2023
DOI: 10.1212/nxi.0000000000200077
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MOG Antibody–Associated Disease and Thymic Hyperplasia

Abstract: Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) is a recently described CNS inflammatory disorder that may manifest with optic neuritis, myelitis, seizures, and/or acute disseminated encephalomyelitis. While MOG-specific antibodies in patients with MOGAD are IgG1, a T-cell–dependent antibody isotype, immunologic mechanisms of this disease are not fully understood. Thymic hyperplasia can be associated with certain autoimmune diseases. In this report we describe a case of MOGAD associated… Show more

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Cited by 4 publications
(2 citation statements)
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“…For example, it is unclear how transient or fluctuating MOG seropositivity, sometimes seen with repeated serum sampling even off treatment, should be applied to MOGAD diagnostic criteria. In addition, MOG-Abs have been reported in conditions considered noncore by the 2023 MOGAD criteria, such as orbital inflammatory disease 31,32 and thymic hyperplasia, 33 so how does one decide whether to include them in future or is the MOG-Ab association spurious for noncore presentations? Furthermore, there are unresolved issues about the role of MOG seropositivity in patients diagnosed with MS. Further basic science and translational research is needed to fully understand the role of MOG-Ab in MOGAD.…”
Section: Discussionmentioning
confidence: 99%
“…For example, it is unclear how transient or fluctuating MOG seropositivity, sometimes seen with repeated serum sampling even off treatment, should be applied to MOGAD diagnostic criteria. In addition, MOG-Abs have been reported in conditions considered noncore by the 2023 MOGAD criteria, such as orbital inflammatory disease 31,32 and thymic hyperplasia, 33 so how does one decide whether to include them in future or is the MOG-Ab association spurious for noncore presentations? Furthermore, there are unresolved issues about the role of MOG seropositivity in patients diagnosed with MS. Further basic science and translational research is needed to fully understand the role of MOG-Ab in MOGAD.…”
Section: Discussionmentioning
confidence: 99%
“…Já na MOGAD, há indícios de que a lesão da mielina seria por ação dos anticorpos que se ligam a MOG e levam a inflamação por ativação do sistema complemento e citotoxidade. Então, provavelmente a ausência de necrose tecidual nos pacientes com MOGAD deve ser responsável pela apresentação relativamente mais branda da doença (HURTUBISE et al, 2023).…”
Section: Snc-unclassified