A CBA did not detect anti-AQP4 or anti-MOG antibodies in the serum. CSF analysis detected pleocytosis, elevations in protein levels and IgG index, and the presence of oligoclonal bands, but not MBP ( Table 1 Patient 2, pre). OCT revealed severe RNFL thinning in the right eye and mild RNFL thinning in the left eye ( Figure 2C). She experienced a severe attack of optic neuritis around the age of 25, as shown on fluid-attenuated inversion recovery (FLAIR) MRI ( Figure 2B). The second patient was a 27-year-old woman who had several attacks of optic neuritis and transverse myelitis involving short lesions in the cervical cord in a year ( Figure 2A). She has had no relapses with subsequent oral prednisolone therapy (20 mg/day) for over 1 year ( Figure 1A). Intravenous methylprednisolone pulse therapy (1 g/day for 3 consecutive days IVMP) markedly decreased symptoms. We reconfirmed that the frozen serum sample from the time of the first CBA was truly seronegative for anti-MOG antibodies. At that time, the second CBA using the same methodology ( 3) revealed seroconversion for anti-MOG antibodies (titer, 1:256 cut-off, ≥1:128). CSF analysis also indicated elevation of protein levels, MBP levels, and IgG index, but pleocytosis and oligoclonal bands were not detected ( Table 1 Patient 1, post). MRI showed T2-hyperintense lesion around the central canal at the C4 level ( Figures 1F,G).

Three months later, she developed a severe relapse of transverse myelitis with a short cervical cord lesion accompanied by recovery from lymphocytopenia ( Figure 1A). Since she desired to have a child, fingolimod was switched to DMF. She had been effectively treated with fingolimod for the diagnosis of atypical MS for 2.5 years. Neither anti-AQP4 nor anti-MOG antibodies were detected in serum samples using an internationally standardized cell-based assay (CBA) ( 2– 4). 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). Optical coherence tomography (OCT) detected a significant decrease in retinal nerve fiber layer (RNFL) thickness in the left eye ( Figure 1E). Magnetic resonance imaging (MRI) showed T2-hyperintense lesions in the left optic nerve ( Figure 1B) and left dorsal horn and fasciculus at the C3 level ( Figures 1C,D). She experienced severe attacks of left retrobulbar neuritis and transverse myelitis at the age of 24. 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). Here we report three cases of MOGAD treated as atypical MS due to negativity for specific antibodies in which seroconversion for anti-MOG antibodies occurred when DMD was switched to dimethyl fumarate (DMF). Whether disease-modifying drugs (DMDs) widely used in MS are also effective in MOGAD remains unclear. Therefore, we suggest that DMF, but not fingolimod, may exacerbate humoral immune imbalance and enhance autoantibody production, leading to aggravation of MOGAD.Īnti-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). MOGAD is considered a humoral immune disease, and DMF reportedly enhances Th2-skewed humoral immune activity. 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. 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. 2Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.1Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan.Keita Takahashi 1 Hideyuki Takeuchi 1 * Ryoko Fukai 1 Haruko Nakamura 1 Keisuke Morihara 1 Yuichi Higashiyama 1 Toshiyuki Takahashi 2 Hiroshi Doi 1 Fumiaki Tanaka 1 *

Anti mog antibody disease