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The relationship between tumour necrosis factor ( TNF )‐α promoter and IL 12 B / IL ‐23 R genes polymorphisms and the efficacy of anti‐ TNF ‐α therapy in psoriasis: a case–control study
Author(s) -
Gallo E.,
Cabaleiro T.,
Román M.,
SolanoLópez G.,
AbadSantos F.,
GarcíaDíez A.,
Daudén E.
Publication year - 2013
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.12425
Subject(s) - tumor necrosis factor alpha , psoriasis , medicine , necrosis , gene , tumor necrosis factor α , genetic enhancement , oncology , immunology , cancer research , gastroenterology , biology , genetics
Summary Background Antitumour necrosis factor (anti‐ TNF )‐α agents can be used successfully to treat patients with psoriasis and other inflammatory diseases. However, very few studies have examined the relationship between TNF ‐α polymorphisms and the response to anti‐ TNF ‐α agents. Objectives To study the association of single nucleotide polymorphisms ( SNP s) of the TNF ‐ α promoter and IL 12B / IL 23 R genes with the response to anti‐ TNF ‐α in patients with psoriasis. Methods SNPs for the TNF ‐α promoter and IL 12B / IL 23 R genes, and the presence of the HLA ‐ C w6 haplotype were genotyped for 109 patients. We studied the association between these SNP s and the efficacy of treatment at 3 and 6 months [ P soriasis A rea and S everity I ndex ( PASI ) and body surface area ( BSA )]. Results Patients with the TNF ‐α‐238 GG genotype more frequently achieved a PASI 75 at 6 months (82·5% vs. 58·8%, P = 0·049). At 6 months, patients with the TNF ‐α‐857 CT / TT genotypes showed greater improvements in PASI score and BSA (83·1% vs. 92·7%, P = 0·004; 82·7% vs. 92·6%, P = 0·009) and more frequently achieved PASI 75 (71·4% vs. 96·3%, P = 0·006). More patients with the TNF ‐α‐1031 TT genotype achieved PASI 75 at 3 months (90·8 vs. 75·7, P = 0·047) and 6 months (85·5% vs. 65·7%, P = 0·038) and demonstrated superior improvements in PASI at 6 months (89·9% vs. 78·7%, P = 0·041). Patients with the IL 23 R ‐ GG genotype (rs11209026) achieved PASI 90 at 6 months more frequently (66·3% vs. 0, P = 0·006) and the improvement of the PASI score was also greater (86·8% vs. 67·8%, P = 0·013). Patients with the HLA ‐ C w6 haplotype showed poorer response than those without this haplotype. Conclusion This study identified a relationship between certain TNF ‐α and IL 12 B / IL 23 R polymorphisms and the short‐term response to anti‐ TNF ‐α drugs. If these results are confirmed, this information will allow for stratified consent with more accurate prediction of response/personalized choice of treatment hierarchy for the patient.