Arthritis Drug May Help Improve Antidepressant Response

Depression may be associated with chronic inflammation
Depression may be associated with chronic inflammation

Adding celecoxib to antidepressant therapy may improve its effectiveness in bipolar patients who have been treatment resistant. Findings from this study were presented at a recent International Congress of Psychiatry and the Neurosciences Meeting.

Previous studies have indicated that depression may be associated with chronic inflammation and that inflammation may hinder the efficacy of antidepressants. Researchers at Loyola University hypothesized that by inhibiting inflammation, celecoxib could potentially increase the effectiveness of antidepressants.

The 8-week study included bipolar patients between the ages of 18 and 65 who were in the depressive phase of their disease and who had not benefited from antidepressant treatment. Patients were randomized to receive either escitalopram + celecoxib (n=31) or escitalopram + placebo (n=24).

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Compared to the placebo group, more patients in the celecoxib group experienced at least a 50% reduction in their depression scores (45% vs. 78%, respectively). In addition, 63% of the celecoxib group reported their depression had gone away completely versus 10% of the placebo group. Patients in the celecoxib group also reported a beneficial effect within a week of starting the combination.

Reducing inflammation with a drug such as celecoxib "reverses treatment resistance and enhances overall antidepressant response," Loyola Medicine psychiatrist Angelos Halaris, MD, PhD wrote in the study. "Such an intervention, if implemented relatively early in the course of the disease, may arrest the neuroprogressive course of bipolar disorder."

Celecoxib (Celebrex; Pfizer) is a non-steroidal anti-inflammatory drug (NSAID) approved for the treatment of osteoarthritis, rheumatoid arthritis, acute pain, ankylosing spondylitis, juvenile rheumatoid arthritis, and primary dysmenorrhea. The mechanism of action of celecoxib is believed to be due to inhibition of prostaglandin synthesis, primarily via inhibition of cyclooxygenase-2 (COX-2).

For more information visit LoyolaMedicine.org.

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