To investigate interleukin-6 (IL-6) as a potential prognostic biomarker in steroid-dependent, relapsing MOG antibody disease (MOGAD). 

MOGAD is an expanding spectrum of central nervous system (CNS) inflammatory-demyelinating disease with diverse clinical phenotypes and treatment response compared to neuromyelitis optica spectrum disorder¹. Patients are often steroid-dependent with relapsing course despite first-line therapy underscoring the need for prognostic biomarkers to guide treatment. IL-6 has been shown to be upregulated in MOGAD and is an emerging therapeutic target^1,2.  

At 34-years-old, the patient presented with right optic neuritis (ON). Investigations were significant for positive MOG-IgG(titer 1:80) and MRI brain with enhancement of right optic nerve and corpus callosal and bilateral cerebellar peduncle lesions. He had complete recovery from index event following corticosteroids; however, experienced relapse with ON and transverse myelitis (TM) two weeks after prednisone taper. Patient had third relapse of ON, and rituximab was initiated. He experienced fourth relapse on rituximab with bilateral ON and focal seizures in setting of enhancing parieto-occipital lesion. Investigations showed suppressed B cells (Abs CD19=0), MOG-IgG titer 1:1000, normal serum IL6 (<1.40 pg/mL). CSF analysis significant for lymphocytic pleocytosis and markedly elevated IL-6 (31.3 pg/mL). CSF B and T cell flow cytometry showed high frequency of T-effector cells. He was initiated on Satralizumab with no relapse to date.  

We report case of relapsing MOGAD refractory to rituximab who was successfully treated with Satralizumab, consistent with research that shows upregulation of CSF IL-6³. Targeted treatment with Satralizumab can block IL-6 differentiation of T cells and stimulation of autoantibody production and highlights IL-6 as potential prognostic marker in MOGAD with therapeutic implications.