Dermatitis atopica

Prim Care Clin Office Pract 35 (2008) 105–117

Atopic Dermatitis
Peck Y. Ong, MDa,*, Mark Boguniewicz, MDb
Division of Clinical Immunology–Allergy, Childrens Hospital Los Angeles, University of Southern California Keck School of Medicine, 4650, Sunset Boulevard, MS# 75, Los Angeles, CA 90027, USA b Division of Pediatric Allergy-Immunology, National Jewish Medical and Research Center, TheUniversity of Colorado Health Sciences Center, 1400 Jackson Street, Denver, CO 80206, USA
a

Atopic dermatitis (AD) is a common chronic inflammatory skin disease in childhood, affecting up to 17% of children in the United States [1]. This skin disease is characterized by intense puritus and cutaneous inflammation. The quality of life of affected individuals can be significantly affected, particularly inthose with moderate to severe disease [2]. In addition, AD patients are predisposed to a variety of skin infections, including Staphylococcus aureus and herpes simplex virus. Up to 50% of children with AD go on to develop asthma [3]. AD also carries with it a significant financial burden to the family and society [4].

Pathogenesis The pathogenesis of AD is complex, involving genetic factors,skin barrier defects, and immune dysregulation (reviewed in reference [5]). The genetics of AD is an area of intense research. Genetic polymorphisms have been associated with chromosome 5q22-23, which contains a cluster of T helper type 2 (Th2) cytokine genes (IL-4 and IL-13). Those genes play a significant role in IgE production and allergic sensitization. More recently, the association of AD withfilaggrin gene mutations has pointed to the role of skin barrier defects in the pathogenesis of AD [6]. Filaggrin is a protein essential to the normal barrier function of the skin. Deficiency in this protein may contribute to the physical barrier defects in AD and predispose patients to increased transepidermal water loss, infections, and inflammation

* Corresponding author. E-mail address:pyong@chla.usc.edu (P.Y. Ong). 0095-4543/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.pop.2007.09.006 primarycare.theclinics.com

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associated with exposure of cutaneous immune cells to allergens [7]. A recent study showed that the level of filaggrin can be modulated by cytokines [8]. This may present specific therapeutic opportunities, although,at this time, maintaining a normal epidermal barrier is key.

Diagnosis There is currently no diagnostic laboratory test for AD. Although the majority of AD patients have elevated total serum IgE, up to 30% of these patients have normal total serum IgE and show no allergic sensitization to food or aeroallergens [9]. The diagnosis of AD is based on clinical criteria. Itch must be present for thediagnosis of AD. In addition, the patient should have three or more of the following criteria [10]:  Visible rashes on the flexural areas (elbows, back of knees, front of neck, or eyelids); in infants, the rash may be present on the cheeks or extensor areas of the knees or elbows  History of rashes on the flexural areas  Personal or family history of respiratory allergies (asthma or allergicrhinitis)  History of dry skin in the past year  Onset before 2 years of age Ninety percent of AD patients have onset of the disease before 5 years. Therefore, new-onset AD in older children or adults should raise suspicion for other skin conditions. Box 1 shows the differential diagnosis of AD.

Management Basic skin care Daily skin care is key in the control of AD symptoms. The following listprovides some of practical actions to take in the treatment of AD:  Rather than soaps, use cleansers with minimal defatting activity and a neutral pH.  Avoid alcohol and astringents in skin care products.  Avoid wool clothing or other materials that may be irritating to the skin; cotton or cotton blends are generally preferred.  Launder clothing to remove formaldehyde and other chemicals. ...