Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement
Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.
The Association of IL-13 Polymorphism with Psoriatic Arthritis among Psoriasis Patients.
Gladman1, Dafna D., Shanmugarajah2, Sutha, Pollock2, Remy, Pellett2, Fawnda, Chandran2, Vinod, Eder2, Lihi
The IL-13 cytokine is involved in T helper type 2 signaling pathway. IL-13 polymorphisms confer a risk for Asthma. Recently, these were found to be associated with a reduced risk for Psoriatic Arthritis (PsA) but not with psoriasis. Smoking was found to abrogate this effect. We aimed to study the association of IL-13 polymorphisms with PsA and psoriasis and their combined effect with smoking.
We genotyped three groups of Caucasian individuals: patients with PsA, patients with psoriasis without arthritis and healthy controls, for the following Single Nucleotide Polymorphisms (SNPs): rs20541 and rs848, an additional SNP, rs1800925, was genotyped only in the PsA and psoriasis groups. The PsA patients were recruited from a large prospective PsA cohort and satisfied the CASPAR criteria. The psoriasis patients were assessed by a rheumatologist to rule out inflammatory arthritis. The control DNA was from healthy volunteers, cadaveric organ donors from laboratories of the University Health Network and from a commercial bio-bank. Smoking status was defined as smoker ever for smokers and lifetime non-smoker. SNP genotyping was performed using TaqMan allelic discrimination assays and SDS 2.2.2 software was used for data collection and allele calling.
The differences in allelic distributions were compared by chi square test using PLINK software. The combined effect of genotype and smoking was tested by comparing the proportions of PsA and psoriasis patients and the different combination groups of rs1800925*CT/TT status and smoking status.
555 PsA patients, 342 psoriasis patients without arthritis and 216 healthy controls were included in the study. Smoking was negatively associated with PsA (258/492 (47.6%) in the PsA group and 139/342 (59.4%) in the psoriasis alone, p<0.0008). The minor alleles of rs20541*A and rs848*A were protective for PsA compared to controls (Odds Ratio (OR) 0.61, p=0.0005, OR 0.62, p=0.0007, respectively). The same alleles were not found to be associated with psoriasis alone (OR 0.75, p=0.06, OR 0.79, p=0.11, respectively). When PsA patients were compared to those with psoriasis alone, the minor alleles of rs1800925*T (OR 0.78, p=0.04) and rs848*A (OR 0.77, p=0.05) were found to be protective. A stronger protection was found with the rs1800925*T/ rs20541*A haplotype (OR 0.64, p=0.007). The combined effect of rs1800925*CT/TT status and smoking status is presented in Table 1. The combination of smoking and the protective genotype rs1800925*CT/TT was the most protective for PsA. Among non-smokers rs1800925*CT/TT was no longer associated with PsA.
Table 1. The combined effect of smoking status and rs1800925*CT/TT genotype status on the prevalence of PsA
An IL-13 polymorphism is protective for PsA among psoriasis patients. This effect was not significant among non-smokers.
To cite this abstract, please use the following information:
Gladman, Dafna D., Shanmugarajah, Sutha, Pollock, Remy, Pellett, Fawnda, Chandran, Vinod, Eder, Lihi; The Association of IL-13 Polymorphism with Psoriatic Arthritis among Psoriasis Patients. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1984