INTRODUCTION
Atopic dermatitis (AD) is a chronic, relapsing skin disease presenting with inflammation, pruritus, and xerosis.1,2 A family history of atopy and related comorbidities such as asthma and allergic rhinitis is often seen in AD patients, particularly associated with severity and early onset.3 Generally, AD is the most common skin disease in young children, and exacerbations are common and may present lifelong.1,2 Flares are associated with sleep deprivation, stigmatization, social withdrawal, anxiety, and depression, and may substantially impact quality of life.4
The main clinical characteristics of AD typically include erythema, edema, excoriations, and xerosis.1 However, characteristics differ depending on age and ethnicity, which trained dermatologists can identify and distinguish, but may be challenging for other healthcare providers such as general practitioners (GPs).2,5
AD is pathologically characterized by its skin barrier dysfunction, which commonly, but not exclusively, is driven by specific filaggrin gene mutations and downregulation of filaggrin and other skin barrier proteins due to inflammation.2,6 Xerosis is a prominent feature that leads to irritation, micro-fissures, and cracks, due to decreased amount of skin lipids in AD-affected skin and increased transepidermal water loss (TEWL). Additionally, the skin barrier dysfunction leaves the skin more susceptible to bacterial colonization, particularly Staphylococcus aureus, contributing to exacerbation and a higher skin infection rate.1,7
The main clinical characteristics of AD typically include erythema, edema, excoriations, and xerosis.1 However, characteristics differ depending on age and ethnicity, which trained dermatologists can identify and distinguish, but may be challenging for other healthcare providers such as general practitioners (GPs).2,5
AD is pathologically characterized by its skin barrier dysfunction, which commonly, but not exclusively, is driven by specific filaggrin gene mutations and downregulation of filaggrin and other skin barrier proteins due to inflammation.2,6 Xerosis is a prominent feature that leads to irritation, micro-fissures, and cracks, due to decreased amount of skin lipids in AD-affected skin and increased transepidermal water loss (TEWL). Additionally, the skin barrier dysfunction leaves the skin more susceptible to bacterial colonization, particularly Staphylococcus aureus, contributing to exacerbation and a higher skin infection rate.1,7
