1. Introduction
Atopic eczema (AE, or atopic dermatitis, AD) is an inflammatory skin disease with involvement of genetic, immunological, and environmental factors which are highly interconnected [1, 2]. The heterogenic disease can be separated into different phenotypes and clinical presentation defined by the ethnicity, disease onset, disease severity, chronic vs acute, intrinsic vs extrinsic (IgE level), pediatric vs adult and inflammatory signature [3-5]. A common feature of all subtypes is a tremendous psychosocial burden for all patients with AE [6]. Prevalence varies by area and is reported to be 15-20% in children in Europe, persisting in up to 5-10 % of adults [7-9]. Although, severe cases are less abundant than mild or moderate disease pattern, 2% of affected children are severely suffering [7, 9]. Therefore, AE remains to be a high and even increasing socioeconomic burden in the United States and in Europe [10, 11], whereas slightly decreasing numbers were reported over the last few years in Japan [12]. Children often overcome atopic eczema, but set off on the so-called ”atopic march”, i.e. begin a classic ”allergy career”. Scientifically, atopic dermatitis is a risk factor for the development of allergies. These are primarily type I allergies with clinical features such as hay fever and asthma. Allergies are increasingly becoming a widespread disease. Currently, almost every fourth person in Europe suffers from symptoms such as asthma or hay fever and the associated restrictions in everyday life or at work. For society, the reduced ability to perform at school, university and at work means great socio-economic damage [13, 14].