Clinical Pearls & Morning Reports
Published March 24, 2021
Atopic dermatitis usually develops in childhood and may persist into adulthood; less frequently, it starts in midlife or late life. Read the NEJM Review Article here.
A: Both sexes are affected, and the prevalence varies among races and ethnic groups. For example, in the United States, the prevalence is higher among Black children (19.3%) than among White children (16.1%). The increasing prevalence in high-income and industrialized countries has been tentatively attributed to environmental factors such as exposure to air pollution and household hygiene products.
A: Among the genetic factors that promote skin barrier dysfunction, mutations in the filaggrin gene (FLG) have emerged as the most prominent, affecting 30 to 50% of White patients. Filaggrin, which is produced by upper-layer epidermal keratinocytes, promotes the production of natural moisturizing factors and the lipid matrix, which acts like mortar, keeping keratinocytes in the horny layer together. A loss-of-function mutation in FLG leads to disturbed skin barrier formation and increased transepidermal water loss, resulting in dry skin. The lack of skin lipids also reduces production of epidermal antimicrobial peptides, leading to increased microbial dysbiosis. This disturbance in the skin barrier makes it possible for allergens to penetrate the skin and induces allergic sensitization.
A: Patients with atopic dermatitis are at risk for an “atopic march,” the sequential development of allergic disorders, including food allergies (especially in children), allergic rhinitis, rhinoconjunctivitis, and asthma. This apparent induction of allergies has been considered to be related to skin barrier leakage, with penetration of allergens and a predisposition of the immune system to react to the allergens with a response in CD4+ type 2 helper T (Th2) cells and subsequent B-cell antibody production. Patients of any age with atopic dermatitis are at risk for the development of bacterial, viral, or fungal skin infections due to skin barrier defects, bacterial skin colonization (especially by Staphylococcus aureus), and an altered skin microbiome. Common skin infections in patients with atopic dermatitis are S. aureus–induced infections (impetigo and abscesses), herpes simplex virus 1–related eczema herpeticum, and molluscum contagiosum infection. Fungal infections such as candidiasis of the skin or nails can also occur.
A: Therapy for atopic dermatitis is selected according to the clinical stage of disease (mild, moderate, or severe), the extent of body-surface area involved, age, coexisting conditions and medications being taken by the patient, the severity of pruritus, the degree to which quality of life is impaired, and the goals of the patient. For all disease stages, including eczema-free intervals, general measures such as the use of emollients (with or without antipruritic agents) and avoidance of infections and trigger factors are advised. When eczema occurs, the use of topical immunosuppressive therapies is recommended as a first approach. Crisaborole, a phosphodiesterase-4 inhibitor, has recently been approved for topical treatment of atopic dermatitis in the United States, but it is not available in all countries.