Date Published: November 10, 2011
Publisher: BioMed Central
Author(s): Wade Watson, Sandeep Kapur.
Atopic dermatitis (AD) is a common, chronic skin disorder that can significantly impact the quality of life of affected individuals as well as their families. Although the pathogenesis of the disorder is not completely understood, it appears to result from the complex interplay between defects in skin barrier function, environmental and infectious agents, and immune abnormalities. There are no specific diagnostic tests for AD; therefore, the diagnosis is based on specific clinical criteria that take into account the patient’s history and clinical manifestations. Successful management of the disorder requires a multifaceted approach that involves education, optimal skin care practices, anti-inflammatory treatment with topical corticosteroids and/or topical calcineurin inhibitors (TCIs), the use of first-generation antihistamines to help manage sleep disturbances, and the treatment of skin infections. Systemic corticosteroids may also be used, but are generally reserved for the acute treatment of severe flare-ups. Topical corticosteroids are the first-line pharmacologic treatments for AD, and evidence suggests that these agents may also be beneficial for the prophylaxis of disease flare-ups. Although the prognosis for patients with AD is generally favourable, those patients with severe, widespread disease and concomitant atopic conditions, such as asthma and allergic rhinitis, are likely to experience poorer outcomes.
Atopic dermatitis (AD) is a chronic, highly pruritic (itchy) inflammatory skin disease, and is one of the most common skin disorders in children . The disorder results in significant morbidity and adversely affects quality of life . Not only are patients affected by the social stigma of a visible skin condition, but the intense itching characteristic of the disease often leads to significant sleep disturbances. In addition, management of the condition necessitates the frequent application of emollients (agents that soothe, moisturize and soften the skin) and topical medications, as well as physician visits. AD also poses a significant economic burden with an estimated annual cost in Canada of $1.4 billion .
The pathogenesis of AD is not completely understood, however, the disorder appears to result from the complex interaction between defects in skin barrier function, immune abnormalities, and environmental and infectious agents. Skin barrier abnormalities appear to be associated with mutations within the filaggrin gene, which encodes a structural protein essential for skin barrier formation. The skin of individuals with AD has also been shown to be deficient in ceramides (lipid molecules) as well as antimicrobial peptides such as cathelicidins, which represent the first-line of defense against many infectious agents. These skin barrier abnormalities lead to transepidermal water loss (passage of water from inside the body through the epidermal layer of the skin to the surrounding atmosphere) and increased penetration of allergens and microbes into the skin. The infectious agent most often involved in AD is Staphylococcus aureus (S. aureus), which colonizes in approximately 90% of AD patients. Defective innate immune responses also appear to contribute to increased bacterial and viral infections in patients with AD. This interplay of factors leads to T-cell responses in the skin (initially a predominantly T helper-2 [Th2] response and later a predominantly Th1 response) with resultant release of chemokines and proinflammatory cytokines (e.g., interleukin [IL]-4, 5 and tumour necrosis factor) that promote immunoglobulin E (IgE) production and systemic inflammatory responses, leading to pruritic inflammation of the skin [6-8].
The prevalence of AD has increased over the past 30 years. It is currently estimated that 10-20% of children and 1-3% of adults in developed countries are affected by the disorder . AD often starts in early infancy; approximately 45% of all cases begin within the first 6 months of life, 60% during the first year, and 85% before 5 years of age. Up to 70% of these children outgrow the disorder before adolescence .
There are no specific diagnostic tests for AD. Diagnosis of the disorder is based on specific criteria that take into account the patient’s history and clinical manifestations. Although various diagnostic criteria for AD have been proposed and validated, the application of many of these criteria is time consuming and necessitates invasive testing. Table 1 provides simplified criteria proposed by Williams et al. that are easy to use, do not require invasive testing, and have been shown to have a high sensitivity and specificity for the diagnosis of AD [11-14]. Using these criteria, the diagnosis of AD requires the presence of an itchy skin condition (or parental/caregiver reports of scratching or rubbing in a child) plus three or more minor criteria, which vary depending on the patient’s age.
The exact role of foods and aeroallergens in the pathogenesis and exacerbation of AD is controversial. Although most patients with AD demonstrate specific IgE antibodies to foods and/or aeroallergens on skin prick testing (SPT) and measurements of serum-specific IgE levels, their clinical significance remains unclear. [6,16] In other words, while a positive SPT or serum specific IgE test indicates sensitization to a particular allergen, this does not prove clinical hypersensitivity or causation.
The treatment of AD should be directed at limiting itching, repairing the skin and decreasing inflammation when necessary. Therefore, the successful management of AD requires a multifaceted approach that involves patient and caregiver education, optimal skin care practices, anti-inflammatory treatment with topical corticosteroids (first-line) and/or topical calcineurin inhibitors (TCIs), the use of first-generation antihistamines to help manage sleep disturbances, and the treatment of skin infections. Systemic corticosteroids may also be considered in severe cases that cannot be controlled with appropriate skin care and topical therapy [1,6,17,18].
The prognosis for patients with AD is generally favourable, with most children outgrowing the condition by early adolescence. However, patients with severe, widespread disease and concomitant atopic conditions, such as asthma and allergic rhinitis, are likely to experience poorer outcomes .
AD is a common, chronic skin disease that starts early in life and can adversely impact the quality of life of patients and their caregivers. Optimal skin care practices and topical corticosteroids remain the cornerstone of therapy for the disease. TCIs have been shown to provide an effective, second-line alternative to topical corticosteroids in appropriate patients prone to frequent flare-ups. Allergy testing to foods and aeroallergens may be considered based on patient history and/or in patients exhibiting a poor response to optimal skin care practices and appropriate pharmacological therapy.
• AD is the most common skin disorder in children, and significantly impacts quality of life.
Dr. Wade Watson is a co-chief editor of Allergy, Asthma & Clinical Immunology. He has received consulting fees and honoraria for continuing education from AstraZeneca, GlaxoSmithKline, King Pharma, Merck Frosst, and Nycomed.