Abs, but 10 (25%) were positive for FL-MOG-Abs (p = 0.0069). Of equal concern, 48% (42/88) of sera from controls (patients with epilepsy) were positive by FL-MOG assay. However, using an IgG1-specific secondary antibody, only 65/1,109 (5.8%) sera were positive on FL-MOG, and AQP4-Ab– positive and control sera were negative. IgM reactivity accounted for the remaining anti-human IgG (H + L) positivity toward FL-MOG. The clinical diagnoses were obtained in 33 FL-MOG–positive patients, blinded to the antibody data. IgG1-Abs to FL-MOG were associated with optic neuritis (n = 11), AQP4-seronegative neuromyelitis optica spectrum disorder (n = 4), and acute disseminated encephalomyelitis (n = 1). All 7 patients with probable multiple sclerosis (MS) were MOG-IgG1 negative. Conclusions: The limited disease specificity of FL-MOG-Abs identified using Alexa Fluor goat anti-human IgG (H + L) is due in part to detection of IgM-Abs. Use of the FL-MOG and restricting to IgG1-Abs substantially improves specificity for non-MS demyelinating diseases. Classification of evidence: This study provides Class II evidence that the presence of serum IgG1- MOG-Abs in AQP4-Ab–negative patients distinguishes non-MS CNS demyelinating disorders from MS (sensitivity 24%, 95% confidence interval [CI] 9%–45%; specificity 100%, 95% CI 88%–100%).

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Journal

Journal ID (iso-abbrev): J Neuroinflammation

Title: Journal of neuroinflammation

Publisher: Springer Nature

ISSN (Electronic): 1742-2094

ISSN (Print): 1742-2094

Publication date (Electronic): Sep 27 2016

Volume: 13

Issue: 1

Affiliations

[1 ] Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany. sven.jarius@med.uni-heidelberg.de.

[2 ] Department of Neurology, Charité University Medicine Berlin, Berlin, Germany.

[3 ] Department of Neurology, Ruhr University Bochum, Bochum, Germany.

[4 ] NeuroCure Clinical Research Center and Clinical and Experimental Multiple Sclerosis Research Center, Department of Neurology, Charité University Medicine, Berlin, Germany.

[5 ] Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité University Medicine Berlin, Berlin, Germany.

[6 ] Department of Neurology and Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.

[7 ] Department of Neurology, Albert Ludwigs University, Freiburg, Germany.

[8 ] Department of Neurology, Hannover Medical School, Hannover, Germany.

[9 ] Department of Neurology, Heinrich Heine University, Düsseldorf, Germany.

[10 ] Department of Neurology, University of Rostock, Rostock, Germany.

[11 ] Molecular Neuroimmunology Group, Department of Neurology, University of Heidelberg, Heidelberg, Germany.

[12 ] Department of Neurology, Julius Maximilians University, Würzburg, Germany.

[13 ] IRCCS, C. Mondino National Neurological Institute, Pavia, Italy.

[14 ] Centro di Riferimento Regionale SM, Azienda Ospedaliero Universitaria San Luigi Gonzaga, Orbassano, Italy.

[15 ] Department of Neuroradiology, Charité University Medicine - Berlin, Berlin, Germany.

[16 ] Department of Neuroradiology, Ruhr University Bochum, Bochum, Germany.

[17 ] Institute of Experimental Immunolog, affiliated to Euroimmun AG, Lübeck, Germany.

[18 ] Department of Neurology, Medical University Innsbruck, Innsbruck, Austria.

Article

Publisher Item ID: 10.1186/s12974-016-0718-0

DOI: 10.1186/s12974-016-0718-0

PMC ID: 5086042

PubMed ID: 27793206

SO-VID: 16fa1946-8549-4e1e-915c-4bf41018cac8

History

Keywords: Aquaporin-4 antibodies (AQP4-IgG, NMO-IgG),Autoantibodies,Azathioprine,Barkhof criteria,Cerebrospinal fluid,Electrophysiology,Evoked potentials,Glatiramer acetate,IPND criteria,Infections,Interferon beta,International consensus diagnostic criteria for neuromyelitis optica spectrum disorders,Longitudinally extensive transverse myelitis,Magnetic resonance imaging,McDonald criteria,Methotrexate,Multiple sclerosis,Myelin oligodendrocyte glycoprotein antibodies (MOG-IgG),Natalizumab,Neuromyelitis optica spectrum disorders (NMOSD),Ofatumumab,Oligoclonal bands,Optic neuritis,Outcome,Pregnancy,Rituximab,Therapy,Transverse myelitis,Treatment,Vaccination,Wingerchuk criteria 2006 and 2015

MOG-IgG in NMO and related disorders: a multicenter study of 50 patients. Part 2: Epidemiology, clinical presentation, radiological and laboratory features, treatment responses, and long-term outcome.

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Most cited references 79

Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients

Overlapping demyelinating syndromes and anti–N-methyl-D-aspartate receptor encephalitis.

MOG cell-based assay detects non-MS patients with inflammatory neurologic disease

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