The epidemiology of alopecia areata: a population-based cohort study in UK primary care.
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ABSTRACT: Background
There is a lack of population-based information on the disease burden and management of alopecia areata (AA).Objectives
To describe the epidemiology of AA, focusing on incidence, demographics and patterns of healthcare utilization.Methods
Population-based cohort study of 4·16 million adults and children, using UK electronic primary care records from the Oxford-Royal College of General Practitioners (RCGP) Research and Surveillance Centre (RSC) network database, 2009-2018. The incidence and point prevalence of AA were estimated. Variation in AA incidence by age, sex, deprivation, geographical distribution and ethnicity was examined. Patterns of healthcare utilization were evaluated in people with incident AA.Results
The AA incidence rate was 0·26 per 1000 person-years. AA point prevalence in 2018 was 0·58% in adults. AA onset peaked at age 25-29 years for both sexes, although the peak was broader in females. People of nonwhite ethnicity were more likely to present with AA, especially those of Asian ethnicity [incidence rate ratio (IRR) 3·32 (95% confidence interval 3·11-3·55)]. Higher AA incidence was associated with social deprivation [IRR most vs. least deprived quintile 1·47 (1·37-1·59)] and urban living [IRR 1·23 (1·14-1·32)]. People of higher social deprivation were less likely to be referred for specialist dermatology review.Conclusions
By providing the first large-scale estimates of the incidence and point prevalence of AA, our study helps to understand the burden of AA on the population. Understanding the variation in AA onset between different population groups may give insight into the pathogenesis of AA and its management.
SUBMITTER: Harries M
PROVIDER: S-EPMC9298423 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAlopecia areata (AA) describes a sudden localized patchy alopecia. The cause of AA is not completely clear and its incidence may be related to genetic, autoimmune, and environmental factors.AimTo explore the possible mechanisms of AA and to provide a basis for the early diagnosis and treatment of AA.MethodsGene microarray data from 122 scalp skin biopsy tissue samples from patients with AA or healthy controls from the Gene-Cloud of Biotechnology Information database were analyzed using bioinformatics analysis methods. Molecular network analysis of the differentially expressed genes (DEGs) was conducted by Cytocluster using the Molecular Complex Detection (MCODE) algorithm.ResultsThe gene expression profile of skin lesions from patients with AA was significantly altered, with 111 DEGs found in the skin lesions of AA, compared with that of the healthy skin. The DEGs were mainly related to biological processes such as the development of the epidermis and inflammatory reaction. The protein-protein interaction network analysis of DEGs revealed bone morphogenetic protein 2 (BMP2) as a core protein interaction network. BMP2 acted not only via the inflammatory response but also via the signaling pathways in epithelial cell development and epidermal cell differentiation to affect the epidermal development. MCODE analysis further showed that keratins (KRTs) and keratin-associated proteins (KRTAPs) can affect the epidermal development via the epidermal development pathway.ConclusionsThe abnormal development of the epidermis and inflammatory reactions in skin tissue play important roles in the pathogenesis of AA and are closely related to BMP2, KRTs, and KRTAPs genes.LimitationsOur study was limited by experimental verification.
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