ABSTRACT
I. INTRODUCTION Atopic dermatitis (AD) is a common chronic pruritic inflammatory skin disorder occurring with increasing frequency in children and adults in western countries. Patients with AD have dry skin (xerosis), eczema, lichenification, and pruritus that is often etremely difficult to treat. The etiology of AD is currently believed to include an immunodysfunction and a skin barrier defect. Immunologically, a Th1/Th2 imbalance appears to result in an allergenspecific hypersecretion of IgE and an increased release of interleukin (IL)-4 and IL-5 but reduced secretion of IL-2 and interferon- (IFN-) (reviewed in Ref. 1). However, as the German synonymon for AD, ‘‘neurodermitis,’’ suggests, neurobiological factors have long been proposed to play an important role in AD. In many anecdotal and investigative reports psychological problems, such as psychic lability, chronic anxiety, mood deviations, or insufficient coping with stress, were delineated as key features of AD [2]. Moreover, as early as 1968, when Szentivanyi formulated his ‘‘-adrenergic theory of the constitutional basis of atopy,’’ neuromediators or neurotransmitters have been implicated in the pathogenesis of atopy [3].
