Tumor Necrosis Factor Inhibitor Therapy and the Risk for Depression Among Working-Age Adults with Rheumatoid Arthritis.

Abstract

Background: Individuals with rheumatoid arthritis (RA) are at high risk for depression because of the overall burden of systemic inflammation. Although some evidence suggests that treatment with powerful anti-inflammatory drugs, such as tumor necrosis factor (TNF) inhibitors, may be effective in reducing the risk for depression in patients with RA, it is unclear whether such reduction in risk is dependent on the response to TNF inhibitor therapy.

Objective: To evaluate the association between the response to TNF inhibitor therapy and the risk for depression among working-age adults with RA.

Method: This retrospective, observational cohort study design was based on data derived from commercial claims data in the QuintilesIMS Real World Data Adjudicated Claims database between October 1, 2009, and September 30, 2015. A total of 4222 working-age adults (18-62 years) with RA who started treatment with TNF inhibitor therapy and were continuously enrolled during the 3 observation periods (ie, 1-year baseline, 1-year treatment, and 1-year follow-up periods) were included in the study. Treatment response to a TNF inhibitor was measured using prescription drug claims based on a published validated algorithm. Multivariable logistic regression was used to examine the association between treatment response to TNF inhibitor therapy and the risk for depression, after controlling for baseline demographic characteristics, clinical characteristics, and RA-related medication use. An inverse probability of treatment weighting technique was used to control for observable differences in TNF inhibitor responders' characteristics versus TNF inhibitor nonresponders.

Results: Overall, 359 (8.5%) patients with RA had depression during the follow-up period and 1679 (39.8%) patients responded to TNF inhibitor treatment during the 1-year treatment period. A significantly lower percentage of TNF inhibitor responders (7.1%, N = 119) had depression than TNF inhibitor nonresponders (9.4%, N = 239). After controlling for other risk factors, responders to TNF inhibitors were 20% less likely to have depression during the follow-up period (adjusted odds ratio, 0.80; 95% confidence interval, 0.64-0.98) than nonresponders to TNF inhibitor therapy.

Conclusion: The risk for depression was significantly reduced among patients with RA who responded to TNF inhibitor therapy compared with those who did not respond to such therapy. To determine whether the lower rate of depression observed with TNF inhibition is a direct effect of treatment with a TNF inhibitor, or whether it could be attributed to improvement in RA disease secondary to treatment, future studies need to also incorporate a control population of patients with RA who receive other antirheumatic regimens, such as disease-modifying antirheumatic drugs.