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Epidemiology and Pathogenesis

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Atopic dermatitis (AD) is a common inflammatory skin disorder that affects 10–20% of children younger than 14 years of age.1,2 The prevalence of AD has increased two- to threefold in the past three decades in industrialized countries and it remains the most common dermatitis of childhood. The pathogenesis of AD is not completely understood and is likely multifactorial, involving complex interactions between environmental triggers, defects in skin barrier function, and systemic and local immunologic responses.3 AD is often the initial presentation of atopic disease in children, and according to the theory of the “atopic march,” poorly controlled AD is believed to contribute to the development of asthma and allergic rhinitis in older children in 50–80% of affected patients.2,3

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Clinical Presentation and Diagnosis

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The diagnosis of AD is made on clinical evaluation. The majority of cases arise within the first 2 years of life.4 The key features of AD as defined by Hanifin and Rajka in 1980 and modified in 2001 include a chronic and relapsing course, typical morphology and distribution of cutaneous findings, and pruritus.5,6 Pruritus is a universal finding in AD and can be severe, leading to sleep disturbances and irritability. Pruritus also leads to scratching, which causes secondary skin changes such as lichenification (thickening and hyperpigmentation of skin with accentuation of skin lines), excoriations, skin breakdown, and infection.

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The cutaneous manifestations of AD may be classified as acute or chronic. In an acute exacerbation of AD, erythematous papules and patches associated with scaling, excoriations, and serous exudates are seen (Figure 58–1). Chronic AD is characterized by hyperpigmented, lichenified plaques and nodules that result from chronic rubbing and scratching (Figure 58–2). Acute and chronic changes may coexist in the same patient. Most AD patients also have dry lackluster skin (xerosis), and a significant number also have ichthyosis vulgaris, a genetic skin disorder that results from mutations in the gene for filaggrin.79 Filaggrin is a key component of the cornified cell envelope, which forms the epidermal skin barrier. Disruption of the epidermal barrier is thought to increase epicutaneous exposure to potential environmental allergens, which can contribute to the development of atopic disease.

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Figure 58–1.
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Acute presentation of AD with erythema and scaling.

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Figure 58–2.
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Chronic AD with the development of hyperpigmentation and lichenification.

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The presentation of AD varies with the patient's age. In infants, AD typically presents acutely with erythematous scaling or crusted patches that involve the face, especially the cheeks, the scalp, and the extensor surfaces of the extremities; the diaper area, periocular areas, and perinasal areas are usually spared (Figure 58–3). In childhood ...

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