The ‘atopic march’ describes the progression from eczema to other atopic conditions, mainly asthma and allergic rhinitis, and there has been a sharp rise in prevalence of all these conditions over the past few decades. Recent research suggests that changes in the skin barrier in early life are central to the development of atopy and there is gathering evidence to suggest that control or prevention of eczema in infancy may prevent future development of other atopic conditions.
Genetic research has shed light on the susceptibility of some individuals to develop atopic conditions through defects in genes involved in skin barrier function. Several studies have demonstrated an increased risk of developing eczema in individuals with defects in the filaggrin gene, which is present in up to 10% of western European populations.1 Filaggrin is one of a number of structural proteins of the epidermis which contribute to maintaining an effective skin barrier. Mutations in the filaggrin gene result in loss of skin barrier function and the presence of atopic diseases, particularly eczema and asthma. Filaggrin gene defects are associated with an increased risk of developing asthma in individuals with eczema, but not those without eczema and, interestingly, filaggrin is not expressed in bronchial mucosa. Therefore, in individuals with filaggrin mutations, it seems that the breakdown in skin barrier plays a role in the development of asthma.2
It is hypothesised that lack of skin barrier function allows exposure to allergens through the skin and that the atopic march arises due to subsequent migration of sensitised T cells to the airways and nose. Mice models have shown that filaggrin mutations lead to increased uptake of …