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  1. C. L. Iñíguez1,
  2. J. A. Mosquera Martínez2,
  3. L. Fernández-Dominguez3,
  4. F. Maceiras-Pan4,
  5. C. García-Porrúa1,
  6. J. L. Guerra-Vázquez5,
  7. V. Quevedo Vila6,
  8. M. Caeiro-Aguado7,
  9. J. Lorenzo-Alvarez8,
  10. J. A. Pinto Tasende7,9
  11. on behalf of GIGAPs
  1. 1Hospital Lucus Augusti, Rheumatology, Lugo, Spain
  2. 2Hospital Montecelo (Pontevedra), Rheumatology, Pontevedra, Spain
  3. 3Complexo Hospitalario Universitario de Ourense, Rheumatology, Ourense, Spain
  4. 4Hospital do Meixoeiro, Rheumatology, Vigo, Spain
  5. 5Hospital Arquitecto Marcide, Rheumatology, Ferrol, Spain
  6. 6Hospital Comarcal de Monforte de Lemos, Rheumatology, Monforte de Lemos, Spain
  7. 7Hospital Universitario da Coruña, Rheumatology, La Coruña, Spain
  8. 8Hospital Universitario da Coruña, Internal Medicine, La Coruña, Spain
  9. 9INIBIC, Rheumatology, A Coruña, Spain


Background: Evidence suggests that inflammation plays a causal role in the development of Metabolic Syndrome (MetS) and elevated peripheral levels of proinflammatory mediators, such as C-reactive protein (CRP) confering cardiovascular and metabolic risk.

Objectives: The objective of this study was to evaluate Metabolic Syndrome among patients with PsA naïve to biologics and to evaluate its association with inflammatory activity status previous start them.

Methods: We performed a retrospective cross-sectional study of a cohort of patients ≥18 years of age, all patients with a diagnosis of PsA (CASPAR criteria), included in the Sueiro Cohort. Patients were managed according to a standard protocol adopted at the Rheumatology outpatient clinic of six hospitals and they were patients on follow-up for at least 6 months. Collected variables included age and gender, blood biochemistry, blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), HLA-B27 and rheumatoid factor, glucocorticoid, NSAID and conventional or biologic DMARD, smoking habit, hyperuricemia, type 2 diabetes mellitus, obesity (BMI kg/m2). MetS was defined by a combination of abdominal obesity, impaired fasting glucose, atherogenic dyslipidemia, and elevated blood pressure. Status of disease activity was supported by tender and swollen joint counts (TJC68 and SJC66) from patients who were going to start treatment with biologics and Patient-reported outcome measure were collected with Patient Global Assessment (0-10 cm) and Patient Pain Assessment (0-10 cm). Remission and low disease activity status was obtained by DAPSA score and its defined cut-off. Tests were two-tailed with a significance level of 5%. Data were analyzed using SPSS V21.0 statistical software (IBM Corp. NY, USA).

Results: A total of 416 were included in the study: 222 PsA patients treated with csDMARD kept in remission or low disease activity and 194 patients needed to be treated with bDMARD. The mean age of the patients was 53.0 years (SD: 11.8). Two hundred and twenty-eight were males (56.2%).

Fifty-six patients had MetS (13.8%) and it was more frequent in patients who were in clinical activity and they needed biologics (17.9% vs 10.4%, p 0.028) with mean (SD) of DAPSA of 16.7 (11.1). Patients starting treatment with biologics and with MetS had more proportion of patients older than 50 years (24.2 % vs 8.3%, p 0.006) and CRP >5 mgr/L (71.4% vs 52.6%, p 0.042) and DAPSA had higher values than in patients without MetS (18.6 vs 16.2) but there were not significant statistical differences. Binary regression analysis showed increased risk of MetS for age > 50 years old (OR 3.287 [95%CI: 1.258-8.591], p 0.015) and CRP > 5 mgr/L (OR 2.684 [95%CI: 1.141-6.313], p 0.024) but not for gender (OR 2.136 [95%CI: 0.932-4.893], p 0.073) neither for DAPSA>14 (OR 1.539 [95%CI: 0.695-3.409], p 0.288).

Conclusion: Patients with PsA active despite csDMARD had more prevalence of MetS and this was associated with those patients over 50 years old and CRP higher than normal values. DAPSA was higher in patients with MetS but without reaching significant statistical difference.

References: [1]Lee YH, Pratley RE. The evolving role of inflammation in obesity and the metabolic syndrome. Current Diabetes Reports. 2005;5:70–75

Acknowledgements: I have acknowledgements to SOGARE.

Disclosure of Interests: None declared.

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