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dc.creatorVejnović, Dubravka
dc.creatorMilić, Vera
dc.creatorPopović, Branka
dc.creatorDamnjanović, Tatjana
dc.creatorMaksimović, Nela
dc.creatorBunjevački, Vera
dc.creatorKrajinović, Maja
dc.creatorNovaković, Ivana
dc.creatorDamjanov, Nemanja
dc.creatorJekić, Biljana
dc.date.accessioned2020-07-13T08:48:00Z
dc.date.available2020-12-21
dc.date.issued2019
dc.identifier.issn1742-5255
dc.identifier.urihttps://smile.stomf.bg.ac.rs/handle/123456789/2526
dc.description.abstractBackground: Methotrexate (MTX), a folate analogue, is the most commonly used disease-modifying drug in the treatment of rheumatoid arthritis (RA). However, high interindividual differences in drug response are present among RA patients.Research design and methods: In a group of 234 RA patients treated with MTX, we investigated whether rs1650697 polymorphism in DHFR gene may have an impact on MTX efficacy and/or adverse drug effects (ADEs). Relative DAS28 values (rDAS28) were used for the estimation of MTX therapy and all ADEs were recorded. Patients were genotyped for selected polymorphism by real-time PCR method. Results: According to the European League Against Rheumatism criteria after 6 months of MTX therapy, 196 patients (83.8%) were classified as responders (25 (10.7%) were good and 171 (73.1%) were moderate) and 38 patients (16.2%) as nonresponders. ADEs were observed in 55 patients (23.5%). Conclusions: Our results showed that the presence of T allele might be protective against MTX hepatotoxicity measured by transaminase levels (p = 0.05). Furthermore, among patients who also received low-dose corticosteroids, we have found a lower rDAS value in patients with CC genotype (p = 0.039).en
dc.publisherTaylor & Francis Ltd, Abingdon
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175091/RS//
dc.rightsembargoedAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
dc.sourceExpert Opinion on Drug Metabolism & Toxicology
dc.subjectDHFRen
dc.subjectgenetic polymorphismen
dc.subjectmethotrexateen
dc.subjectpharmacogeneticsen
dc.subjectrheumatoid arthritisen
dc.subjecttoxicityen
dc.titleAssociation of C35T polymorphism in dihydrofolate reductase gene with toxicity of methotrexate in rheumatoid arthritis patientsen
dc.typearticle
dc.rights.licenseBY-NC-ND
dcterms.abstractДамњановић, Татјана; Вејновић, Дубравка; Милић, Вера; Поповић, Бранка; Максимовић, Нела; Буњевачки, Вера; Крајиновић, Маја; Новаковић, Ивана; Дамјанов, Немања; Јекић, Биљана;
dc.citation.volume15
dc.citation.issue3
dc.citation.spage253
dc.citation.epage257
dc.citation.other15(3): 253-257
dc.citation.rankM21
dc.description.otherThis is the peer-reviewed version of the article: Vejnović, D.; Milić, V.; Popović, B.; Damnjanović, T.; Maksimović, N.; Bunjevački, V.; Krajinović, M.; Novaković, I.; Damjanov, N.; Jekić, B. Association of C35T Polymorphism in Dihydrofolate Reductase Gene with Toxicity of Methotrexate in Rheumatoid Arthritis Patients. Expert Opinion on Drug Metabolism & Toxicology 2019, 15 (3), 253–257. [https://doi.org/10.1080/17425255.2019.1563594]
dc.identifier.wos000458880400007
dc.identifier.doi10.1080/17425255.2019.1563594
dc.identifier.pmid30583708
dc.identifier.scopus2-s2.0-85059575374
dc.identifier.fulltexthttps://smile.stomf.bg.ac.rs/bitstream/id/5271/Association_of_C35T_acc_2019.pdf
dc.type.versionacceptedVersion


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