Polymorphisms involved in response to biological agents used in rheumatoid arthritis

Abstract

Rheumatoid arthritis (RA) is a systemic disease that leads to joint destruction. During the last decade, the therapy of RA has been principally based on biological drugs. Although the efficacy of biological therapy has been established, patients demonstrated a high heterogeneity in clinical response to treatment. Several genetic polymorphisms play a part in the different response to biological drugs. This review summarizes the pharmacogenetics of biological agents approved for clinical RA treatment. We reviewed PubMed papers published over the past 20 years (2000–2020), inserting as the search term “rheumatoid arthritis and polymorphisms”. Despite some studies showing important correlations between genetic polymorphisms and response to biological therapy in RA patients, most of these findings are still lacking and inconsistent. The personalized treatment according to a pharmacogenetics approach is promising but the available pharmacogenetics data on biological treatment in RA are not adequate and reliable to recommend pharmacogenetic tests before starting biological therapy in RA patients. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

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Keywords

Cd20, Cd80, Cd86, Il-1, Il-6, Polymorphism, Rheumatoid arthritis, Tnf-α, Arthritis, rheumatoid, Biological factors, Humans, Polymorphism, single nucleotide, Adalimumab, Etanercept, Infliximab, Interleukin 6, Tocilizumab, Tumor necrosis factor, Biological factor, Biological therapy, Clinical outcome, Das28, Disease activity, Dna polymorphism, Dual antiplatelet therapy, Enzyme linked immunosorbent assay, Gene frequency, Genetic analysis, Genetic association, Genetic polymorphism, Genetic variation, Genome-wide association study, Genotype, Haplotype, Human, Pharmacogenetics, Phase 3 clinical trial (topic), Restriction fragment length polymorphism, Review, Single nucleotide polymorphism, Treatment response, Drug effect, Genetics

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