{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T19:25:00Z","timestamp":1793215500405,"version":"4.5.0"},"reference-count":52,"publisher":"American Medical Association (AMA)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Netw Open"],"abstract":"<jats:sec id=\"ab-zoi250491-4\">\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-5\">\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To determine the phenotypes of AD expression across 12 US birth cohorts and identify factors associated with phenotype and development of allergic diseases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-6\">\n                    <jats:title>Design, Setting, and Participants<\/jats:title>\n                    <jats:p>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\u2019s 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-7\">\n                    <jats:title>Exposures<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-8\">\n                    <jats:title>Main Outcomes and Measures<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-9\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-zoi250491-10\">\n                    <jats:title>Conclusions and Relevance<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1001\/jamanetworkopen.2025.15094","type":"journal-article","created":{"date-parts":[[2025,6,12]],"date-time":"2025-06-12T11:00:57Z","timestamp":1749726057000},"page":"e2515094","source":"Crossref","is-referenced-by-count":18,"title":["Phenotypes of Atopic Dermatitis and Development of Allergic Diseases"],"prefix":"10.1001","volume":"8","author":[{"given":"Alexandra R.","family":"Sitarik","sequence":"first","affiliation":[{"name":"Department of Public Health Sciences, Henry Ford Health, Detroit, Michigan"},{"name":"Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy A.","family":"Eapen","sequence":"additional","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of Medicine, Henry Ford Health, Detroit, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jocelyn M.","family":"Biagini","sequence":"additional","affiliation":[{"name":"Division of Asthma Research, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio"},{"name":"Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J.","family":"Jackson","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Allergy, Immunology, and Rheumatology, University of Wisconsin School of Medicine and Public Health, Madison"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine L. M.","family":"Joseph","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, Henry Ford Health, Detroit, Michigan"},{"name":"Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haejin","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Allergy and Clinical Immunology, Department of Medicine, Henry Ford Health, Detroit, Michigan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa J.","family":"Martin","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio"},{"name":"Department of Pediatrics, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine","family":"Rivera-Spoljaric","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Washington University School of Medicine, St Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric M.","family":"Schauberger","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Allergy, Immunology, and Rheumatology, University of Wisconsin School of Medicine and Public Health, Madison"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ganesa","family":"Wegienka","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, Henry Ford Health, Detroit, Michigan"},{"name":"Department of Obstetrics, Gynecology and Reproductive Biology, College of Human Medicine, Michigan State University, East Lansing"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Casper","family":"Bendixsen","sequence":"additional","affiliation":[{"name":"National Farm Medicine Center, Marshfield Clinic Research Institute, Marshfield, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agust\u00edn","family":"Calatroni","sequence":"additional","affiliation":[{"name":"Rho Inc, Federal Research Operations, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soma","family":"Datta","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane R.","family":"Gold","sequence":"additional","affiliation":[{"name":"Channing Division of Network Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts"},{"name":"Department of Environmental Health, Harvard T. 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