Atopic dermatitis is one of the most common skin diseases in children. Genetic disorders that determine the development of persistent dysfunction of cellular immunity play an important role in the development of clinical symptoms of atopic dermatitis. In the new concept of the occurrence of clinical manifestations of atopic dermatitis (AD), T-regulatory lymphocytes are assigned, in the form of CD4+CD25+ phenotype, which is controlled by the transcription factor FoxP3. The study of the mechanism of itching, which is more or less observed in all children with blood pressure, showed that in the case of the island-inflammatory course of Th2-dependent blood pressure, itching is histamine-conditioned. According to the concept of «Outside to Inside – outside – inside», the most significant mechanisms causing the appearance of blood pressure are a genetic predisposition that causes the formation of allergic reactions, changes in the permeability of the epidermal barrier, against the background of transepidermal moisture loss, the occurrence of xerosis phenomena and a decrease in the itching threshold. Significant abnormalities in the state of the skin microbiota were found in children with AD. The species composition of the intestinal microbiota in children with AD differs significantly from that in children with healthy skin. Intestinal microbiocenosis largely determines the direction of morphofunctional processes in the epidermis, by means of translocation of intestinal bacteria regulating the humoral response directly in the skin. Most often, allergic reactions are triggered when food proteins enter the body. Among other allergens, cow’s milk protein is the most significant in the development of allergic reactions in young children. In many cases, in 1-year-old children with AD, goat’s milk mixtures are a good alternative to cow’s milk-based milk mixtures. At the present stage, the most important in the complex of therapeutic measures in children with blood pressure from the first year of life are diet therapy and active external therapy, including the phased use of topical steroids, calcineurin inhibitors, emollients.
