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. A 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, then chronic lichenified AD develops, which features accentuated skin markings with hyperpigmentation. Trigger avoidance, skin hydration, and topical steroids are the first steps
for improvement. In acute lesions of AD, the T-helper type 2 cells produce interleukin (IL) 4, IL-13, and IL-31, which may potentiate barrier dysfunction and contribute to pruritus. In chronic lesions, the T-helper type 1 cells predominate and secrete interferon γ 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 patients with AD.
Possible pathogenic role of T helper type 9 cells and interleukin (IL)-9 in atopic dermatitis