Possible causes, ways of development and stages of formation of atopic dermatitis in children

Background. Atopic dermatitis is a common chronic inflammatory skin disease affecting 2.6 % of the global population (204.05 million people), of which 102.78 million are children. Atopic dermatitis has a complex multifactorial nature. According to current understanding, the development of the disease is influenced by genetic predisposition, skin barrier dysfunction, imbalance of surface microflora, immune mechanisms, food allergies, and sensitization to aeroallergens. There is a challenge in determining the contribution of each of these mechanisms to the development of atopic dermatitis. The purpose was to analyze and systematize current data on the etiology, pathogenesis, and stages of atopic dermatitis development in children. Materials and methods. A comprehensive analysis of current scientific sources concerning various aspects of atopic dermatitis pathogenesis was conducted, including genetic, immunological, microbiological, and environmental factors. Some interest was given to studying the possibilities of fetal food sensitization. Results. It has been found that atopic dermatitis has a multifactorial nature with a key role played by genetic predisposition, particularly mutations in the filaggrin gene, which leads to impaired skin barrier function. The pathogenesis includes immune mechanisms with predominance of T helper 2 cells in the acute phase and production of pro-inflammatory cytokines (IL-4, IL-5, IL-13). Imbalance of skin and gut microbiome, epicutaneous sensitization to food and aeroallergens, intrauterine sensitization, as well as environmental factors (birth season, vitamin D levels, air pollutants) are important modifying factors for the development of atopic dermatitis. Conclusions. Atopic dermatitis is a complex and multifaceted disease caused by a combination of various pathological mechanisms, which cumulatively may contribute to the early formation of the disease with clinical manifestation in the first years of a child’s life. A leading role in the formation of atopic dermatitis is played by a defect in the gene encoding filaggrin protein synthesis. This, in turn, leads to a defect in the skin barrier functions, through which transepidermal water loss increases, leading to the penetration of allergens, pathogenic microorganisms, and pollutants into the skin. Epicutaneous sensitization through an altered skin barrier forms food allergies, and food allergies lead to exacerbations of atopic dermatitis. The shift of the immune response from T helper 1 cells in favor of T helper 2 cells stimulates the release of pro-inflammatory cytokines and promotes the activation of atopic dermatitis exacerbation. Depleted skin and gut microbiome, negative influences on the mother’s body during pregnancy (alcohol consumption, smoking, stress, excessive consumption of potentially allergenic food products), and air pollutants all stimulate the development of atopic dermatitis in the newborn child. Therefore, the formation of atopic dermatitis is the result of a complex interaction between genetic predisposition, immune dysregulation, significant disruption of skin and gut microbiome, as well as intrauterine exposure to negative factors, sensitization to food and aeroallergens, and other less significant factors. Understanding and further study of this interaction is necessary for developing effective approaches to the prevention and treatment of atopic dermatitis.