Disease management of atopic dermatitis: a practice parameter

INTRODUCTION Atopic dermatitis is an important manifestation of the atopic diathesis.1,2 It not only frequently accompanies allergic respiratory disease but often precedes it as the initial clinical manifestation of allergic disease. The evaluation and management of patients with atopic dermatitis is therefore an integral part of an allergist’s practice and training. Since atopic dermatitis affects more than 10% of children, it is important for the primary care physician/provider to be familiar with the evaluation and management of this common skin condition, and know when to consult a qualified subspecialist, particularly when the diagnosis may not be established (Table 1). Although the exact role of IgE antibodies in the pathogenesis of atopic dermatitis is not clear, most individuals with atopic dermatitis have elevated serum IgE levels and there is evidence that the eosinophil plays a role in disease pathogenesis, based on elevated tissue and serum levels of eosinophil derived cationic proteins.3,4 Research into the pathogenesis of allergic disease continues to suggest a complex inflammatory process involving mast cells, lymphocytes, and infiltrating leukocytes which are orchestrated by a cytokine profile that has been identified with the T Helper Type 2 (TH2) lymphocyte.5 Recent advances in our understanding of the immunopathogenesis of atopic dermatitis are leading to the development of novel forms of therapy that may be helpful in selected patients. The response to topical corticosteroids as the mainstay of treatment for atopic dermatitis is likely to be the result of corticosteroid reduction of cellular immune activation. CLINICAL CRITERIA FOR DIAGNOSIS Intense pruritus and cutaneous reactivity associated with a lowered “itch threshold” are hallmarks of atopic dermatitis.6,7 Several skin lesions are commonly seen in atopic dermatitis. Acute lesions are characterized by intensely pruritic, erythematous papules and vesicles over erythematous skin. These are frequently associated with extensive excoriations and erosions which are accompanied by a serous exudate. Subacute lesions are characterized by erythema, excoriation, and scaling. Chronic lesions are characterized by thickened plaques of skin, accentuated skin markings (lichenification), and fibrotic papules (prurigo nodularis). In patients with chronic atopic dermatitis, all three skin reaction patterns may coexist in the same individual. Although atopic dermatitis may present at any age, it often begins between 2 and 6 months of age. The infantile form of atopic dermatitis involves the extensor surfaces of extremities, face, trunk and neck areas early, whereas the flexural aspects of the antecubital fossa and the popiliteal fossa become involved in chronic childhood and adult atopic dermatitis. Frequently, atopic dermatitis subsides in severity as the child matures, leaving an adult with skin that is prone to itching and inflammation when exposed to exogenous irritants.8 Last, chronic hand eczema may be the primary manifestation of many adults with atopic dermatitis. The American Academy of Allergy, Asthma and Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing atopic dermatitis parameters. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these Practice Parameters. Any request for information about or an interpretation of these Practice Parameters by the AAAAI or the ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. This document has been approved and endorsed by the Allergy & Immunology subsection of the American Academy of Pediatrics. ‡ Reviewers. Sami L Bahna, MD; Jean A Chapman, MD; John M James, MD; Gail G Shapiro, MD; F Estelle R Simons, MD; and Betty B Wray, MD Received for publication May 23, 1997. Accepted for publication in revised form June 24, 1997.