Anti-Inflammatories Linked to Lower Use of Psychotropic Medications in AS Patients

Anti-Inflammatories Linked to Lower Use of Psychotropic Medications in AS Patients
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Taking certain anti-inflammatory medications is associated with lower use of antidepressants and benzodiazepine-related hypnotics (BRH) among people with ankylosing spondylitis (AS) and other inflammatory disorders, a nationwide study from Sweden suggests.

The study, “Use of antidepressants and benzodiazepine-related hypnotics before and after initiation of TNF-α inhibitors or non-biological systemic treatment in patients with rheumatoid arthritis, psoriatic arthritis or ankylosing spondylitis,” was published in the journal BMC Rheumatology.

AS, rheumatoid arthritis (RA), and psoriatic arthritis (PsA) are chronic inflammatory diseases that primarily affect the joints. All three are associated with higher risks for depression, anxiety, and sleeping problems.

Although the reasons for the links to mental health problems remain unclear, a growing body of evidence suggests that communication between the immune system and the brain via molecules known as cytokines are a possible explanation.

Studies have shown that anti-inflammatory medications, including those targeting cytokines, are effective in easing symptoms of depression. Therapies that block the tumor necrosis factor (TNF) protein have also been associated with lower rates of depression in RA patients.

Researchers analyzed the use of antidepressants and the BRH class of psychotropics before and after starting anti-inflammatory treatments with anti-TNF compounds or non-biological systemic (NBS) therapies among patients with AS, RA, or PsA.

They intended to address the scarce information regarding the use of treatments for psychiatric manifestations among these patients.

The study included 6,256 patients starting anti-TNF treatment (mean age 52), and 13,241 taking NBS therapies (mean age 56.1). Among those with AS, 1,336 patients started on TNF inhibitors and 1,970 on NBS treatments.

Using a series of nationwide Swedish public databases, the researchers assessed use of psychiatric medications from two years before starting anti-inflammatory therapy until two years after the start of treatment.

Results showed that in contrast to the increasing use of antidepressants among controls, patients had a markedly lower use of such therapies after starting on anti-TNF or NBS treatments.

Those taking anti-TNF therapies experienced a steady decrease in the use of antidepressants over the one-year duration of follow-up. In turn, patients receiving NBS treatments showed a greater use of antidepressants in the first six months after beginning anti-inflammatory treatment, then halting thereafter.

“Decreased rates of dispensed psychotropic drugs after the time of anti-TNF and NBS treatment initiation were seen among patients with autoimmune disorders, but not population controls,” the investigators wrote.

Whether the lower rates of psychiatric medication in treated patients are due to direct anti-inflammatory effects, indirect effects on metal health via lessened disease, or both remains to be determined, they said.

“Further research involving participants with inflammatory disorders and concurrent psychiatric symptoms should assess this interesting question,” the scientists said.

Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has also studied Biochemistry at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario in London, Ontario, Canada. His work has ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Forest Ray received his PhD in systems biology from Columbia University, where he developed tools to match drug side effects to other diseases. He has since worked as a journalist and science writer, covering topics from rare diseases to the intersection between environmental science and social justice. He currently lives in Long Beach, California.
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