@article{
author = "Jančić, Ivan and Šefik-Bukilica, Mirjana and Živojinović, Slađana and Damjanov, Nemanja and Spasovski, Vesna and Kotur, Nikola and Karan-Đurašević, Teodora and Pavlović, Sonja and Bufan, Biljana and Arsenović-Ranin, Nevena",
year = "2015",
abstract = "Uvod: Genetički faktori su značajni za predviđanje ishoda lečenja bolesnika sa reumatoidnim artritisom (RA). Cilj studije bio je da se ispita uticaj-308G/A TNF-α (rs 1800629) i -174G/C IL-6 (rs1800795) promotorskih polimorfizama na terapijski odgovor na etanercept. Metode: U studiju su bila uključena 73 pacijenta sa aktivnim RA. Terapijski odgovor je procenjivan posle 6 i 12 meseci terapije po kriterijumima Evropske lige protiv reumatizma. Genotipizacija pacijenata za polimorfizme -308G/A TNF-α i -174G/C IL-6 urađena je PCR-RFLP metodom i procenjivan je uticaj genotipova na odgovor na etanercept. Rezultati: Nije bilo razlike u procentu respondera (pacijenti kod kojih se DAS28 popravio gt 1,2) između pacijenata sa TNF-α -308GG, GA i AA genotipom ni posle 6 ni posle 12 meseci tretmana. Posle 12 meseci lečenja procenat respondera je bio značajno veći kod pacijenata sa IL-6 -174GG u odnosu na pacijente sa GC ili CC genotipom (p= 0,006, x2 test). Poređenje pacijenata prema kombinovanim IL-6/TNF-α genotipovima pokazalo je da je IL-6 -174GG / TNF-α -308GG genotip učestaliji kod respondera u odnosu na druge kombinovane genotipove (p= 0.022, x2 test). Tačnije, svi pacijenti sa kombinovanim IL-6 -174GG / TNF-α -308GG genotipom bili su responderi posle 12 meseci terapije etanerceptom. Zaključak: Studija pokazuje da bolesnici sa genotipovima koji se povezuju sa manjom produkcijom TNF-α i IL-6 najbolje odgovaraju na terapiju etanerceptom., Background: The study was undertaken to assess the influence of functional -308G /A TNF-α (rs 1800629) and -174G/C IL-6 (rs1800795) promoter polymorphisms on the therapeutic response to etanercept, a TNF-α blocker, in patients with rheumatoid arthritis (RA). Methods: Seventy-three patients suffering from active RA were studied, at baseline and 6 and 12 months after therapy. The therapeutic response was estimated according to the European League Against Rheumatism response criteria. Patients were genotyped for -308G /A TNF-α and -174G/C IL-6 polymorphisms by the PCR-RFLP method, and the influence of genotype on etanercept response was assessed. Results: No difference in the percentage of responders (patients who had DAS28 improvement gt 1.2) between patients with the TNF-α -308GG and GA and AA genotype was detected after 6 and 12 months of treatment. After 12 months of treatment the percentage of responders was significantly increased in patients with the IL-6 -174GG genotype compared with those with the GC or CC genotype (p=0.006 by Chi-square test). Evaluation of the patients according to their combined IL-6/TNF-α genotypes showed that patients with the IL-6 -174GG / TNF-α -308GG genotype were more frequent among the responders compared to those with other combined genotypes (p=0.022 by Chisquare test). More precisely, all patients with the combined IL-6 -174GG / TNF-α -308GG genotype were responders after 12 months of etanercept treatment. Conclusions: The study suggests that patients who are genetically low TNF-α and IL-6 producers are the best responders to etanercept therapy.",
publisher = "Društvo medicinskih biohemičara Srbije, Beograd i Versita",
journal = "Journal of Medical Biochemistry",
title = "Uticaj polimorfizama TNF-α (-308G/A) i IL-6 (-174G/C) gena na terapijski odgovor na etanercept u reumatoidnom artritisu, Influence of promoter polymorphisms of the TNF-α (-308G/A) and IL-6 (-174G/C) genes on therapeutic response to etanercept in rheumatoid arthritis",
pages = "421-414",
number = "4",
volume = "34",
doi = "10.2478/jomb-2014-0060"
}
