Abstract
Nowadays, it is well established a link between psoriasis and cardiovascular (CV) diseases. A series of different overlapping mechanisms including inflammation, homeostasis dysregulation, and genetic susceptibility are thought to underlie this association. Advances in understanding the molecular patterns involved in the complex scenario of psoriasis have highlighted a tight correlation with atherosclerosis. Indeed, common profiles are shared in term of inflammatory cytokines and cell types. In the last decade, the management of psoriasis patients has been revolutionized with the introduction of biological therapies, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-12/23, and IL-17 inhibitors. In clinical setting, the effectiveness of these therapies as well as the incidence of CV events is related to the type of biologics. In particular, anti-TNF-α agents seem to reduce these events in psoriasis patients whereas anti-IL-12/23 agents related CV events reduction still remain to clarify. It has to be taken into account that IL-12/23 inhibitors have a shorter post-marketing surveillance period. An even more restricted observational time is available for anti-IL-17 agents. IL-17 is associated with psoriasis, vascular disease, and inflammation. However, IL-17 role in atherosclerosis is still debated, exerting both pro-atherogenic and anti-atherogenic effects depending on the specific context. In this review, we will discuss the differences between the onset of CV events in psoriasis patients, referred to specific biological therapy and the underlying immunological mechanism. Given the development of new therapeutic strategies, the investigation of these inhibitors impact on heart failure outcome is extremely important.
Highlights
Giuseppina Caiazzo1, Gabriella Fabbrocini1, Roberta Di Caprio1, Annunziata Raimondo1, Emanuele Scala1, Nicola Balato1 and Anna Balato2*
Since systemic inflammation is currently considered the main cause of cardiovascular disease (CVD) risk in Pso, it has been thought that biological therapies might be helpful in treating cutaneous manifestations but have positive or negative CV effects depending on the specific cytokine target and molecular mode of action
Despite the recognized efficacy of biological agents in psoriasis treatment, little is known about their impact on risk of major adverse cardiovascular events (MACEs) in these patients
Summary
The growing body of evidences pointing to increases in MI and CV events in psoriatic patients has raised the question whether treating cutaneous disease might prevent heart attacks and decrease CVD risk development. Demonstrated that a continuous systemic therapy with fumaric acid esters, behind reducing Pso severity, was able to improve the endothelial vasodilator function, reduce serum levels of CRP, and increase the potentially cardioprotective adiponectin [33]. It has been with the introduction of biological therapies that Pso treatment expectations and long-term control have greatly improved and the idea that these therapies, more than the systemic ones, might reduce the risk of CVD reinforced [34]. IL-23 regulates the maintenance of Th17 cells, whereas IL-17 and TNF mediate effector functions of innate (TNF) and adaptive (TNF, IL-17) immune cells
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