Artigo Revisado por pares

Influence of −308 A/G polymorphism in the tumor necrosis factor α gene on etanercept treatment in rheumatoid arthritis

2007; Wiley; Volume: 57; Issue: 8 Linguagem: Inglês

10.1002/art.23092

ISSN

2151-4658

Autores

Sandrine Guis, Nathalie Balandraud, J. Bouvenot, Isabelle Auger, Éric Toussirot, Daniel Wendling, Jean‐Pierre Mattei, Léonor Nogueira, Bénédicte Mugnier, Pierre Legeron, Olfert Landt, Guy Serre, Jean Roudier, C Roudier,

Tópico(s)

Autoimmune and Inflammatory Disorders Research

Resumo

Abstract Objective To determine whether the −308 A/G tumor necrosis factor α (TNFα) gene polymorphism can predict the outcome of etanercept therapy in 86 patients with rheumatoid arthritis (RA), as already observed in patients treated with infliximab. Methods Eighty‐six RA patients treated with etanercept were genotyped for −308 A/G TNFα gene polymorphism by polymerase chain reaction and melting curve analysis, using specific gene primers and probes. Patients were subdivided into group A (G/A genotype) and group G (G/G genotype). We compared clinical responses to etanercept between groups A and G after 6 months, using the Disease Activity Score in 28 joints (DAS28). After 12‐month treatment, 48 of 86 patients were evaluated again. Results Of 86 patients, 18 (21%) belonged in group A and 68 (79%) belonged in group G. After 6‐month treatment, 55.6% of patients in group A and 82.4% of patients in group G had DAS28 improvement >1.2 ( P = 0.027 by chi‐square). The mean ± SD DAS28 improvement was 1.69 ± 1.31 in group A and 2.23 ± 1.19 in group G ( P = 0.098 by t ‐test). After 1‐year treatment 48 patients were tested again: 10 (21%) belonged in group A and 38 (79%) belonged in group G. Forty percent of patients in group A and 87% in group G had DAS28 improvement >1.2 ( P = 0.005 by chi‐square). The mean ± SD DAS28 improvement was 1.334 ± 1.37 in group A and 2.29 ± 1.47 in group G (Mann‐Whitney U test = 115, P = 0.0057). Conclusion RA patients with a −308 G/G TNFα genotype respond to etanercept better than patients with a −308 A/G genotype.

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