4.7 Article

Longitudinal atopic dermatitis endotypes: An atopic march paradigm that includes Black children

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 149, Issue 5, Pages 1702-+

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2021.09.036

Keywords

Atopic march; atopic dermatitis; race; genetic ancestry; environmental exposure; skin barrier; biomarker

Funding

  1. National Institutes of Health [U19AI070235]

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This study investigates the atopic march in Black and White children and identifies distinct allergic trajectories in these populations. It reveals that Black children have a higher risk of asthma despite a more intact skin barrier and less sensitization, food allergy, and allergic rhinitis. Conversely, White children have a lower risk of asthma despite a more dysfunctional skin barrier and higher rates of sensitization, food allergy, and allergic rhinitis.
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 5 601), 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.

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