The Allergy March

What is the Allergy March?
The term “allergy march” describes how allergic diseases develop throughout a person’s life. Allergies usually begin with eczema – a dry, red skin rash that causes intense itching and discomfort. Eczema is most commonly diagnosed within the first few months of life. For 1/3 to 1/2 of children, eczema is associated with underlying food allergies.

Food allergies (such as peanut allergy) typically begin to appear within the first three years of a child’s life. As children grow older, allergies may continue to develop in the form of asthma or conjunctivitis.

Current scientific knowledge indicates that certain types of allergies are more prevalent, and the onset of allergic symptoms can be linked to age. Eczema traditionally represents the first symptom in the youngest age group, followed by gastrointestinal symptoms. Inhalant allergies occur later, with a marked increase in incidence and prevalence by the age of three years.

Biological markers include skin prick tests for inhaled and/or food allergens, and the presence in the blood of specific immunoglobulin E (IgE) molecules that recognize these allergens. This is called the clinical and biological response “atopy.” When this term was coined in the 1920s, it was observed that atopic diseases are a group of conditions that tend to occur in families. Since then, we have come to understand that environments and lifestyles within families also contribute, alongside genetic aspects, to shaping the likelihood of developing atopic diseases.

It has been known for many years that atopic diseases run in families. The risk of developing atopic symptoms in newborns during the first two decades of life strongly depends on the presence of specific symptoms in their parents and siblings. There is a close relationship between specific symptoms such as asthma or eczema in a child and the symptoms in parents or siblings from atopic manifestations in the family. These clinical observations suggest a specific genetic phenotype. To date, a variety of markers within specific chromosomal regions have been linked to either eczema or asthma, while other regions appear to be related to other atopic conditions. If genetic studies become more useful, they could help identify candidate targets for primary prevention measures, as well as individuals who might respond to certain therapeutic interventions in the future.

Over the past two decades, two general hypotheses have been proposed in the literature regarding the observed increase in atopic diseases and childhood asthma. New risk factors related to nutrition, environmental exposure, or lifestyle that were not known several decades ago have become closely associated. The lack of protective factors associated with traditional lifestyles in the past has led to an increased exposure to atopic diseases.

How can I stop or reduce the allergy march?
If your infant has eczema or egg allergy, it does not necessarily mean that it will continue to develop into other, more severe forms of allergy. However, they are at increased risk of the subsequent allergy march. 20% of children with eczema will develop another form of allergy, namely peanut allergy, by the time they reach 3 years of age, and 80% of these children will continue to suffer from it throughout their lives.

Currently, a major study is being conducted in the United Kingdom to investigate various prevention methods to achieve this goal. Three categories of interventions have been described that may lead to better outcomes in children with atopic conditions; these are interventions that may reduce the risk of persistent asthma:

1. Early intervention: Targets early disease processes in an attempt to normalize conditions for lung growth and development. Examples of this approach include studies using asthma controller therapies (e.g., Inhaled Corticosteroids (ICS), Leukotriene antagonists) in young children with recurrent wheezing who are at risk of developing persistent asthma. These recent studies have shown that these conventional therapies have worked to reduce the severity and exacerbations of asthma in young children, similar to their effectiveness in older children and adults. However, those treated with ICS for two years are not more likely to remain free of symptoms after stopping ICS treatment. No side effects of such “therapy” based on leukotriene antagonists have been investigated or reported so far.

2. Secondary preventive measures: These are measures taken with children at risk before the onset of chronic lung disease. Examples of recent studies addressing this aspect include:

   • Cetirizine for the treatment of young children with Atopic Dermatitis.

   • The Early Treatment of Atopic Dermatitis in Children (ETAC) study for young children with allergic dermatitis (The Atopic Dermatitis March study).

   • Immunotherapy for pollen dust in children with Allergic Rhinitis.

   • Calcineurin inhibitors.

3. Primary preventive measures: Aim to shape and improve early immune development, and by doing so, other risk factors can be overcome. Examples of previous studies, starting from birth or before birth, include:

   • Dietary supplementation using Lactobacillus or antioxidants (such as omega-3 fatty acids).

   • Reducing exposure to house dust mite allergens and other indoor allergens.

   • Reducing exposure to allergenic foods.