Abstract

Atopic dermatitis (AD), or atopic eczema, is a pruriginous inflammatory dermatosis with a genetic predisposition evolving in recurrent flare-ups on a background of chronicity, affecting essentially infants and small children. The clinical phenotype of AD results from interactions between genes and susceptibility, a defect in the cutaneous barrier function (abnormalities in filaggrin and the proteins of the epidermic differentiation complex) and dysfunction of the innate and/or adaptive immune response. With its multifactorial origin, it is dependent on the TH2 lymphocyte system, with a tendency to produce immunoglobulin E (IgE) and the risk of asthma, rhinitis, or allergic conjunctivitis define an atopic susceptibility. Staphylococcus aureus colonization plays a vital role in the perpetuation of the inflammatory phenomena. The disease often regresses in older children. Its prevalence is on the rise in industrialized countries. Diagnosis is clinical, facilitated by certain criteria initially proposed by Hanifin and Rajka and then simplified by Williams. The allergological investigation is reserved for cases that are stubborn, severe, or associated with respiratory symptoms. AD is a dermatosis that evolves in erratic and often unpredictable flare-ups. AD flare-up treatment is based on local corticosteroid therapy. Maintenance therapy attempts to correct the cutaneous dryness with hydrating products whose efficacy has now been proven. Optimal management includes the family's and/or the child's comprehension of the treatment, explaining to them that the goal to reach is not only to relieve the child, but also to attempt to modify the course of the disease. AD is thus a star disease and a public health problem. The major progress made in the comprehension of the physiopathological mechanisms of AD promise targeted therapies from new biotechnologies.

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