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<0.001) (Table 1). In the principal component analysis the clinical co-variables were reduced to 3 components explaining 63% of experienced fatigue (figure 1); The first component, contributing to 31%, was mainly constituted by inflammatory factors as swollen and tender joints, doctors-global evaluation, higher CRP, and pain score, whereas the second component mainly consisted of contributions from age and disease duration, explaining 17% of experienced fatigue. The third component, contributing to 15%, consisted of patient pain, tender joint count, increasing age, and by concomitant low CRP. The remaining 37% was considered residuals.

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Figure 1

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

1. 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.

References

Acknowledgements This study was supported by the Oak Foundation. Data was extracted from the DANBIO Registry.

Disclosure of Interest M. Skougaard: None declared, T. Jørgensen 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. Højgaard Speakers bureau: Celgene, UCB, J. Guldberg-Møller 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.