Tocilizumab treatment in severe recurrent anti-MOG-associated optic neuritis

Patients presenting with a clinical phenotype indicative of neuromyelitis optica spectrum disease (NMOSD) including its limited variants such as recurrent optic neuritis (ON) or longitudinally extensive transverse myelitis negative for AQP-4 antibodies may test positive for immunoglobulin G antibodies against myelin oligodendrocyte glycoprotein (MOG), a transmembrane protein expressed on oligodendrocytes and the outer layers of the myelin sheath. MOG antibody-associated autoimmunity has gained increasing attention over recent years due to its clinical overlap with NMOSD, despite the latter being considered an autoimmune astrocytopathy. Anti-MOG antibody-positive patients show a relapsing disease course that can lead to substantial visual loss and spinal cord involvement.^1–3 Data on therapy in MOG antibody-associated disease as of yet is limited, but similar to NMOSD, it appears critical to start an efficacious treatment early in order to prevent severe functional sequelae including blindness. Tocilizumab (TCZ), a humanized antibody targeting the interleukin-6 (IL-6) receptor, has shown promise in patients with breakthrough disease and highly active forms of AQP-4 antibody-positive NMOSD.^4,5 Prolonged treatment with TCZ has been reported both efficacious and safe⁵ and leading to a reduction of AQP-4 antibody titers.^4,5