Atopic dermatitis (AD) is a common chronic inflammatory skin condition, primarily affecting children in urban and high-income areas. Its prevalence has increased significantly over the past 30 years, with up to 20% of children affected, often within their first year of life. AD is characterized by erythematous, scaly, pruritic lesions, xerosis, and frequent atopy, with distinct clinical features in children compared to adults.
The pathophysiology of AD involves skin barrier dysfunction, immune response alterations, and environmental triggers. Genetic factors, particularly mutations in the filaggrin gene, play a significant role in severe AD, leading to increased water loss and skin dehydration. Immunologically, a Th2-predominant response drives inflammation, and environmental exposures, such as air pollutants and irritants, exacerbate the condition.
Recent studies suggest that dietary habits, particularly a high intake of ultra-processed foods (UPFs), may contribute to AD by activating inflammatory pathways. UPFs, rich in advanced glycation end products (AGEs), induce oxidative stress and inflammation, potentially worsening skin damage. This study aims to explore the potential role of UPF-derived compounds, especially AGEs, in the pathogenesis of pediatric AD.