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Atopic dermatitis (AD) is the most common inflammatory skin disease. Recent research findings have provided an insight into the complex pathogenic mechanisms involved in this disease. Despite a rising prevalence, effective and safe therapeutics for patients with moderate-to-severe AD are still lacking. Biomarkers of lesional, nonlesional skin, and blood have been developed for baseline as well as after treatment with broad and specific treatments (i.e., cyclosporine A and dupilumab). These biomarkers will help with the development of novel targeted therapeutics and assessment of disease reversal, with the promise of a more personalized treatment approach. Since AD involves more than one subtype (i.e., intrinsic/extrinsic, pediatric/adult, etc.), these molecular fingerprints needs to be validated in all subpopulations with AD.

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Phase 2 randomized, double-blind study of IL-17 targeting with secukinumab in atopic dermatitis To the Editor:Atopic dermatitis (AD) affects 3% to 10% of adults. 1 Recently, the increased understanding of AD pathogenesis has led to development of new treatments, including dupilumab, the first US Food and Drug Administration-approved biologic for moderate-to-severe AD. Although T H 2 skewing is common across all AD subtypes, as suggested by the efficacy of dupilumab across populations with AD, it is a highly heterogeneous disease with diverse subtypes characterized by varying immune activation, perhaps requiring additional therapeutic approaches. 2,3 Recent studies have shown increased T H 17 skewing in several AD subtypes, including intrinsic, 3 Asian, 2 and pediatric AD, 4 and have also shown that T H 17-related markers are significantly correlated with AD severity. [2][3][4] An Asian patient with AD demonstrated clinical and tissue improvement with secukinumab, a selective IL-17A inhibitor. 5 However, controlled trials with IL-17 antagonists in patients with moderate-to-severe AD (including T H 17-high subtypes) are FIG 1. Epidermal thickness, epidermal hyperplasia markers, and clinical outcomes. A-C, Box plots depicting fold change (FCH) in epidermal thickness (A), Ki67 level (B), and K16 level (C) in lesional skin at week 4 (W4) and W16 versus at baseline (BL) (W0); red stars indicate significance of comparison with baseline. 1 P < .1 and **P < .01. D and E, Mean percentage change 6 SEM for the Scoring Atopic Dermatitis (SCORAD) (D) and the Eczema Area and Severity Index (EASI) (E) scores in all patients with AD receiving secukinumab or placebo from baseline to W16. Red and blue numbers in (D) and (E) represent numbers of patients receiving secukinumab and placebo remaining at each time point, respectively.

Epstein-Barr virus (EBV) is a human B-lymphotropic herpes virus and one of the most common viruses in humans. Specific skin signs related to EBV infection are the exanthem of mononucleosis, which is observed more frequently after ingestion of amoxicillin, and oral hairy leukoplakia, a disease occurring mostly in immunocompromised subjects with HIV infection. Other more uncommon cutaneous disorders that have been associated with EBV infection include virus-related exanthems or diseases such as Gianotti-Crosti syndrome, erythema multiforme, and acute genital ulcers. Other skin manifestations, not correlated to virus infection, such as hydroa vacciniforme and drug-induced hypersensitivity syndrome have also been linked to EBV. The putative involvement of EBV in skin diseases is growing similarly to other areas of medicine, where the role of EBV infection is being investigated in potentially debilitating inflammatory diseases. The prognosis of EBV infection in healthy, immunocompetent individuals is excellent. However, lifelong infection, which is kept in check by the host immune system, determines an unpredictable risk of pathologic unpredictable scenarios. In this review, we describe the spectrum of non-tumoral dermatological manifestations that can follow EBV primary infection or reactivation of EBV in childhood.