Pos1532 what is the real impact of depression on clinical response to therapy in patients with psoriatic arthritis treated with biologic disease-modifying antirheumatic drugs?

Background The estimated prevalence of depression in patients with psoriatic arthritis (PsA) ranges from 20 to 30% and is higher than in the general population. The relationship between depression, systemic inflammation, disease activity and response to therapy in PsA patients remains unclear and under investigation. Patients with depression seems to have overexpression of pro-inflammatory cytokines involved in the pathogenesis of PsA, such as interleukin (IL)-6, IL-17 and tumor necrosis factor-alpha (TNF-α). On the other hand, depression leads to pain sensitization and plays a pivotal role in the shaping of pain responses and patient reported outcome measures (PROMs). Objectives To compare the response to therapy in PsA patients with or without depression, treated with biologic disease-modifying antirheumatic drug (bDMARD) for the first time. Methods An observational monocentric retrospective cohort study of patients with PsA (according to CASPAR criteria) registered in the national database (Reuma.pt), who started their first bDMARD between June 2010 and December 2021, was conducted. Demographic data, disease activity data, functional parameters and response to therapy 12 months after the start of bDMARD were collected. Depression was defined according to Hospital Anxiety and Depression scale (HADS). In patients who didn’t fill out the questionnaire, depression was identified by consulting medical records. For patients with peripheral involvement, DAS28 (4V), CDAI and SDAI were collected at baseline. For patients with axial involvement, Ankylosing Spondylitis Disease Activity Score (ASDAS)-C-reactive protein (CRP) was also collected. American College of Rheumatology (ACR) response criteria, change in Ankylosing Spondylitis Disease Activity Score (ΔASDAS), BASDAI50 response, change in HAQ (ΔHAQ) and EULAR response (good, moderate or no response) were calculated at month 12. Chi-square test and t-test were conducted (for categorical and normally distributed continuous variables, respectively). A p-value <0.05 was considered statistically significant. Results 129 PsA patients were included (66 females, 51.2%). The mean age was 52.2±10.9 years and the disease duration was 13.9±7.2 years. All patients were treated with bDMARD, 122 (94.6%) with anti-TNFα agents and 7 (5.4%) with anti-IL-17 agents. Thirty-two (24.8%) patients had depression and the mean value of HADS was 10.0±3.8. The majority of these patients were treated with antidepressants (n=25, 78.1%). Patients with and without depression had similar sociodemographic characteristics, except for gender, since there were significantly more females in the depression group (p<0.001). These 2 groups had similar disease activity scores at baseline. Patients with depression and peripheral involvement had a significantly lower ACR20/50/70 responses (p=0.001, p=0.002 and p=0.001 respectively) after 12 months of therapy. Also, these patients had a significantly poorer EULAR response (p=0.002). Furthermore, patients with depression and axial involvement had a lower Δ-ASDAS (p=0.03) and a lower BASDAI50 response (p=0.06), after 12 months of therapy. Switch due to ineffectiveness in the first 12 months was higher in patients with depression (p=0.002). Conclusion In our study, depression was associated with poorer response to therapy and higher bDMARD discontinuation rates. Depression might be associated with a pro-inflammatory state but also has a close relationship with chronic widespread pain which can influence some composite disease activity measures. Clinical judgement of the degree of disease activity, using objective measures of disease activity, is important in patients with depression, in order to avoid inappropriate escalation of therapy. Furthermore, recognition and treatment of depression in patients with PsA are crucial, as this might improve their quality of life and also their ability to manage their rheumatic disease. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests None Declared.