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Depression linked to non-adherence to TNF-a inhibitors in patients with ankylosing spondylitis
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Depression and anxiety were associated with the discontinuation of tumor necrosis factor-alpha inhibitors in patients with ankylosing spondylitis, according to recently presented data.
Using the Swedish biologics register, ARTIS, which includes data on patients previously naïve to biologic therapy, researchers identified 965 patients with ankylosing spondylitis (AS) who began treatment with a tumor necrosis factor-alpha (TNF-a) inhibitor between July 1, 2006, and Dec. 31, 2010. Patients with anxiety or depression were identified using the National Patient Register and the Prescribed Drug Register.
The continuation of the TNF-a inhibitor was assessed by univariate and multivariate Cox regression analysis with covariates for age, sex, TNF-a therapy type; treatment starting year; co-medications; income; education; civil status; the number of hospitalizations in the prior 2 years; and comorbidities, such as diabetes, IBD and psoriasis.
The criteria for depression or anxiety was met by 123 of the 965 patients. Patients with depression or anxiety were more likely to be female and have lower baseline erythrocyte sedimentation rates and C-reactive protein, but higher scores on patients and global pain, according to the researchers.
The hazard ratio (HR) for discontinuation of anti-TNF-a treatment was 1.78 during a 3-year period in patients with AS with comorbid depression or anxiety compared with patients who had AS but not depression or anxiety. Multivariate analysis revealed HR for the risk of discontinuation was 1.53 in patients with AS and comorbid depression or anxiety, and 2.39 when factored with primary inefficacy. Other factors that influenced TNF-a inhibitor discontinuation were higher age, lower education level, no history of uveitis and single marital status.
“Depression [or] anxiety may have influenced the patients’ symptoms before and during TNF-a treatment, including aggravation of back symptoms that are not caused by inflammation and, thus, not likely to improve upon TNF-a therapy,” the researchers wrote. – by Shirley Pulawski
Reference:
Lie E, et al. Paper #OP0289. Presented at: European League Against Rheumatism Annual European Congress of Rheumatology; June 10-13, 2015; Rome.
Disclosures: Lie reports she is a consultant for AbbVie, Bristol-Myers Squibb, Hospira, Pfizer and UCB. She is also on the speakers bureau for AbbVie and Bristol-Myers Squibb. Please see the full study for a list of all other authors’ relevant financial disclosures.