Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyel...
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Frontiers Media S.A.
2025-01-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2024.1510097/full |
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author | Chen Min Bi Zhuajin Liu Peidong Li Ruoyu Liu Ju Liu Hongbo |
author_facet | Chen Min Bi Zhuajin Liu Peidong Li Ruoyu Liu Ju Liu Hongbo |
author_sort | Chen Min |
collection | DOAJ |
description | Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. At present, the mechanism underlying the disease is unknown. Herein, we report two cases of MOGAD accompanied by Epstein-Barr virus (EBV) infection. Both presented inflammation response in the cerebrospinal fluid (CSF), demonstrating elevated level of cell accounts and protein. EBV genomic sequence was also detected in the CSF samples. The patients recovered substantially after 3 months following a combination treatment with methylprednisolone and immunosuppressive therapy with ofatumumab. These cases provide new insight into the production of MOG-IgG and the possible pathological mechanisms underlying MOGAD. The cases also confirm the association with EBV, a virus that infects human B cells and has been proposed to be a trigger for MOGAD. This is the first report on subcutaneous ofatumumab treatment for MOGAD triggered by EBV, suggesting that this is a potentially valuable therapeutic option. |
format | Article |
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institution | Kabale University |
issn | 1664-3224 |
language | English |
publishDate | 2025-01-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Immunology |
spelling | doaj-art-ee9b57163ead4feead0e214edcaec9c42025-01-07T06:40:23ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-01-011510.3389/fimmu.2024.15100971510097Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case seriesChen Min0Bi Zhuajin1Liu Peidong2Li Ruoyu3Liu Ju4Liu Hongbo5Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaDepartment of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, ChinaMyelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) caused by pathogenic immunoglobulin G antibodies to myelin oligodendrocyte glycoprotein is a rare demyelinating disease of the central nerve system (CNS). The clinical phenotypes of MOGAD include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. At present, the mechanism underlying the disease is unknown. Herein, we report two cases of MOGAD accompanied by Epstein-Barr virus (EBV) infection. Both presented inflammation response in the cerebrospinal fluid (CSF), demonstrating elevated level of cell accounts and protein. EBV genomic sequence was also detected in the CSF samples. The patients recovered substantially after 3 months following a combination treatment with methylprednisolone and immunosuppressive therapy with ofatumumab. These cases provide new insight into the production of MOG-IgG and the possible pathological mechanisms underlying MOGAD. The cases also confirm the association with EBV, a virus that infects human B cells and has been proposed to be a trigger for MOGAD. This is the first report on subcutaneous ofatumumab treatment for MOGAD triggered by EBV, suggesting that this is a potentially valuable therapeutic option.https://www.frontiersin.org/articles/10.3389/fimmu.2024.1510097/fullMOG-IgG associated encephalitisEpstein-Barr virusofatumumabneuron damagecase report |
spellingShingle | Chen Min Bi Zhuajin Liu Peidong Li Ruoyu Liu Ju Liu Hongbo Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series Frontiers in Immunology MOG-IgG associated encephalitis Epstein-Barr virus ofatumumab neuron damage case report |
title | Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series |
title_full | Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series |
title_fullStr | Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series |
title_full_unstemmed | Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series |
title_short | Ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody-associated disease accompanied by Epstein-Barr viral infection: a case series |
title_sort | ofatumumab successfully treats myelin oligodendrocyte glycoprotein antibody associated disease accompanied by epstein barr viral infection a case series |
topic | MOG-IgG associated encephalitis Epstein-Barr virus ofatumumab neuron damage case report |
url | https://www.frontiersin.org/articles/10.3389/fimmu.2024.1510097/full |
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