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Neurodermatitis : Atopic dermatitis - current insights into path physiology and management


Schmid-Grendelmeier, P; Ballmer-Weber, B K (2010). Neurodermatitis : Atopic dermatitis - current insights into path physiology and management. Therapeutische Umschau. Revue thérapeutique, 67(4):175-185.

Abstract

Atopic eczema (AE) is a multifaktoriell skin disease caused by a variety of factors such as genetic conditions, alterated skin structure, immunologic deviations, psychological and environmental factors, among others. There are two main subtypes of AE, i.e. the IgE-associated ("extrinsic atopic eczema") and the non-IgE-associated type ("intrinsic atopic eczema") with different prognosis concerning the development of respiratory diseases ("atopy march"). The role of allergens varies: while in early childhood food allergens may play a role, mites and microbial antigens may become more relevant in adolescence and adulthood. Recently, it was demonstrated that Filaggrin is a major gene for atopic eczema. The altered skin structure and a deficiency in antimicrobial peptides favour colonization with Staphylococcus aureus; their enterotoxins with superantigenic activity stimulate activation of T cells and macrophages. Also sensitization to the yeast Malassezia spp. occurs almost exclusively in AE patients. So far, AE skin lesions are orchestrated by the local tissue expression of proinflammatory cytokines and chemokines with activation of T lymphocytes, dendritic cells, macrophages, keratinocytes, mast cells, and eosinophils which lead to the skin inflammatory responses. From the therapeutic point of view, a step wise approach using emollients as a basic treatment is recommended. Modern topical corticosteroids of moderate to medium potency applied once per day and only on several days per week offer an efficient anti-inflammatory treatment with moderate side effects. Topic immunomodulatory drugs (tacrolimus and pimecrolimus) have in addition substantially improved the treatment of AE. Proactive treatment approaches also in disease-free intervals may reduce exacerbations and total drug use. Phototherapy and wet dressings are both efficient and safe additional tools in more severe forms. For generalized severe forms systemic drugs such as Cyclosporin A are very helpful. Various Biologicals and antipruriginous substances are under clinical investigation and may add to an improved therapy in the future.

Abstract

Atopic eczema (AE) is a multifaktoriell skin disease caused by a variety of factors such as genetic conditions, alterated skin structure, immunologic deviations, psychological and environmental factors, among others. There are two main subtypes of AE, i.e. the IgE-associated ("extrinsic atopic eczema") and the non-IgE-associated type ("intrinsic atopic eczema") with different prognosis concerning the development of respiratory diseases ("atopy march"). The role of allergens varies: while in early childhood food allergens may play a role, mites and microbial antigens may become more relevant in adolescence and adulthood. Recently, it was demonstrated that Filaggrin is a major gene for atopic eczema. The altered skin structure and a deficiency in antimicrobial peptides favour colonization with Staphylococcus aureus; their enterotoxins with superantigenic activity stimulate activation of T cells and macrophages. Also sensitization to the yeast Malassezia spp. occurs almost exclusively in AE patients. So far, AE skin lesions are orchestrated by the local tissue expression of proinflammatory cytokines and chemokines with activation of T lymphocytes, dendritic cells, macrophages, keratinocytes, mast cells, and eosinophils which lead to the skin inflammatory responses. From the therapeutic point of view, a step wise approach using emollients as a basic treatment is recommended. Modern topical corticosteroids of moderate to medium potency applied once per day and only on several days per week offer an efficient anti-inflammatory treatment with moderate side effects. Topic immunomodulatory drugs (tacrolimus and pimecrolimus) have in addition substantially improved the treatment of AE. Proactive treatment approaches also in disease-free intervals may reduce exacerbations and total drug use. Phototherapy and wet dressings are both efficient and safe additional tools in more severe forms. For generalized severe forms systemic drugs such as Cyclosporin A are very helpful. Various Biologicals and antipruriginous substances are under clinical investigation and may add to an improved therapy in the future.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
Dewey Decimal Classification:610 Medicine & health
Language:German
Date:2010
Deposited On:07 Jan 2011 15:21
Last Modified:09 Mar 2017 08:20
Publisher:Hogrefe Verlag
ISSN:0040-5930
Free access at:Related URL. An embargo period may apply.
Publisher DOI:https://doi.org/10.1024/0040-5930/a000031
Related URLs:http://www.zora.uzh.ch/43901/
http://www.zora.uzh.ch/43890/
PubMed ID:20336617

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