The -308 TNFα and the -174 IL-6 promoter polymorphisms associate with effective anti-TNFα treatment in seronegative spondyloarthritis

The genetic predisposition to a long-term efficacy of anti-tumor necrosis factor (TNF)α treatment in seronegative spondyloarthritis (SpA) was investigated by analysing the possible correlation between several single nucleotide gene polymorphisms and the retention rate of anti-TNFα therapies. We comp...

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Veröffentlicht in:The pharmacogenomics journal 2016-06, Vol.16 (3), p.238-242
Hauptverfasser: Fabris, M, Quartuccio, L, Fabro, C, Sacco, S, Lombardi, S, Ramonda, R, Biasi, D, Punzi, D, Adami, S, Olivieri, I, Curcio, F, De Vita, S
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Sprache:eng
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Zusammenfassung:The genetic predisposition to a long-term efficacy of anti-tumor necrosis factor (TNF)α treatment in seronegative spondyloarthritis (SpA) was investigated by analysing the possible correlation between several single nucleotide gene polymorphisms and the retention rate of anti-TNFα therapies. We compared patients needing to switch the first anti-TNFα (Sw, No. 64) within at least 12 months of follow-up with patients not needing to switch (NSw, No. 123), observing at least 6 months of treatment to establish anti-TNFα failure, leading to treatment change. Response to treatment was evaluated by standardised criteria (BASDAI for axial involvement, DAS28-EULAR for peripheral involvement). The TNFα -308 A allele and the interleukin (IL)-6 -174GG homozygosis resulted as independent biomarkers predicting survival of the first anti-TNFα therapy in SpA patients ( P =0.007, odds ratio (OR): 4.4, 95% confidence interval (CI)=1.5–13.1 and P =0.035, OR: 2.1, 95% CI=1.1–4.4). Also, the male gender ( P =0.001, OR: 3.4, 95% CI=1.6–7.1) associated with the NSw phenotype, whereas no association was found either with the specific diagnosis or the predominant joint involvement.
ISSN:1470-269X
1473-1150
DOI:10.1038/tpj.2015.49