A case of concurrent anti-myelin oligodendrocyte glycoprotein antibody-associated myelitis and subacute combined degener
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LETTER TO THE EDITOR
A case of concurrent anti-myelin oligodendrocyte glycoprotein antibody-associated myelitis and subacute combined degeneration Keisuke Mizutani 1
&
Keita Sakurai 2
&
Toshiyuki Takahashi 3,4 & Hiroyuki Yuasa 1
Received: 28 July 2020 / Accepted: 16 November 2020 # Fondazione Società Italiana di Neurologia 2020
Dear Editor, Myelin oligodendrocyte glycoprotein (MOG) is expressed on the surface of oligodendrocytes. Anti-MOG antibodies have been linked to encephalitis and myelitis, with several studies reporting the coincidence of anti-MOG antibody-associated disease and other diseases [1]; however, the detail of this relationship is unclear. Here, we describe the first case of anti-MOG antibody-associated myelitis with subacute combined degeneration (SCD) due to autoimmune gastritis (AIG). The patient provided written informed consent, and the study was approved by the appropriate ethics review board. A 58-year-old woman with chronic thyroiditis presented with progressive left hemiplegia for two weeks. She noticed numbness in her limbs beginning one year prior to admission and had no history of alcohol abuse, gastrectomy, or unbalanced diet. Neurological examination revealed left hemiplegia, with partial loss of deep sensations and positive Tromner, Hoffmann, and Babinski reflexes on the left side. She did not have anemia (hemoglobin: 12.1 g/mL, normal range [NR]: 10.8–15.0 g/mL; mean corpuscular volume: 104.9 fL, NR: 83.5–101.6 fL), and her serum folate, copper, and ceruloplasmin levels were normal. Collagen and tumor marker tests were negative, except for anti-thyroid peroxidase (>2000 IU/
* Keisuke Mizutani [email protected] 1
Department of Neurology, Tosei General Hospital, 160 Nishioiwake-cho, Seto, Aichi 489-8642, Japan
2
Department of Radiology, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan
3
Department of Neurology, Tohoku University Hospital, Sendai, Miyagi, Japan
4
Department of Neurology, National Hospital Organization Yonezawa National Hospital, Yonezawa, Yamagata, Japan
mL, NR: ≤ 5.61 IU/mL) and anti-thyroglobulin antibody (258 IU/mL, NR: ≤ 4.11 IU/mL), respectively. Her cerebrospinal fluid (CSF) contained 7 lymphocytes/μL (NR: ≤ 5 /μL), normal protein levels (38 mg/dL, NR: ≤ 45 mg/dL), elevated levels of myelin basic protein (MBP) (614 pg/mL, NR: ≤ 102 pg/mL: measured using enzyme-linked immune-sorbent assay), and no evidence of oligoclonal immunoglobulin G (IgG) bands. Magnetic resonance imaging (MRI) showed hyperintense lesions (T2-weighted images) and abnormal enhancement (contrast-enhanced T1-weighted images) in the cervical spine (Fig. 1a–c). Due to suspected acute myelitis, methylprednisolone was administered intravenously (two 3day cycles of 1000 mg/day), and her left hemiplegia improved rapidly. Subsequently, this was replaced by oral prednisolone, with the treatment tapered by 5 mg/day every week and maintained at 5 mg daily. Two weeks after the intravenous steroid therapy, the abnormal enhancement on contrast-enhanced T1-weighted MRI was
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