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].