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Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Online ISSN 1827-1820
UPDATE ON CONTACT DERMATITIS
Jensen J. M., Fölster-Holst R., Proksch E.
Department of Dermatology University of Kiel, Kiel, Germany
A defect in barrier function is present in atopic dermatitis, potentially playing the causative role in the development of atopic lesions by enabling the penetration of type I environmental allergens into the skin, which consequently initiates immunological reactions and inflammation. This defect may be caused by genetic defects associated with the atopic syndrome (in particular filaggrin gene mutations) causing impaired nasal, bronchial, and intestinal mucous membranes. This leads to an enhanced penetration of environmental allergens such as those from house dust mite, cat dander and grass pollen into the skin which than leads to atopic dermatitis, allergic rhinitis, bronchial asthma. The immunological reaction results in increased epidermal proliferation and disturbed differentiation, accompanied by changes in lipid composition. Increased proliferation and disturbed differentiation have been identified in both lesional and non-lesional skin in atopic dermatitis. Because impaired epithelial defense appears to play a central role in the pathogenesis of atopic dermatitis, treatment strategies which address the long-term maintenance of barrier function by restoring lost lipid content and skin barrier hydration are of great importance for atopic patients.