What is the pathophysiology of pediatric atopic dermatitis (AD)?

Updated: Jun 03, 2020
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Answer

Clinically unaffected skin in patients with atopic dermatitis has increased numbers of T-helper type 2 (Th2) cells compared with skin in patients without atopic dermatitis. Increased levels of interleukin (IL)-4 and IL-13 (Th2 cytokines) are seen in acute atopic dermatitis skin lesions, whereas chronic atopic dermatitis lesions show increased expression of IL-5 (Th2 cytokine) and IL-12 and interferon (IFN)-γ (Th1 cytokines). Chronic atopic dermatitis lesions also exhibit greater eosinophil infiltration compared with skin in patients without atopic dermatitis.

IL-4 enhances differentiation of T-helper cells along the Th2 pathway, and IL-13 acts as a chemoattractant for Th2 cells to infiltrate atopic dermatitis lesions. IL-13 may also directly induce IL-5 expression and eosinophil infiltration, thereby facilitating the transition from acute lesions into chronic lesions. [2]

In addition, patients with atopic dermatitis appear to have significantly decreased levels of skin barrier molecules compared with normal controls. Ceramide lipids in the stratum corneum, which are responsible for water retention and permeability functions, and skin barrier proteins such as filaggrin are expressed at significantly lower levels in the skin of patients with atopic dermatitis compared with the skin of patients without atopic dermatitis. [2, 3]

Significant evidence favors the hygiene hypothesis for the development of atopic dermatitis. An inverse relationship is recognized between helminth infections and atopic dermatitis but no other pathogens. [4] In addition, early day care, endotoxin, unpasteurized farm milk, and animal exposure appear to be beneficial, likely because of a general increase in exposure to nonpathogenic microbes.

Positive association was shown between maternal exposure to increased concentrations of particulate matter and atopic dermatitis. [5]


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