Atopic Dermatitis



Atopic Dermatitis


Lauren Fried

Gabriela A. Cobos

David Cohen



BACKGROUND

Atopic dermatitis (AD) is a chronic and relapsing condition associated with pruritus and inflammation. The pathophysiology of AD is complex and involves both overactivity of the immune system and epidermal barrier dysfunction.

AD is the most common chronic inflammatory skin disease. It affects 15% to 30% of children and 1% to 3% of adults in the United States, and the prevalence is increasing.1,2 AD most often presents within the first 5 years of life, with 10% to 30% of cases persisting into adulthood. However, it may have a later onset, with about 20% of cases first presenting in adulthood.3


PRESENTATION

Patients may present with an acute or chronic report of pruritic, red papules or plaques. In young children, the affected areas typically include the face, hands, and extensors. In older children and adults, flexural regions, such as the antecubital fossae, are often involved.




PATHOGENESIS

Immune overactivity in AD lesions is evidenced by increased prevalence of TH2 cells, which produce inflammatory cytokines, including interleukin (IL)-4, IL-13, and IL-31.10 These and other cytokines increase IgE production, activate additional TH2 cells, cause pruritus, and impair proper epidermal keratinocyte differentiation, thus promoting inflammation and contributing to barrier dysfunction.11

Epithelial barrier dysfunction allows for increased penetration of allergens and antigens, which leads to increased TH2 activation and amplifies the inflammatory cascade. The barrier dysfunction also leads to increased transepidermal water loss, causing xerosis and increased susceptibility to viral and bacterial infections, including Staphylococcus aureus, herpes simplex virus, and molluscum contagiosum.12

There is still ongoing debate on whether the inappropriate immune activation with production of inflammatory cytokines, IgE, and pruritus-derived scratching engenders damage in the epidermal barrier or whether inherent barrier dysfunction allowing for increased
penetration by allergens triggers the inappropriate inflammation.13

There is also a significant genetic component in the pathogenesis, as evidenced by a higher concordance rate for AD among monozygotic twins (80%) compared with dizygotic twins (20%).14 Additionally, mutations in the filaggrin gene (FLG), which lead to loss-of-function variants, have been found in high proportions in both European and Asian populations with AD. The FLG encodes a protein that is vital for epidermal barrier function. These mutations are associated not only with an increased risk of developing AD (odds ration >4, compared with noncarriers) but also with an earlier onset of disease and more severe, persistent phenotype.15

Jun 29, 2020 | Posted by in Dermatology | Comments Off on Atopic Dermatitis
Premium Wordpress Themes by UFO Themes