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Complete remission induced by rituximab in refractory, seronegative, muscle-specific, kinase-positive myasthenia gravis
  1. William S Baek1,
  2. Asad Bashey2,
  3. Geoffrey L Sheean3
  1. 1Department of Neurophysiology, UCSD Perlman Ambulatory Care Center, San Diego, California, USA
  2. 2Rebecca and John Moores UCSD Cancer Center, San Diego, California, USA
  3. 3Department of Neurophysiology, UCSD Perlman Ambulatory Care Center, San Diego, California, USA
  1. Correspondence to:
 Dr G L Sheean
 Department of Neurosciences, UCSD Medical Center, University of California, San Diego, 200 West Arbor Drive (8465), San Diego, CA 92103-8465, USA; gsheean{at}ucsd.edu

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Rituximab is a chimeric IgG1 κ monoclonal antibody that targets CD20, a transmembrane phosphoprotein on most B cells. Rituximab depletes B cells by binding to the CD20 molecule and initiating complement-dependent cytolysis or antibody-dependent cell-mediated cytotoxicity.1

Recently, there was a case of muscle-specific kinase (MuSK)-positive myasthenia gravis (MG) successfully treated with rituximab.2

We report a patient with MuSK-positive generalised MG who achieved complete remission with rituximab, after being refractory to steroids, intravenous immunoglobulin, immunosuppressants, thymectomy and less responsive to plasmapheresis.

A 32-year-old man was referred for refractory MG. He gave a 2.5-year history of mild bulbar and generalised weakness, mostly in proximal extremities, without sensory symptoms. He denied ptosis and diplopia but reported mild dysphagia and dysarthria. Family history was negative for neuromuscular disorders. He was receiving no medications. He denied any history of smoking and drank socially.

The general physical examination was unremarkable. Neurological examination demonstrated diplopia on extreme lateral gaze without fatigable ptosis or Cogan’s lid twitch sign. There was moderate weakness of facial muscles bilaterally and of the tongue, without …

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