###### Abstract  
Atopic dermatitis is a chronic and multifactorial inflammatory dermatosis. Recurrent eczematous lesions and intense pruritus very often reduce the quality of life of patients, affecting their mental health. For this reason, it is necessary to undertake treatment. Treatment should be characterized by an individual approach to the patient, taking into account the predominant pathogenetic factors in the development of atopic dermatitis and systematic skin care. Sothing the typical symptoms of AD, i.e., dry skin and persistent itching, involves emollients, which counteract xerosis and reduce the feeling of itching. Studies confirm that the regular use of emollients in patients with AD prolongs the period between relapses and alleviates the intensity of symptoms during periods of disease severity. This review paper aims to highlight the challenges that patients with atopic dermatitis face. This work will also present an indication of the rationale for the use of emollients in this condition, as well as an indication of the forms of their application in therapeutic and care preparations. a +
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Skin barrier defect is a key element in the course of atopic dermatitis [7]. It consists of abnormalities of the stratum corneum, disorders of tight junctions or antimicrobial peptides [7; 8]. The aforementioned elements are responsible for the clinical manifestations of patients with AD such as dry skin. This parameter in turn generates increased transepidermal water loss (TEWL), facilitates the penetration of allergens and disrupts the microbial balance of the skin surface [7; 8]. The genetic determinants of AD include a mutation of the filaggrin structural protein (FLG) [7]. The authors of [9] report that the effect of mutations in the filaggrin gene predisposing to atopic dermatitis was noted in 2006. The role of this protein is primarily based on maintaining the structure of the epidermis by synthesizing molecules that retain water. Filaggrin deficiency results in keratinocyte abnormalities and causes impairment of the epidermal barrier, which allows exogenous molecules to penetrate the epidermis [9]. Mutations in filaggrin occurring in C-terminal repeats cause a significant reduction in filaggrin in the epidermis of AD patients. This is because the C-terminal region is essential for the proper processing of profilaggrin into filaggrin [10]. Abnormalities in filaggrin synthesis reduce the amount of natural moisturizing factor and cause an increase in skin pH as a result of the decreased production of transurocapnic acid [11]. Another factor in the defect of the skin barrier is a decrease in cutaneous ceramides, which results in a decrease in TEWL and increases the possibility of allergens and microorganisms penetrating deep into the skin [6] (Figure 1). According to statistics, the incidence of AD is steadily increasing [1]. According to the Global Report on Atopic Dermatitis 2022, about 223 million people worldwide struggle with AD [12]. Atopic dermatitis affects about 25% of children [11]. During the first years of a person's life, the prevalence of the disease is comparable in both sexes; it is only after the age of six that the diagnosis of atopic dermatitis increases in females [11]. In a retrospective study that was conducted in South Korea, atopic dermatitis was diagnosed in 944,559 children and in more than one million adults (1,066,453) [2]. In contrast, according to a compilation of information in a publication [7], 3.91% of children in Poland suffer from AD. The primary goals of treating atopic dermatitis are to reduce inflammation, decrease pruritus or redness and restore the normal skin barrier [13]. Therapeutic strategies in the treatment of AD target the skin--that is, skin care and topical medications, most commonly corticosteroids (ICS) or calcineurin inhibitors. The mainstay of atopic dermatitis treatment used for more than 60 years has been topical corticosteroids [14].