Background Depression is a common comorbid condition in rheumatoid arthritis (RA) patients that may influence the evolution of disease progression, and consequently, affect response to therapeutic treatments.
Objectives The aim of this study was to determine if depression is a moderator of clinical response to biologic disease modifying anti-rheumatic drug (DMARD) therapy.
Methods RA patients initiating a biologic DMARD with a 6 or 12 months (±2 months) follow-up visit were identified from a national RA registry sample (Consortium of Rheumatology Researchers of North America; CORRONA). Patients with self-reported depression at treatment initiation or a clinical visit within 6-months prior were classified as depressed. They were compared to controls with no self-reported history of depression with respect to achieving remission or low disease activity (LDA) based on the clinical disease activity index (CDAI). To account for confounders, particularly differences in baseline disease severity, inverse probability weighting was used due to the high correlation between disease activity measures and their strong association with the outcomes. Predicted probabilities for depression at treatment initiation were used to derive inverse probability weights from propensity score models incorporating baseline values for variables selected a priori that were associated with depression. Logistic regression was then used to estimate unadjusted odd ratios (ORs) and 95% confidence intervals (CIs) for the likelihood of response, and adjusted associations were assessed with weighted models.
Results Response rates were significantly different between patients with and without reports of depression receiving biologic treatment at 6 and 12 months follow-up: 15.51% vs. 6.59, 16.71% vs. 9.52%, 36.99% vs. 27.15%, 35.84% vs. 25.24 for remission and LDA, respectively. The corresponding ORs for remission and LDA in the depressed were 0.38 [0.25-0.58] and 0.64 [0.49-0.83] at 6 months and 0.53 [0.36-0.77] and 0.60 [0.45-0.81] at 12 months, respectively. The remission ORs from propensity score weighted models displayed similar patterns: 0.48 [0.30-0.77] at 6 months and 0.67 [0.44-1.04] at 12 months. Although, adjusted LDA effect estimates indicated only a slightly lower likelihood of response: 0.90 [0.66-1.22] at 6 months and 0.88 [0.63-1.23] at 12 months.
Conclusions The findings indicate that depression is associated with a lower likelihood of response, particularly CDAI remission, but not LDA. However, it is unclear whether this association with achieving clinical remission is related to depression having a substantive impact on disease expression or is due to the effect on patient's experience of their symptoms. Nonethelss, these data suggest that rheumatologists should consider the presence of affective symptoms when treating their patients to provide the best care possible and address any challenges due to depression
Acknowledgements This study is sponsored by CORRONA. In the last 2 years, AbbVie, Amgen, AstraZeneca, Genentech, Horizon Pharma, Eli Lilly, Novartis, Pfizer, Vertex, and UCB have supported CORRONA through contracted subscriptions.
Disclosure of Interest A. Rathbun: None declared, L. Harrold Consultant for: CORRONA Inc., G. Reed Employee of: CORRONA Inc.
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