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. 2022 May;149(5):1702-1710.e4.
doi: 10.1016/j.jaci.2021.09.036. Epub 2021 Oct 18.

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

Affiliations

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

Jocelyn M Biagini et al. J Allergy Clin Immunol. 2022 May.

Abstract

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.

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

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Conflict of interest statement

The authors have no conflicts of interest.

Figures

Figure 1.
Figure 1.
Progressor Phenotypes of Black and White MPAACH Children. A. Progressor phenotype across V1 and V2 by race (n=456). B. Children with at least one co-morbidity across V1 and V2 (n=325). *children that did not have a co-morbidity at V1 and did not yet complete V2 were not included in the non-progressor phenotype (n=145).
Figure 2.
Figure 2.
Sensitization patterns Food Allergy and Allergic Rhinitis in Black and White MPAACH children at visit 1.
Figure 3.
Figure 3.
A) maximum respiratory symptom frequency score and B) Pediatric Asthma Risk Scores (PARS) in Black and White MPAACH children at visit 1.
Figure 4.
Figure 4.
Skin FLG expression and TEWL in non-lesional and lesional skin in Black and White MPAACH children at visit 1.
Figure 5.
Figure 5.
Parental AD, asthma and environmental allergies/hay fever in Black and White MPAACH children.

Comment in

References

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