Study links early childhood eczema timing to risk of allergies like food allergy, asthma, and rhinitis, with five distinct disease phenotypes identified.
Atopic dermatitis phenotypes and allergic disease development in children | Image Credit: © lial88 - © lial88 - stock.adobe.com.
A newly published cohort study of over 5,000 children has identified 5 distinct phenotypes of atopic dermatitis (AD) expression across early childhood, each associated with varying risks of food allergy, allergic rhinitis, and asthma.1
The analysis, published in JAMA Network Open and conducted using data from 12 US birth cohorts enrolled between 1980 and 2019, included 5,314 children who had at least 3 clinical assessments for the chronic inflammatory skin diseased (characterized by pruritus and eczematous lesions)2 within their first 84 months of life. Cohorts were from the Environmental Influences on Child Health Outcomes (ECHO) program, with follow-up continuing through September 2022. The final population included both population-based (63.6%) and high-risk (36.4%) cohorts, with diverse racial and ethnic representation.1
Researchers used longitudinal latent class analysis to define 5 AD phenotypes:
AD prevalence ranged from 24.1% to 28.4%, overall common among study participants. The phenotype of AD expressed in a child—particularly the age of onset and whether the condition persisted or resolved—was associated with risk of developing other allergic diseases.
Children with early-onset AD phenotypes were significantly more likely to have food allergies. For those with transient early AD, the adjusted odds ratio (aOR) for food allergy was 2.15 (95% CI, 1.48–3.08). Children with early AD and potential reoccurrence had an aOR of 2.43 (95% CI, 1.66–3.50), while persistent AD was associated with an aOR of 2.26 (95% CI, 1.84–2.78) for food allergy.
In contrast, late-onset and persistent AD were most strongly linked to allergic rhinitis. Children with late-onset AD had an aOR of 1.84 (95% CI, 1.38–2.43), and persistent AD was associated with an aOR of 2.02 (95% CI, 1.64–2.48) for rhinitis.
All phenotypes of AD were associated with an increased risk of asthma. This supports the long-standing understanding of the skin-lung connection and the role of skin barrier dysfunction in the atopic march.
Black children were more likely than White children to experience certain AD phenotypes. For example, Black children had higher odds of transient early AD (aOR, 3.26; 95% CI, 2.06–5.18), early AD with potential reoccurrence (aOR, 3.72; 95% CI, 2.35–5.90), and persistent AD (aOR, 2.01; 95% CI, 1.54–2.63). Children of other reported race—including multiracial children and those not otherwise specified—also had increased odds for some AD phenotypes.
In addition, female children were significantly less likely than male children to develop certain types of AD. Girls had a lower risk of early AD with reoccurrence (aOR, 0.45; 95% CI, 0.27–0.74) and persistent AD (aOR, 0.60; 95% CI, 0.49–0.74).
According to the study authors, these results suggest that the timing of skin barrier dysfunction may be a critical factor in the development of allergic disease. The findings reinforce the importance of early identification and monitoring of AD in pediatric patients.
"In this cohort study, timing of AD expression was associated with development of other allergic diseases, suggesting that the timing of skin barrier disruption plays an important role in atopic march pathways," the authors concluded.
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