[Abnormal vasomotor, sudoral and sebaceous reactions in atopic dermatitis (author's transl)].

Putting forward disturbances of cutaneous vasomotricity, sweating and sebaceous excretion is of slight diagnostical value in atopy, but contributes to a better knowledge of its physiopathology. Abnormal vascular reactions are probably correlated with a functional disturbance of beta-adrenergic receptors of the blood vessels; clinical symptoms of apparently paradoxical vasoconstriction occur in most cases of atopic dermatitis, i. e. white dermographism in 80 p. 100, delayed cholinergic blanch in 70 p. 100 or absence of erythema to rubefacients in 55 to 70 p. 100. The troubles of eccrine sweating are more complex: in the eczematous lesions there is a spontaneous and experimentally provoked increase of sweating; in atopic patients the level of acetylcholine induced sweating is lowered and the mean excretion rate is increased; these parameters are not modified by beta-blockers which enhance cholinergic sweating in normals. On the contrary, in atopics beta 2-agonists increase eccrine sweating in summer, but become inefficient in autumn and winter, just as if there was a less severe beta-blockade during warm season. In atopics, sweat is mainly of the cholinergic type and contains more chlorides and less acid mucopolysaccharides; therefore its tensio-activity is increased and its thermolytic evaporative rate correlatively decreased; eccrine sweat glands of atopics are less able to adapt to wintry adrenergic stress, because catecholamines stimulate in preference the dark muciparous cells of the glomerular coil. Eccrine sweat of atopics contains also high amounts of IgE and that is probably the reason of its whealing effect by intradermal injection. The cutaneous dryness of atopic patients seems unrelated to these sudoral troubles, but rather to a excessive transepidermal water loss due to the extensive eczematous microscopical spongiosis of the epidermis and the loss of the barrier function of its horny layer. Decrease of the sebaceous secretion contributes also to the xerosis and following disturbances have been registered: decrease of the total excretion rate, decrease of the lipids of sebo-glandular origin such as waxes, squalen and triglycerides, higher amount of cholesterol, decrease of surfaces and density of sebaceous glands and lower labelling of cells in S phase. Troubles of apocrine sweating have not yet been reported. Abnormal vasomotor, sudoral and sebaceous functions in atopic patients can be satisfactorily interpreted if one accepts the theory of a constitutional blockade of beta 2- and H2-receptors.