Is Atopic March Real?
Other than managing eczema, the other question that will be on the minds of parents with eczema children would be WILL MY CHILD GET ASTHMA OR HAY FEVER NEXT?
The atopic march refers to the progression from atopic dermatitis (AD) to allergic asthma (AA) and to allergic rhinitis (AR, hay fever). Does this decades-long hypothesis still hold true?
To find out, I have looked at all the studies on atopic march (and allergic march) and compiled the conclusions stated in the papers that I came across:
The Canadian researchers looked at past studies and below are some of the observations stated in their paper:
- AD, AR and AA are temporally associated and may be causally related
- Not universal, i.e. not all AD progressed to AA
- Only 3.1% of the children in one study progressed from AD to AA, and from AA to AR (traditional model)
- If the atopic march model is expanded to include AD to AA or AD to AR, about 10.5% of the children gone through this allergic progression
Whether or not the traditional model holds true, there are risk factors for atopic march, i.e. should these factors be present, they increases the likelihood of eczema progressing to asthma or hay fever:
- Early persistent (for 3 years) onset of AD is associated with AA
- Ig-E eczema is related to AA. Not all eczema has an underlying allergic condition, meaning there is no hypersensitivity seen from allergy testing (also known as non-atopic eczema). For children with allergic eczema, there is a stronger relationship to AA and AR
- Filaggrin mutations predisposes AD, which then predisposes AA (also known as the outside-in hypothesis). Filaggrin (FLG) is a key epidermal protein that "holds" the skin together by being an insoluble skin barrier. When this is defective, the skin will allow allergen, pathogen to penetrate which stimulates inflammation. More studies on this in these food allergy research & food sensitization from eczema posts.
- TSLP-overexpression associated with allergic asthma. TSLP is thymic stromal lymphopoietin which is an IL-7-like cytokine, which stimulates immune response. When there is over-expression of TSLP, there is hypersensitivity to inhaled allergen.
Published in the Annals of Allergy, Asthma and Immunology (Feb 2018), the Australian and US researchers looked into the published studies on this, and reported:
- Strong link between AD and sensitization, food allergy, asthma, and allergic rhinitis, particularly AD that is severe and commences in the first 6 months of life.
- Regular use of prophylactic emollients can significantly decrease the expression of AD, at least while treatment continues.
Published in the Acta Pædiatrica (July 2016), the Swedish researched compiled their findings from a longitudinal birth cohort study using questionnaires. 3,382 questionnaires were analysed, which was a major strength of this study. The findings were:
- Strong link between having an allergic condition during infancy and having one at 8 years old
- Stronger link between having more than one allergic conditions during infancy, and having an allergic condition at 8 years old
- Recurrent wheeze at infancy only increased risk of asthma at 8 years old
- Eczema and food allergy independently increased risk of all four allergic conditions at 8 years old (eczema, food allergy, asthma or rhinitis)
- Data suggest co-existence of allergic conditions, rather than a progressive development of the same disease. Therefore, it is more likely that certain allergic conditions have the same underlying causes.
Published in the Journal of Clinical & Cellular Immunology (April 2014), the US researchers looked into the studies on Atopic March:
- Atopy is the personal or familial propensity to produce IgE antibodies and sensitization in response to environmental triggers
- The first step of the Atopic March is Atopic Dermatitis (AD)
- Unfortunately, AD is increasing in prevalence and remains chronic, evident from only 60% of the children outgrowing eczema by adulthood
- The last step of the Atopic March is Allergic Rhinitis and Asthma
- Children with specific IgE antibodies to common environmental allergens are more likely than those with intrinsic eczema (ie no allergy) to have allergic rhinitis and asthma
- Risk factors include IgE sensitization and early onset and severity of AD
- 70% of patients with severe eczema develop asthma compared to 20-30% of those with mild eczema, and 8% for general population
- The dysfunctional skin barrier serves as a site for allergic sensitization to antigens and colonization of bacterial super antigens
> Defective skin barrier meant that the skin has less lipids (ceramides and sphingosines) and dysfunctional skin protein (filaggrin) that led to abnormal skin barriers (generally understood as being more 'porous' and susceptible to allergens, irritants and pollutants)
> Defective skin barrier can be observed by increased TEWL (transepidermal water loss)
> Increased TEWL correlates with eczema severity
> Eczema skin predisposes to staph bacteria colonization, and these staph bacteria secretes superantigens that stimulate TSLP which activates immune cells and promote inflammation
- The sensitization led to Th2 which predisposes patients to allergic nasal responses and promotes airway hyper reactivity