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Long‐term response to rituximab and fludarabine combination in IgM anti‐myelin‐associated glycoprotein neuropathy
Author(s) -
Gruson Berengere,
Ghomari Kamel,
Beaumont Marie,
Garidi Reda,
Just Alain,
Merle Philippe,
Merlusca Lavinia,
Marolleau Jean P.,
Royer Bruno
Publication year - 2011
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1111/j.1529-8027.2011.00343.x
Subject(s) - medicine , rituximab , fludarabine , macroglobulinemia , waldenstrom macroglobulinemia , gastroenterology , monoclonal gammopathy of undetermined significance , immunology , monoclonal , immunoglobulin m , oncology , antibody , chemotherapy , monoclonal antibody , multiple myeloma , immunoglobulin g , lymphoma , cyclophosphamide
We report the clinical response and biological effects of treatment with rituximab and fludarabine (RF) in five patients with IgM anti‐myelin‐associated glycoprotein (MAG) demyelinating neuropathy. Between November 2006 and October 2009, four men and one woman aged 52–85 years received intravenous rituximab at 375 mg/m 2 on day 1 and oral fludarabine at 40 mg/m 2 /day from days 1 to 5, in a treatment cycle that was repeated every month for up to 6 months. Two patients had IgM monoclonal gammopathy of undetermined significance and three low tumor mass Waldenstrom's macroglobulinemia. Four patients showed a major hematological response with a decrease in anti‐MAG titer in three and clearing in one. One patient did not respond. For the responding patients, symptoms and electrophysiological parameters improved significantly. No patient relapsed at post‐RF treatment follow‐up (12–45 months), and no toxicity was reported. The combination of RF induced significant responses in IgM anti‐MAG demyelinating neuropathies, without toxicity. Clinical improvements were correlated to hematological and immunological results.