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Atopic dermatitis (AD) is an inflammatory skin disorder that can be acute, subacute, or chronic relapsing in presentation. The condition is one of the most common skin ailments in children and often begins in infancy. Characterized by dry skin that is intensely pruritic, the itch-scratch cycle of incessant rubbing and scratching leads to increased skin thickness termed lichenification.1  In many patients, the disease is associated with significant morbidity and decreased quality of life. Scratching predisposes the skin to secondary infections, and itching results in significant sleep disturbance.

Structural abnormalities of the skin and dysregulation of the immune system play crucial roles in the pathophysiology of AD. For optimal outcomes, a multifaceted approach should be used for management of patients with the condition. Treatment is aimed at repairing the diseased skin, protecting and rebuilding the skin barrier, and addressing immune dysfunction.2


The prevalence of AD has been increasing over the past 30 years, affecting 10% to 20% of children and 1% to 3% of adults in developed countries.3 The condition frequently presents in infancy, with 45% of cases beginning within the first 6 months of life, 60% in the first year of life, and 85% before 5 years of age.4 The incidence of AD is slightly higher in males than females.5 Approximately 70% of children with AD will have clinical remission of the disease before they reach adolescence.5,6 In children who develop AD before 2 years of age, approximately 50% will also develop asthma.2 Individuals with concomitant asthma and allergic rhinitis are much more likely to have a severe form of AD.7 Although infrequent, initial presentation of AD can occur in adulthood.

Atopic dermatitis exhibiting excoriations and lichenification.


The pathogenesis of AD is not entirely understood. Complex interactions between immune dysregulation, skin barrier defects, and environmental and infectious factors have been implicated. Skin barrier abnormalities have been linked to a mutation or impaired expression of the filament aggregating protein (filaggrin) gene, which encodes for proteins essential for skin barrier maintenance.8 Patients with AD often have skin that is deficient in lipid molecules known as ceramides and antimicrobial peptides such as cathelicidins, which serve as the first line of defense against infectious agents. Skin barrier dysfunction also leads to transepidermal water loss, surface pH changes, and enhanced penetration of allergens and microbes into the skin. Colonization of Staphylococcus aureus, the most common infectious agent, has been identified in approximately 90% of AD cases, and up to 12% have methicillin-resistant S aureus.9

Also contributing to increased bacterial infections is a defective immune response that induces chemokines, proinflammatory cytokines, and elevated serum immunoglobulin E (IgE) levels.1 Skin inflammation in patients with AD is often associated with biphasic activation of helper T cell type 2 (TH2). In acute AD, T-cell infiltration orchestrates expression predominance of the cytokines interleukin-4 (IL-4) and interleukin-13 (IL-13). In chronic inflammation, an increase in interleukin-5 (IL-5), granulocyte-macrophage colony-stimulating factor, and interferon (IFN)-γ is seen.9

The role of allergens in the exacerbation and pathogenesis of AD is still being debated. Patients with AD often demonstrate specific IgE antibodies to foods and aeroallergens with elevated serum IgE levels and a positive skin prick test, although the clinical significance is unclear. Exposure to animal dander, pollen, house dust mites, and mold may exacerbate AD. Implementation of avoidance measures for patients who notice a worsening of their AD with allergen exposure is prudent.2

Severe AD in infancy may predispose patients to developing allergies to egg and peanuts. In a subset of infants and children with AD, flares may be triggered by exposure to eggs, milk, peanuts, soybeans, fish and wheat.2

Disruption in the skin barrier function leading to increased transepidermal water loss and reduced ceramide levels will exacerbate AD. Skin barrier disruptions may be induced by frequent hand washing or bathing. Exotoxins of S aureus can activate T cells and macrophages by acting as superantigens.4 A temperate climate usually helps to improve AD, while flares are commonly seen in the winter months. Clothing, particularly wool or fur, exacerbates AD. Emotional stress, whether from the disease itself or other elements, is an important exacerbating factor associated with flares of AD.