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Myasthenia Gravis During the Course of Neuromyelitis Optica Publisher



Etemadifar M1, 2, 3 ; Abtahi SH1, 2, 3 ; Dehghani A1, 5 ; Abtahi MA1, 5 ; Akbari M1, 6 ; Tabrizi N4 ; Goodarzi T7, 8, 9
Authors
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Authors Affiliations
  1. 1. Medical School, Isfahan University of Medical Sciences, Iran
  2. 2. Isfahan Medical Students Research Committee (IMSRC), Iran
  3. 3. Isfahan Research Committee of Multiple Sclerosis, Iran
  4. 4. Department of Neurology, Medical School, Isfahan University of Medical Sciences, Iran
  5. 5. Ophthalmology Ward, Feiz Hospital, Isfahan University of Medical Sciences, Iran
  6. 6. Department of Epidemiology and Statistics, Isfahan University of Medical Sciences, Isfahan, Iran
  7. 7. National Institute of Genetic Engineering and Biotechnology, Iran
  8. 8. Department of Plant Biotechnology, Canker Group, Tehran, Iran
  9. 9. S.H.A. Official Research Center of Neurological-Ophthalmological Sciences (SHARNOS Co.), Seyed-Alikhan, Chaharbagh Abbasi Isfahan 81448-14581, No. 9, Boroomand, Iran

Source: Case Reports in Neurology Published:2011


Abstract

Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder of the central nervous system that has been thought to be a severe subtype of multiple sclerosis for a long time. The discovery of aquaporin-4 (AQP4) antibody as a highly specific marker responsible for the pathogenesis of NMO, not only has made a revolutionary pace in establishing a serologic distinction between the two diseases, but it has also classified NMO as an antibody-mediated disorder. Similarly, myasthenia gravis (MG) is a well-known antibody-mediated disorder. In this report, we describe the case of a middle-aged female patient who experienced definite MG with an unclear clinical picture of chronic demyelinating disease that initially reflected the diagnosis of MS, but further imaging and paraclinical workup (e.g. positive AQP4 antibody test) revealed NMO. The coexistence of NMO and MG is previously described. However, this is the first case with NMO symptoms preceding the onset of MG. Of note, the development of MG occurred after a 2-year period of interferon β-1b (IFN β-1b) administration. This calls the question to mind of whether in our case MG is induced by the administration of interferon, instead of an original pathogenic link between MG and NMO. In other words, immunomodulatory treatments can slip the immunity towards T-helper II predominant pathways that can trigger MG. However, if we assume that such an explanation (i.e. increased susceptibility to autoantibody-mediated disorders) is true, our case can be considered the first case of NMO who developed MG following IFN β-1b treatment. © 2011 S. Karger AG, Basel.
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