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Summary

Background  Recently, a number of non-HLA (human leucocyte antigen) psoriasis genetic susceptibility loci have been identified through genome-wide association studies, but data on their association with psoriatic arthritis (PsA) are lacking.

Objectives  To investigate recently identified psoriasis susceptibility loci in a cohort of Chinese patients with PsA, psoriasis vulgaris (PsV) and healthy controls.

Methods  Twenty single-nucleotide polymorphisms (SNPs) from 20 loci were selected for genotyping in 379 patients with PsA, 595 patients with PsV and 1181 healthy controls using the MassARRAY platform (Sequenom, San Diego, CA, U.S.A.). Data handling, quality control and association were performed using PLINK software, v. 1.07. The Cochran–Armitage trend test was used to test the genotype–phenotype association.

Results  PsA showed a significant association with markers at TNIP1 (rs17728338, P = 2·20 × 10−8), IL28RA (rs4649203, P = 5·04 × 10−6), IL12B (rs2082412, P = 3·82 × 10−5), ERAP1 (rs27524, P = 1·25 × 10−3), PTTG1 (rs2431697, P = 1·22 × 10−3) and GJB2 (rs3751385, P = 1·48 × 10−3) when compared with the control group. In PsV a significant association was found for IL28RA (rs4649203, P = 9·53 × 10−7), TNIP1 (rs17728338, P = 1·21 × 10−4) and ERAP1 (rs27524, P = 1·17 × 10−3). The allele frequencies were not statistically different between PsA and PsV except for SNPs at IL12B and ZNF816A with a nominal P-value of 0·04 and 0·01, respectively.

Conclusions  This study provides evidence for the involvement of ERAP1, IL28RA, GJB2 and PTTG1 loci in PsA susceptibility and confirmed the previously reported association with PsA and PsV. These results support the hypothesis that genetic aetiology of psoriasis is the same in both PsA and PsV and also support the higher genetic component of PsA than PsV.