Abstract

The development of atopic dermatitis (AD) in infancy and subsequent allergic rhinitis and asthma in later childhood is known as the atopic march. This progressive atopy is dependent on various underlying factors such as the presence of filaggrin mutations as well as the time of onset and severity of AD. Clinical manifestations vary among individuals. Previously it was thought that atopic disorders may be unrelated with sequential development. Recent studies support the idea of a causal link between AD and later onset atopic disorders. These studies suggest that a dysfunctional skin barrier serves as a site for allergic sensitization to antigens and colonization of bacterial super antigens. This induces systemic Th2 immunity that predisposes patients to allergic nasal responses and promotes airway hyper reactivity. While AD often starts early in life and is a chronic condition, new research signifies that there may be an optimal window of time in which targeting the skin barrier with therapeutic interventions may prevent subsequent atopic disorders. In this review we highlight recent studies describing factors important in the development of atopic disorders and new insights in our understanding of the pathogenesis of the atopic march.

Highlights

  • Atopic diseases, including atopic dermatitis, allergic rhinitis, and asthma have increased in frequency in recent decades and affect approximately 20% of the population worldwide

  • Patients with eczema with specific IgE antibodies to common environmental allergens present by 2 to 4 years of age are at higher risk for progressing in the atopic march to allergic rhinitis and asthma than those with eczema without IgE sensitization [10,22]

  • The Tasmanian Longitudinal Health (TLH) Study investigated the influence of eczema on the development of asthma from childhood to adult life and found that childhood eczema was significantly associated with new-onset asthma in three separate life stages: pre-adolescence, adolescence (2.14; 1.33-3.46), and adult life (1.63; 1.28-2.09) as well as over the life-span from the ages of 8 to 44 years (1.73; 1.42-2.12) [25]

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Summary

Introduction

Atopic diseases, including atopic dermatitis, allergic rhinitis, and asthma have increased in frequency in recent decades and affect approximately 20% of the population worldwide. Patients with eczema with specific IgE antibodies to common environmental allergens (extrinsic AD) present by 2 to 4 years of age are at higher risk for progressing in the atopic march to allergic rhinitis and asthma than those with eczema without IgE sensitization (intrinsic AD) [10,22]. A population-based prevalence estimate of eczema in U.S adults found that the 1 year eczema prevalence of adults is 10.2%, with 3.2% of the adult population ever having a history of asthma, hay fever, or both [26] These studies strongly suggest that the atopic march progresses well past childhood. It is still unclear why some infants with AD outgrow the disease with increasing age, whereas others will "march" to develop other atopic conditions such as allergic rhinitis and/or asthma in later stages. This provides further credence that it might be possible to prevent hay fever in children with eczema by controlling their eczema and improving skin barrier function [35]

Role of Food Allergy in the Atopic March
Animal Models Supporting the Atopic March
Potential Mechanisms and Speculations Underlying the Atopic March
Skin Barrier Defects in AD and the Atopic March
Role of Filaggrin Mutation in AD and in the Atopic March
Findings
Conclusion
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