Introduction
Atopic dermatitis (AD) is a chronic relapsing disease, which most often
debuts in early childhood and remits later in childhood. It is
characterized by defects in the barrier function due to an abnormal
stratum corneum in both affected and nonaffected
skin1,2. Several lines of evidence indicate that an
epidermal barrier impairment in the skin of children with AD is involved
in the development of allergic sensitization3,4.
Recently, it has been proposed that early exposure to foods via the skin
in children with AD may allow penetration of food allergens through the
skin leading to development of sensitization and subsequent food
allergy5,6. This is in contrast to an early,
continuous oral exposure to some allergenic foods such as peanuts and
egg, which may lead to development of immune tolerance and reduced risk
of food allergy in young children6–8.
The development of specific IgE (sIgE) to environmental allergens has
also been associated with a defective skin barrier
function4; e.g. one study showed association between
increasing total epidermal water loss and prevalence of sensitization to
aeroallergens4. Another study used a chemical
sensitizer to show that sensitization through the skin in AD induced a
persistent skewing towards antigen-specific Th2 responses regardless of
Filaggrin (FLG ) mutation status3. FLG is
a key protein that assists in the final differentiation of the epidermis
and formation of the skin barrier2. FLGmutation status leads to functional loss of barrier function in the skin
and other mucosal surfaces2,9. A previous literature
review described that up to 2/3 of patients with AD will develop
allergic rhinitis10, and particularly earlier debut of
AD seemed to impose a higher risk. To our knowledge, no previous studies
have investigated the association between AD severity and later
development of aeroallergen sensitization and allergic rhinitis, and
none included FLG mutation status.
We hypothesized that the epidermal barrier defect in early-onset, more
severe AD in infancy compared to late-onset AD may facilitate
penetration of aeroallergens via the skin and increase the risk of
developing aeroallergen sensitization and allergic rhinitis in
childhood. To test this hypothesis, we used data from the Copenhagen
Prospective Studies on Asthma in Childhood2000(COPSAC2000) at-risk mother-child cohort to determine
whether early-onset vs. late-onset AD and severity of AD are associated
with development of aeroallergen sensitization and allergic rhinitis at
6-7 and 12 years of age.