INTRODUCTION
Atopic dermatitis (AD) is one of the most common dermatologic disorders encountered in both pediatric and general dermatologic practices in the United States and globally, especially in well-developed countries with multiple urban areas.1-3 The complexity of AD is typified by multiple pathogenic associations, including genetic factors, environmental influences, lifestyle, dietary exposures, innate abnormalities of multiple epidermal barrier functions, hyper-responsiveness to both cutaneous allergens and irritants, impact from increased bacterial colonization with Staphylococcus aureus, and neurogenic/neuroimmunological factors.1-33 Importantly, these pathogenic factors do not operate in a vacuum, with supporting evidence from the observation that filaggrin (FLG) null mutations alone do not appear to cause AD.33 Rather, the pathogenic factors of AD interact to produce a varied spectrum of phenotypes that present every day in clinical practice to dermatologists, allergists, and primary care physicians.1-3,20 Independently and collectively, these pathogenic factors may also correlate directly to AD severity, persistence and/or frequency of recurrence, and response to therapy.5-7,13,14,21-26 Further details on these pathogenic associations are outlined in Table 1, which depict important pathophysiologic reference points that relate to the common clinical features of AD.1-45
Clinical Overview of Atopic Dermatitis
Atopic dermatitis is one of the most common dermatoses encountered in pediatric and general dermatology practice, and most commonly presents initially in infancy or early childhood.It has been estimated that 45% of patients with AD present within the first 6 months of life, 60% within the first 12 months of life, and 85% before 5 years of age.1 The association of polyvalent immunoglobulin E sensitization to inhalant and/or food allergens characterizes extrinsic AD and explains the subsequent development of asthma, seasonal rhinitis, and sometimes food hypersensitivity in many patients with AD, as extrinsic AD accounts for 60% to 90% of AD cases.1,46 The clinical presentations and associated manifestations of AD, as well as its range of severity and the course of the disease over time, are well covered in virtually all major general and pediatric dermatology textbooks for the interested reader who is less familiar with AD.
The heavy educational and research emphasis on pediatric and adolescent AD often results in adult AD being overlooked as a diagnostic consideration, especially as the eczematous presentations of AD in adults are often localized. Although AD is most predominant during childhood and adolescence and may “burn out†after the teenage years in some cases, persistence into adulthood is still common. Many cases of AD in adults present as various recurrent forms of eczema and pruritus, often with associated allergic sinusitis (and sometimes adult asthma) noted in the medical history.47-50 Some of the localized eczematous presentations commonly affecting adults with AD include lichen simplex, chronic/recurrent hand eczema, eyelid dermatitis, genital pruritus (including vulvar pruritus, vulvar hyperplastic dystrophy [lichen simplex], and scrotal pruritus often with lichen
