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Key clinical point: Both the age of onset and persistence of atopic dermatitis (AD) are differentially associated with the expression and progression of other atopic diseases during childhood.

Major finding: Children who developed AD at 1 year of age (persistent AD) showed significantly higher rates of food allergy (P = .004), asthma (P < .001), and self-reported rhinitis (P < .001) during childhood compared with children without AD at age 1 year (none/intermittent AD [never had AD or had an intermittent course] or late-onset AD [onset from 4-6 years of age]).

Study details: This study included 285 children from the Childhood Origins of ASThma cohort with a history of physician-diagnosed asthma or respiratory allergies who were followed up to 18 years of age and categorized based on AD phenotypes into none/intermittent (n = 180), late-onset (n = 38), or persistent (n = 67) AD groups.

Disclosures: This study was funded by the US National Institutes of Health (NIH) and the US National Heart, Lung, and Blood Institute. Two authors declared receiving funding from or having other ties with various sources, including NIH.

Source: Taki MH, Lee KE, Gangnon R, et al. Atopic dermatitis phenotypes impact expression of atopic diseases despite similar mononuclear cell cytokine responses. J Allergy Clin Immunol. 2024 (Mar 2). doi: 10.1016/j.jaci.2024.02.015 Source

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Key clinical point: Both the age of onset and persistence of atopic dermatitis (AD) are differentially associated with the expression and progression of other atopic diseases during childhood.

Major finding: Children who developed AD at 1 year of age (persistent AD) showed significantly higher rates of food allergy (P = .004), asthma (P < .001), and self-reported rhinitis (P < .001) during childhood compared with children without AD at age 1 year (none/intermittent AD [never had AD or had an intermittent course] or late-onset AD [onset from 4-6 years of age]).

Study details: This study included 285 children from the Childhood Origins of ASThma cohort with a history of physician-diagnosed asthma or respiratory allergies who were followed up to 18 years of age and categorized based on AD phenotypes into none/intermittent (n = 180), late-onset (n = 38), or persistent (n = 67) AD groups.

Disclosures: This study was funded by the US National Institutes of Health (NIH) and the US National Heart, Lung, and Blood Institute. Two authors declared receiving funding from or having other ties with various sources, including NIH.

Source: Taki MH, Lee KE, Gangnon R, et al. Atopic dermatitis phenotypes impact expression of atopic diseases despite similar mononuclear cell cytokine responses. J Allergy Clin Immunol. 2024 (Mar 2). doi: 10.1016/j.jaci.2024.02.015 Source

Key clinical point: Both the age of onset and persistence of atopic dermatitis (AD) are differentially associated with the expression and progression of other atopic diseases during childhood.

Major finding: Children who developed AD at 1 year of age (persistent AD) showed significantly higher rates of food allergy (P = .004), asthma (P < .001), and self-reported rhinitis (P < .001) during childhood compared with children without AD at age 1 year (none/intermittent AD [never had AD or had an intermittent course] or late-onset AD [onset from 4-6 years of age]).

Study details: This study included 285 children from the Childhood Origins of ASThma cohort with a history of physician-diagnosed asthma or respiratory allergies who were followed up to 18 years of age and categorized based on AD phenotypes into none/intermittent (n = 180), late-onset (n = 38), or persistent (n = 67) AD groups.

Disclosures: This study was funded by the US National Institutes of Health (NIH) and the US National Heart, Lung, and Blood Institute. Two authors declared receiving funding from or having other ties with various sources, including NIH.

Source: Taki MH, Lee KE, Gangnon R, et al. Atopic dermatitis phenotypes impact expression of atopic diseases despite similar mononuclear cell cytokine responses. J Allergy Clin Immunol. 2024 (Mar 2). doi: 10.1016/j.jaci.2024.02.015 Source

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