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.

Keywords: adipokines; cardiovascular risk; metabolic syndrome; obesity; pathophysiology; psoriatic arthritis; treatment.

Figure 1

Interaction between obesity and adipokines in the development of psoriasis, psoriatic arthritis, and cardiovascular disease. In obese patients, the adipose tissue presents cellular changes due to greater infiltration of pro-inflammatory cells with a decrease in the anti-inflammatory cell population. In this way, it becomes dysfunctional and acts as an endocrine organ, increasing the secretion of pro-inflammatory adipokines. A systemic inflammatory state is generated that, in genetically predisposed subjects, favors the appearance of skin psoriasis. On the other hand, the increased mechanical load at the enthesis sites contributes to the onset of psoriatic arthritis. The inflammation characteristic of the disease added to the sedentary lifestyle secondary to joint involvement perpetuates the growth of adipose tissue. Finally, both due to the presence of classical and non-classical factors associated with obesity, cardiovascular risk increases.