ABSTRACT
The skin is much more than just a protective coat and encounters a high number of antigens at the interface between the body and the surrounding environment.1,2
Atopic dermatitis (AD) is a chronic inflammatory skin disease, clinically and histologically very similar to contact dermatitis. AD can occur at any age and has a high prevalence in children. In past years, the rising interest in this disease has been forced by its increasing prevalence in Western societies and its contribution to the worsening of health care costs.3 AD offers a wide clinical spectrum ranging from minor forms presented by a few dry eczematous patches to major forms with erythematous rash.4 Cardinal features of AD are erythematous eczematous skin lesions, flexural lichenifications or papules which go along with an intense pruritus and cutaneous hyperreactivity.5,6 Various names, such as atopic eczema, neurodermitis constitutionalis, endogenous eczema, eczema flexurarum, Besnier’s prurigo, asthma eczema, or hay fever eczema have been created for this disease and indicate that still no precise clinical definition of AD exists.7 Additionally, the exact pathophysiosiological mechanisms leading to AD are still elusive and various studies have tried to unravel the key factors leading to this disease.8
