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Published on: September 27, 2017
Severe Atopic Dermatitis in Children
1Division of General Pediatrics, Children's Hospital Los Angeles, 4650 Sunset Blvd., Los Angeles, CA, 90027, USA.
Insights
Understanding atopic dermatitis (AD) mechanisms is key to developing safer treatments. Targeting Th2 inflammation pathways and other factors like skin microbiota offers promising therapeutic avenues for severe childhood AD.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Severe atopic dermatitis (AD) in children causes significant health issues, including psychosocial and infectious complications.
- Current treatments like topical corticosteroids and tacrolimus have potential side effects, necessitating safer alternatives.
Purpose of the Study:
- To review current understanding of atopic dermatitis pathogenesis.
- To identify potential therapeutic targets for improved and safer AD treatments.
Main Methods:
- Review of recent findings on AD mechanisms.
- Analysis of the role of skin barrier defects and Th2 inflammation in AD persistence.
- Identification of key cytokines and other molecular targets involved in AD.
Main Results:
- Primary skin barrier defects and Th2 inflammation significantly contribute to AD.
- Key Th2 cytokines (IL-4, IL-13, TSLP, IL-25, IL-31, IL-33) are identified as potential therapeutic targets.
- Other targets include Janus kinase, phospholipase A2, aryl hydrocarbon receptor, and skin microbiota.
Conclusions:
- A deeper understanding of AD pathogenesis is crucial for developing novel and safer treatment strategies.
- Targeting specific molecular pathways and factors offers promising directions for future AD therapies.
Purpose Of Review:
Severe atopic dermatitis (AD) in childhood leads to significant morbidity including psychosocial problems and infectious complications. There are only a few approved treatment options for these patients. These include topical corticosteroids and tacrolimus ointment, which are associated with potential side effects.
Recent Findings:
In order to find better and safer treatments, further understanding of AD mechanisms is needed. Primary skin barrier defects play an important role in the pathogenesis of AD. In addition, the suppression of skin barrier functions by Th2 inflammation also plays an important role in the persistence and recurrence of AD. Cytokines in the Th2 pathway, which includes IL-4, IL-13, TSLP, IL-25, IL-31, and IL-33, are potential therapeutic targets in AD. Other potential targets of AD are Janus kinase, phospholipase A2, aryl hydrocarbon receptor, and skin microbiota. A better understanding of the pathogenesis of AD will provide future direction for treatment.
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