DESCRIPTION

Atopic dermatitis (AD) is a chronic inflammatory state of the skin characterized by pruritus, erythema, induration, and scale of the skin. It is the result of chronic inflammation resulting from abnormalities of skin barrier structures, an immunologic response to environmental allergens, defects in innate immunity, and an altered microbiome.

EPIDEMIOLOGY

• 45% of those with AD have symptoms in the first 6 months of life; 60% during the 1st year and 85% before the age of 5 years
• There is higher prevalence in urban versus rural populations.
• Prevalence of AD is 20% in the United States. Internationally, estimates range widely between 0.3% and 20.5%.

ETIOLOGY

• The exact cause of AD is still under debate, but it is the result of dysfunction of the innate skin barrier, genetic predisposition, environmental exposures, and immune dysregulation. Increased viral (warts and molluscum) and dermatophyte infections seen in atopic patients appear to be related to cytokine-induced suppression of endogenous antimicrobial peptides.
• Patients often have elevated IgE levels and decreased chemotaxis of neutrophils.

RISK FACTORS

GENERAL PREVENTION

• One key factor in preventing AD flares is through using emollients to retain moisture of the skin.
• Another useful tactic is the avoidance of exacerbating factors. These include heat, low humidity, sweat, excess saliva, nonbreathable clothing fabrics, infections, bathing without moisturizing immediately afterward, harsh solvents, and detergents.

PATHOPHYSIOLOGY

• AD is due to a combination of impairment of skin barrier and an abnormal immune response.
• Defects in skin barrier integrity result in increased water loss in both skin marked with lesions as well as unaffected skin. Irritants and allergens impair the skin’s barrier functions leading to cytokine production, inflammation, and development of eczematous lesions. Defects in the skin barrier lead to allergen penetration leading to sensitization.
• Abnormalities of the immunologic reaction such as a strong type 2 T-helper cell (TH₂) response to environmental allergens and defects in innate immunity lead to an increased inflammatory state.
• On histology, typical findings of AD include spongiosis (edema of the epidermis), acanthosis, hyperkeratosis, and lymphohistiocytic infiltrate of the dermis. Spongiosis leads to stretching and rupture of intercellular attachments with vesicle formation.
• AD is a disorder of immune dysregulation with increased T-cell activation and increased cytokine production of interleukin (IL)-4, IL-5, and IL-13, which lead to increased IgE production.