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Primary skin diseases that principally affect the epidermis may be categorized as either a dermatitis or a papulosquamous disorder. Dermatitis commonly denotes inflammation of the epidermis. Eczema generically denotes edema within the epidermis. Many primary dermatitides are eczematous in nature, although the term eczema is often misused interchangeably for atopic dermatitis. In its mildest or chronic form, edema is seen histopathologically as prominent, toothlike interconnections between keratinocytes (spongiosis). With more intracellular fluid accumulation, intraepidermal vesicles are formed. Vesicles are often subclinical in subacute or chronic eczemas where edema is mild but present as grossly evident vesicles and bullae in acute eczemas. Papulosquamous eruptions are characterized by the presence of erythematous papules or plaques with overlying scale. While eczematous processes clinically manifest with weeping or crusting, papulosquamous disorders are associated with little to no edema and thus clinically tend to be dry.


Atopic dermatitis is the most common chronic inflammatory childhood skin disease, characterized by intense itching, dry skin, inflammation, and exudation. The typical clinical finding is an ill-defined patch or plaque of scaling and erythema. Pruritus is a constant feature. Chronic scratching results in dramatic accentuation of the skin markings (lichenification), sometimes with postinflammatory hyperpigmentation, whereas the chronic eczematous process itself may result in hypopigmentation.


The exact prevalence of atopic dermatitis is not known but has been reported to be 15% to 20% lifetime prevalence. Symptoms begin during the first 6 months in 45% of children, first year of life in 60%, and before the age of 5 years in at least 85% of affected individuals.1


The pathogenesis of atopic dermatitis is not completely understood. It is likely multifactorial involving interplay between immune, genetic, metabolic, infectious, and environmental factors.2 Abnormalities of the epidermal barrier paired with immune dysregulation culminate in expression of this disease. A genetic basis for abnormal barrier function in some patients with atopic dermatitis has recently been linked to the FLG gene, the gene in which null mutations result in ichthyosis vulgaris, a scaly skin disorder in which 20% to 25% of people are also atopic.3 The FLG gene encodes filaggrin, a protein essential for epidermal barrier formation and hydration. The role of filaggrin (or of its absence) in the development of atopic dermatitis is not completely understood.


In infancy, involvement of the face, particularly the cheeks (Fig. 358-1), and of extensor surfaces of the extremities is typical, but involvement of the scalp and trunk is also common. In older children, atopic dermatitis favors the flexures such as the antecubital and popliteal fossae. Ankles, wrists, and dorsa of hands and feet are also commonly involved (eFig. 358.1). Occasionally, disease is widespread and severe. A papular variant may be seen, particularly in African American patients (eFig. 358.2). Several subtle physical findings may support the diagnosis, including accentuation of skin markings on palms and soles, double or triple creases under the lower eyelid (Dennie-Morgan folds), ...

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