Atopic dermatitis

Abstract

Atopic dermatitis (AD) is a chronic and relapsing disease affecting an increasing number of patients. Usually starting in early childhood, AD can be the initial step of the so-called atopic march, i.e. followed by allergic rhinitis and allergic asthma. AD is a paradigmatic genetically complex disease involving gene-gene and gene-environment interactions. Genetic linkage analysis as well as association studies have identified several candidate genes linked to either the epidermal barrier function or to the immune system. Stress, bacterial or viral infections, the exposure to aero- or food-allergens as well as hygienic factors are discussed to aggravate symptoms of AD. Athough generalized Th2-deviated immune response is closely linked to the condition of AD, the skin disease itself is a biphasic inflammation with an initial Th2 phase and while chronic lesions harbour Th0/Th1 cells. Regulatory T cells have been shown to be altered in AD as well as the innate immune system in the skin. The main treatment-goals include the elimination of inflammation and infection, preserving and restoring the barrier function and controlling exacerbating factors. The overall future strategy in AD will be aimed to control skin inflammation by a more proactive management in order to potentially prevent the emergence of sensitization as well as to design customized management based on genetic and pathophysiologic information.

Keywords: Atopic dermatitis; Pathophysiology; Proactive management; Therapy.

Fig. 1

Genotype-phenotype relation in atopic dermatitis.

Fig. 2

FcεRI+ Langerhans cells and inflammatory dendritic epidermal cells (IDEC) exhibit distinct functional properties upon activation via the IgE receptor.

Fig. 3

Staphycoccus aureus exhibits a wide spectrum of biological activities which all can contribute to aggravate sensitization and inflammation in atopic dermatitis.

Fig. 4

Schematic view of the reactive and proactive management of atopic dermatitis. The goal of the new approach should be: an early intervention as the flare start, an almost clearance of the lesions and an intermittent application (one or twice/week) of anti-inflammatory compounds.