Psoriasis is a chronic, immune-mediated, inflammatory skin disease, affecting 1–3% of the white population. Although the existence of two psoriasis incidence peaks has been suggested (one in adolescence before 20 years of age and another in adulthood), its onset may occur at any age, including childhood and adolescence, in which the incidence is now estimated at 40.8 per 100,000. As for adult psoriasis, pediatric psoriasis has recently been associated with obesity, metabolic syndrome, increased waist circumference percentiles and metabolic laboratory abnormalities, warranting early monitoring and lifestyle modifications. In addition, due to psoriasis' chronic nature and frequently occurring relapses, psoriatic patients tend to have an impaired quality of life, often requiring long-term treatment. Therefore, education of both pediatric patients and their parents is essential to successful and safe disease management. Given the lack of officially approved therapies, the very limited evidence-based data from randomized controlled trials, and the absence of standardized guidelines, to date, pediatric psoriasis treatment is primarily based on published case reports, case series, guidelines for adult psoriasis, expert opinions and experience with these drugs in other pediatric disorders coming from the disciplines of rheumatology, gastroenterology and oncology. This review focuses on the use of systemic treatments in pediatric psoriasis and their specific features, analyzing the few literature evidences available, expanding the treatment repertoire and guiding dermatologists in better managing of recalcitrant pediatric psoriasis.

IL-33 is a novel pro-inflammatory cytokine and ligand for the orphan receptor ST2. Although originally defined as an inducer of Th2-mediated responses, IL-33 was recently found to be involved in arthritis, a Th1/Th17-mediated disease. Here, we assessed the ability of IL-33 to promote inflammation via mast cells (MCs) and keratinocytes (KCs) activation in psoriasis. IL-33 resulted elevated in the skin but not in the serum of psoriasis patients. IL-33 was secreted by psoriasis KCs and HaCaT cells after TNF-a stimulation. In HMC-1, TNF-a, but not IL-17, could induce a robust increase in IL-33 expression. In HaCaT cells, TNF-a was able to induce IL-6, MCP-1 and VEGF, and the addition of IL-33 reinforced these increases. TNF-a + IL-33 combination showed similar results in primary KCs and ex vivo skin organ culture. In conclusion, our study suggests that IL-33 may be involved in psoriasis biology via MCs and KCs.

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Sandoz and Sanofi. A. Cristaudo has been principal investigator in clinical trials sponsored by Abbvie, Leo Pharma and Pfizer. F. Cusano received honoraria as speaker and advisory board member from Sanofi Genzyme. M. Esposito has served as a speaker for Sanofi-Genzyme.

Our study identifies the presence of shiny white to red areas, SFTs and "erosions" as main dermoscopic criteria of superficial BCC. Other dermoscopic features, such as leaf-like areas, arborizing telangiectasias, blue-gray globules and large blue-gray ovoid nests, are not strongly associated with the diagnosis of superficial BCC but they are useful in the differential diagnosis from other pigmented and nonpigmented skin lesions.