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Atopic dermatitis (AD) is a chronic, heterogenous, inflammatory skin disorder associated with a high skin‐related health burden, typically starting in childhood and often persisting into adulthood. AD is characterized by a wide range of clinical phenotypes, reflecting multiple underlying pathophysiological mechanisms and interactions between genetics, immune system dysregulation and environmental factors. In this review, we describe the diverse cellular and molecular mechanisms involved in AD, including the critical role of T‐cell‐driven inflammation, primarily via T helper (Th) 2‐ and Th17‐derived cytokines, many of which are mediated by the Janus kinase (JAK) signaling pathway. These local inflammatory processes interact with sensory neuronal pathways, contributing to the clinical manifestations of AD, including itch, pain and sleep disturbance. The recent elucidation of the molecular pathways involved in AD has allowed treatment strategies to evolve from broad‐acting systemic immunosuppressive therapies to more targeted agents, including JAK inhibitors and cytokine‐specific biologic agents. Evidence from the clinical development of these targeted therapies has reinforced and expanded our understanding of the pathophysiological mechanisms underlying AD and holds promise for individualized treatment strategies tailored to specific AD subtypes. [ABSTRACT FROM AUTHOR]

Background: Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease with different clinical phenotypes based on factors such as age, race, comorbidities, and clinical signs and symptoms. The effect of these factors on therapeutic responses in AD has only been scarcely studied and not for upadacitinib. Currently, there is no biomarker predicting response to upadacitinib. Objectives: Evaluate the efficacy of the oral Janus kinase inhibitor upadacitinib across patient subgroups (baseline demographics, disease characteristics and prior treatment) in patients with moderate‐to‐severe AD. Methods: Data from phase 3 studies (Measure Up 1, Measure Up 2 and AD Up) were utilized for this post hoc analysis. Adults and adolescents with moderate‐to‐severe AD were randomized to receive once daily oral upadacitinib 15 mg, upadacitinib 30 mg or placebo; patients enrolled in the AD Up study received concomitant topical corticosteroids. Data from the Measure Up 1 and Measure Up 2 studies were integrated. Results: A total of 2584 patients were randomized. A consistently greater proportion of patients achieved at least 75% improvement in the Eczema Area and Severity Index, a 0 or 1 on the validated Investigator Global Assessment for Atopic Dermatitis, and improvement in itch (including an achievement of a reduction of ≥4; and score of 0/1 in Worst Pruritus Numerical Rating Scale) with upadacitinib compared with placebo at Week 16, regardless of age, sex, race, body mass index, AD severity, body surface area involvement, history of atopic comorbidities or asthma, or previous exposure to systemic therapy or cyclosporin. Conclusions: Upadacitinib had consistently high skin clearance rates and itch efficacy across subgroups of patients with moderate‐to‐severe AD through Week 16. These results support upadacitinib as a suitable treatment option in a variety of patients. TRIAL REGISTRATION: ClinicalTrials.gov Identifiers: NCT03569293 (Measure Up 1), NCT03607422 (Measure Up 2) and NCT03568318 (AD Up). [ABSTRACT FROM AUTHOR]

The evidence‐ and consensus‐based guideline on atopic eczema was developed in accordance with the EuroGuiDerm Guideline and Consensus Statement Development Manual. Four consensus conferences were held between December 2020 and July 2021. Twenty‐nine experts (including clinicians and patient representatives) from 12 European countries participated. This second part of the guideline includes recommendations and detailed information on basic therapy with emollients and moisturizers, topical anti‐inflammatory treatment, antimicrobial and antipruritic treatment and UV phototherapy. Furthermore, this part of the guideline covers techniques for avoiding provocation factors, as well as dietary interventions, immunotherapy, complementary medicine and educational interventions for patients with atopic eczema and deals with occupational and psychodermatological aspects of the disease. It also contains guidance on treatment for paediatric and adolescent patients and pregnant or breastfeeding women, as well as considerations for patients who want to have a child. A chapter on the patient perspective is also provided. The first part of the guideline, published separately, contains recommendations and guidance on systemic treatment with conventional immunosuppressive drugs, biologics and janus kinase (JAK) inhibitors, as well as information on the scope and purpose of the guideline, and a section on guideline methodology. [ABSTRACT FROM AUTHOR]

The evidence‐ and consensus‐based guideline on atopic eczema was developed in accordance with the EuroGuiDerm Guideline and Consensus Statement Development Manual. Four consensus conferences were held between December 2020 and July 2021. Twenty‐nine experts (including clinicians and patient representatives) from 12 European countries participated. This first part of the guideline includes general information on its scope and purpose, the health questions covered, target users and a methods section. It also provides guidance on which patients should be treated with systemic therapies, as well as recommendations and detailed information on each systemic drug. The systemic treatment options discussed in the guideline comprise conventional immunosuppressive drugs (azathioprine, ciclosporin, glucocorticosteroids, methotrexate and mycophenolate mofetil), biologics (dupilumab, lebrikizumab, nemolizumab, omalizumab and tralokinumab) and janus kinase inhibitors (abrocitinib, baricitinib and upadacitinib). Part two of the guideline will address avoidance of provocation factors, dietary interventions, immunotherapy, complementary medicine, educational interventions, occupational and psychodermatological aspects, patient perspective and considerations for paediatric, adolescent, pregnant and breastfeeding patients. [ABSTRACT FROM AUTHOR]

Background and objectives: The economic burden of atopic dermatitis (AD) is of particular interest. The present study aims to analyse the association of disease‐related characteristics, annual costs and treatment benefits in AD. Methods: Between August 2017 and June 2019, a cross‐sectional observational study in patients with AD was conducted in Germany. Cost‐of‐illness data were assessed from the societal perspective. Disease characteristics included severity, time since diagnosis and therapy, as well as atopic comorbidity and the implementation of prevention measures. Subgroup analyses of the total costs were conducted for these characteristics. A linear regression model was applied to analyse the impact of disease characteristics on the costs. Furthermore, associations of biologic treatment with outcome parameters were analysed. Results: A total of 1291 patients from 111 centres were included in the analyses. The total costs amounted on average to € 3660 ± € 6428 per patient and year. Higher costs were shown in various patient groups, for example, in patients using biologics (€ 20 983 vs. € 2470). In a regression analysis, gender, education and the number of implemented prevention measures were identified as significant predictors of costs. Patients treated with biologics showed consistently better outcome parameters and were more often satisfied with their treatment. Conclusions: Gender, education and implemented prevention measures are significant cost determinants in AD. The results confirm that treatment with biologics is the main cost driver in AD. However, incremental patient‐relevant benefits of high‐priced therapy are reflected by the significantly better clinical outcomes in the group treated with biologics. [ABSTRACT FROM AUTHOR]

Background: Epigallocatechin‐3‐gallate (EGCG) has been proven effective in treating viral warts. Since anticarcinogenic as well as anti‐inflammatory properties are ascribed to the substance, its use has been evaluated in the context of different dermatoses. The effect of EGCG on interface dermatitis (ID), however, has not yet been explored. Objectives: In this study, we investigated the effect of EGCG on an epidermal human in vitro model of ID. Methods: Via immunohistochemistry, lesional skin of lichen planus patients and healthy skin were analysed concerning the intensity of interferon‐associated mediators, CXCL10 and MxA. Epidermal equivalents were stained analogously upon ID‐like stimulation and EGCG treatment. Monolayer keratinocytes were treated likewise and supernatants were analysed via ELISA while cells were processed for vitality assay or transcriptomic analysis. Results: CXCL10 and MxA are strongly expressed in lichen planus lesions and induced in keratinocytes upon ID‐like stimulation. EGCG reduces CXCL10 and MxA staining intensity in epidermis equivalents and CXCL10 secretion by keratinocytes upon stimulation. It furthermore minimizes the cytotoxic effect of the stimulus and downregulates a magnitude of typical pro‐inflammatory cytokines that are crucial for the perpetuation of ID. Conclusions: We provide evidence concerning anti‐inflammatory effects of EGCG within a human in vitro model of ID. The capacity to suppress mediators that are centrally involved in disease perpetuation suggests EGCG as a potential topical therapeutic in lichen planus and other autoimmune skin diseases associated with ID. [ABSTRACT FROM AUTHOR]

All patients continued to use TCS, one patient received concomitant acitretin, which had been initiated approximately 5 years before the anti-IL-23 treatment, and one patient received concomitant methotrexate, which was initiated 16 weeks after the beginning of the biological therapy. 56.3% (9/16) and 25.0% (4/16) of the patients reached PPPASI-50 and PPPASI-75 improvement at week 12, respectively, and at 12 months of treatment PPPASI-50 and PPPASI-75 response was observed in 62.5% (10/16) and 43.8% (7/16) of patients, respectively (Figure 1a-c). The patients in this manuscript have given written informed consent to the publication of their case details (photographs). [Extracted from the article]

Atopic dermatitis (AD) is a chronic and relapsing, inflammatory skin disease characterized by impaired skin barrier function and immune system dysregulation that results in dryness, skin microbiome dysbiosis and intense pruritus. It is highly heterogeneous, and its management is demanding. Patients with AD are at greater risk of comorbidities such as attention‐deficit hyperactivity disorder as well as other atopic diseases. Early‐onset AD cases typically improve or resolve in late childhood; however, it is proposed that the prevalence of persistent or adult‐onset AD is higher than previously thought. Basic therapy consists of emollient application and trigger avoidance, and when insufficient, topical corticosteroids (TCS) are the first‐line treatment. However, corticophobia/steroid aversion and TCS side‐effects, particularly on sensitive skin areas, lead to low compliance and insufficient disease control. Several long‐ and short‐term randomized controlled and daily practice studies have demonstrated that topical calcineurin inhibitors, such as pimecrolimus, have similar anti‐inflammatory effects to low‐to‐medium strength TCS, reduce pruritus and improve the quality of life of patients. In addition, pimecrolimus does not cause skin atrophy, is steroid‐sparing and has a good safety profile, with no evidence for an increased risk of malignancies or skin infections. In general, pimecrolimus cream is well‐accepted and well‐tolerated, encouraging patient adherence and leading to its use by many physicians as a preferred therapy for children and sensitive skin areas. [ABSTRACT FROM AUTHOR]