[Allergic contact dermatitis].

Clinical definition of eczema is based on the presence of multiform erythematous, papular and vesicular lesions which are followed by marked desquamation. When the underlying mechanism is allergic, skin lesions are mediated by inflammatory Th1 lymphocytes recognizing hapten determinants, i.e. IVth allergic mechanism in allergic contact dermatitis. This mechanism is responsible also for allergy to bacterial proteins in nummular eczema, or to fungal and bacterial proteins, atopens and nickel in dyshidrotic eczema. Eczematous lesions can develop after damage to the skin barrier by toxic chemical or irritating substances, as non-allergic irritation eczema. These substances non-specifically stimulate the Langerhans cells and keratinocytes to produce numerous cytokines inducing expression of adhesion molecules on the endothelial cells. This is responsible for non-specific mobilization of Th1 cells to the skin. A model example is dermatitis induced by mercury salts and/or sodium lauryl sulfate. Intermediate position between allergic and non-allergic eczema is occupied by atopic dermatitis/eczema. In addition to classical IgE-dependent mechanism leading to degranulation of mast cells, there is generation of specific population of Th2 lymphocytes recognizing food and air-borne atopens. This reaction is responsible for skin inflammation in the late-phase response, in which allergic process started by Th2 cells switches to non-specific migration of Th1 cells attracted by cytokines released from eosinophils, keratinocytes and Th2 lymphocytes.