AI Article Synopsis
- Rituximab treatment may improve symptoms in some patients with polyneuropathy linked to IgM monoclonal gammopathy, and the effectiveness can depend on specific genetic variations in immune receptors.
- Polymorphisms in FcγRIIA and FcγRIIIA genes were examined in 27 patients to see how they impacted response to rituximab.
- Results indicated that the FcγRIIIA-V/V158 genotype was linked to better patient outcomes after one year of treatment, suggesting these genetic markers could help predict treatment success.
Article Abstract
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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| http://dx.doi.org/10.1136/jnnp-2013-306958 | DOI Listing |
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