Adipokines, Cardiovascular Risk, and Therapeutic Management in Obesity and Psoriatic Arthritis

Abstract

Psoriatic arthritis is a chronic inflammatory disease with skin and joint pathology as the dominant characteristics. Scientific evidence supports its systemic nature and relevant relationship with obesity, metabolic syndrome, and associated conditions. Metabolic syndrome and obesity share common signaling pathways with joint inflammation, reinforcing the idea that adipose tissue is a major contributor to disease development and severity. The adipose tissue is not a mere energy store but also an endocrine organ participating in the immune response. In the search for the best therapeutic strategy for a patient, we should appraise the adipose tissue as an endocrine and immune organ responsible for mild chronic inflammation. Today, our challenge is not only to achieve disease remission but to control the associated comorbidities as well. In light of the high prevalence of obesity in psoriatic arthritis patients and the importance of the adipose tissue in the development of chronic inflammation, we aimed to identify the most relevant articles in this regard published in English until June 2020 using the PubMed database. Search terms included psoriatic arthritis, in combination with metabolic syndrome, obesity, adipokines, cardiovascular disease, and treatment. This review summarizes the current evidence regarding the role of adipose tissue as an adipokine-secreting endocrine organ, discussing its influence on disease development and severity, and ultimately in meeting successful disease management.

Minimal disease activity and remission in patients with psoriatic arthritis with elevated body mass index: an observational cohort study in the Swiss Clinical Quality Management cohort

“… 5 17 18 In short, obesity has been described as a low-grade inflammatory disease, 18 and both obesity and PsA share pathological inflammatory pathways. 5 18 19 Further evidence supporting the association between obesity and a worse PsA clinical outcome is the association of weight loss with higher rate of achieving MDA. 20 Additionally, obesity is a well-known contributor to the metabolic syndrome (MetS), and MetS was similarly associated with lower likelihood of achieving MDA in patients with PsA.…”

“…Psoriatic arthritis (PsA) is an immune-mediated rheumatic disease,1 with an estimated prevalence of 0.05%–0.42%,2–4 and 5%–41% among patients with psoriasis 3. PsA is a complex and multifactorial disease,5 for which pathological features include musculoskeletal involvement, such as inflammation of the peripheral joints (arthritis), the entheses (enthesitis), the axial skeleton (spondylitis) and the finger and toe digits (dactylitis), as well as extra-articular manifestations involving skin and nails, and potentially other organs 6. Pharmacological treatments include conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) and biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) 3.…”

“…The rationale behind the association between obesity and PsA has been previously discussed 5 17 18. In short, obesity has been described as a low-grade inflammatory disease,18 and both obesity and PsA share pathological inflammatory pathways 5 18 19.…”

“…The rationale behind the association between obesity and PsA has been previously discussed 5 17 18. In short, obesity has been described as a low-grade inflammatory disease,18 and both obesity and PsA share pathological inflammatory pathways 5 18 19. Further evidence supporting the association between obesity and a worse PsA clinical outcome is the association of weight loss with higher rate of achieving MDA 20.…”

Prevention and risk assessment of cardiovascular events in a population of patients with psoriasis and psoriatic arthritis

“…Previous studies indicate a positive correlation between Ps and calcium deposition in coronary arteries, as well as endothelial dysfunction caused by chronic inflammation, which is the starting point for atherosclerosis [20]. The combination of these two phenomena -atherosclerotic plaque formation and skin plaques that appear in Ps -is described in the literature as two plaques for one syndrome [21] because they share a similar profile of cytokines secreted by Th1 (tumor necrosis factor α [TNF-α] and interferon γ [IFN-γ]) and Th17 (interleukin 17 and IL-22) lymphocytes [22,23]. A study by Yamazaki [24] indicated that the pro-inflammatory cytokine TNF-α has the greatest impact on atherosclerosis formation.…”