Phänotypen der atopischen Dermatitis

Abstract

Atopic dermatitis (AD) is a common disease affecting both children and adults. AD develops from a complex interplay between environmental, genetic, immunologic and biochemical factors. Genetic factors predispose atopic subjects to mount exaggerated Th2 responses and to a poorly efficient epidermal barrier, which may be sufficient to initiate inflammation in the skin and may favor allergic sensitization. Thus AD can present with different clinical pheno-types. AD is classically distinguished into an intrinsic and extrinsic form, which are clinically identical but the former lacks high level specific IgE and is not associated with respiratory atopy. Although in many cases AD presents with monotonous eczematous lesions on the face, neck and skin folds, it may also present with other features. Very common is nummular eczema, which in many instances may be the dominant expression of AD. In other patients, AD affects limited areas (periorificial eczema, nipple eczema, cheilitis, hand eczema) or its main presentation is with excoriated papules and nodules (atopic prurigo). In conclusion, AD is a multifaceted disease affecting patients with epidermal barrier dysfunction and dry and sensitive skin. The recognition of the less common AD phenotypes is essential for proper patient management.

Bathing effects of east saline groundwater concentrates on allergic (atopic) dermatitis-like skin lesions induced by 2,4-dinitrochlorobenzene in hairless mice

“…Due to an imbalanced immune response to various allergens (3), there are a number of symptoms, such as erythema, keratosis and scaling, that occur during AD. Another characteristic of the allergic immune system is the ability to produce a greater number of immunoglobulin E (IgE) antibodies and type 2 helper T cells (Th2), which are pivotal for IgE synthesis (4,5). Th2 cells predominantly induce the production of interleukin (IL) families and these cytokines are associated with the specific function of immune cells in AD (5).…”

“…Another characteristic of the allergic immune system is the ability to produce a greater number of immunoglobulin E (IgE) antibodies and type 2 helper T cells (Th2), which are pivotal for IgE synthesis (4,5). Th2 cells predominantly induce the production of interleukin (IL) families and these cytokines are associated with the specific function of immune cells in AD (5). IgE is used as an indicator of AD severity and abnormalities of the skin barrier, a key feature of AD (6).…”

“…IgE is used as an indicator of AD severity and abnormalities of the skin barrier, a key feature of AD (6). During allergic inflammation, IgE and IgE-mediated mast cell and eosinophil activation contribute to AD (4,5). In addition, IgE is able to sensitize mast cells in the skin when cell-bound IgE is cross-linked by allergens, culminating in the production of inflammatory mediators, such as interleukins (IL)-4, −5 and −13 and tumor necrosis factor (TNF)-α (5).…”

“…During allergic inflammation, IgE and IgE-mediated mast cell and eosinophil activation contribute to AD (4,5). In addition, IgE is able to sensitize mast cells in the skin when cell-bound IgE is cross-linked by allergens, culminating in the production of inflammatory mediators, such as interleukins (IL)-4, −5 and −13 and tumor necrosis factor (TNF)-α (5). The cytokines IL-4 and IL-13 released by mast cells contribute to the Th2 response (5).…”

“…In addition, IgE is able to sensitize mast cells in the skin when cell-bound IgE is cross-linked by allergens, culminating in the production of inflammatory mediators, such as interleukins (IL)-4, −5 and −13 and tumor necrosis factor (TNF)-α (5). The cytokines IL-4 and IL-13 released by mast cells contribute to the Th2 response (5). TNF-α produced by macrophages also serves an important role in the acute phase of AD (7) and it has been demonstrated that oxidative stress is involved in the pathogenesis of AD (3,8).…”