Abstract

Here we report three cases of anti-myelin oligodendrocyte glycoprotein (MOG) antibody–associated disease (MOGAD) mimicking multiple sclerosis in which seropositivity for anti-MOG antibodies occurred during disease-modifying drug dimethyl fumarate (DMF) treatment. These patients developed relapses with anti-MOG antibody seroconversion after switching from fingolimod or steroid pulse therapy to DMF, which was associated with peripheral lymphocyte recovery. MOGAD is considered a humoral immune disease, and DMF reportedly enhances Th2-skewed humoral immune activity. Therefore, we suggest that DMF, but not fingolimod, may exacerbate humoral immune imbalance and enhance autoantibody production, leading to aggravation of MOGAD.

Highlights

  • Anti-myelin oligodendrocyte glycoprotein (MOG) antibody–associated disease (MOGAD), which makes up ∼40% of anti-aquaporin 4 (AQP4) antibody–negative neuromyelitis optica spectrum disorders, is often difficult to distinguish from multiple sclerosis (MS) [1]

  • A recent report mentioned that dimethyl fumarate (DMF) is ineffective but not harmful in a patient with MOGAD [8], the effectiveness of DMF has yet to be determined

  • Our patients were diagnosed with atypical MS because they were seronegative for specific antibodies and had good response to IVMP and fingolimod

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Summary

Introduction

Anti-myelin oligodendrocyte glycoprotein (MOG) antibody–associated disease (MOGAD), which makes up ∼40% of anti-aquaporin 4 (AQP4) antibody–negative neuromyelitis optica spectrum disorders, is often difficult to distinguish from multiple sclerosis (MS) [1]. The first patient was a 27-year-old woman who experienced two attacks of optic neuritis and transverse myelitis with short cervical and thoracic cord lesions in 4 years (Figure 1A). Cerebrospinal fluid (CSF) analysis revealed a slight elevation in protein levels and increases in myelin basic protein (MBP) levels and IgG index, but not in cell count or oligoclonal bands (Table 1; Patient 1, pre). She developed a severe relapse of transverse myelitis with a short cervical cord lesion accompanied by recovery from lymphocytopenia (Figure 1A).

Results
Conclusion

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