Nomenclature and clinical phenotypes of atopic dermatitis

Abstract

Atopic dermatitis is a heterogeneous disease and resists classification. In this review, we discuss atopic dermatitis nomenclature and identify morphologic phenotypes, which will facilitate correct diagnoses and development of treatment strategies. We support using the term ‘atopic dermatitis’ rather than eczema, because it describes the allergic background and inflammation (‘itis’) as drivers of the disease. Atopic dermatitis has many morphologic manifestations that vary by topographic area affected, age, or race and require consideration in differential diagnosis. Different phenotypes based on morphology and topographic location, ethnicity, and age are discussed. A better-defined phenotype identification for atopic dermatitis will facilitate earlier and correct diagnosis of this complex condition and inform selection of the most appropriate treatment choice in an era in which targeted therapies may generate more individualized patient care.

Immunophenotypes in Atopic Dermatitis

“…All the patients have epithelial barrier defects due to genetic and environmental factors [2,4,5]. Epidermal abnormalities in AD affect the barrier's permeability, allowing allergen penetration into the skin and enhancing Staphylococcus aureus skin colonization [2,4,5].…”

“…All the patients have epithelial barrier defects due to genetic and environmental factors [2,4,5]. Epidermal abnormalities in AD affect the barrier's permeability, allowing allergen penetration into the skin and enhancing Staphylococcus aureus skin colonization [2,4,5]. In response to barrier disruption, keratinocytes express various cytokines and chemokines, which act on immune cells to drive inflammation [2,[4][5][6][7].…”

“…Epidermal abnormalities in AD affect the barrier's permeability, allowing allergen penetration into the skin and enhancing Staphylococcus aureus skin colonization [2,4,5]. In response to barrier disruption, keratinocytes express various cytokines and chemokines, which act on immune cells to drive inflammation [2,[4][5][6][7]. Type 2 mediators, such as Thymic Stromal Lymphopoietin (TSLP), Interleukin (IL) 33, and IL-25 are produced by activated keratinocytes [4][5][6][7].…”

“…Atopic Dermatitis (AD), the most prevalent chronic inflammatory skin condition globally, is characterized by itch and dry skin with eczema flares, affecting both children and adults [1,2]. The disease is associated with an extensive burden on the patients and also a significant impact on the lives of caregivers and family members [3].…”

“…Etiopathogenesis of AD is complex and multifactorial, including genetic, immunological, and environmental factors that cause skin barrier abnormalities and immune dysfunction [4,5]. Moreover, clinical features of the eczema lesions "acute" (oozing, edema and erythema) or "chronic" (dyspigmentation, xerosis, and lichenification), its topography, and the immunological phenotypes are heterogeneous [2].…”