Lihi Eder1,2, Fatima Abji3,4, Cheryl F Rosen3,4, Vinod Chandran3,4, Dafna D Gladman3,4. 1. From the Division of Rheumatology, Women's College Research Institute, Women's College Hospital; Department of Medicine, University of Toronto; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; Division of Dermatology, Toronto Western Hospital, Toronto, Ontario, Canada. lihi.eder@wchospital.ca. 2. L. Eder, MD, PhD, Division of Rheumatology, Women's College Research Institute, Women's College Hospital, and Department of Medicine, University of Toronto; F. Abji, MSc, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; C.F. Rosen, MD, FRCPC, Division of Dermatology, Toronto Western Hospital; V. Chandran, MD, DM, PhD, Department of Medicine, University of Toronto, and Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; D.D. Gladman, MD, FRCPC, Department of Medicine, University of Toronto, and Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital. lihi.eder@wchospital.ca. 3. From the Division of Rheumatology, Women's College Research Institute, Women's College Hospital; Department of Medicine, University of Toronto; Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; Division of Dermatology, Toronto Western Hospital, Toronto, Ontario, Canada. 4. L. Eder, MD, PhD, Division of Rheumatology, Women's College Research Institute, Women's College Hospital, and Department of Medicine, University of Toronto; F. Abji, MSc, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; C.F. Rosen, MD, FRCPC, Division of Dermatology, Toronto Western Hospital; V. Chandran, MD, DM, PhD, Department of Medicine, University of Toronto, and Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital; D.D. Gladman, MD, FRCPC, Department of Medicine, University of Toronto, and Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital.
Abstract
OBJECTIVE: To assess whether obesity is associated with distinct psoriatic arthritis (PsA) features and whether it interacts with PsA HLA susceptibility alleles. METHODS: Patients with early PsA were compared with patients with psoriasis without arthritis (PsC). The primary predictor was the body mass index (BMI) at the first visit to the clinic. The clinical features across 3 BMI groups were compared by linear trend test and Cochrane-Armitage trend test. The interaction between BMI and HLA risk alleles for psoriatic disease (HLA-B*27, B*3901, B*3801, B*0801, B*4402, B*4403, and C*0602) were assessed using logistic regression analysis. RESULTS: There were 314 patients with early PsA, and 498 patients with PsC were analyzed. Obesity was more frequent in patients with PsA compared with PsC (OR 1.77; p = 0.002). Higher BMI was associated with older age at onset of PsA (p < 0.0001) and psoriasis (p = 0.009). The frequency of HLA-B*27 was higher in patients with normal weight compared with those with higher BMI (p = 0.002). A significant interaction was found for the combined effect of HLA-B*27 and obesity in logistic regression analysis (p = 0.036). In patients who were HLA-B*27-negative, the association between obesity and PsA was statistically significant (OR 2.39; p < 0.001), but obesity was less frequent in patients with PsA who were HLA-B*27-positive. CONCLUSION: Obesity is linked with late-onset psoriasis and PsA, while normal weight is associated with the presence of the HLA-B*27 allele and an earlier onset of the disease. These results highlight the differential risk factors that may drive the inflammatory process in psoriatic disease.
OBJECTIVE: To assess whether obesity is associated with distinct psoriatic arthritis (PsA) features and whether it interacts with PsA HLA susceptibility alleles. METHODS:Patients with early PsA were compared with patients with psoriasis without arthritis (PsC). The primary predictor was the body mass index (BMI) at the first visit to the clinic. The clinical features across 3 BMI groups were compared by linear trend test and Cochrane-Armitage trend test. The interaction between BMI and HLA risk alleles for psoriatic disease (HLA-B*27, B*3901, B*3801, B*0801, B*4402, B*4403, and C*0602) were assessed using logistic regression analysis. RESULTS: There were 314 patients with early PsA, and 498 patients with PsC were analyzed. Obesity was more frequent in patients with PsA compared with PsC (OR 1.77; p = 0.002). Higher BMI was associated with older age at onset of PsA (p < 0.0001) and psoriasis (p = 0.009). The frequency of HLA-B*27 was higher in patients with normal weight compared with those with higher BMI (p = 0.002). A significant interaction was found for the combined effect of HLA-B*27 and obesity in logistic regression analysis (p = 0.036). In patients who were HLA-B*27-negative, the association between obesity and PsA was statistically significant (OR 2.39; p < 0.001), but obesity was less frequent in patients with PsA who were HLA-B*27-positive. CONCLUSION:Obesity is linked with late-onset psoriasis and PsA, while normal weight is associated with the presence of the HLA-B*27 allele and an earlier onset of the disease. These results highlight the differential risk factors that may drive the inflammatory process in psoriatic disease.
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