ABSTRACT
Introduction
Psoriasis is an inflammatory disease nowadays considered not only as a cutaneous but as a systemic disease. Among the numerous comorbidities, psoriatic arthritis (PsA), depression, obesity, and cardiovascular disease (CVD) are considered the most frequent. In addition, metabolic syndrome (MetS), which involves hypertension, dyslipidemia, obesity, and atherosclerosis, has presented a higher prevalence in recent years, especially in psoriatic patients.
Areas covered
The mechanism linking anti-tumor necrosis factor (TNF) to MetS and CVD has been widely explained, while there are unknowns about inhibitors of interleukin (IL)-17 and −23. Considering the growing incidence of CVD in the world’s population and in particular the strict correlation in patients with psoriasis, it is important to identify therapeutic options able to avoid a negative impact on patients with both conditions. The aim of this paper is to perform a review of the scientific literature with a focus on the pathogenetic mechanism linking psoriasis to CVD and MetS.
Expert opinion
The scientific evidence currently available allows us to consider and support the use of anti-IL-17 and anti-IL-23 as a first-line therapy choice in psoriatic patients with high risk of CVDs or MetS.
Article highlights
The growing impact of cardiovascular pathologies and metabolic syndrome in the world’s population and in psoriatic patients highlights the need for therapies that do not damage the patient’s equilibrium.
The advent of IL-17/23 inhibitory monoclonal antibodies has allowed us to change the therapeutic approach to psoriasis with growing scientific evidence supporting its use as a first-line therapy in patients with cardiovascular comorbidities and metabolic syndrome.
The IL-17/23 axis has a principal role in modulating the low inflammatory chronic state, explaining the link between psoriasis and metabolic comorbidities.
In obese patients, there is a shift from an anti-inflammatory subset to a pro-inflammatory one, with higher expression of adiponectin that supports the chronic low-grade inflammatory state.
The identification, through the collection of anamnesis and laboratory tests, of any metabolic and cardiovascular comorbidity would allow one to start anti-IL-17/23 therapy with a better impact on the patient’s life.
Declaration of interest
E Trovato and F Prignano are both involved in an intermittent project focused on consulting and/or advisory relationships or/and travel-congress support with Eli-Lilly, Novartis, Janssen-Cilag, Abbvie and Almirall. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
A reviewer on this manuscript has disclosed involvement with Pfizer, Novartis, Eli Lilly, Janssen, Abbvie, Amgen, Almirall, Boehringer, Sanofi, Union Chimique Belge and Leo Pharma. Peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.
Author contributions
E Trovato: writing and original draft preparation; F Prignano: review and editing; P Rubegni: supervision. All authors have read and agreed to the published version of the manuscript.