Atopic dermatitis is a chronic, non-infectious inflammatory dermatosis. Acharacteristic feature is persistent itching of the skin. The chronic, relapsing course of the disease, economic burden, and the whole family’s involvement in the treatment process immensely reduce the quality of life of patients and their families. The disease emerges as a social problem by increasing indirect costs, such as visiting a doctor, absenteeism from work and school, and avoiding social interactions. Thepathophysiology of atopic dermatitis is complex and multifactorial. It includes genetic disorders, a defect in the epidermal barrier, an altered immune response, anddisruption of the skin’s microbial balance. The numerous complex changes at thegenetic level and innate and adaptive immunity provide the basis for characterizing the various phenotypes and endotypes of atopic dermatitis. Emerging therapies rely on the action of specific molecules involved in the disease’s pathogenesis. It may be the starting point for the individualization of atopic dermatitis treatment. This paper will try to present some molecular mechanisms of atopic dermatitis and their clinical implications.

Dupilumab is a monoclonal antibody against the α subunit of the receptor for interleukin 4 and interleukin 13. It is the first biological drug registered in the world for the treatment of atopic dermatitis. Dupilumab turned out to be a milestone in the treatment of atopic dermatitis and an alternative to standard immunosuppressive drugs. In numerous multicenter studies, including real-life studies, it has been proven that dupilumab brings a significant improvement in subjective and objective clinical symptoms in atopic dermatitis. Conjunctivitis is one of the side effects of dupilumab treatment. It is estimated that it affects about 14% of patients with atopic dermatitis. The mechanisms leading to it are not yet fully understood.

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