Atopic Dermatitis

Atopic dermatitis, commonly referred to as eczema, is a chronic, relapsing, pruritic inflammatory skin disorder. The etiology of atopic dermatitis is complex and multifactorial. Although the exact mechanism is unknown, it is believed that AD arises from an interplay of epidermal barrier dysfunction, immune dysregulation and microbiome alterations. Additionally, genetic predispositions, such as loss-of-function mutations in the filaggrin gene, may set the stage for the immune-driven inflammation. This condition often begins in infancy (60% by age 1, 90% by age 5).

In lighter skin tones, Fitzpatrick I–III and in Figure I, eczema is typically visualized as red, erythematous patches with scaling in skin fold areas and creases on the body. In darker skin, Fitzpatrick IV–VI and in Figures II, III and IV, erythema is often less evident or appears violaceous, grayish, or hyperpigmented rather than bright red. Additionally, the dryness may show as ashen. In Fitzpatrick IV-VI, hyperpigmentation is more prominent and lesions may assume a more papular form pattern. 

Delayed recognition is common in Fitzpatrick IV-VI. Erythema is masked in darker skin which contributes to a later diagnosis and higher rates of uncontrolled disease (up to 32% uncontrolled disease in Black patients). 

The treatment for atopic dermatitis is stepped based on disease severity and patient preference. Foundational measures include regular emollients, avoidance of triggers, bathing practices, and educational support. Topical anti-inflammatory therapy, such as corticosteroids, topical calcineurin inhibitors, ayrl hydrocarbon inhibitors, and PDE-4 inhibitors like crisaborole are standard for flares and maintenance. More advanced options include systemic immunomodulators, such as IL-4, IL-13 inhibitorsdupilumab and/or JAK inhibitors, for moderate-to-severe disease.

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