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Main Outcomes and Measures Presence of anti-MOG antibodies was blindly assessed in serial samples collected over a median of 4 years. Data were analyzed from May to October 2018. Of 156 excluded participants, 154 were excluded owing to missing baseline samples and 2 owing to incomplete clinical information. Of 430 participants with acquired demyelinating syndrome recruited, 274 were included in analyses. Inclusion criteria included (1) incident central nervous system demyelination, (2) at least 1 serum sample obtained within 45 days from onset, and (3) complete clinical information. Objective To characterize serial anti-MOG antibody serologies and clinical and imaging features at presentation and during follow-up in an inception cohort of prospectively monitored children with acquired demyelination.ĭesign, Setting, and Participants In this prospective cohort study, study participants were recruited from July 2004 to February 2017 through the multicenter Canadian Pediatric Demyelinating Disease Study.
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Importance Identifying the course of demyelinating disease associated with myelin oligodendrocyte glycoprotein (MOG) autoantibodies is critical to guide appropriate treatment choices.
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Participants with ADEM had a considerably shorter time to seroconversion than participants without ADEM. C, Kaplan-Meier curves in participants with acute disseminated encephalomyelitis (ADEM) vs non-ADEM presentations. B, Kaplan-Meier curve for the time to conversion to seronegative status in all participants who were positive for anti-MOG antibodies at time of presentation. Of the 10 participants with borderline results at onset, 7 became seronegative, 2 fluctuated between negative and borderline status and 1 became seropositive in the last follow-up sample (7 years from onset titer, 1:200). Only 2 of 139 participants who were negative for anti-MOG antibodies at presentation changed serological status in subsequent examinations: 1 participant became seropositive at 3 months and was persistently positive for the subsequent 8 years and 1 had an isolated finding of a borderline result at 2 years from onset. All rights reserved.A, Evolution of serologic status in participants with follow-up greater than 1 year. In this review, we examine the history of the MOG antibody and its relevance to demyelinating disease, as well as compare the clinical, radiographic and serological profiles of patients with MOG antibody with patients with AQP4 antibody.Ĭopyright © 2018 Elsevier B.V. MOG antibody disease has thus recently emerged as a distinct entity carved out of the patient population diagnosed with NMOSD. In recent studies around the world where MOG testing is available, up to 42% of NMOSD patients who test seronegative for the AQP4 antibody test positive for MOG antibodies. In addition, acute disseminated encephalomyelitis (ADEM) is a well-recognized phenotype of MOG antibody disease in children. Clinically, the disease resembles neuromyelitis optica spectrum disorders in the predilection for relapses of optic neuritis and transverse myelitis. MOG is a glycoprotein expressed on the outer membrane of myelin and solely found within the central nervous system, including in the brain, optic nerves and spinal cord. MOG antibody disease is an autoimmune disease of the central nervous system associated with a serological antibody against MOG, myelin oligodendrocyte glycoprotein.