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      Epicutaneous sensitization in the development of food allergy: What is the evidence and how can this be prevented?

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          Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis.

          Atopic disease, including atopic dermatitis (eczema), allergy and asthma, has increased in frequency in recent decades and now affects approximately 20% of the population in the developed world. Twin and family studies have shown that predisposition to atopic disease is highly heritable. Although most genetic studies have focused on immunological mechanisms, a primary epithelial barrier defect has been anticipated. Filaggrin is a key protein that facilitates terminal differentiation of the epidermis and formation of the skin barrier. Here we show that two independent loss-of-function genetic variants (R510X and 2282del4) in the gene encoding filaggrin (FLG) are very strong predisposing factors for atopic dermatitis. These variants are carried by approximately 9% of people of European origin. These variants also show highly significant association with asthma occurring in the context of atopic dermatitis. This work establishes a key role for impaired skin barrier function in the development of atopic disease.
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            Consensus-based European guidelines for treatment of atopic eczema (atopic dermatitis) in adults and children: part I

            This guideline was developed as a joint interdisciplinary European project, including physicians from all relevant disciplines as well as patients. It is a consensus-based guideline, taking available evidence from other guidelines, systematic reviews and published studies into account. This first part of the guideline covers methods, patient perspective, general measures and avoidance strategies, basic emollient treatment and bathing, dietary intervention, topical anti-inflammatory therapy, phototherapy and antipruritic therapy, whereas the second part covers antimicrobial therapy, systemic treatment, allergen-specific immunotherapy, complementary medicine, psychosomatic counselling and educational interventions. Management of AE must consider the individual clinical variability of the disease; highly standardized treatment rules are not recommended. Basic therapy is focused on treatment of disturbed barrier function by hydrating and lubricating topical treatment, besides further avoidance of specific and unspecific provocation factors. Topical anti-inflammatory treatment based on glucocorticosteroids and calcineurin inhibitors is used for flare management and for proactive therapy for long-term control. Topical corticosteroids remain the mainstay of therapy, whereas tacrolimus and pimecrolimus are preferred in sensitive skin areas and for long-term use. Topical phosphodiesterase inhibitors may be a treatment alternative when available. Adjuvant therapy includes UV irradiation, preferably with UVB 311 nm or UVA1. Pruritus is targeted with the majority of the recommended therapies, but some patients may need additional antipruritic therapy. Antimicrobial therapy, systemic anti-inflammatory treatment, immunotherapy, complementary medicine and educational intervention will be addressed in part II of the guideline.
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              The Public Health Impact of Parent-Reported Childhood Food Allergies in the United States

              A 2015–2016 population-based, cross-sectional survey was administered to a sample of US households to estimate current FA prevalence, severity, and health care use. Video Abstract BACKGROUND: Childhood food allergy (FA) is a life-threatening chronic condition that substantially impairs quality of life. This large, population-based survey estimates childhood FA prevalence and severity of all major allergenic foods. Detailed allergen-specific information was also collected regarding FA management and health care use. METHODS: A survey was administered to US households between 2015 and 2016, obtaining parent-proxy responses for 38 408 children. Prevalence estimates were based on responses from NORC at the University of Chicago’s nationally representative, probability-based AmeriSpeak Panel (51% completion rate), which were augmented by nonprobability-based responses via calibration weighting to increase precision. Prevalence was estimated via weighted proportions. Multiple logistic regression models were used to evaluate FA predictors. RESULTS: Overall, estimated current FA prevalence was 7.6% (95% confidence interval: 7.1%–8.1%) after excluding 4% of children whose parent-reported FA reaction history was inconsistent with immunoglobulin E–mediated FA. The most prevalent allergens were peanut (2.2%), milk (1.9%), shellfish (1.3%), and tree nut (1.2%). Among food-allergic children, 42.3% reported ≥1 severe FA and 39.9% reported multiple FA. Furthermore, 19.0% reported ≥1 FA-related emergency department visit in the previous year and 42.0% reported ≥1 lifetime FA-related emergency department visit, whereas 40.7% had a current epinephrine autoinjector prescription. Prevalence rates were higher among African American children and children with atopic comorbidities. CONCLUSIONS: FA is a major public health concern, affecting ∼8% of US children. However, >11% of children were perceived as food-allergic, suggesting that the perceived disease burden may be greater than previously acknowledged.
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                Author and article information

                Contributors
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                Journal
                Allergy
                Allergy
                Wiley
                0105-4538
                1398-9995
                May 18 2020
                Affiliations
                [1 ]Paediatric Allergy Group Department of Women and Children’s Health School of Life Course Sciences King’s College London St. Thomas’ Hospital London UK
                [2 ]Paediatric Allergy Group Peter Gorer Department of Immunobiology School of Immunology & Microbial Sciences King’s College London Guys’ Hospital London UK
                [3 ]Children’s Allergy Service Evelina Children’s Hospital Guy’s and St. Thomas’ Hospital NHS Foundation Trust London UK
                [4 ]Sean N. Parker Center for Allergy and Asthma Research at Stanford University Stanford University Stanford CA USA
                [5 ]Department of Medicine Division of Pulmonary and Critical Care Medicine Stanford University Stanford CA USA
                [6 ]Department of Medicine Division of Allergy, Immunology and Rheumatology Stanford University Stanford CA USA
                [7 ]Benaroya Research Institute and Immune Tolerance Network Seattle WA USA
                [8 ]Department of Pediatrics Division of Pediatric Allergy‐Immunology National Jewish Health Denver CO USA
                Article
                10.1111/all.14304
                32249942
                caaad6db-1aca-41f0-a8da-91f5cfcb6a40
                © 2020

                http://creativecommons.org/licenses/by-nc-nd/4.0/

                http://doi.wiley.com/10.1002/tdm_license_1.1

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