Demystifying MOGAD and Double Seronegative NMOSD Further With IL-6 Blockade.

Abstract

Myelin oligodendrocyte glycoprotein-IgG (MOG-IgG)-associated disorder (MOGAD) is a recently de fi ned neuroimmunologic disorder a ff ecting the CNS, commonly presenting with acute disseminated encephalomyelitis in children and with optic neuritis and/or myelitis in adults. Although some patients, especially children, may exhibit a monophasic course, there are others who tend to run a highly relapsing course, potentially resulting in long-lasting neurologic disability, akin to those with neuromyelitis optica spectrum disorder (NMOSD). 1 In fact, up to almost half of patients with NMOSD without aquaporin-4 (AQP4-IgG) harbor MOG-IgG. 2 In addition, despite comprehensive testing for aquaporin-4 antibodies, there remains a proportion of patients who phenotypically resemble those with NMOSD but are seronegative for both AQP4-IgG and MOG-IgG. 3 Recent key phase II and III international, randomized, double-blind, placebo-controlled trials in patients with NMOSD, AQP4-IgG, drugs speci fi c immunopathogenic of humanized monoclonal antibody targeting interleukin-6 e cacy interleukin-6 of with