It is the the development of atopic dermatitis (AD) or eczema in infancy to allergic rhinitis and asthma in later childhood. This progression is dependent on various underlying factors such as the presence of filaggrin mutations as well as the time of onset and severity of AD. Clinical manifestations vary among individuals. Recent studies show that there is a causal link between AD and later onset atopic disorders. Environmental and genetic studies provide evidence that a dysfunction skin barrier serves as a site for allergic sensitization to antigens/allergens which leads to phenotypes of AD systemic sensitization and increased risk of allergic rhinitis, lung inflammation and airway hyperresponsiveness. While AD often starts early in life and is a chronic condition, new research signifies that there may be an OPTIMAL WINDOW OF TIME IN WHICH TARGETING THE SKIN BARRIER WITH THERAPEUTIC INTERVENTIONS MAY PREVENT SUBSEQUENT ATOPIC DISORDERS. The mainstays of therapy for AD include frequent moisturizing barrier cream, optimal skin hygiene, avoidance of allergic triggers, topical corticosteroids, and calcineurin inhibitors. Antihistamines can help control itch. Emollients improve the barrier function of the stratum corneum by providing water and lipids. Sufficient lipid replacement therapy reduces the inflammation and restores epidermal function. Some products have therapeutic efficacy in improving clinical and biophysical parameters of patients with AD. Long-term studies are found to be important to evaluate whether lipid barrier replacement therapy reduces bacterial colonization or prevents progression of the atopic march.


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