Fcγ receptor IIIA genotype is associated with rituximab response in antimyelin-associated glycoprotein neuropathy.
case_series · Level IV
Where this comes from
- Record sourced from PubMed, PMID 24487381.
- Also identified by DOI 10.1136/jnnp-2013-306958.
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Abstract
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. 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. We determined FcγRIIA-R/H131 and FcγRIIIA-V/F158 genotypes in 27 patients with PNP-IgM using allele-specific PCR and Sanger sequencing. The FcγRIIIA-V/V158 genotype was associated with functional improvement (p=0.02) after 1 year. FcγRIIIA polymorphisms are potential biomarkers for response to rituximab treatment in polyneuropathy associated with IgM monoclonal gammopathy.
Medical subject headings
- Antibodies, Monoclonal, Murine-Derived
- Glycoproteins
- Myelin Sheath
- Polyneuropathies
- Receptors, IgG