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Atopic dermatitis (AD), or atopic eczema, is a common inflammatory skin disorder characterized by pruritus, a chronic and recurrent course, and a distinctive anatomic distribution and morphology. It is often accompanied by a personal or family history of other allergic disorders. Epidemiologic data indicate that AD has been increasing in prevalence, with rates as high as 18% in the United States.1,2 Socioeconomic studies estimate that the annual financial impact of AD may be as high as $4400 per patient and $364 million to $3.8 billion per year in the United States.3,4 Although most patients are treated in the outpatient setting, one third to one half of the yearly expenditures for AD are directly related to the costs of hospitalization.

Patients may require hospitalization because of the severity of their primary skin disease or as a result of secondary complications, predominantly bacterial or viral superinfections. Some patients presenting with an eczematous dermatitis along with other comorbidities may require inpatient evaluation for potential underlying causes, such as Wiskott-Aldrich syndrome, hyper-IgE syndrome, or a variety of metabolic disorders.


AD appears to be a multifactorial disease that involves dysregulation of the immune response, with resulting alterations in skin barrier integrity and associated cutaneous hyperreactivity. Studies suggest that T cells, particularly those expressing markers for the Th2-response, are up-regulated in acute AD. The elaboration of Th2-related cytokines such as interleukin (IL)-4, IL-5, and IL-13 indirectly results in increased immunoglobulin E (IgE) production and eosinophilia. In the chronic phase of AD, there is a switch to the Th1-related cytokines IL-12 and interferon-γ. Other pathobiologic abnormalities noted in patients with AD include a genetic background of atopy, disturbed essential fatty acid metabolism, increased leukocyte phosphodiesterase activity, autonomic nervous system dysregulation, pruritus,5-7 and a predisposition to infection.8

The specific genetic basis of the disease has yet to be elucidated. Studies of twins and families clearly indicate a familial predisposition in approximately two-thirds of patients. Twin studies suggest an 85% concordance among monozygotic twins, but only a 21% concordance among dizygotic twins and nontwin siblings.9 If one parent has AD, 59% of offspring will develop AD; if both parents have AD, 81% of offspring will develop the disease. It now appears unlikely that AD is the result of a single gene; rather, it appears to be the result of multiple genes interacting to produce the disorder. Recent research does, however, suggest that filaggrin mutations may play a central role in many patients with atopic dermatitis and indicates that filaggrin and other defects in barrier function, such as kallikrein 7 and cystatin A, are important in the pathogenesis of atopic dermatitis.10

Patients with AD have an increased propensity for other atopic diseases such as asthma and allergic rhinitis. Based on clinical observations, patients sometimes progress sequentially from AD to the development of asthma and allergic rhinitis in ...

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