OBJECTIVE: To investigate the effect of pharmacological treatment of SpA on depressive symptoms, and explore whether this effect differs between drug classes.
METHODS: Data from the observational ASAS Health Index Validation Study were used. Patients were assessed at baseline and after initiation of NSAID/conventional synthetic (cs)DMARD/TNFi. Depressive symptoms were assessed with the Hospital Anxiety and Depression Scale depression-subscale (HADS-D, 0-21 [best-worst]). Covariables included demographics and disease characteristics, including disease activity (ASDAS/BASDAI). Change in HADS-D from baseline was compared between treatments (NSAID/csDMARD/TNFi) with ANOVA and multivariable regression analysis.
RESULTS: 304 patients were included; 102/45/157 initiated NSAID/csDMARD/TNFi and 260/44 (85%/15%) had axial/peripheral SpA. At baseline, mean (SD) HADS-D was 6.9 (4.2), 126 (42%) were possibly depressed (HADS-D≥8) and 66 (22%) probably depressed (HADS-D≥11). At follow-up, depressive symptoms significantly improved in all treatment groups. In multivariable regression without disease activity measures, initiating TNFi compared to NSAID was associated with greater improvement in depressive symptoms (B=-1.27, 95%CI -2.23 to -0.32) and lower odds of possible depression at follow-up (OR = 0.47, 95%CI 0.23-0.94). This association was attenuated after additional adjustment for disease activity (ASDAS/BASDAI) but not CRP. csDMARDs did not differ from NSAIDs regarding their effect on HADS-D. Between-drug class results were confirmed in axSpA, although less clear in pSpA.
CONCLUSION: Treatment of active SpA also improves depressive symptoms. Especially in axSpA, TNFi have a larger effect than NSAIDs, which is mainly explained by a stronger effect on disease activity. We found no evidence for a direct link between CRP-mediated inflammation and depressive symptoms in SpA.
|Number of pages||8|
|Publication status||E-pub ahead of print - 7 Oct 2022|