Abstract
SummaryPsoriasis (PsO) is a chronic immune-mediated inflammatory skin disorder associated with numerous co-morbidities. This descriptive review focuses on the cardiometabolic co-morbidities of PsO with reference to the epidemiology and pathogenetic mechanisms linking PsO and cardiometabolic disease (CMD). Registry-based studies have shown PsO to be associated with an increased risk of cardiovascular morbidity and mortality. Factors linking PsO and CMD include: chronic inflammation, obesity, classic cardiovascular risk factors, and the effects of systemic therapy used to treat PsO. Chronic inflammation is associated with PsO itself, and with obesity. Adipose tissue is responsible for the secretion of various adipokines, which together with pro-inflammatory cytokines arising from the psoriatic plaque, contribute to the proinflammatory and pro-atherogenic environment. Systemic therapy aimed at decreasing inflammation has been shown to improve CMD in PsO. Screening for and treating CMD and initiating lifestyle modifications will remain the most important interventions until further data emerge regarding the effect of systemic therapy on CMD progression.
Highlights
Immunopathogenesis of psoriasisThe interplay between genetic factors and environmental triggers results in the classic psoriatic plaque, characterised histologically by epidermal hyperplasia, vascular hyperproliferation and chronic inflammation.[4] Common triggers for the disease are local skin trauma (Koebner phenomenon), stress, Streptococcus pyogenes, infection and smoking.[4] About a third of patients have a family history of PsO and genome-wide analysis studies have shown the PSORS1 gene, located on chromosome 6p, accounts for between 35 and 50% of the heritability of PsO.[24]
Psoriasis (PsO) is a chronic immune-mediated inflammatory skin disorder associated with numerous co-morbidities
We examine the epidemiological and pathological evidence linking PsO and cardiometabolic disorders, with a particular focus on cardiovascular disease (CVD)
Summary
The interplay between genetic factors and environmental triggers results in the classic psoriatic plaque, characterised histologically by epidermal hyperplasia, vascular hyperproliferation and chronic inflammation.[4] Common triggers for the disease are local skin trauma (Koebner phenomenon), stress, Streptococcus pyogenes, infection and smoking.[4] About a third of patients have a family history of PsO and genome-wide analysis studies have shown the PSORS1 gene, located on chromosome 6p, accounts for between 35 and 50% of the heritability of PsO.[24]. Psoriasis (PsO) is a complex, chronic, immune-mediated inflammatory skin disorder, which has a global prevalence ranging between 0.91 and 8.5%.1. It is recognised by the World Health Organisation as a major global health challenge,[2] and is associated with impaired psychological quality of life, which. Pro-angiogenic factors produced by keratinocytes such as vascular endothelial growth factor drive abnormal vascular proliferation within the psoriatic plaque.[4,25]
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