Atopic dermatitis (AD), also known as atopic eczema, is a chronic relapsing inflammatory dermatosis characterized by pruritus, xerosis, and a close association with IgE-mediated sensitization to aeroallergens and foods. More than 60% of children with AD are at risk to develop allergic
rhinitis or asthma (the atopic march). The distribution of lesions varies by age. Infants tend to have lesions on the cheeks and scalp, and very young children typically have involvement over the extremities cheeks, forehead, and neck. Rash in the diaper area of infants is rarely AD. Lesions
in older children and adults are usually located in flexural areas, such as the antecubital and popliteal fossae, along with the head and neck. Acute lesions of AD begin as erythematous papules and serous exudates. Secondary lesions include excoriations and crusted erosions due to scratching.
Subacute lesions appear as erythematous scaling papules and plaques. If the itch and rash progress uncontrolled, chronic lichenified AD develops featuring accentuated skin markings with hyperpigmentation. Trigger avoidance, skin hydration, and topical steroids are the first steps for improvement.
In acute lesions of AD, the Th2 cells produce IL-4, IL-13, and IL-31, which may potentiate barrier dysfunction and contribute to pruritus. In chronic lesions, the Th1 cells predominate and secrete interferon gamma and IL-12. Barrier dysfunction from filaggrin predisposes patients to AD. Skin
superinfection, particularly with Staphylococcus aureus, is common, and cultures of affected lesions help guide therapy. Eczema herpeticum from herpes simplex virus can be life-threatening in AD patients.
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