Investigation of 20 non‐HLA (human leucocyte antigen) psoriasis susceptibility loci in Chinese patients with psoriatic arthritis and psoriasis vulgaris. (25th April 2013)

• Record Type: Journal Article
• Authors: Yang, Q.; Liu, H.; Qu, L.; Fu, X.; Yu, Y.; Yu, G.; Tian, H.; Yu, Y.; Sun, D.; Peng, J.; Bao, F.; Yuan, C.; Lu, N.; Li, J.; Zhang, Y.; Zhang, F.
• Is Part Of: British journal of dermatology. Volume 168:Number 5(2013:May)
• Page Start: 1060
• Page End: 1065
• Publication Date: 2013-04-25
• Subjects: Dermatology -- Periodicals; Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/bjd.12142
• Languages: English
• ISSNs: 0007-0963

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Summary</title> <p> <bold>Background </bold> 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.</p> <p> <bold>Objectives </bold> To investigate recently identified psoriasis susceptibility loci in a cohort of Chinese patients with PsA, psoriasis vulgaris (PsV) and healthy controls.</p> <p> <bold>Methods </bold> 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.</p> <p> <bold>Results </bold> PsA showed a significant association with markers at <italic>TNIP1</italic> (rs17728338, <italic>P</italic> = 2·20 × 10<sup>−8</sup>), <italic>IL28RA</italic> (rs4649203, <italic>P</italic> = 5·04 × 10<sup>−6</sup>), <italic>IL12B</italic> (rs2082412, <italic>P</italic> = 3·82 × 10<sup>−5</sup>), <italic>ERAP1</italic> (rs27524, <italic>P</italic> = 1·25 × 10<sup>−3</sup>), <italic>PTTG1</italic> (rs2431697, <italic>P</italic> = 1·22 × 10<sup>−3</sup>) and <italic>GJB2</italic> (rs3751385, <italic>P</italic> = 1·48 × 10<sup>−3</sup>) when compared with the control group. In PsV a significant association was found for <italic>IL28RA</italic> (rs4649203, <italic>P</italic> = 9·53 × 10<sup>−7</sup>), <italic>TNIP1</italic> (rs17728338, <italic>P</italic> = 1·21 × 10<sup>−4</sup>) and <italic>ERAP1</italic> (rs27524, <italic>P</italic> = 1·17 × 10<sup>−3</sup>). The allele frequencies were not statistically different between PsA and PsV except for SNPs at <italic>IL12B</italic> and <italic>ZNF816A</italic> with a nominal <italic>P</italic>‐value of 0·04 and 0·01, respectively.</p> <p> <bold>Conclusions </bold> This study provides evidence for the involvement of <italic>ERAP1</italic>, <italic>IL28RA</italic>, <italic>GJB2</italic> and <italic>PTTG1</italic> 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.</p> </abstract>