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Atopic dermatitis is a common inflammatory skin disorder that affects 10–20% of children younger wthan 14 years of age.1,2

The prevalence of atopic dermatitis has increased two- to threefold since the 1980s in industrialized countries, and it remains the most common dermatitis of childhood. The pathogenesis of atopic dermatitis, although not completely understood, is likely multifactorial, involving complex interactions between environmental triggers, defects in skin barrier function, and systemic and local immunologic responses.3 atopic dermatitis is often the initial presentation of atopic disease in children, and according to the theory of the “atopic march,” poorly controlled atopic dermatitis is believed to contribute to the development of asthma and allergic rhinitis in older children in 50–80% of affected patients.2,3


The diagnosis of atopic dermatitis is made on clinical evaluation. Most cases arise within the first 2 years of life.4 The key features of atopic dermatitis 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 atopic dermatitis 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.

The cutaneous manifestations of atopic dermatitis may be classified as acute or chronic. In an acute exacerbation of atopic dermatitis, ery­thematous papules and patches associated with scaling, excoriations, and serous exudates are seen (Figure 62-1). Chronic atopic dermatitis is characterized by variably hyperpigmented, lichenified plaques and nodules that result from chronic rubbing and scratching (Figure 62-2). Acute and chronic changes may coexist in the same patient. Most atopic dermatitis 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.7–9 Filaggrin is a key component of the cornified cell envelope, which forms the epidermal skin barrier. Disruption of the epidermal barrier increases transepidermal water loss and is thought to increase epicutaneous exposure to potential environmental allergens, which can contribute to the development of atopic disease.

FIGURE 62-1.

Acute presentation of atopic dermatitis with erythema and scaling.

FIGURE 62-2.

Chronic atopic dermatitis with the development of hyperpigmentation and lichenification.

The presentation of atopic dermatitis varies with the patient’s age. In infants, atopic dermatitis 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 ...

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