Complete remission induced by rituximab in refractory, seronegative, muscle-specific, kinase-positive myasthenia gravis

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...

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Veröffentlicht in:Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 2007-07, Vol.78 (7), p.771-771
Hauptverfasser: Baek, William S, Bashey, Asad, Sheean, Geoffrey L
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Sprache:eng
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Zusammenfassung: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 chimeric murine/human IgG1 [kappa] monoclonal antibody against CD20, rituximab depletes B cells by binding to the CD20 molecule and initiating complement-dependent cytolysis or antibody-dependent cell-mediated cytotoxicity, 1 hence providing therapeutic benefit for many B cell-mediated diseases.
ISSN:0022-3050
1468-330X
DOI:10.1136/jnnp.2006.093567