Transient MOG antibody seroconversion associated with immunomodulating therapy

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Bibliographic Details
Main Authors: Pawlitzki, Marc (Author) , Campe, Christin (Author) , Rolfes, Leoni (Author) , Heinze, Hans-Jochen (Author) , Leypoldt, Frank (Author) , Wandinger, Klaus-Peter (Author) , Reindl, Markus (Author) , Wildemann, Brigitte (Author) , Jarius, Sven (Author) , Körtvélyessy, Péter (Author)
Format: Article (Journal)
Language:English
Published: 2020
In: Multiple Sclerosis and Related Disorders
Year: 2019, Volume: 37
ISSN:2211-0356
DOI:10.1016/j.msard.2019.101420
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.msard.2019.101420
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Author Notes:Marc Pawlitzki, Christin Campe, Leoni Rolfes, Hans-Jochen Heinze, Frank Leypoldt, Klaus-Peter Wandinger, Markus Reindl, Brigitte Wildemann, Sven Jarius, Peter Körtvelyessy
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Item Description:Gesehen am 04.05.2020
Available online: 28 September 2019
Immunoglobulin G (IgG) autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG) have recently been associated with autoimmune CNS demyelination. We present the case of a 35-year-old patient who was seronegative for MOG-IgG (as confirmed by means of three independent immunoassays) during two corticosteroid-responsive attacks of brainstem encephalitis and optic neuritis, respectively, but turned positive for MOG-IgG under treatment with interferon-beta (IFN-beta), which was commenced 6 months after onset of the first attack. MOG-IgG serum levels declined after therapy was switched to glatiramer acetate. The fact that seroconversion was first observed under treatment with IFN-beta is in accordance with previous evidence suggesting a role of IFN-beta in disease exacerbation in antibody-mediated disorders
Physical Description:Online Resource
ISSN:2211-0356
DOI:10.1016/j.msard.2019.101420