• The Allergy March

    What is the Allergic March?

    The “Allergic March” is a term that describes how allergic diseases progress throughout one’s life.The Allergic March usually begins with eczema – a dry, red, scaly rash that causes considerable itching and discomfort. Eczema is most commonly diagnosed within the first few months of life. In 1/3 to 1/2 of children, eczema is associated with an underlying food allergy. Food allergies (peanut allergy, for instance) generally begin to appear within the first three years of a child’s life. As children age further, the allergic march may proceed to the development of asthma and/or rhino-conjunctivitis.

    Current literature suggests the prevalence of specific allergen sensitivities and the incidence of allergic symptoms can be linked to age. Eczema is typically the first symptom in the youngest age group, followed by gastrointestinal symptoms.Sensitization to inhalant allergens occurs next, with a marked increase in incidence and prevalence by age 3.

    The biological markers include skin-test sensitivities to inhale and/or food allergens and the presence in the blood of specific immunoglobulin E molecules that recognize these allergens. This clinical and biological allergic response is called “atopy”. In the 1920s, when this term was developed, atopy was observed to be a cluster of diseases that would tend to occur in families. Since then, we have come to understand that environments and lifestyles within families also contribute to genetic aspects to form the likelihood of developing atopic diseases.

    It has been known for many years that atopic diseases run in families. The risk that neonates will develop atopic symptoms during the first two decades of life strongly depends on the manifestation of the same specific symptoms in their parents and siblings: there is a closer association between specific symptoms like asthma or atopic dermatitis in the child and the same symptoms in parents or siblings than with other atopic manifestations in the family. These clinical observations suggest the presence of phenotype-specific genes. To date, a variety of markers within specific chromosomal regions have been linked to either atopic dermatitis or asthma, whereas other regions seem to be linked to other atopic phenotypes. If genetic studies turn out to be fruitful, they might help to identify candidate targets for primary prevention measures, as well as individuals who may respond to certain therapeutic interventions in the future.

    During the last two decades, two general hypotheses have been proposed in the literature in connection with the observed increase of atopy and asthma in childhood.New risk factors connected to nutrition, environmental exposure or lifestyle that were not known several decades ago have become relevant.Protective factors related to a more traditional lifestyle in the past have been lost, leading to a greater susceptibility to atopic diseases.

     

    Can we stop or prevent the allergy March?

    If your infant has eczema or egg allergy, it doesn’t necessarily mean that they will go on to develop other, more serious allergic conditions. However, it does mean that they have an increased risk of following the allergic march. Up to 20% of children with eczema go on to develop peanut allergy by the age of 3, and 80% of these children will remain allergic for life.

    Currently, a major study running in United Kingdom looking into different prevention methods to achieve this objective. Three categories of interventions have been described that may lead to optimal outcomes in children with atopy, that is interventions that may reduce the risk of developing persistent asthma. The first of these, “early interventions” targets disease processes early in an attempt to normalize conditions for lung growth and development. Examples of this approach include studies of the use of asthma controller therapies (e.g., inhaled corticosteroids (ICS), and leukotriene antagonists in young children with recurrent wheezing who are at risk for developing persistent asthma. These recent studies showed that these conventional controller therapies reduce asthmaseverity and exacerbations in young children, similar to their efficacy in older children and adults. However, those treated with ICS therapy for 2 years were not more likely to remain symptom-free after ICS was discontinued; such a “curative” effect has not yet been investigated or reported for leukotriene antagonists.

     

    Secondary preventions” are those that take place in young at-risk children prior to the establishment of chronic lung processes. Examples of some recent studies include:

    • Cetirizine in young children with atopic dermatitis (Early Treatment of the Atopic Child [ETAC] study)

    • Topical calcineurin inhibitor in young children with new-onset atopic dermatitis (Study the Atopic March [SAM] study)

    • Pollen allergen immunotherapy in children with allergic rhinitis (PAT study)

    The third group, “primary preventions” aim to shape and optimize early immune development and, in doing so, override other aspects of risk. Examples of previous studies, beginning from birth or prior to birth, include supplementing the diet with lactobacillus or antioxidants (e.g., omega-3 fatty acids), reducing exposure to dust mite allergen and other major indoor allergens, and reducing exposure to allergenic foods.

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