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Observational Study
. 2025 Jun 2;8(6):e2515094.
doi: 10.1001/jamanetworkopen.2025.15094.

Phenotypes of Atopic Dermatitis and Development of Allergic Diseases

Alexandra R Sitarik  1   2 , Amy A Eapen  3 , Jocelyn M Biagini  4   5 , Daniel J Jackson  6 , Christine L M Joseph  1   2 , Haejin Kim  3 , Lisa J Martin  5   7 , Katherine Rivera-Spoljaric  8 , Eric M Schauberger  6 , Ganesa Wegienka  1   9 , Casper Bendixsen  10 , Agustín Calatroni  11 , Soma Datta  12 , Diane R Gold  12   13 , Lisa Gress  6 , Tina V Hartert  14   15 , Christine C Johnson  1 , Gurjit K Khurana Hershey  4 , Fernando D Martinez  16   17 , Rachel L Miller  18 , Christine M Seroogy  6 , Sweta Singh  19 , Anne L Wright  16   17 , James E Gern  6 , Anne Marie Singh  6 ; ECHO Children’s Respiratory and Environmental Workgroup
Collaborators, Affiliations
Observational Study

Phenotypes of Atopic Dermatitis and Development of Allergic Diseases

Alexandra R Sitarik et al. JAMA Netw Open. .

Abstract

Importance: Atopic dermatitis (AD) is the most common inflammatory disease in childhood, and children with AD are more likely to develop other allergic diseases, including food allergy, allergic rhinitis, and asthma.

Objective: To determine the phenotypes of AD expression across 12 US birth cohorts and identify factors associated with phenotype and development of allergic diseases.

Design, setting, and participants: This cohort study compiled longitudinal data from 12 observational US birth cohorts across decades (children born from April 1980 to June 2019) in the Environmental Influences on Child Health Outcomes (ECHO) Children's Respiratory and Environmental Workgroup with follow-up to September 2022. Participants were enrolled prenatally; children with 3 or more AD assessments across the first 84 months of life were included in analyses. Data were analyzed from December 2020 to April 2024.

Exposures: Exposures included decade of birth, cohort type (population-based or high-risk), family history of asthma (mother, father, or sibling), birth order, gestational age at birth, delivery mode, breastfeeding, pet exposure, antibiotic use, environmental tobacco smoke exposure, allergic sensitization, peripheral blood eosinophil count, and total IgE.

Main outcomes and measures: Primary outcomes were AD phenotype, food allergy, allergic rhinitis, asthma, and wheeze. Longitudinal latent class analysis was used to identify underlying longitudinal patterns of AD expression, and associations of AD phenotype with allergic outcomes were examined using logistic regression, multinomial logistic regression, and linear regression.

Results: In 5314 children from 9 cohorts (1896 born in the 2000s [35.7%]; 2585 female [48.6%]; 1083 Black or African American [20.4%]; 3344 White [62.9%]; 350 other reported race [6.6%; including 8 American Indian or Alaska Native (0.2%); 58 Asian (1.1%); 4 Native Hawaiian or Pacific Islander (0.1%) and 280 multiracial or with any race not otherwise specified (5.3%)]), 3382 (63.6%) were from a population-based cohort, while 1932 (36.4%) were from a high-risk cohort. AD prevalence ranged from 24.1% (540 children) to 28.4% (1156 children) at each time point, and 5 phenotypes of AD were identified: transient early AD, early AD with potential reoccurrence, late-onset AD, persistent AD, and minimal or no AD. Compared with White children, Black children were at higher risk for AD (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; persistent AD: aOR, 2.01; 95% CI, 1.54-2.63), as were children with other reported race (transient early AD: aOR, 2.31; 95% CI, 1.13-4.70; early AD with potential reoccurrence: aOR, 3.27; 95% CI, 1.73-6.18). Female children were significantly less likely to have early AD with potential reoccurrence (aOR, 0.45; 95% CI, 0.27-0.74) and persistent AD (aOR, 0.60; 95% CI, 0.49-0.74) than male children. Compared with miniml or no AD, phenotypes with early AD expression were associated with food allergy (transient early AD: adjusted odds ratio [aOR], 2.15; 95% CI, 1.48-3.08; early AD with potential reoccurrence: aOR, 2.43; 95% CI, 1.66-3.50; persistent AD: aOR, 2.26; 95% CI, 1.84-2.78), later AD expression was associated with allergic rhinitis (late-onset AD: aOR, 1.84; 95% CI, 1.38-2.43; persistent AD: aOR, 2.02; 95% CI, 1.64-2.48), and any AD disease was associated with asthma.

Conclusions and relevance: In this birth cohort study of 5314 children, timing of AD expression was associated with increased risk for atopic march pathways. Identifying risk factors for AD phenotypes may inform targeted therapeutic prevention strategies.

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Conflict of interest statement

Conflict of Interest Disclosures: Dr Eapen reported receiving grants from the National Institute of Allergy and Infectious Diseases and the National Institutes of Health outside the submitted work. Dr Jackson reported receiving personal fees from Avillion (consulting), Areteia (consulting), AstraZeneca (data safety monitoring board), Genentech (consulting), GlaxoSmithKline (consulting), Regeneron (consulting), Sanofi (consulting), Upstream Bio (data safety monitoring board), and Pfizer (data safety monitoring board); and grants from GlaxoSmithKline and Regeneron outside the submitted work. Dr Kim reported receiving grants from the National Institute of Allergy and Infectious Diseases and the National Institutes of Health outside the submitted work. Dr Martin reported receiving grants from the National Institutes of Health outside the submitted work. Dr Rivera-Spoljaric reported receiving grants from the National Institutes of Health (grant No. UG3/UH3, R56) and personal fees from Sanofi-Genzyme (no-branded disease state lectures) outside the submitted work. Dr Schauberger reported a patent (WO2018161062) for noninvasive methods for skin sample collection and analysis outside the submitted work. Dr Wegienka reported receiving grants from the National Institutes of Health outside the submitted work. Dr Hartert reported receiving personal fees from the American Thoracic Society (co-chair of the vaccine and immunization initiative), personal fees from National Institutes of Health and National Heart, Lung, and Blood Institute (member and council), Parker B Francis Council of Scientific Advisors (grant reviewer), UpToDate (content contributor author), and Pfizer (vaccine data safety monitoring board) outside the submitted work. Dr Martinez reported receiving grants from the National Institutes of Health and National Heart, Lung and Blood Institute, National Institute of Environmental Health Sciences, and Cystic Fibrosis Foundation; and consulting fees from OM Pharma (consulting) outside the submitted work. Dr Seroogy reported receiving grants from the National Institutes of Health honoraria from UpToDate outside the submitted work. Dr Wright reported receiving grants from the National Institutes of Health outside the submitted work. Dr Gern reported receiving grants from the National Institutes of Health outside the submitted work. Dr A. Singh reported receiving personal fees from Genetech (advisory board) and grants from the National Institutes of Health and US Department of Agriculture outside the submitted work. No other disclosures were reported.

Figures

Figure 1.
Figure 1.. Prevalence of Atopic Dermatitis (AD) by Age and Cohort
Each individual cohort is represented by a distinct color. General-risk (or population-based) cohorts are represented with circles and solid lines, and high-risk cohorts are represented with triangles and dotted lines. CAS indicates Childhood Allergy Study; CCAAPS, Cincinnati Childhood Allergy and Air Pollution Study; CCCEH, Columbia Center for Children’s Environmental Health; COAST, Childhood Origins of Asthma; EHAAS, Epidemiology of Home Allergens and Asthma Study; IIS, Infant Immune Study; INSPIRE, Respiratory Syncytial Virus Infection During Infancy and Asthma During Childhood in the USA; URECA, Urban Environment and Childhood Asthma; WISC, Wisconsin Infant Study Cohort.
Figure 2.
Figure 2.. Description of the 5 Atopic Dermatitis (AD) Phenotypes Identified in the Children’s Respiratory and Environmental Workgroup
Summary of AD expression across time for each phenotype identified is shown.
Figure 3.
Figure 3.. Atopic Dermatitis (AD) Phenotype and Allergic Disease Outcomes
Odds ratios (ORs) are adjusted for cohort type, decade of birth, child sex, and child race. Orange squares represent AD phenotypes with significantly increased odds (relative to the minimal or no AD phenotype) for the allergic disease shown. Blue squares represent nonsignificant ORs. Columns show the total number of events relative to the total number of children for each allergic outcome and comparison (each AD phenotype vs minimal or no AD), as well as ORs and 95% CIs.
See this image and copyright information in PMC

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