• J. Neurol. Neurosurg. Psychiatr. · Aug 2014

    Fcγ receptor IIIA genotype is associated with rituximab response in antimyelin-associated glycoprotein neuropathy.

    • Abraham C J Stork, Nicolette C Notermans, Leonard H van den Berg, Raymond D Schellevis, Jikke-Mien F Niermeijer, Maaike Nederend, Jeanette H W Leusen, and W-Ludo van der Pol.
    • Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, The Netherlands.
    • J. Neurol. Neurosurg. Psychiatr. 2014 Aug 1; 85 (8): 918-20.

    BackgroundTreatment with anti-B cell antibody rituximab may ameliorate the disease course in a subgroup of patients with polyneuropathy associated with IgM monoclonal gammopathy. Polymorphisms of leukocyte IgG receptors (FcγR) that influence efficiency of antibody-dependent cell-mediated cytotoxicity determine rituximab efficacy in patients with lymphoma and autoimmune disease.ObjectiveTo investigate the association of FcγRIIA and FcγRIIIA polymorphisms with the response to rituximab treatment in a cohort of patients with polyneuropathy associated with IgM monoclonal gammopathy (PNP-IgM) with and without antimyelin-associated glycoprotein antibodies.MethodsWe determined FcγRIIA-R/H131 and FcγRIIIA-V/F158 genotypes in 27 patients with PNP-IgM using allele-specific PCR and Sanger sequencing.ResultsThe FcγRIIIA-V/V158 genotype was associated with functional improvement (p=0.02) after 1 year.ConclusionsFcγRIIIA polymorphisms are potential biomarkers for response to rituximab treatment in polyneuropathy associated with IgM monoclonal gammopathy.Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

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