A skin disease of major importance, atopic dermatitis (AD) is characterized by pruritus and a typical morphology and distribution of skin lesions. It is a chronic relapsing inflammatory process often occurring in patients with a personal or family history of other atopic conditions such as bronchial asthma and allergic rhinoconjunctivitis.

AD is one of the most common skin disorders in the developed world. The prevalence of AD is increasing not only in the United States but worldwide. AD affects up to 20% of children and from 1% to 3% of adults.1 Although one common misconception is that AD is linked to unhygienic conditions, the prevalence of AD is higher in urban and high-income areas than in rural and low-income locations.

The pathophysiology of atopic dermatitis is a multifactorial and heterogeneous process involving allergic and nonallergic factors. Understanding this complex process is important in the management of individuals with AD. Skin barrier dysfunction, alterations in cell-mediated immune responses, immunoglobulin E (IgE)-mediated hypersensitivity, and environmental factors are common contributors to the development of AD.2 AD has been shown to have a strong genetic influence (80% concordance in monozygous twins and 20% in heterozygous twins),3 which can influence the severity of symptoms.

Epidermal barrier dysfunction caused by abnormal lipid metabolism and/or epidermal structural protein formation, such as filaggrin mutation or protease inhibitor deficiency, contributes to dry skin and epidermal skin dysfunction. In this state of weakened barrier there is a shift of Th1 to Th2 cells in the initiation phase of AD, with consequent increased IgE production. In addition, normal skin is colonized with Staphylococcus epidermidis; however, recent studies have shown that abnormal microbial colonization with organisms such as S aureus or Malassezia furfur leads to increased susceptibility to skin infection.4

Recent research has enabled better understanding of the role of various cytokines in the AD disease process.5 Cytokines such as IL-31 are responsible for the itch process along with neuropeptides, proteases, and kinins. It has been found that IL-31 receptors, such as receptor A and oncostatin M receptor β protein, are overexpressed in AD lesions and hence responsible for the itching associated with AD.6 Along with cytokines and immunologic disruption, psychosomatic influences also lead to the increased formation of inflammatory cells, worsening the symptoms of AD.