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Fcγ receptor IIIA genotype is associated with rituximab response in antimyelin-associated glycoprotein neuropathy
  1. Abraham C J Stork1,
  2. Nicolette C Notermans1,
  3. Leonard H van den Berg1,
  4. Raymond D Schellevis1,
  5. Jikke-Mien F Niermeijer2,
  6. Maaike Nederend3,
  7. Jeanette H W Leusen3,
  8. W-Ludo van der Pol1
  1. 1Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, The Netherlands
  2. 2Department of Neurology, Academic Medical Center, Amsterdam, The Netherlands
  3. 3Laboratory for Translational Immunology, University Medical Center Utrecht, Utrecht, The Netherlands
  1. Correspondence to W-Ludo van der Pol, Department of Neurology, HP F02.226, Brain Center Rudolf Magnus, UMC Utrecht, Heidelberglaan 100, Utrecht 3584 CX, The Netherlands; wpol2{at}


Background Treatment 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.

Objective To 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.

Methods We determined FcγRIIA-R/H131 and FcγRIIIA-V/F158 genotypes in 27 patients with PNP-IgM using allele-specific PCR and Sanger sequencing.

Results The FcγRIIIA-V/V158 genotype was associated with functional improvement (p=0.02) after 1 year.

Conclusions FcγRIIIA polymorphisms are potential biomarkers for response to rituximab treatment in polyneuropathy associated with IgM monoclonal gammopathy.


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