The pathogenesis of this disease is more complex, with genetic, physiological and pharmacological immune response to media-related abnormalities, environmental factors also play an important Benbingfasheng. About 70% of patients with a genetic family of atopic dermatitis, asthma or allergic rhinitis, such as genetic history of allergy.


Parents have a genetic history of allergy, which occurred in children allergic to genetic diseases than their parents, only one has a genetic history of allergies to high. Recently found that chromosome 11ql3 parts of the gene and the disease incidence of allergic asthma-related. In the abnormal immune performance for high blood IgE, recently pointed out that the study of skin Langerhans cells with high affinity IgE Fc receptor (Fc e RI). "Inhalation" genetic antigens into the skin of atopic dermatitis, caused by the activation of Langerhans cells, the release of IL-1β atopic make specific sub-type of T helper cell activation and TH-2 have


IL-4, IL-5 cytokines, such as to stimulate B cells to produce IgE, while IL-5 is eosinophilic differentiation and proliferation of white blood cells, an important factor. In patients with atopic dermatitis, by the environmental allergens (house dust mites, pollen) test spot caused by eczema-like skin reactions with the performance of delayed reaction skin (cutaneous late-phase reaction) is similar. In the lesions in the white blood eosinophilic infiltration, so that the IgE-mediated "contact allergy" in the genetic pathogenesis of atopic dermatitis mechanism played an important role. Physiological aspects of pharmacology, patients with skin and white blood cells to β-adrenergic agonists of the slow, produced by the level of cAMP and inhibition of epidermal cell nuclear split function, β-adrenergic receptor stimulants and β decreased affinity, a Adrenergic receptor ratio increased, and so on. In addition yet found a single cell nuclear cAMB phosphodiesterase (PDE) activity increased, so that the reduction in the level of cAMP.