Polymorphisms involved in response to biological agents used in rheumatoid arthritis

dc.contributor.authorPallio, Giovanni
dc.contributor.authorMannino, Federica
dc.contributor.authorIrrera, Natasha
dc.contributor.authorEid, Ali H.
dc.contributor.authorSquadrito, Francesco
dc.contributor.authorBitto, Alessandra
dc.contributor.departmentPharmacology and Toxicology
dc.contributor.facultyFaculty of Medicine (FM)
dc.contributor.institutionAmerican University of Beirut
dc.date.accessioned2025-01-24T11:39:44Z
dc.date.available2025-01-24T11:39:44Z
dc.date.issued2020
dc.description.abstractRheumatoid 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.
dc.identifier.doihttps://doi.org/10.3390/biom10091203
dc.identifier.eid2-s2.0-85089808827
dc.identifier.pmid32825059
dc.identifier.urihttp://hdl.handle.net/10938/29337
dc.language.isoen
dc.publisherMDPI AG
dc.relation.ispartofBiomolecules
dc.sourceScopus
dc.subjectCd20
dc.subjectCd80
dc.subjectCd86
dc.subjectIl-1
dc.subjectIl-6
dc.subjectPolymorphism
dc.subjectRheumatoid arthritis
dc.subjectTnf-α
dc.subjectArthritis, rheumatoid
dc.subjectBiological factors
dc.subjectHumans
dc.subjectPolymorphism, single nucleotide
dc.subjectAdalimumab
dc.subjectEtanercept
dc.subjectInfliximab
dc.subjectInterleukin 6
dc.subjectTocilizumab
dc.subjectTumor necrosis factor
dc.subjectBiological factor
dc.subjectBiological therapy
dc.subjectClinical outcome
dc.subjectDas28
dc.subjectDisease activity
dc.subjectDna polymorphism
dc.subjectDual antiplatelet therapy
dc.subjectEnzyme linked immunosorbent assay
dc.subjectGene frequency
dc.subjectGenetic analysis
dc.subjectGenetic association
dc.subjectGenetic polymorphism
dc.subjectGenetic variation
dc.subjectGenome-wide association study
dc.subjectGenotype
dc.subjectHaplotype
dc.subjectHuman
dc.subjectPharmacogenetics
dc.subjectPhase 3 clinical trial (topic)
dc.subjectRestriction fragment length polymorphism
dc.subjectReview
dc.subjectSingle nucleotide polymorphism
dc.subjectTreatment response
dc.subjectDrug effect
dc.subjectGenetics
dc.titlePolymorphisms involved in response to biological agents used in rheumatoid arthritis
dc.typeReview

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