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Atopic dermatitis (AD) is a common inflammatory skin disease characterized by the development of highly pruritic eczematous lesions [ 1 , 2 ]. AD often begins in infancy and follows a chronic, relapsing course [ 1 , 2 , 3 ]. Diagnosis is based on patient and family history, as well as clinical characteristics of the disease, and is guided by several sets of diagnostic criteria, most of which derive from the 1980 Hanifin and Rajka criteria [ 3 ]. A 2003 update of the Hanifin and Rajka criteria by the American Academy of Dermatology (AAD) established essential, important, and associated features of AD [ 1 , 2 ]. Essential features include pruritus and eczematous lesions that can be acute (erythema and vesicular eruptions), subacute (ill-defined weepy crusted plaques), or chronic (well-defined, dry lichenified plaques). Skin lesions often show age-specific morphology and distribution patterns [ 2 ]. Important features include early onset, dryness, and increased immunoglobulin E (IgE) level (atopy), although about 20% of patients with AD do not have elevated IgE levels [ 2 ]. Associated features assist in diagnosis and can include numerous secondary signs such as hyperlinear palms and atypical vascular responses [ 2 ]. A diagnosis of AD requires the exclusion of numerous other dermatologic conditions (e.g., scabies, seborrheic dermatitis, contact dermatitis, ichthyoses, cutaneous T cell lymphoma, psoriasis, photosensitivity dermatoses, immunodeficiency disorders, erythroderma of other causes) [ 2 , 4 ]. Evidence of neuroimmune dysregulation (e.g., abnormal levels of interleukin [IL]-31, IL-4, IL-13, brain-derived natriuretic peptide) may further assist in differential diagnosis [ 5 , 6 , 7 , 8 , 9 , 10 ].
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Al-Afif et al. (2019) studied this question.
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