Abstract
Psoriasis is a chronic inflammatory disease characterized by erythematous scaly plaques, accompanied by systemic damage that leads to the development of multiple comorbidities. In particular, the association between psoriasis and cardiometabolic comorbidities, including cardiovascular diseases (CVDs), obesity, diabetes mellitus, and metabolic syndrome, has been verified in a considerable number of clinical trials. Moreover, the increased risk of cardiometabolic comorbidities positively correlates with psoriasis severity. Biologic therapy targeting inflammatory pathways or cytokines substantially improves the life quality of psoriasis patients and may affect cardiometabolic comorbidities by reducing their incidences. In this review, we focus on exploring the association between cardiometabolic comorbidities and psoriasis, and emphasize the benefits and precautions of biologic therapy in the management of psoriasis with cardiometabolic comorbidities. The pathogenic mechanisms of cardiometabolic comorbidities in psoriasis patients involve common genetic factors, lipid metabolism, insulin resistance, and shared inflammatory pathways such as tumor necrosis factor-α and interleukin-23/Th-17 pathways.
Highlights
Psoriasis is a chronic immune-mediated inflammatory disease characterized by erythematous scaly plaques that commonly develop on extensor surfaces
Psoriasis is typically related to metabolic diseases including obesity, diabetes mellitus, and metabolic syndrome, which manifests as a combination of central obesity, hypertension, insulin
We explored the association between biologics and cardiometabolic comorbidities in patients with psoriasis to determine optimal systemic management of psoriasis by early screening and intervention for cardiometabolic comorbidities
Summary
Psoriasis is a chronic immune-mediated inflammatory disease characterized by erythematous scaly plaques that commonly develop on extensor surfaces. An increased risk of inflammatory comorbidities such as cardiovascular diseases (CVDs) and metabolic diseases, collectively called cardiometabolic comorbidities, has been reported in psoriasis patients. Second-generation biologics are composed of IL-12/23 and IL-17 inhibitor family: anti–IL12/23p40 antibody ustekinumab; anti–IL-23p19 antibodies guselkumab, risankizumab, and tildrakizumab; anti–IL-17A antibodies secukinumab and ixekizumab; and anti–IL-17 receptor a antibody brodalumab (Rønholt and Iversen, 2017) They have become prevalent regimens for the induction and maintenance of curative effect in patients with severe psoriasis that a higher proportion of patients have achieved Psoriasis Area Severity Index 75 (PASI 75) and PASI 90 after long-time treatment (Papp et al, 2005; Reich et al, 2005; Saurat et al, 2008). Other overlapping pathogenic mechanisms between psoriasis and comorbid cardiometabolic disorders have been proposed to be caused by common genetic factors (Lu et al, 2013), secretion of adipokines (Deng and Scherer, 2010; Robati et al, 2014), lipoprotein particles (Salahuddin et al, 2015), insulin resistance (Gyldenløve et al, 2015), angiogenesis (Malecic and Young, 2017), endothelial dysfunction (Karbach et al, 2014), and oxidative stress (Armstrong et al, 2011; Lockshin et al, 2018)
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