Longitudinal atopic dermatitis endotypes: An atopic march paradigm that includes Black children
| Autor: | Gurjit K. Khurana Hershey, Mariana L. Stevens, Jocelyn M. Biagini, Rahul Patel, Daniel Spagna, John Kroner, Liza Bronner Murrison, Michael G. Sherenian, Hua He, Lisa J. Martin, Asel Baatyrbek Kyzy, Brittany Grashel, Samuel Paul, Alexandra Gonzales, Angelo Bucci |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Immunology Article Dermatitis Atopic Food allergy medicine Immunology and Allergy Humans SCORAD Child Sensitization Asthma medicine.diagnostic_test business.industry Water Environmental exposure Atopic dermatitis medicine.disease Dermatology Rhinitis Allergic medicine.anatomical_structure Cohort Disease Progression business Food Hypersensitivity Filaggrin |
| Zdroj: | J Allergy Clin Immunol |
| Popis: | BACKGROUND The atopic march has been studied mostly in White populations, biasing our current paradigms. OBJECTIVE We sought to define the atopic march in Black and White children and explore mechanisms for racial differences. METHODS Utilizing the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort (n = 601), we assessed longitudinal sensitization, food allergy (FA), allergic rhinitis, risk of asthma development (through the Pediatric Asthma Risk Score), Scoring for Atopic Dermatitis (SCORAD), transepidermal water loss, skin filaggrin (FLG) expression, exposures, and genetic heritability to define AD progression endotypes in Black and White children. RESULTS White MPAACH children were more likely to be sensitized to aero and food allergens (P = .0001) and over 3 times more likely to develop FA and/or allergic rhinitis (AR) without asthma risk (P < .0001). In contrast, Black children were over 6 times more likely to proceed to high asthma risk without FA, sensitization, or AR (P < .0001). White children had higher lesional and nonlesional transepidermal water loss (both P < .001) as well as decreased nonlesional keratinocyte FLG expression (P = .02). Black children had increased genetic heritability for asthma risk and higher rates of exposures to secondhand smoke and traffic-related air pollution. CONCLUSIONS Black and White children with AD have distinct allergic trajectories defined by different longitudinal endotypes. Black children exhibit higher asthma risk despite a more intact skin barrier and less sensitization, FA, and AR. White children have less asthma risk, despite a more dysfunctional skin barrier, and more FA, AR, and sensitization. The observed racial differences are likely due in part to increased genetic heritability for asthma risk and harmful environmental exposures in Black children. Collectively, our findings provide a new paradigm for an atopic march that is inclusive of Black children. |
| Databáze: | OpenAIRE |
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