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Objective: To study whether obesity increases the risk of psoriatic arthritis (PsA), given that obesity is a risk factor for psoriasis and is associated with more severe disease., Design: Case series. We used Cox regression analysis to study the relationship between obesity and PsA while controlling for age at psoriasis onset, current body mass index (BMI), sex, family history of psoriasis, worst-ever body surface area (BSA) involvement, Koebner phenomenon, and nail involvement., Setting: Dermatology clinics at the University of Utah School of Medicine. Patients Volunteer sample of patients with dermatologist-diagnosed psoriasis enrolled in the Utah Psoriasis Initiative from November 2002 to October 2008 (943 subjects; 50.2% women, 49.8% men)., Main Outcome Measures: Physician diagnosis of PsA from self-report questionnaire., Results: In our subjects, we found that BMI at age 18 years was predictive of PsA (odds ratio [OR], 1.06) (P < .01) over and above control variables. Other variables that were predictors of PsA included younger age at psoriasis onset (odds ratio [OR], 0.98) (P < .01), female sex (OR, 1.45) (P = .01), higher worst-ever BSA involvement with psoriasis (OR, 1.01) (P = .04), Koebner phenomenon (OR, 1.59) (P < .01), and nail involvement (OR, 1.76) (P < .01). Current BMI and family history of psoriasis were not significant predictors of PsA., Conclusions: This study suggests that obesity at age 18 years increases the risk of developing PsA. Adiposity is associated with higher levels of inflammatory cytokines known to be associated with psoriasis. This inflammatory milieu could increase the risk of PsA in predisposed subjects. Prevention and early treatment of obesity may decrease the risk of PsA.

Genetic and environmental factors influence the development of psoriasis (Ps) and psoriatic arthritis (PsA). Recently, we reported that three IL13 polymorphisms, rs1800925, rs20541, and rs848, on chromosome 5q31 conferred the risk for Ps. IL13 encodes IL-13, a Th2 cytokine, and rs1800925 and rs20541 confer risk of asthma. Further, smoking may increase the risk of developing Ps. We examined the association between IL13 polymorphisms, smoking, and PsA in two Ps sample sets genotyped for rs1800925, rs20541, and rs848. We found that the minor alleles (rs1800925*T, rs20541*A, and rs848*A) were significantly associated with protection from PsA versus controls, and that no association with Ps is seen when the PsA cases are excluded. This effect was strongest with rs1800925*T (odds ratio (OR) 0.40, P(allelic) 0.000067). The prevalence of PsA in cases with the rs1800925*CT or TT genotype is about half that of those with the CC genotype (15.5 vs 32.1%, P=0.0002). However, smoking appears to abrogate this effect (CT/TT/non-smoker, prevalence of PsA 13%, OR 0.20, P=0.0001; CT/TT/smoker, prevalence 38%, OR 0.88, P=0.74, CC/non-smoker, prevalence 42% (reference), CC/smoker prevalence 47%, OR 1.21, P=0.47). This study suggests that IL13 polymorphisms associate most strongly with PsA and that smoking may modulate this effect.