Contact dermatitis in the atopic child.

The two major forms of contact dermatitis are irritant contact dermatitis and allergic contact dermatitis. Irritant contact dermatitis is seen in roughly 80% of contact dermatitis cases.1 Irritant contact dermatitis is an inflammatory, but nonimmunologic doseand time-dependent skin response to direct cellular injury caused by a skin irritant, and it does not require prior sensitization.2,3 Common irritants in the pediatric age group include excessive bathing, urine and feces in the diaper area, bubble baths, cleansers, or wipes.4 Allergic contact dermatitis (ACD) is a delayed-type, T-cell mediated hypersensitivity reaction (type IV immune response) wherein the allergens are small haptens that bind to epidermal carrier proteins to form complete antigens. Dermal dendritic cells in the skin process these antigens and present them to naive T cells in the lymph nodes, stimulating an immune response that results in T-cell activation and memory T-cell clonal expansion. Upon re-exposure to the same allergen, the sensitized T cells, primarily T helper 1 (Th1) type, hone to the skin and release inflammatory mediators, producing intercellular edema of the epidermis and the clinical manifestations of ACD.2,3 Susceptibility to ACD varies according to age, frequency, type, and duration of allergen exposure.1 The pathogenesis of allergic dermatitis (AD) is complex and multifactorial. Traditionally, AD has been categorized as an immunemediated condition driven primarily by Th2 cells,5 yet many now believe that the primary defect in AD is a disrupted skin barrier.6 AD patients often have insufficient amounts of filaggrin, which is critical for the skin to absorb atmospheric water and, thus, maintain moisturization. In addition, decreased amounts of ceramides, fatty molecules that promote water retention within the epidermis and prevent the ingress of foreign harmful substances, have also been demonstrated in the skin of atopics. The resulting compromised epidermal barrier facilitates the passage of pathogens, allergens, and irritants through the skin, leading to a cascade of events that initiates a Th2 response and the clinical manifestations of AD. Im ag e co ur te sy o f S ha ro n E. J ac ob , M D. R ep rin te d w ith p er m is si on .