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Failure of alemtuzumab therapy to control MOG encephalomyelitis

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Myelin oligodendrocyte glycoprotein (MOG) immunoglobulin G (IgG)–associated encephalomyelitis (EM) is a rare autoimmune disorder that displays substantial clinicoradiologic overlap with aquaporin-4 (AQP4)-IgG-seropositive neuromyelitis optica spectrum disorders (NMOSD) and classic multiple… Click to show full abstract

Myelin oligodendrocyte glycoprotein (MOG) immunoglobulin G (IgG)–associated encephalomyelitis (EM) is a rare autoimmune disorder that displays substantial clinicoradiologic overlap with aquaporin-4 (AQP4)-IgG-seropositive neuromyelitis optica spectrum disorders (NMOSD) and classic multiple sclerosis (MS).1–3,e1 The long-term outcome is often poor.2,3,e1 Recent evidence suggests that many disease-modifying agents approved for the treatment of MS may be ineffective or even harmful in AQP4-IgG-positive and MOG-IgG-positive patients.2–4

Keywords: igg; failure alemtuzumab; encephalomyelitis; therapy control; alemtuzumab therapy; mog

Journal Title: Neurology
Year Published: 2017

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