title: Treatment of IgM antibody associated polyneuropathies using rituximab.
abstract: OBJECTIVE
  Polyneuropathies with associated serum IgM antibodies are often difficult to treat. Rituximab is a monoclonal antibody directed against the B cell surface membrane marker CD20. Rituximab eliminates B cells from the circulation, and, over time, could reduce cells producing autoantibodies. This study tested the ability of rituximab to produce changes in serum antibody titres, and improvement in strength, in patients with neuromuscular disorders and IgM autoantibodies.
  
  
  METHODS
  Over a period of two years, the authors evaluated changes in strength, measured by quantitative dynamometry, and concentrations of several types of serum antibodies in patients with polyneuropathies and serum IgM autoantibodies. Twenty one patients treated with rituximab were compared with 13 untreated controls.
  
  
  RESULTS
  Treatment with rituximab was followed by improved strength (an increase of mean (SEM) 23% (2%)of normal levels of strength), a reduction in serum IgM autoantibodies (to 43% (4%) of initial values), and a reduction in total levels of IgM (to 55% (4%) of initial values). There was no change in levels of serum IgG antibodies. There were no major side effects, even though B cells were virtually eliminated from the circulation for periods up to two years.
  
  
  CONCLUSIONS
  In patients with IgM autoantibody associated peripheral neuropathies, rituximab treatment is followed by reduced serum concentrations of IgM, but not IgG, antibodies, and by improvement in strength. Additional studies, with placebo controls and blinded outcome measures, are warranted to further test the efficacy of rituximab treatment of IgM associated polyneuropathies.
authors.affiliation: Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA. pestronk@kids.wustl.edu
authors.forename: A
authors.initials: A
authors.lastname: Pestronk
authors.forename: J
authors.initials: J
authors.lastname: Florence
authors.forename: T
authors.initials: T
authors.lastname: Miller
authors.forename: R
authors.initials: R
authors.lastname: Choksi
authors.forename: M T
authors.initials: MT
authors.lastname: Al-Lozi
authors.forename: T D
authors.initials: TD
authors.lastname: Levine
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000009:adverse effects* / Q000097:blood; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D005500:Follow-Up Studies; D006801:Humans; D007075:Immunoglobulin M / Q000009:adverse effects* / Q000097:blood; D007136:Immunoglobulins / Q000097:blood; D009142:Musculoskeletal Physiological Phenomena / Q000187:drug effects; D017063:Outcome Assessment, Health Care; D011115:Polyneuropathies / Q000097:blood / Q000139:chemically induced* / Q000188:drug therapy*; D000069283:Rituximab; D013997:Time Factors
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D000970:Antineoplastic Agents; D007075:Immunoglobulin M; D007136:Immunoglobulins; D000069283:Rituximab