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Pathways to managing atopic dermatitis: consensus from the experts.

Atopic dermatitis (AD) is a chronic, relapsing, inflammatory skin disease that typically starts in early childhood and can persist into adulthood in some cases. AD is characterized by highly pruritic outbreaks, xerosis, and cutaneous inflammation manifesting as acute, subacute, or chronic eczematous dermatitis.1 Although multiple treatment algorithms for AD have been suggested, they have failed to simplify decision making sufficiently to encourage their routine incorporation into patient management. The primary objectives of this expert roundtable are to document current treatment approaches in an algorithm that is both therapeutically comprehensive and practical for patients and parents (where applicable), with utility in everyday practice. 
 
The prevalence of AD has been increasing worldwide, with rates in the United States (US) ranging from 10 to 25 percent in children and approximately 3 to 5 percent in adults, depending on the population. The annual prevalence of new AD cases among children less than 17 years of age in the US is reported to be approximately 11 percent.2,3 However, accurate diagnosis may be complicated by the wide variability in clinical presentation and the lack of consensus around diagnostic criteria, especially in adults.4 Eighty-five percent of AD cases start before the age of five years.5 Some patients outgrow the disease around puberty, while others continue to suffer throughout their lives. Various reports set the prevalence of adult-onset AD at between 13 and 47 percent.6 
 
Published criteria for diagnosing AD are as varied as the clinical presentation of AD itself. AD is typically diagnosed based on clinical manifestations and patient history. Itchy skin is the cornerstone of the diagnosis, followed by several other criteria, such as age of onset, sites of predilection, family or personal history of atopy, distribution, xerotic skin changes, tendency to relapse, and appearance of lesions.3,4 Patients are often classified as having mild, moderate, or severe disease, which is then used as a guide for treatment selection. Several instruments are used to assess the clinical status of patients and establish severity, but the two most common are the SCORing Atopic Dermatitis (SCORAD) tool7 and the Eczema Area and Severity Index (EASI), which were recently found to be comparable (Table 1).8 There is a paucity of data on the distribution of AD severity, with mild, moderate, and severe AD reported to affect 84, 14, and 2 percent of cases, respectively, in the pediatric population, with much higher percentages of patients with moderate-to-severe AD in the adult population.9 
 
 
 
 
 
 
 
The etiology of AD is not well understood. Evidence suggests that AD is a multifactorial disease with complex interplay between genetic and environmental factors. Clinical phenotypes include xerotic skin changes, eczematous plaques in various stages, lichenification, marked pruritus, associated sleep disturbance, increased Staphylococcus aureus colonization, and predisposition to skin infection, with laboratory assessments showing increased immunoglobulin E (IgE) and eosinophil counts in most cases.10 
 
It is abundantly clear that there is a genetic predisposition to AD. A child has a twofold increased risk of developing AD if one parent has the disease and a threefold increased risk if both parents are affected.10 Evidence overwhelmingly suggests a pathological link between AD, allergic rhinitis, and asthma, with AD being the skin manifestation of a systemic disorder. Data have suggested that AD is often the first step in the emergence of an allergic triad that is often referred to as the “atopic march.” This refers to a progression of atopic disease that is believed to start with atopic dermatitis and subsequently progresses to asthma and allergic rhinitis.5