Anti-inflammatories linked to reduced depression in spondyloarthritis patients

For patients with spondyloarthritis (SpA), anti-inflammatory medications help reduce symptoms of depression, but it may be due more to improved symptoms of the SpA itself. A study recently published in Rheumatology. examined the effects of different pharmacological treatments of SpA on depression. While various studies suggest an inflammation-depression link, “We found no evidence for a direct link between C-reactive protein (CRP)-mediated inflammation and depressive symptoms in SpA,” the study read. At the same time, the researchers did find that different anti-inflammatory drugs used for SpA have different impacts on depressive symptoms. Spondyloarthropathy or spondyloarthrosis refers to any joint disease in the vertebral column and is a group of inflammatory diseases rather than a single entity. Conditions include ankolysing spondylitis (the most common form), reactive arthritis, psoriatic arthritis or enteropathic arthritis. It can also cause inflammation in areas where ligaments and tendons attach to bones. SpA can be considered axial (axSpA) or peripheral (pSpA). The disease leads to pain, stiffness and impaired physical functioning plus the prevalence of mental health disorders such as depression and anxiety is increased in these patients relative to the general population. Depression can be related to the symptoms and impact of SpA on daily life, including stigmatization due to physical disability, and worry. But “SpA and depression could share a common pathophysiological pathway,” the researchers said. Previous studies demonstrated inflammatory biomarkers, such as TNF-a and CRP, are increased in people with depression, including in people with no rheumatic diseases, the study said. In general, there is growing evidence for an inflammatory hypothesis of depression which suggests inflammation is a direct cause of depression. Some studies suggest TNFis can improve depressive symptoms in SpA, but little is known about the effect of non-steroidal anti-inflammatory drugs (NSAIDS) or csDMARDs. For this study, researchers used data from the observational, longitudinal Assessment of SpondyloArthritis international Society Health Index Validation Study (ASAS HI). Patients all had either axSpA or pSpA, and were assessed at baseline as well as after initiation of NSAIDs, conventional synthetic DMARDs (csDMARDs) orTNF inhibitors (TNFis). A total of 304 patients were included in the analyses. They had a mean age of 37.3 years, 190 (63%) were male, and 260 (85%) had axSpA. At baseline, SpA scores were measured and mental health was assessed. Twenty patients (6.6%) reported they got treatment for depression. A total of 102 patients started NSAIDS, 45 csDMARD, and 157 initiated TNFis, 260 (85%) had axial SpA and 44 (15%) had peripheral SpA. At basleine, disease activity, physical function and inflammation were similar between the treatment groups. The mean time between the baseline and follow-up assessment was 6.3 weeks for NSAIDs, 15.0 weeks for csDMARDs and 15.6 weeks for TNFis. At follow-up, most patients, 244 (80.8%) reported that that the impact of their disease had improved compared to baseline, and measures also showed improvements, with rates of depression falling. At baseline, possible depression occurred in 126 (42%) of patients, and 66 (22%) had probable depression. At follow-up this dropped to 85 (28%) and 31 (10%) patients respectively, a difference that was statistically significant. The biggest decrease in possibly and probably depressed patients occurred among those who received a TNFi. NSAIDs and csDMARDs also improved depressive symptoms in SpA, but to a lesser extent than TNFis. The study noted that the effect on depression “could largely be explained through improvement of disease activity and/or physical function, while CRP-mediated inflammation did not seem to contribute directly.” “Although we did observe differences between drug classes regarding depressive symptoms—which might suggest that inflammation in some way contributes to depression in SpA, as these drugs influence the immune system in different ways—this could be mainly attributed to differences between these drug classes regarding improvement of symptoms of SpA . . .. It is important to emphasize that this does not necessarily indicate that inflammation does not play a role in the pathophysiology of depression in SpA.” Yet various studies in the medical literature suggest an association between depression and inflammation. A 2021 study in Molecular Psychiatry concluded that inflammation was associated with core depressive symptoms. It noted that previous studies have shown that “inflammation is present in about a quarter of depressed patients as evidenced by elevated CRP levels.” The researchers analyzed data on 147,478 individuals from the UK Biobank (UKB) where there were data on CRP and depressive or anxiety symptoms, and 2,905 people from the Netherlands Study of Depression and Anxiety (NESDA). They investigated whether inflammation was consistently associated with depressive and anxiety symptoms. CRP was measured in both cohorts, and interleukin-6 (IL-6) in NESDA. Genetic analyses were included, and depressive and anxiety symptoms were assessed with self-report questionnaires. That study concluded that inflammation is associated with specific aspects of depression. “Inflammation does not map uniformly onto all affective symptoms, but rather are more consistently associated with specific depressive symptoms of fatigue, altered appetite, sleep problems (in particular hypersomnia), and the core symptom of depressed mood as compared to other symptoms of depression and anxiety. Furthermore, we provide evidence consistent with a potentially causal role of IL-6 in fatigue and sleep alterations,” it read.

Anti-inflammatories linked to reduced depression in spondyloarthritis patients

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