Dermatoses precipitated or perpetuated by emotional factors
Popular candidates for inclusion in this group of diseases are psoriasis, urticaria, atopic eczema, pom-pholyx, discoid eczema, alopecia areata, lichen sim-plex and lichen planus. Fancy rather than fact still rules here, but a scientific basis for these effects is gradually being established. For example, in psoriasis, stress increases the neuropeptide content of lesions, with a concomitant drop in the activity of enzymes that degrade neuropeptides, especially mast-cell chy-mase. In addition, the blood concentrations of certain neuromediators, especially β-endorphin, changes during exacerbations. Yet an aura of doubt lingers onafor a variety of reasons. The concept of stress is not a simple one, and the terms in which it is discussed are sometimes used rather vaguely. Each type of stress may well provoke its own pattern of response. For this reason many investigators have preferred to record damaging life events rather than to speculate about the presence of stress itself. However, there are problems with this approach too, as a barrage of minor daily annoyances may well be more important than major life events. Every dermatologist will have seen apparent examples of associations between external stress and exacerbations of most of these conditions, but proof that stress causes them is hard to find. Some studies suggest that even hyperhidrosis of the palms and soles, once thought to be an accentu-ated response to stress, has no relationship to chronic anxiety at all. No one questions that stress can cause sweating of the palms, but some studies suggest that chronic hyperhidrosis of the palms and soles, once thought to be simply an accentuated response to stress, has no relationship to chronic anxiety at all.
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