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A 1-year-old Asian American girl is brought to her family physician for a new rash on her face and legs (Figures 130-1 and 130-2). The child is scratching both areas but is otherwise healthy. There is a family history of asthma, allergic rhinitis, and atopic dermatitis (AD) on the father’s side. The child responded well to low-dose topical corticosteroids and emollients.
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AD is a chronic and relapsing inflammatory skin disorder characterized by itching and inflamed skin that is triggered by the interplay of genetic, immunologic, and environmental factors.
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AD is the most frequent inflammatory skin disorder in the US and the most common skin condition in children.1
Worldwide prevalence in children is 15 to 20 percent and is increasing in industrialized nations.2
Sixty percent of cases begin during the first year of life and 90 percent by 5 years of age.1 1/3 will persist into adulthood.2
Sixty percent of adults with AD have children with AD (Figure 130-3).1
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Etiology and Pathophysiology
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Strong familial tendency, especially if atopy is inherited from the maternal side.
Associated with elevated T-helper (Th) 2 cytokine response, elevated serum immunoglobulin (Ig) E, hyperstimulatory Langerhans cells, defective cell-mediated immunity, and loss of function mutation in filaggrin, an epidermal barrier protein.
Exotoxins of Staphylococcus aureus act as superantigens and stimulate activation of T-cells and macrophages, worsening AD without actually showing signs of superinfection.
Patients may have a primary T-cell defect. This may be why they can get more severe skin infections caused by herpes simplex virus (eczema herpeticum as seen in Figure 130-4) or bacteria (widespread impetigo). They are also at risk of a bad reaction to the smallpox vaccine with dissemination of the attenuated virus beyond the vaccination site. Eczema vaccinatum is a potentially deadly complication of smallpox vaccination (Figure 130-5).
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