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.

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EditorAmong the basic protective measures against COVID-19, the need to wash hands frequently and in a prolonged way using soap and to regularly use alcohol-based hand sanitizers is well established for the whole population. Healthcare workers in general, and particularly those involved in the direct care of COVID-19-infected patients, have to wear personal protective equipment (PPE) daily for many hours and also accomplish general preventive measurements outside their work. Cutaneous adverse reactions can develop that need to be prevented, identified and therapeutically managed. According to the data reported by Lin et al., 1 based on the experience from healthcare workers in Wuhan, adverse skin reactions were reported in 74% of responders (n = 376) to a general survey. The most commonly reported types of eruptions were skin dryness or desquamation (68.6%), papules or erythema (60.4%) and maceration (52.9%). Hands, cheeks and nasal bridge were the top three most commonly affected areas. Adverse skin reactions showed in the univariate analysis a significant association with sex, epidemic level, working place, duration of full-body PPE use, getting soaking wet after work and frequency of handwashing. The multivariate analysis showed an increased number of reactions in females, who work at the hospitals, in inpatient wards and use full-body PPE for over 6 h per day. Similar results were reported from Chengdu, with 198 of 404 (49.0%) respondents to an online survey from the healthcare sector reporting mask-related skin reactions, mostly, in 169, in the face following prolonged use of N95 and medical-grade masks. Of note, worsening of preexisting facial skin problems such as acne or rosacea was frequently reported. 2 This scenario is certainly similar to what the health care personnel is suffering nowadays in Europe. 3 The identification of these cutaneous reactions, how to prevent and treat them is the objective of this document.

Psoriasis is a chronic skin disorder associated with several comorbid conditions. In psoriasis pathogenesis, the role of some cytokines, including TNF-α and IL-17, has been elucidated. Beside their pro-inflammatory activity, they may also affect glucose and lipid metabolism, possibly promoting insulin resistance and obesity. On the other hand, adipose tissue, secreting adipokines such as chemerin, visfatin, leptin, and adiponectin, not only regulates glucose and lipid metabolism, and endothelial cell function regulation, but it may contribute to inflammation. Areas covered: This review provides an updated 'state-of-the-art' about the reciprocal contribution of a small subset of conventional cytokines and adipokines involved in chronic inflammatory pathways, upregulated in both psoriasis and increased adiposity. A systematic search was conducted using the PubMed Medline database for primary articles. Expert commentary: Because psoriasis is associated with increased adiposity, it would be important to define the contribution of chronic skin inflammation to the onset of obesity and vice versa. Clarifying the pathogenic mechanism underlying this association, a therapeutic strategy having favorable effects on both psoriasis and increased adiposity could be identified.

Interleukin (IL)-36 cytokines are new members of the IL-1 family, which include pro-inflammatory factors, IL-36α, IL-36β and IL-36γ, and a natural receptor antagonist IL-36Ra. Over recent years, much has been learned on their important functions in the regulation of immune response and, especially, on their role in many inflammatory skin diseases. However, to date, no data have been reported on their possible involvement in acne and hidradenitis suppurativa (HS). Here, we have shown that IL-36α, IL-36β, and IL-36γ are increased in lesional skin of acne and HS, highlighting their possible pathogenetic contribution to these two skin conditions. In contrast, IL-36Ra (the anti-inflammatory member of IL-36 sub-family) was increased just in psoriasis, suggesting that an imbalance in IL-36/IL36Ra functions could play a role in the phenotype of skin damage. One of the consequences of this imbalance may be the increased induction of IL-8 that we found higher in acne, HS, and ACD respect to psoriasis.