Case Studies:AetiopathogenesisThis is probably multifactorial and most studies investigating the causes of atopic eczema deal with children. There is little to suggest that adult atopic eczema should have a different aetiopathogenesis apart from some clinical features, such as the predominant involvement of the hands and head and neck (Sandstrom Falk MH et al 2006).GeneticsPopulation based family studies in Europe suggest that in atopic families up to 50% of offspring will have atopic eczema (Schults Larsen F 2000). Twin studies show a concordance rate for atopic eczema of 0.75 for monozygotic twins compared to 0.20 for dizygotic twins support a genetic basis for atopic eczema (Schultz Larsen F 2000 and 1993, Morar N 2006). Further evidence for a genetic predisposition to atopic eczema is the finding of candidate genes (Schults Larsen F 2000, Morar N 2006, Cork MJ 2006).The predisposition for IgE hyper-responsiveness to allergens defines the term atopy (Johansson SGO 2005). A systematic review of the published evidence for allergic sensitisation and eczema in 12 population studies from around the world has shown that IgE hyper-responsiveness does not necessarily equate to atopic eczema even though it may be associate with the disease phenotype, especially those with severe disease (Flohr C et al 2004; Williams H et al 2006). Amongst those with atopic dermatitis up to 60% were not atopic. Geographic location was associated with the risk of being atopic amongst those with atopic eczema as compared to normal healthy controls. In 5 studies that included adolescents and adults the findings were essentially similar. In the single cross-sectional household survey from Ethiopia, which included adults, 15% of those with atopic eczema and 8 % of those without atopic eczema were atopic by skin prick testing (Yemaneberhan H et al 2004). This was lack of association between atopic eczema and allergen sensitisation was confirmed in a cross-sectional survey and nested case controlled study of children (Abraham H et al 2005). EnvironmentA documented increasing prevalence of atopic eczema over the last 30 years is not consistent with genetic drift alone (Williams HC 1995, 1992; Diepgen T 2000) but supports a strong environmental influence as evidenced by population migration studies (Burrell-Morris C et al 2000). These environmental influences, which affect initial disease expression or aggravation of established disease, are summarised in Table 1. More detailed information can be obtained from published reviews on gene-environment interactions (Morar N 2006; Cork J 2006; Flohr C et al 2005; Akdis CA et al 2006; Taieb A et al 2005; McNally et al 2000; Godfrey K 2000; Schafer T et al 2000; Burrell-Morris C et al 2000; Kolmer H et al 2000; McNally et al 2000; Braae Olesen A et al 2000; Schultz Larsen F 2000).The concept of a damaged barrier function (whether intrinsically normal or dysfunctional) inducing a state of epidermal repair coupled with aberrant responses to epidermal insults in the affected skin, best explains the aetiopathogenesis of atopic eczema (Morar N et al 2006; Cork MJ et al 2006; Taib A et al 2006). |
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