Do Analgesics Interfere with Efficacy of Selective Serotonin Reuptake Inhibitors?

Jonathan Silver, MD

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In This Article

Abstract and Introduction

Abstract

Results from an animal study and from reanalyzed STAR*D data suggest so, although unexamined confounders may exist.

Introduction

Cytokines may be important in depression. These immunomodulators are produced by glial cells, regulate brain serotonin and noradrenergic systems, and activate the hypothalamic-pituitary-adrenal axis. Antidepressants increase levels of p11, a specific protein that regulates depression in rodent models and interacts with the serotonin receptor. To learn about possible interactions of antidepressants, cytokines, p11, and anti-inflammatory drugs (NSAIDs), researchers conducted experiments in mice and reanalyzed data from the large STAR*D study.

The selective serotonin reuptake inhibitors citalopram and fluoxetine increased p11 levels in mouse frontal cortex, but coadministered ibuprofen (IBU) or acetylsalicylic acid (ASA) blocked this increase. IBU lowered plasma citalopram levels. The tricyclic desipramine produced a small p11 increase, which was not affected by IBU or ASA. Antidepressant-related p11 increases were dependent on signaling by two cytokines (interferon-gamma and tumor necrosis factor-alpha). In a mouse model of depression, IBU, ASA, and acetaminophen prevented the behavioral response to SSRIs but not to antidepressants of other types.

Of STAR*D patients who took citalopram for 12 weeks, significantly fewer achieved remission if taking NSAIDs than if not taking NSAIDs (45% vs. 55%). Findings were similar in a comparison of other analgesic use with nonuse (37% vs. 54%).

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