Atopic Dermatitis

Published on 06/06/2015 by admin

Filed under Pediatrics

Last modified 06/06/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2857 times

19 Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease affecting 10% to 20% of children and accounting for approximately 1 million outpatient visits per year. More than half of patients affected present before 12 months of age with an itchy rash on the face and extremities. AD is often associated with asthma, allergic rhinitis, and food allergy. The natural history of atopic disease, progressing from AD to asthma and allergic rhinitis, is often referred to as the atopic march.

Etiology and Pathogenesis

The chronic skin lesions of AD result from a complex interplay of genetic, immune, infectious, and environmental factors. In combination, these factors produce areas of persistently pruritic, inflamed skin that significantly impact the quality of life of patients. Immunologically, the systems affected most are the epidermal barrier, the first line of defense for the immune system, and the humoral immune system, which modulates the immune response to antigenic challenges by regulating antibody production.

The epidermis provides a critical barrier to keep infectious organisms, irritants, and allergens from entering the body. Genes encoding epithelial structural proteins have been strongly implicated in the pathogenesis of AD. Filaggrin is a key protein involved in keratinization that is encoded by a gene within the epidermal differentiation complex on chromosome 1q21. Defects in the gene encoding Filaggrin have been named as major causes of AD. Spink 5 is a protease inhibitor involved in intercellular attachment, which is also important in maintaining an intact epidermal barrier. It is deficient in Netherton’s syndrome, a disorder that includes severe AD.

In addition to the genes encoding epidermal barrier components, genes encoding cytokines produced by type 1 and type 2 helper T cells have also been implicated in AD. These cytokines, including interleukins (ILs) 4, 5, 12, and 13 and granulocyte-macrophage colony-stimulating factor, are important in the regulation of immunoglobulin E (IgE) synthesis. IL-18, also implicated in AD, is involved in the switching between type 1 and type 2 helper T cell responses. Children with AD have an imbalance toward a type 2 helper T cell response, resulting in a switch in B cell antibody production toward an IgE response, contributing to the development of atopic disease.

A number of other factors are important in the pathogenesis of AD. Reduced levels of ceramide, lipid molecules that make up an important component of the epidermal barrier, contribute to the compromised epidermal barrier function. The barrier is further compromised by increased proteolytic enzyme activity via increased production and a decrease in endogenous protease inhibitors. External factors, including mechanical injury from scratching affected skin, proteases from bacteria and dust mites, and the use of pH-altering soaps also contribute to a weakened skin barrier, facilitating bacterial colonization and penetration of allergens. The combination of defects in the immune system, compromised skin barrier integrity, and external pathogens and irritants sets up the cycle of chronic inflammation characteristic of AD.

Clinical Presentation

Most children with AD initially present at a very young age, with more than half presenting in the first year of life and more than two-thirds presenting before age 5 years.


The defects in the epithelial barrier leave the skin susceptible to invasion by viruses and bacteria. Two common secondary infections include superinfection with Staphylococcus aureus and eczema herpeticum.

Evaluation and Management

Laboratory Testing

Buy Membership for Pediatrics Category to continue reading. Learn more here