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Myasthenia Gravis during the Course of Neuromyelitis Optica

Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder of the central nervous system that has been thought to be a severe subtype of multiple sclerosis for a long time. The discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not...

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Autores principales: Etemadifar, Masoud, Abtahi, Seyed-Hossein, Dehghani, Alireza, Abtahi, Mohammad-Ali, Akbari, Mojtaba, Tabrizi, Nasim, Goodarzi, Tannaz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: S. Karger AG 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224523/
https://www.ncbi.nlm.nih.gov/pubmed/22125527
http://dx.doi.org/10.1159/000334128
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author Etemadifar, Masoud
Abtahi, Seyed-Hossein
Dehghani, Alireza
Abtahi, Mohammad-Ali
Akbari, Mojtaba
Tabrizi, Nasim
Goodarzi, Tannaz
author_facet Etemadifar, Masoud
Abtahi, Seyed-Hossein
Dehghani, Alireza
Abtahi, Mohammad-Ali
Akbari, Mojtaba
Tabrizi, Nasim
Goodarzi, Tannaz
author_sort Etemadifar, Masoud
collection PubMed
description Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder of the central nervous system that has been thought to be a severe subtype of multiple sclerosis for a long time. The discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not only has made a revolutionary pace in establishing a serologic distinction between the two diseases, but it has also classified NMO as an antibody-mediated disorder. Similarly, myasthenia gravis (MG) is a well-known antibody-mediated disorder. In this report, we describe the case of a middle-aged female patient who experienced definite MG with an unclear clinical picture of chronic demyelinating disease that initially reflected the diagnosis of MS, but further imaging and paraclinical workup (e.g. positive AQP4 antibody test) revealed NMO. The coexistence of NMO and MG is previously described. However, this is the first case with NMO symptoms preceding the onset of MG. Of note, the development of MG occurred after a 2-year period of interferon β-1b (IFN β-1b) administration. This calls the question to mind of whether in our case MG is induced by the administration of interferon, instead of an original pathogenic link between MG and NMO. In other words, immunomodulatory treatments can slip the immunity towards T-helper II predominant pathways that can trigger MG. However, if we assume that such an explanation (i.e. increased susceptibility to autoantibody-mediated disorders) is true, our case can be considered the first case of NMO who developed MG following IFN β-1b treatment.
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spelling pubmed-32245232011-11-28 Myasthenia Gravis during the Course of Neuromyelitis Optica Etemadifar, Masoud Abtahi, Seyed-Hossein Dehghani, Alireza Abtahi, Mohammad-Ali Akbari, Mojtaba Tabrizi, Nasim Goodarzi, Tannaz Case Rep Neurol Published: October, 2011 Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder of the central nervous system that has been thought to be a severe subtype of multiple sclerosis for a long time. The discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not only has made a revolutionary pace in establishing a serologic distinction between the two diseases, but it has also classified NMO as an antibody-mediated disorder. Similarly, myasthenia gravis (MG) is a well-known antibody-mediated disorder. In this report, we describe the case of a middle-aged female patient who experienced definite MG with an unclear clinical picture of chronic demyelinating disease that initially reflected the diagnosis of MS, but further imaging and paraclinical workup (e.g. positive AQP4 antibody test) revealed NMO. The coexistence of NMO and MG is previously described. However, this is the first case with NMO symptoms preceding the onset of MG. Of note, the development of MG occurred after a 2-year period of interferon β-1b (IFN β-1b) administration. This calls the question to mind of whether in our case MG is induced by the administration of interferon, instead of an original pathogenic link between MG and NMO. In other words, immunomodulatory treatments can slip the immunity towards T-helper II predominant pathways that can trigger MG. However, if we assume that such an explanation (i.e. increased susceptibility to autoantibody-mediated disorders) is true, our case can be considered the first case of NMO who developed MG following IFN β-1b treatment. S. Karger AG 2011-10-21 /pmc/articles/PMC3224523/ /pubmed/22125527 http://dx.doi.org/10.1159/000334128 Text en Copyright © 2011 by S. Karger AG, Basel http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial-No-Derivative-Works License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Users may download, print and share this work on the Internet for noncommercial purposes only, provided the original work is properly cited, and a link to the original work on http://www.karger.com and the terms of this license are included in any shared versions.
spellingShingle Published: October, 2011
Etemadifar, Masoud
Abtahi, Seyed-Hossein
Dehghani, Alireza
Abtahi, Mohammad-Ali
Akbari, Mojtaba
Tabrizi, Nasim
Goodarzi, Tannaz
Myasthenia Gravis during the Course of Neuromyelitis Optica
title Myasthenia Gravis during the Course of Neuromyelitis Optica
title_full Myasthenia Gravis during the Course of Neuromyelitis Optica
title_fullStr Myasthenia Gravis during the Course of Neuromyelitis Optica
title_full_unstemmed Myasthenia Gravis during the Course of Neuromyelitis Optica
title_short Myasthenia Gravis during the Course of Neuromyelitis Optica
title_sort myasthenia gravis during the course of neuromyelitis optica
topic Published: October, 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224523/
https://www.ncbi.nlm.nih.gov/pubmed/22125527
http://dx.doi.org/10.1159/000334128
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