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Published on: September 26, 2019
From Skin Barrier Dysfunction to Systemic Impact of Atopic Dermatitis: Implications for a Precision Approach in
Laura Maintz1,2, Thomas Bieber1,2,3, Helen D Simpson4
1Department of Dermatology and Allergy, University Hospital Bonn, 53127 Bonn, Germany.
Insights
Atopic dermatitis (AD) in children can lead to other allergies and asthma. Early, tailored treatments targeting skin barrier and inflammation may prevent systemic effects and comorbidities.
Area of Science:
- Dermatology
- Immunology
- Pediatrics
Background:
- Atopic dermatitis (AD) affects up to 20% of children, often initiating the atopic march.
- AD presents heterogeneous phenotypes involving skin barrier dysfunction, T cell activation, and microbiome dysbiosis.
- Cutaneous inflammation in AD has systemic effects and increases comorbidity risk, particularly in severe cases.
Purpose of the Study:
- To review evidence on the systemic impact of atopic dermatitis.
- To discuss implications for preventive and therapeutic strategies.
- To explore precision medicine approaches for AD management.
Main Methods:
- Review of current scientific literature.
- Analysis of pathogenetic mechanisms in AD.
- Discussion of comorbidity data and therapeutic interventions.
Main Results:
- AD is linked to a higher risk of asthma and other comorbidities, especially severe or persistent AD.
- Early intervention to restore skin barrier, modify microbiome, and target inflammation is crucial.
- Stratification of AD patients by endotype can guide precision medicine.
Conclusions:
- Tailored, early therapy for AD can mitigate systemic impact and comorbidities.
- Precision medicine, guided by biomarkers, offers improved long-term control of AD.
- Understanding comorbidities informs preventive and therapeutic strategies for AD and associated conditions.
Abstract:
Atopic dermatitis (AD) affects up to 20% of children and is considered the starting point of the atopic march with the development of food allergy, asthma, and allergic rhinitis. The heterogeneous phenotype reflects distinct and/or overlapping pathogenetic mechanisms with varying degrees of epidermal barrier disruption, activation of different T cell subsets and dysbiosis of the skin microbiome. Here, we review current evidence suggesting a systemic impact of the cutaneous inflammation in AD together with a higher risk of asthma and other comorbidities, especially in severe and persistent AD. Thus, early therapy of AD to restore the impaired skin barrier, modified microbiome, and target type 2 inflammation, depending on the (endo)phenotype, in a tailored approach is crucial. We discuss what we can learn from the comorbidities and the implications for preventive and therapeutic interventions from precision dermocosmetics to precision medicine. The stratification of AD patients into biomarker-based endotypes for a precision medicine approach offers opportunities for better long-term control of AD with the potential to reduce the systemic impact of a chronic skin inflammation and even prevent or modify the course, not only of AD, but possibly also the comorbidities, depending on the patient's age and disease stage.
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