Atopic Dermatitis
Atopic dermatitis (AD) and eczema are often used interchangeably. AD is a common, pruritic, chronic inflammatory dermatosis characterized clinically by relapsing episodes of flares of intensely pruritic, inflammatory skin lesions. AD is predominantly medi
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Tanja Bohl
20.1 Introduction and Terminology Atopic dermatitis and eczema are often used interchangeably. Other terms used include endogenous eczema and flexural eczema. Atopic dermatitis (AD) is the term that will be used in this article. AD is favoured because it indicates the inflammation of the skin and the presence of atopy in the affected individual. AD is a common, pruritic, chronic inflammatory dermatosis characterized clinically by relapsing episodes of flares of intensely pruritic, inflammatory skin lesions. Overall incidence in the USA is 17% and varies with 10–20% of children and 2–5% of adults affected in western countries particularly those of European and Asian ethnicity. The onset is primarily in childhood, and although AD may improve after childhood, dry, easily irritated, sensitive skin persists. Vulvar AD may occur alone or in the presence of AD elsewhere and is associated with significant impairment of quality of life in either.
20.1.1 Atopic March Atopic march refers to the progression of AD from a cutaneous disorder alone, to a systemic one. It begins with AD and a dysfunctional epidermal barrier function. This affects allergen presentation to the cutaneous and systemic immune systems, resulting in systemic effects that include increased IgE-mediated, Type 1 hypersensitivity, allergic reactions. The increased incidence of food allergy in individuals with AD is an example of this.
20.1.2 Atopic Diathesis Individuals with AD have an increased incidence of extrinsic asthma, allergic rhinitis and allergic conjunctivitis. This is referred to as an atopic diathesis or atopic phenotype. The presence of an atopic diathesis is an important diagnostic criterion for AD. Common associations seen in this population include ichthyosis vulgaris, keratosis pilaris, Staphylococcus colonization, and infection and eczema herpeticum.
T. Bohl (*) Jean Hailes for Women’s Health, Clayton, VIC, Australia © Springer International Publishing AG, part of Springer Nature 2019 J. Bornstein (ed.), Vulvar Disease, https://doi.org/10.1007/978-3-319-61621-6_20
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20.2 Pathogenesis The aetiology and pathogenesis of AD is multifactorial and incompletely understood [1–18]. It involves a complex interaction of genetic and environmental factors. The mechanisms involved in this interaction are subsequently the focus of research into AD pathogenesis. AD is predominantly mediated by T-helper cells with T-helper 2 (Th2) primarily in acute AD and T-helper 1 (Th-1) in chronic AD. A dysfunctional epidermal barrier function is integral to the development of AD and is present in most if not all atopic individuals. Genetic, inflammatory, immunologic and environmental factors affect epidermal barrier function in AD.
20.2.1 Genetics A genetic component to the aetiology of AD is supported by the familial clustering of the atopic phenotype. Twin studies also support a genetic component. Identical and fraternal twins have a seven- and threefold increase of AD, respectively. There is no single genetic trait that ex
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