Atopic Dermatitis Knowledge Centre
Understanding
Causes
There are two recognised types of atopic dermatitis: extrinsic, which accounts for 70–80% of all cases and is mediated by elevated levels of the allergy-related antibody, IgE and intrinsic; which is non-IgE-dependent and affects 20–30% of all patients.
The precise cause of the disease is poorly understood but the most common form, extrinsic atopic dermatitis, is strongly associated with a hypersensitivity reaction to environmental allergens which can include foods, air-borne particles (e.g. cigarette smoke), soaps and perfumes, and fabrics. The presence of an allergen stimulates the activation of a cascade of molecules that mediate the inflammatory response. Specifically, the activation of T-cells in the affected area induces release of cytokines, which draw in B-cells that in turn respond by overproducing IgE.
IgE binds to mast cells that, in the presence of an allergen, release histamine, which contributes to the development of pruritus. Recently, several new mediators have been associated with pruritus in atopic dermatitis, including serine proteases, interleukin 31 and nerve growth factor.
Scratching further stimulates immune reactions within the skin and a cyclical pattern is established as demonstrated in the diagram below.24, 25
Cyclical pattern of inflammation in atopic dermatitis
Adapted from Figure 1 of “Self-sustaining atopic dermatitis feedback loop” published in Actas Dermosifiliogr 2008;99:690-700, with permission of Elsevier Doyma, S.L
Patients with intrinsic atopic dermatitis develop identical symptoms to their extrinsic counterparts but do not exhibit the initial hypersensitive response. The underlying processes by which intrinsic atopic dermatitis develops remain elusive and have been the subject of intense research. Differences in the patterns of cytokine expression observed between extrinsic and intrinsic atopic dermatitis, and the influence of specific genetic variations have been implicated as critical factors associated with intrinsic atopic dermatitis.
References:
24. Conde-Taboada A, Gonzalez-Barcala FJ, Toribio J. [Review and update of current understanding of childhood atopic dermatitis.]. Actas Dermosifiliogr 2008; 99: 690-700.
25. Maintz L, Novak N. Getting more and more complex: the pathophysiology of atopic eczema. Eur J Dermatol 2007; 17: 267-83
© February 2010 Astellas Pharma Europe LTD.
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