4.7 Article

Genetic ancestry does not explain increased atopic dermatitis susceptibility or worse disease control among African American subjects in 2 large US cohorts

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出版社

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2019.06.044

关键词

Atopic dermatitis; eczema; genetic ancestry; disease control; racial/ethnic disparities

资金

  1. Robert Wood Johnson Foundation
  2. National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) [K23 AR073915]
  3. National Eye Institute [R01 EY027004]
  4. National Institute of Diabetes and Digestive and Kidney Diseases [R01 DK116738]
  5. National Institute on Aging
  6. National Institute of Mental Health
  7. National Institute of Health Common Fund [RC2 AG036607]

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Background: Atopic dermatitis (AD) is more common among African American children. Whether there are racial/ethnic difference among adults with AD and the causes for those disparities are unclear. Objective: We sought to examine the relationship between self-reported race/ethnicity and AD and determine whether African genetic ancestry is predictive of these outcomes among African American subjects. Methods: We analyzed data from 2 independent multiethnic longitudinal studies: 86,893 subjects aged 18 to 100 years from the Kaiser Permanente Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort and 5467 subjects aged 2 to 26 years from the national Pediatric Eczema Elective Registry (PEER) cohort. The primary outcomes were physician-diagnosed AD in GERA and repeated measures of self-reported disease control among patients with physician-diagnosed AD at 6-month intervals in PEER. We examined whether self-identified African American race/ ethnicity was predictive of these outcomes and then tested whether a continuous measure of African genetic ancestry was associated with outcomes within the African American group. Results: AD was more common among self-identified African American subjects than non-Hispanic white subjects in GERA (4.4% vs 2.1%; odds ratio, 2.06; 95% CI, 1.70-2.48) and less well-controlled in PEER subjects (odds of 1-level worse control, 1.91; 95% CI, 1.64-2.22). However, African genetic ancestry was not associated with AD risk or control among self-identified African American subjects in either cohort, nor did an AD polygenic risk score or genetic skin pigment score explain the AD disparities in patients with AD. Conclusion: Ancestry-related genetic effects do not explain increased AD prevalence or poorer disease control among African American subjects.

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