Autor: |
McSweeney, S.M., Christou, E.A.A., Dand, N., Boalch, A., Holmes, S., Harries, M., Palamaras, I., Cunningham, F., Parkins, G., Kaur, M., Farrant, P., McDonagh, A., Messenger, A., Jones, J., Jolliffe, V., Ali, I., Ardern‐Jones, M., Mitchell, C., Burrows, N., Atkar, R. |
Předmět: |
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Zdroj: |
British Journal of Dermatology; Dec2020, Vol. 183 Issue 6, p1136-1138, 3p |
Abstrakt: |
Dear Editor, Frontal fibrosing alopecia (FFA) is an inflammatory primary scarring alopecia of uncertain aetiology that represents a variant of lichen planopilaris.1 It predominantly, although not exclusively, affects postmenopausal women.2 Its pathogenesis is characterized by immune-mediated follicular destruction at the level of the hair bulge, which leads to a clinical phenotype of progressive frontotemporal hair and eyebrow loss that is often preceded by widespread body-hair loss.2 Histologically, a lichenoid inflammatory infiltrate surrounds the isthmus and infundibulum of the hair follicle, and this progresses to follicular scarring and dropout in advanced disease.2 We recently completed the first genome-wide association study (GWAS) in FFA coupled with transcriptomic and metabolomic analyses, which have provided important insights into its pathogenesis.3 We have conducted and herein present a descriptive cross-sectional study of the clinical phenotype in women from the FFA UK GWAS Cohort. Patients with a formal diagnosis of FFA made by a consultant dermatologist from 20 secondary care dermatology departments across the UK were eligible for inclusion. In keeping with the immune-mediated pathogenesis of FFA, 20-7% of participants reported at least one comorbid autoimmune disease (Table 1). [Extracted from the article] |
Databáze: |
Complementary Index |
Externí odkaz: |
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