Depression in Psoriatic Arthritis: Dimensional Aspects and Link with Systemic Inflammation

Abstract

Studying comorbidities in patients with psoriatic arthritis (PsA) provides a better understanding of the extended burden of the disease. Depression and anxiety are well recognized but understudied comorbidities in patients with PsA. The prevalence of depression is significantly higher in this patient population than in the general population, with far reaching consequences in terms of long-term quality of life. Over the past few years there has been an increasing interest in the link between inflammation and depression, with several novel studies being conducted. 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. Depression in PsA is multidimensional, with recognized phenotypes, including cognitive disorder, alexithymia and anhedonia. The paucity of standardized, validated tools to screen these dimensional phenotypes remains an unmet need. Prevalence studies on depression in patients with PsA, mostly based on patient-reported outcomes, are only able to highlight the tip of the iceberg. A comprehensive, multidisciplinary approach addressing the subdomains of depression is imperative for a better understanding of depression in PsA patients, as well as to find a way forward for improving their quality of life. In this scoping review, we explore existing evidence on the burden of depression in PsA patients, the link between inflammation and depression in these patients and the screening tools used to evaluate the subdomains of depression.

Patient-Centered Care in Psoriatic Arthritis—A Perspective on Inflammation, Disease Activity, and Psychosocial Factors

“…Therapy response in PsA with concurrent depression is suboptimal. Intricate relationships between depression, pain, and inflammation have been described [ 62 ]. Systematic reviews indicate that DMARDs (TNFα, IL-12/23, IL-17, or phosphodiesterase 4 inhibition) lead to significant, but small improvements in fatigue.…”

“…The shift from the monoaminergic theory of depression to recognizing the importance of cytokine signaling, neuroinflammatory, and neuroendocrine pathways with external stressors creates a complex and multifaceted model of depression [ 62 , 72 , 73 ]. Imaging studies have tied peripheral inflammation to altered brain structure integrity in depression [ 74 ].…”

“…The concept of pro-inflammatory shifts in immune populations, based on the perpetual perception of threat, leading to early development of symptoms (hypervigilance, sensitivity to pain, social anxiety), which gradually progress to chronic pain, depressive mood, and precipitate inflammatory, is postulated [ 75 ]. Depression shares a close relationship with inflammation in PsA, though the efficacy of disease modifying anti-rheumatic drugs is not optimal [ 62 ]. Data from RA suggests that the presence of depressive symptoms reduces the likelihood of attaining good responses and controlling disease over time [ 76 ].…”

“…Data for PsA are scarce as comprehensive reviews examining depression and anxiety in PsA have found only one study that met inclusion criteria to explore treatment effects and reflects a high risk of bias that indicates quality data are necessary [ 83 ]. It has been noticed that although cytokines involved in PsA (IL-6, IL-17, TNFα) can be elevated in depression or anxiety, conflicting data indicate no apparent link between depression and circulating IL-23 or IL-17 [ 62 ]. Meta-analyses in depression have indicated responders to antidepressants have a unique cytokine profile and specific shifts can be tied to therapy success [ 82 ].…”

“…Clinicians themselves often do not have time or relevant training to provide different modalities of psychotherapy [ 94 ]. Moreover, the synergistic effect of DMARDs and antidepressants remains an open question for investigation and it has been noted that placebo effects on depression and anxiety have to be scrutinized with regard to the relative benefits attributed to antidepressants [ 62 ]. Bridging the divide between psychotherapy and management of difficult manifestations of rheumatic disease is a unique opportunity to improve patient satisfaction and translate multidisciplinary care into better clinical outcomes.…”