Topical Treatment for the Management of Atopic Dermatitis
February 2019 | Volume 18 | Issue 2 | Supplement | s112 | Copyright © 2019
Peter W. Hashim MD MHS,a Tinley Chen BA,a Adelaide A. Hebert MD,b Leon H. Kircik MDa-c
aThe Icahn School of Medicine at Mount Sinai, Department of Dermatology, New York, New York BIndiana University School of Medicine, Indianapolis, IN cUTHealth McGovern Medical School-Houston, Houston, TX DPhysicians Skin Care PLLC, Louisville, KY
Atopic dermatitis affects up to 20% of children and continues to increase in prevalence. Effective disease control is aimed at decreasing symptoms and reducing the frequency of flares, which may be complicated by secondary bacterial infections. Although recent advances have produced a number of non-systemic treatment options, topical corticosteroids remain a fundamental component of treatment algorithms. J Drugs Dermatol. 2019;18(2 Suppl):s112-116.
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Atopic Dermatitis (AD) is a chronic, relapsing, pruritic inflammatory skin disease with an estimated prevalence of 15-20% in children.1 The onset of AD occurs within the first year of life for approximately 60% of children, most commonly at 6 months of age.2 While the presentation of AD can vary widely in morphology and distribution depending on age and chronicity, pediatric AD is typically characterized by facial, neck, and extensor involvement. Lesions may manifest as papular, vesicular, erythematous, or lichenified pruritic patches on a background of dry skin.3The pathogenesis of AD involves a complex interplay of genetic, immunologic, and environmental factors that combine to produce a defective skin barrier and dysregulated immune system. A family history of atopic disease is strongly associated with the development of AD, with the odds of development being two-fold higher in children with one atopic parent, and three-to-five-fold higher in children with two atopic parents.4 Among many heritable immune defects, mutations in the filaggrin gene have been prominently implicated. The gene encodes profilaggrin, which then degrades to filaggrin, a critical epidermal barrier protein.5 Functional impairments in filaggrin lead to decreased epidermal hydration and disruption of barrier function. A null mutation in the filaggrin gene confers a three-fold increased risk for earlier-onset AD and is associated with more severe forms.5,6 Genetic alterations producing a defective epidermal barrier contribute to epidermal water loss, a predisposition to infection by pathogenic microbes, and the penetration of environmental allergens.Topical CorticosteroidsThe topical management of AD is focused on symptomatic relief, increasing the duration of intervals between flares, and the management of acute flares. The regular application of emollients, preferably soon after bathing in order to improve hydration, is an integral component of topical regimens. Consistent use can ease the symptoms of AD, prevent flares, reduce the severity of disease, and possibly avoid the need for more aggressive pharmacological intervention. There is limited evidence regarding the benefit of adding oils, emollients, or other additives to bath water. Soaps that can damage and further irritate the skin should be avoided.7Topical corticosteroids remain the first-line treatment for AD and continue to be used in conjunction with systemic therapies for severe cases. Topical agents provide a multi-pronged effect due to their anti-inflammatory, immunosuppressive, anti-proliferative, and vasoconstrictive properties. These qualities of corticosteroids are thought to arise through genomic mechanisms.8 Lipophilic glucocorticoid molecules passively diffuse through cell membranes and bind to cytoplasmic glucocorticoid-specific receptors in keratinocytes and fibroblasts within the epidermis and dermis. A conformational change in the receptor-corticosteroid dimer complex allows entry into the nucleus to bind to specific glucocorticoid-response elements. This process induces the synthesis of anti-inflammatory proteins and regulatory proteins, thereby modulating the inflammatory response. Corticosteroids are also able to indirectly and directly regulate pro-inflammatory gene transcription factors, such as nuclear factor k B (NFkB), activator protein-1, and interferon regulatory factor-3.9 The upregulation of phospholipase A2 inhibitory protein lipocortin-1 prevents the release of arachidonic acid, a precursor of inflammatory mediators such as prostaglandins and leukotrienes.When selecting an appropriate potency and formulation of topical corticosteroid, it is important to consider the treatment area and length of treatment, while balancing the efficacy and