Epidemiology
The prevalence of atopic dermatitis has increased rapidly in industrialized countries since the early sixties{Devenny, 2004 #725}. Now about 15-25% child and 2-8% of adults are affected{Williams, 2006 #728}. There is a true aspiration to explain the global rise in the prevalence of atopic dermatitis. Trend data imply that the developing world may soon display a picture which resemble that of affluent nations, hence AD is no longer something troubling only the wealthy – it is a worldwide challenge{Flohr, 2014 #726}. Several epidemiologic studies of AD have described a broad palette of influential factors possibly driving the pandemic like representation of AD. The protective effects of rural upbringing, diverse diet, early exposure to infectious agents or the lack of such has been deem responsible{Flohr, 2004 #11}, however their importance is not likely to be a simple cause-and-effect relationship and newer studies confront this concept of disease. Epidemiologic studies conducted at a population level can not alone provide a balanced understanding of the enigma of atopic dermatitis{Flohr, 2014 #726}.
Aetiology
The impact of genetics on AD development, prognosis and course of disease is with out a doubt a keystone in understanding this disease. Concordance rates among monozygotic twins (77%) being much higher than among dizygotic twins (15%), and 1. degree relatives with atopy being a solid AD risk factor suggests atopic dermatitis–specific genes{Morar, 2006 #729}. The genomic region of primary interest is a family of epithelium-associated genes named the epidermal differentiation complex{Cookson, 2004 #730}. With in this complex we find the single most studied gene in AD; filaggrin. After the pivotal discoveries by McLean and co-workers{Palmer, 2006 #720}, it is now common knowledge that loss-of-function mutations with this gene heavily increase the risk of AD, albeit just as important is the fact that not all individuals with loss-of-function filaggrin mutations develop AD, and only one in four of AD patients carry a mutation within this gene. These findings have triggered a cascade of studies involving genes and encoded proteins within the epidermal differentiation complex, that has ultimately lead to a more comprehensive understanding of AD.
Due to the rise in AD prevalence an interest in identification of environmental risk and protective factors is growing. Climate is a possible explanation for the differences in prevalence between populations. Results suggest that AD symptoms correlate negatively with annual outdoor temperatures, which likewise is an AD flare factor, findings that could be due to higher UV light exposure in warmer countries{Silverberg, 2013 #731}. However, this relationship is quite complexed reflected by the inconsistency in season variations from patient to patient{Kramer, 2005 #735}.
The possible protection from rural living and likewise the risk factor of urban residency is well examined and supported{Schram, 2010 #733}, a cause-relationship that has birthed the “hygiene hypothesis”. A third explanatory factor could be the ‘Western’ affluent diet leading to an increase in AD risk. This is possibly attributed the low content of anti-inflammatory n-3 polyunsaturated fatty acids of such diets{Ellwood, 2001 #734}. Many other hypotheses have been explored, from the immunomodulation by measures of hygiene, individual gut microbiota diversity, and endotoxin exposure through animal husbandry to the effects of air pollution, tobacco smoke, and domestic hard water{Flohr, 2014 #726}. In summary the environmental factors possibly involved in AD development and disease aggravation are many and epidemiological studies will keep supplying the field of basic research with new causalities to explore.
There has been several paradigm shifts in our common perception of the primary cause of AD. The concept of immune dysregulation, with the involvement of T-helper (Th) cells, IgE-mediated sensitization and cytokine release, leading to skin inflammation and disrupted epidermal barrier function has been the leading a dominating theory. Todays knowledge do not contest these relationships, however the view is less parochial today than ever and the feedback-loop between skin barrier dysfunction and immunomodulation is highly complicated and definitely not a one-way track.