A recent review published in Pediatric Allergy and Immunology investigates the significance of skin barrier dysfunction in atopic dermatitis (AD) and food allergies in infants. Dr. Ji Hyun Kim, a professor of pediatrics at Samsung Medical Center and the Sungkyunkwan University School of Medicine, and his colleagues emphasize that AD, the most prevalent chronic inflammatory skin condition in children, is marked by severe itching and results from a complex interplay of skin barrier dysfunction, immune dysregulation, and changes in skin microbiota.
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The research highlights that defects in the skin barrier, whether genetic or acquired, enhance the entry of allergens through the skin, increasing the risk of sensitization. Specifically, the loss of function of the filaggrin (FLG) gene is notably linked to the development of AD and other allergic disorders. Additionally, there is growing evidence that compromised skin barriers may contribute to the onset of food allergies, particularly during infancy. The dual-allergen exposure hypothesis proposes that exposure to allergens through a faulty skin barrier can promote sensitization to food allergens.
For predicting AD and food allergies in infants, the researchers discuss that although there is a heightened risk for skin barrier issues in those with either condition, both are complex with distinct pathophysiological pathways. Certain biomarkers associated with AD, but not food allergies, include structural skin barrier abnormalities, mutations in the FLG gene, and altered lipid composition. Alterations in ceramides and FLG protein expression disrupt the skin's structural integrity. Factors such as cytokines, particularly interleukin (IL)-13 and thymic stromal lymphopoietin, as well as microbial imbalances linked to Staphylococcus species, also contribute to skin barrier damage.
In managing skin barrier-related issues in AD and food allergies, Dr. Kim and his team suggest that for high-risk infants showing signs of subclinical AD, the use of emollients and environmental controls can help prevent the progression to clinical AD. While the efficacy of emollients remains somewhat mixed, further studies are needed to assess their formulation and application. Oral probiotics have produced varied results in preventing AD.
When preventive measures are ineffective, treatment strategies may include topical corticosteroids for milder cases and more proactive treatments for moderate to severe AD. AD is identified as a significant risk factor for food allergies. Effective prevention not only involves skin barrier techniques but also the early introduction of allergenic foods to promote immune tolerance. When food allergies present, avoiding problematic foods is crucial, with spontaneous remission possible. If no remission occurs by age one, immunotherapy may be an option.
Dr. Kim and colleagues conclude that the skin barrier is central to the pathogenesis of both AD and food allergies, particularly in infancy when it is still developing. They call for future research to refine predictive biomarkers and develop safe strategies that encompass both prevention and treatment to alleviate the impact of AD and food allergies from a young age.