Apparent Links Emerging Among Psoriatic Arthritis, Depression, and Inflammation

Investigators still have a lot to learn about the links among psoriatic arthritis, inflammation, and depression, but a growing body of evidence suggests significant interplay.

Depression is a common comorbidity in patients with psoriatic arthritis (PsA), but more work is needed to fully understand the links between the conditions and the implications for treatment of patients, according to a new review article.

A pair of investigators from the University of Toronto write that recent research into PsA has attempted to better understand links between inflammation and depression. As the body of knowledge grows, the authors say clinicians need to take a multidimensional approach to treating patients with depression and PsA. The article is published in the journal Rheumatology and Therapy.

Depression and anxiety are seen in about one-third of patients with PsA, including a depression rate of about 20%. Still, co-authors Ashish J. Mathew, MD, and Vinod Chandran, MD, PhD, note that relatively little research has been done into depression as a comorbidity for PsA when compared with metabolic comorbidities. That is beginning to change, in part because investigators better understand the complex interplay between the 2 conditions.

“In patients with psoriasis, psychiatric disorders can both result from and contribute to disease progression, suggesting overlapping biological mechanisms,” Mathew and Chandran write. “The synthesis of psoriasis and destructive inflammatory arthritis in PsA patients should arguably lead to a higher point prevalence of comorbid depression and anxiety.”

Yet, it remains difficult to fully ascertain the cause-and-effect relationship between depression and PsA, the authors say. Inflammatory responses appear to have a role to play in the pathophysiology of depression, and investigators have increasingly focused on the idea that inflammation is the link between depression and chronic illness.

“Levels of pro-inflammatory cytokines involved in the pathogenesis of PsA, such as interleukin (IL)-6, IL-17 and tumor necrosis factor-alpha (TNFα), are raised in patients with depression and anxiety,” Mathew and Chandran note, adding that patients with autoimmune diseases face a higher risk of mood disorders when treated with inflammation-based therapies.

“However, much as inflammation is considered to be central to the pathogenesis of depression in PsA, inflammation in itself cannot explain the complete link, with some studies failing to find an association between depression and inflammation,” they add.

Another question raised by the research is the extent to which treatment for PsA might affect depression. Patients with comorbid depression and PsA tend to have poor response to treatment for PsA, partly due to lower rates of patient adherence to treatment. However, the authors say the reasons are multifactorial.

On the other hand, there is evidence that newer drugs for PsA might be able to positively impact a patient’s depression.

“Recent evidence suggests a significant improvement of depression in PsA patients treated with biologic disease-modifying anti-rheumatic drugs (bDMARDs) as compared to conventional DMARDs,” they write.

With investigators circling important links but many questions still remaining, Mathew and Chandran say physicians will need to keep abreast of the emerging research in order to be able to treat patients with PsA and comorbidities.

“Physicians should be conversant with the comprehensive assessment of subdomains of depression as this knowledge will effectively enhance remission rates and the quality of life in patients with PsA,” they say.


Mathew AJ, Chandran V. Depression in psoriatic arthritis: dimensional aspects and link with systemic inflammation [published online April 22, 2020]. Rheumatol Ther. doi: 10.1007/s40744-020-00207-6.