[Then physiopathology of atopic dermatitis]

Atopic dermatitis is transmitted as an autosomal dominant trait. Its expressivity is variable, and flare-ups are triggered by environmental factors such as air-borne allergens, cutaneous flora or foodstuffs. Elevation of serum IgE levels is inconstant and not specific; it is associated with a deficiency of suppressor T cell population. The epidermis contains IgE bound to the surface of Langerhans cells; this abnormality seems to be specific as it is not found in atopic or non atopic healthy subjects. The lack of beta-adrenergic response is partially explained by the hyperactivity of the cyclic AMP-degrading phosphodiesterase. Disturbances in essential fatty acid metabolism (inactivation of delta 6 desaturase) are thought to be responsible for abnormalities in the permeability of epithelial structures. The relationships between pharmacological, biochemical and immunological dysregulations are unknown.