Guidelines on the Management of Atopic Dermatitis ... - Dermatology

dermatitis of 0.75 for monozygotic twins compared to 0.20 for dizygotic twins support a
genetic basis for atopic dermatitis. 10,11,12 Further evidence for a genetic predisposition to
atopic dermatitis is the finding of candidate genes. 1,10,12
Allergic sensitisation
The predisposition for IgE hyper-responsiveness to allergens defines the term atopy. 13 A
systematic review of the published evidence for allergic sensitisation and dermatitis in 12
population studies from around the world has shown that IgE hyper-responsiveness does not
necessarily equate to atopic dermatitis, even though it may be associated with the disease
phenotype, especially those with severe disease. 14,15 Amongst those with atopic dermatitis,
up to 20 - 60% were not atopic per definition. Geographic location was associated with the
risk of being atopic, amongst those with atopic dermatitis as compared to normal healthy
controls.
In five studies that included adolescents and adults, the findings were essentially similar. In a
cross-sectional household survey from Ethiopia, which included adults and children, 15% of
those with atopic dermatitis and 8% of those without atopic dermatitis were atopic by skinprick
testing. 16 This lack of association between atopic dermatitis and allergen sensitisation
was confirmed in a cross-sectional survey and nested case controlled study of children. 17
Environment
A documented increasing prevalence of atopic dermatitis over the last 50 years is not
consistent with genetic drift alone, 18,19,20 but supports a strong environmental influence as
evidenced by population migration studies. 21,22 These environmental influences, which affect
initial disease expression or aggravation of established disease, are summarised in Table 1.
Population studies from Africa seldom confirm a role for these environmental factors. 16,17,23
Interestingly, many are surrogate markers of urbanisation 21,22 and increased socio-economic
status, 24 which appear to be the only fairly consistent association across all population
groups*. More detailed information can be obtained from published reviews on geneenvironment
interactions. 1,10,12,21,25-40
The aetiopathogenesis of atopic dermatitis is best explained by the concept of a damaged
barrier function, whether intrinsically normal or dysfunctional, that induces a state of
epidermal repair, coupled with aberrant responses to epidermal insults in the affected
skin. 2,3,4,8,10,12,24,27,41,42,43 In Africa this hypothesis has still not been validated. A novel filaggrin
gene defect has been documented in a single Ethiopian case of atopic dermatitis 44 . What
evolutionary advantage the skin barrier defect conveyed to the populations now exposed to
environmental influences precipitating atopic disease is unknown.
Table 1: Environmental influences on atopic dermatitis
Environmental factor Effect on atopic dermatitis References
Rural compared to urban
living (hygiene hypothesis)
Increased risk with urbanisation 21, 22, 24,
25, 38
*Socioeconomic status Increased risk with higher socio-economic status 16, 17, 24,
28, 45
*Education level of parents Increased risk with higher level of education 29
*Family size (hygiene
hypothesis)
Increased risk with decreasing family size 25, 29