IJCS | Volume 33, Nº2, March / April 2020

psoriasis skin lesions and atherosclerosis vascular lesions are very similar, showing increased number of Th1 and Th17 lymphocytes. The Th1 and Th17 cytokine pathways have been shown to be involved in the pathogenesis of both psoriasis and atherosclerosis. The overexpression of Th17 cytokines in patients with psoriasis maymediate vascular inflammation and the development of atherosclerosis and CV comorbidities. Other mechanisms proposed are shared genetic factors, secretion of adipokines, lipoprotein composition and function, angiogenesis, oxidative stress, microparticles and hypercoagulability. 8 Whilemetabolic comorbidities are still underdiagnosed and undertreated in patientswith long-standing psoriasis, the question arises whether earlier and more stringent control of the disease-driving inflammatory processes could potentially prevent the development andworsening of comorbidities. In this context, canwe consider psoriasis as an independent risk factor for CV disease? Several factors are associated with a higher risk of developing CV disease, including age, high blood pressure, obesity, smoking, stress and family history. Many (if not all) of these risk factors are also present in psoriatic patients. 9 Metabolic syndrome is more frequent in patients with psoriasis than in general population. Campos et al. 1 found dyslipidemia in 93%, hypertension in 46%, obesity in 40% and diabetes in 33% of the sample studied (psoriatic arthritis patients aged between 30 to 74 years, without other chronic inflammatory diseases, seen at the rheumatology outpatient clinic of a referral hospital in Jo o Pessoa / Paraiba). Su et al., 10 found that the risk of developing severe vascular events is higher when psoriasis acts as a disease amplifier (i.e., when metabolic disorder precedes psoriasis), compared towhen it acts as the disease initiator. Reich 2 proposed a simplifiedmodel, based on the excellent paper byDavidovici et al., 11 that illustratesmany potential functional interplays between shared genetic risk factors that drive both psoriasis and obesity, and may promote the development of CV comorbidities (Figure 2). There are, however, opposing arguments to thismodel, and the debate so far has been whether there is a causal relationship between psoriasis and CV diseases. 9 Campos et al., 1 found a high prevalence of cardiovascular risk factors in psoriatic arthritis patients, and the majority of the samplewas stratified into high or intermediateCV risk. This raises important issues regarding this association, including determining the minimum degree of psoriasis severity required to significantly increase the CV risk. So, despite not being a (yet) consensual topic, there is strong evidence to suggest that psoriasis is an independent risk factor for the development ofmetabolic and CV comorbidities. In this regard, treatment of psoriasis might be expected to reduce the risk of developing these diseases. 2,9 Although inflammation suppression, mainly by immunomodulatory agents, has been suggested as a promising target for the management of CV diseases, Campos et al., 1 found no significant difference in CV parameters with the different drugs used by the study population. Nevertheless, other studies have shown positive effects with the new cytokine-targeted therapies, mainly anti-TNF α . 8 A limitation of the study by Campos et al. 1 is, in fact, its cross-sectional nature and absence of a control group. In conclusion, since optimal treatment of psoriasis is the one that not only ameliorates skin condition but also decreases the risk for CV and metabolic disorders, an early diagnosis and appropriate intervention made by internal medicine physicians, dermatologists and immunologists, are mandatory. 9 Campos et al., 1 highlight the importance of assessing CV risk in psoriasis patients (mainly, but not exclusively with the severe forms of the disease), reinforcing this new perspective for inflammatory skin conditions. SHARED GENETIC RISK FACTORS OBESITY PSORIASIS Cardiovascular disease Figure 2 – Model of interplay between metabolic co-morbidities and psoriasis. Modified from ref 2,11 . 110 Boechat Psoriatic March Int J Cardiovasc Sci. 2020; 33(2):109-111 Editorial