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Background <p>Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an autoimmune inflammatory demyelinating disease typically characterized by recurrent myelitis and optic neuritis. Its pathogenesis is primarily mediated by MOG-immunoglobulin G (IgG), a pathogenic autoantibody targeting central nervous system myelin. Efgartigimod, a human IgG antibody Fc fragment and natural ligand for the neonatal Fc receptor, promotes degeneration of circulating pathogenic IgG, potentially positioning it as a novel therapeutic option for MOGAD. Case presentation</p> Case presentation <p>We present the case of a 41-year-old Chinese male with MOGAD. During his third acute attack, he developed bilateral lower limb paralysis, sensory deficits, and urinary retention. Spinal magnetic resonance imaging revealed longitudinally extensive T2-hyperintense lesions extending from C7 to T5. Cerebrospinal fluid analysis showed mildly elevated protein (49 mg/dL) without pleocytosis. Serum anti-MOG IgG titer was positive at 1:100 (via cell-based assay). First-line immunotherapy, comprising intravenous methylprednisolone and immunoglobulin, failed to elicit clinical improvement. Subsequent administration of efgartigimod (10 mg/kg weekly for 4 doses) led to serological improvement and substantial functional recovery. At the 3-week post-treatment assessment, the patient achieved independent ambulation. </p> Conclusions <p>This is the first documented use of efgartigimod as a rescue therapy for an acute, severe myelitis attack in a patient with isolated MOGAD, expanding on recent observations in overlap syndromes. These findings highlight its potential role as a promising treatment alternative for MOGAD.</p>

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Successful treatment with efgartigimod as rescue therapy in acute attack of MOGAD: a case report

  • 期刊论文

  • 发表日期：

    2026年4月2日

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  • Yi-Xiao Li,
  • Rui-Yun Wang,
  • Ming-Qiu Wang,
  • Yan-Lei Hao

摘要

Background

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an autoimmune inflammatory demyelinating disease typically characterized by recurrent myelitis and optic neuritis. Its pathogenesis is primarily mediated by MOG-immunoglobulin G (IgG), a pathogenic autoantibody targeting central nervous system myelin. Efgartigimod, a human IgG antibody Fc fragment and natural ligand for the neonatal Fc receptor, promotes degeneration of circulating pathogenic IgG, potentially positioning it as a novel therapeutic option for MOGAD. Case presentation

Case presentation

We present the case of a 41-year-old Chinese male with MOGAD. During his third acute attack, he developed bilateral lower limb paralysis, sensory deficits, and urinary retention. Spinal magnetic resonance imaging revealed longitudinally extensive T2-hyperintense lesions extending from C7 to T5. Cerebrospinal fluid analysis showed mildly elevated protein (49 mg/dL) without pleocytosis. Serum anti-MOG IgG titer was positive at 1:100 (via cell-based assay). First-line immunotherapy, comprising intravenous methylprednisolone and immunoglobulin, failed to elicit clinical improvement. Subsequent administration of efgartigimod (10 mg/kg weekly for 4 doses) led to serological improvement and substantial functional recovery. At the 3-week post-treatment assessment, the patient achieved independent ambulation.

Conclusions

This is the first documented use of efgartigimod as a rescue therapy for an acute, severe myelitis attack in a patient with isolated MOGAD, expanding on recent observations in overlap syndromes. These findings highlight its potential role as a promising treatment alternative for MOGAD.