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.
Highlights
Rheumatoid arthritis (RA) is a crippling chronic inflammatory and autoimmune disease
IL-6 −174 G/G genotype was associated with better response to anti-TNF agent and anti-CD20 rituximab (Table 2), suggesting that a pharmacogenetic pre-evaluation of patients could be useful for a targeted treatment of RA patients
Numerous papers have reported that some single nucleotide polymorphism (SNP) might have a linkage to biological treatment response and could have a potential role as possible predictors of response in particular for TNF-α inhibitors, anti-IL-6R drugs, and CD20 inhibitor
Summary
Rheumatoid arthritis (RA) is a crippling chronic inflammatory and autoimmune disease. Before the advent of biologic therapy, most RA cases were treated using a combination of DMARDs; for refractory and severe cases, anti-TNF therapy has become a foundation of RA treatment These anti-TNF biological drugs are divided into two classes: the TNF-receptor fusion protein (certolizumab, etanercept), which prevents TNF action by binding to its cell surface receptor, and TNF-binding monoclonal antibodies (adalimumab, golimumab, and infliximab). Patients with single nucleotide polymorphism (SNP) in +1970 position of the gene coding for IL-1 receptor (IL-1R) exhibited higher levels of this receptor and were more susceptible to developing a severe form of AR [18] This may explain how the C/C genotype in this SNP could influence the efficacy of biological agent. In light of all these observations, we review the pharmacogenetic biological treatment of RA, focusing on TNF-α, IL6, and anti-CD20
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call