Pos0883 predictors of patient-reported treatment success in patients with psoriatic arthritis

Background Determinants of patient-reported treatment success in psoriatic arthritis (PsA) have not been defined. Objectives To determine predictors of patient-reported treatment success in PsA. Methods Rheumatologist-diagnosed PsA patients, who met the CASPAR classification, were recruited from a single center. PsA outcome measures included 68/66 joint counts, enthesitis, dactylitis, psoriasis body surface area (BSA), patient reported outcomes including PROMIS CAT. The study primary outcome was patient-reported treatment success: “Today, considering the level of control of your psoriatic arthritis and psoriasis, do you consider your treatment has been successful?” with response options Yes/No. Multivariate logistic regression analyses were performed to determine predictors of patient-reported treatment success in PsA. We hypothesized that disease activity measures, including arthritis, psoriasis, enthesitis, and dactylitis, symptoms, and treatment type would contribute to patient-reported treatment success. We did not include multiple patient-reported outcomes in a model due to collinearity. Results A total of 178 participants had a baseline visit. Mean (SD) CASPAR score was 3.7 (0.9) age 51.7 (13.5) years, BMI 31.3 (7.2), while 52.2% were women, and 86.0% Caucasian. Treatment success was reported by 116 patients (65%). Overall, 105 participants had complete data for all the variables included in the logistic regression models. The total joint swelling 66, total joint tenderness 68, PROMIS pain interference, and PROMIS fatigue were significantly negatively associated with treatment success while controlling for age, race, gender, and BMI. Each additional swollen joint was associated with a 23% decreased odds of treatment success, each tender joint was associated with 17% decreased odds of success, each additional point on the PROMIS fatigue and on the PROMIS pain interference was associated with 6% and 15% decreased odds of success, respectively (Table 1). Patients receiving a tumor necrosis factor inhibitor (TNFi) had approximately 11-13 times increased odds of reporting treatment success compared to patients on a classical synthetic DMARD alone, while controlling for age, race, gender, and BMI. Conclusion Patient-reported treatment success was independently associated with control of tender and swollen joints, pain, fatigue, and with receiving a TNF-inhibitor medication. This supports the use of biological treatments as standard of care in PsA. Table 1. Two models of predictors of patient-reported treatment success Model 1 Model 2 Variable Odds Ratio 95% Confidence Interval P-value Variable Odds Ratio 95% Confidence Interval P-value Total joint swelling 66 0.77 0.604-0.991 0.04 Total joint tenderness 68 0.83 0.70-0.97 0.02 SPARCC Enthesitis Index 1.78 0.479-6.591 0.39 SPARCC Enthesitis Index 2.22 0.53-9.26 0.28 Psoriasis BSA 0.85 0.71-1.020 0.08 Psoriasis BSA 0.83 0.69-1.00 0.05 LDI Total Score 2.61 0.265-25.639 0.41 LDI Total Score 1.67 0.21-13.40 0.63 PROMIS pain interference 0.85 0.772-0.931 0.00 PROMIS fatigue 0.94 0.88-0.99 0.03 Medication MOA Classical synthetic DMARD (reference) TNFi PDE4i IL-17i IL-23i Multiple MOAs No MOA Ref 12.86 12.53 1.90 2.17 6.74 0.34 Ref 1.497-110.47 0.64-245.168 0.332-10.847 0.227-20.824 0.792-57.295 0.002-49.204 Ref 0.02 0.10 0.47 0.50 0.08 0.67 Medication MOA Classical synthetic DMARD (reference) TNFi PDE4i IL-17i IL-23i Multiple MOA No MOAs Ref 10.61 13.22 1.16 0.84 3.27 0.46 Ref 1.3-86.9 0.80-219.5 0.31-8.31 0.10-7.08 0.41-25.95 0.01-14.34 Ref 0.03 0.07 0.57 0.87 0.26 0.66 BMI 1.06 0.977-1.154 0.16 BMI 1.05 0.97-1.14 0.19 Age at enrollment 1.01 0.966-1.064 0.57 Age at enrollment 1.00 0.95-1.04 0.90 Gender Female (reference) Male Ref 0.90 Ref 0.258-3.150 Ref 0.87 Gender Female (reference) Male Ref 0.70 Ref 0.21-2.37 Ref 0.57 Race White Black Asian Ref 0.24 0.81 Ref 0.017-3.359 0.035-18.923 Ref 0.29 0.90 Race White (Reference) Black Asian Ref 0.38 1.18 Ref 0.03-4.28 0.07-19.37 Ref 0.44 0.91 Ref , reference group; i = inhibitor Model 1: N=105; R 2 = 0.36 Model 2: N=104, R 2 =0.32 REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests Christeen Samuel: None declared, Amanda Grace-Finney: None declared, Thomas Grader-Beck: None declared, Uzma Haque: None declared, John Miller: None declared, Suzanne Grieb: None declared, Laura Prichett: None declared, Ana-Maria Orbai Consultant of: Bristol-Myers Squibb, Janssen, UCB, Grant/research support from: Amgen, Celgene, AbbVie/Abbott.