The following is a summary of “Effect of anti-inflammatory treatment on depressive symptoms in spondyloarthritis: does the type of drug matter?,” published in the June 2023 issue of Rheumatology by Webers, et al.
For a study, researchers sought to examine the impact of pharmacological treatment on depressive symptoms in patients with Spondyloarthritis (SpA) and investigate potential differences in this effect across different drug classes.
Data from the Assessment of SpondyloArthritis International Society Health Index Validation Study were utilized for this analysis. Baseline and post-treatment assessments were conducted after initiation of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), conventional synthetic Disease-Modifying Antirheumatic Drugs (csDMARDs), or Tumor Necrosis Factor inhibitors (TNFis). Depressive symptoms were evaluated using the Hospital Anxiety and Depression Scale depression subscale (HADS-D), scored from 0 to 21 (with 0 indicating the best and 21 indicating the worst). Covariables, including demographics and disease characteristics, were considered, such as disease activity assessed by Ankylosing Spondylitis Disease Activity Score (ASDAS) or Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). The change in HADS-D scores from baseline was compared among the different treatment groups using analysis of variance and multivariable regression analysis.
The study included 304 patients, among whom 102 initiated NSAIDs, 45 initiated csDMARDs, and 157 initiated TNFis. Of the participants, 260 (85%) had axial SpA, while 44 (15%) had peripheral SpA. At baseline, the mean HADS-D score was 6.9 (S.D. 4.2), with 126 patients (42%) classified as possibly depressed (HADS-D ≥8) and 66 patients (22%) classified as probably depressed (HADS-D ≥11). Following treatment, depressive symptoms significantly improved in all treatment groups. In multivariable regression analysis without considering disease activity measures, initiating TNFis compared to NSAIDs was associated with a greater improvement in depressive symptoms [β = -1.27 (95% CI -2.23, -0.32)] and lower odds of possible depression at follow-up [odds ratio 0.47 (95% CI 0.23, 0.94)]. However, this association was attenuated after additional adjustment for disease activity (ASDAS/BASDAI) but not C-reactive protein (CRP). The effect of csDMARDs on HADS-D did not differ significantly from NSAIDs. These between-drug class findings were consistent in patients with axial SpA but less conclusive in those with peripheral SpA.
The findings suggested that treatment of active SpA can lead to improvements in depressive symptoms. Specifically, in axial SpA, TNFis have a greater effect on depressive symptoms than NSAIDs, primarily attributed to their stronger impact on disease activity. The study did not find direct evidence for a link between CRP-mediated inflammation and depressive symptoms in SpA.