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Background Pain is a major concern for patients with psoriatic arthritis (PsA) in spite of treatment with biologic/conventional disease modifying drugs (b/csDMARDS). Studies on the prognostic role of pain mechanisms in PsA, are scarce. Objectives To investigate the presence of widespread non-arthritic pain (WP) in patients with PsA, and determine its relation to patient-reported, clinical- and ultrasound (US) disease measures, as well as to achievement of 4 months response to b/csDMARD therapy. Secondly, to study if US Colour Doppler activity (CD) at baseline is associated to treatment response. Methods A prospective cohort study was performed following a protocol.1Patients initiating b/csDMARDs for PsA were recruited from rheumatology clinics in Copenhagen. Clinical- and US examinations and patient-reported outcomes (PROs) were performed at baseline and after 4 months. WP was defined as a Widespread Pain Index≥4, and pain in ≥4/5 regions. CD activity in selected joints, entheses and tendons (73 projections) was summed. Response was assessed by American College of Rheumatology 20% (ACR20), Disease Activity in Psoriatic Arthritis 50% (DAPSA 50) and Minimal Disease Activity (MDA). Main response analyses were based on intention to treat with non-responder imputation, and consisted of logistic regressions adjusting for gender and age. Results Of 123 screened patients, 69 were included. Of these, 24 (35%) fulfilled the WP definition. At baseline (Table), WP was associated with worse PROs and composite scores, while CD activity and clinical measures were similar to those without WP. WP profile was significantly related to achievement of MDA at follow-up but not to other response criteria (table 1). Presence of CD activity at baseline was not significantly associated to 4 months response by any criteria, e.g. 19%/31% with CD=0/CD >0, reached ACR20, (p=0.262). Conclusions WP was present in 1/3 of patients, and associated with worse PROs, composite measures, and failure to achieve MDA at follow-up. Neither WP nor CD at baseline was related to other response measures. Reference Hojgaardet al. BMJ Open2006;6. doi:10.1136/bmjopen-2015-010650 Acknowledgements Thanks to: The Oak foundation, Danish Rheumatism Association, Centre for Rheumatology Gentofte Hospital. Disclosure of Interest None declared

Background Fatigue has been identified as one of the most significant symptoms and an outcome of great importance to patients with psoriatic arthritis (PsA), but the association between underlying components of experienced fatigue and the disease has been sparsely investigated. [1] Objectives To describe the degree of fatigue in a PsA population. Secondly, to explore which components of inflammation and non-inflammatory factors contribute to experienced fatigue. Methods The study was designed as a cross-sectional survey including patients registered in DANBIO, the Danish nationwide rheumatologic registry, from December 2013 to June 2014. Principal component analysis was used to identify clustering factors associated with fatigue Results A total of 1,062 PsA patients were included in the study. The median Visual Analog Scale (VAS) fatigue score was 57mm. Patients with moderate to severe fatigue (VAS score ≥57) had higher scores of pain, DAS28, HAQ, patient global assessment, and more tender and swollen joints (p Conclusions Clinical inflammatory disease activity, chronification, as well as pain in the absence of inflammation were all identified as important factors explaining 63% of moderate to severe fatigue in the current PsA population. References Orbai AM, Mease PJ, de WM et al. Report of the GRAPPA-OMERACT Psoriatic Arthritis Working Group from the GRAPPA 2015 Annual Meeting. J Rheumatol 43; 965–9. Acknowledgements This study was supported by the Oak Foundation. Data was extracted from the DANBIO Registry. Disclosure of Interest M. Skougaard: None declared, T. Jorgensen Speakers bureau: Abbvie, Roche, UCB, Novartis, Biogen, S. Rifbjerg-Madsen: None declared, L. Coates Grant/research support from: Abbvie, BMS, Celgene, Jannsen Pharmaceuticals, Lilly, MSD, Novartis, Pfizer, Sun Pharma, UCB, A. Egeberg Grant/research support from: Pfizer, Eli Lilly, Speakers bureau: Pfizer, Eli Lilly, Novartis, Galderma, Janssen Pharmaceuticals, K. Amris: None declared, L. Dreyer: None declared, P. Hojgaard Speakers bureau: Celgene, UCB, J. Guldberg-Moller Paid instructor for: Abbvie, J. Merola Grant/research support from: Biogen IDEC, Amgen, Pfizer, Boehringer Ingelheim, Consultant for: Biogen IDEC, Eli Lilly, Novartis, Momenta, UCB, Kiniksa, AbbVie, Amgen, Pfizer, Janssen Pharmaceuticals, Momenta, Mallinckrodt, Speakers bureau: AbbVie, Eli Lilly, P. Frederiksen: None declared, H. Gudbergsen Speakers bureau: MSD, Pfizer, L. E. Kristensen Speakers bureau: Pfizer, AbbVie, Amgen, UCB, Celgene, BMS, MSD, Novartis, Eli Lilly, Janssen Pharmaceuticals.