Atopic dermatitis (AD) is a hereditary disease, the degree of clinical manifestations of which largely depends on the influence of environmental factors and the body’s resistance. The modern pathogenetic model of AD can be represented as a chain, the genetic links of which are considered to be: a set of predisposition genes, a reduced skin barrier function, a violation of innate immunity, which are joined by external factors and features of the adaptive immune response. The most significant genetically determined disorders in this disease are changes in the immune system and skin barrier, the dysfunction of which is a favorable background for the development of AD. The second group of factors that influence the development of the disease is the triggers of the external environment: various chemical substances, food and medicinal irritants, infectious agents, etc. Bacteriological research data indicate high rates of colonization density of lesions and conditionally intact skin areas of AD patients with moderately severe and severe severity [(6.5±0.2) lg CFU/cm2 and (6.3±0.1) lg CFU/cm2 and (6.9±0.2) lg CFU/cm2 and (6.8±0.2) lg CFU/cm2, respectively, against 4.1±0.1 lg CFU/cm2 on the skin of healthy persons, p ≤ 0.05]. When using narrow-spectrum UVB therapy as part of complex treatment of severe forms of AD, regression of clinical signs of pyococcal infection was noted in 72.2% of people. Clinical remission was achieved in 27.7% of patients, significant improvement in 55.5%, improvement in 16.7%.
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