Cross-sectional study of blood biomarkers of patients with moderate to severe alopecia areata reveals systemic immune and cardiovascular biomarker dysregulation - 11/01/21
Abstract |
Background |
Although there is increased understanding of the alopecia areata (AA) pathogenesis based on studies in scalp tissues, little is known about its systemic profile.
Objective |
To evaluate the blood proteomic signature of AA and determine biomarkers associated with increased disease severity.
Methods |
In a cross-sectional study, we assessed 350 inflammatory and cardiovascular proteins using OLINK high-throughput proteomics in patients with moderate to severe AA (n = 35), as compared with healthy individuals (n = 36), patients with moderate to severe psoriasis (n = 19), and those with atopic dermatitis (n = 49).
Results |
Seventy-four proteins were significantly differentially expressed between AA and control individuals (false discovery rate, <.05) including innate immunity (interleukin [IL] 6/IL-8), T helper (Th) type 1 (interferon [IFN] γ/CXCL9/CXCL10/CXCL11), Th2 (CCL13/CCL17/CCL7), Th17 (CCL20/PI3/S100A12), and cardiovascular-risk proteins (OLR1/OSM/MPO/PRTN3). Eighty-six biomarkers correlated with AA clinical severity (P < .05), including Th1/Th2, and cardiovascular/atherosclerosis-related proteins, including SELP/PGLYRP1/MPO/IL-18/OSM (P < .05). Patients with AA totalis/universalis showed the highest systemic inflammatory tone, including cardiovascular risk biomarkers, compared to control individuals and even to patients with atopic dermatitis and those with psoriasis. The AA profile showed some Th1/Th2 differences in the setting of concomitant atopy.
Limitations |
Our analysis was limited to 350 proteins.
Conclusion |
This study defined the abnormalities of moderate to severe AA and associated circulatory biomarkers. It shows that AA has systemic immune, cardiovascular, and atherosclerosis biomarker dysregulation, suggesting the need for systemic treatment approaches.
Le texte complet de cet article est disponible en PDF.Key words : Alopecia areata, atherosclerosis, atopic dermatitis, biomarkers, blood, cardiovascular, inflammation, OLINK, proteomics, psoriasis
Abbreviations used : AA, AD, AT, AU, CVD, DEP, FDR, GSVA, IFN, IL, MMP, MPO, SALT, SCORAD, Th
Plan
Funding sources: None. |
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Disclosure: Dr Guttman-Yassky is an employee of Mount Sinai and has received research funds (grants paid to the institution) from AbbVie, Celgene, Eli Lilly, Janssen, MedImmune/AstraZeneca, Novartis, Pfizer, Regeneron, Vitae, Glenmark, Galderma, Asana, Innovaderm, Dermira, UCB and is a consultant for Sanofi Aventis, Regeneron, Stiefel/GlaxoSmithKline, MedImmune, Celgene, Anacor, AnaptysBio, Dermira, Galderma, Glenmark, Novartis, Pfizer, Vitae, Leo Pharma, AbbVie, Eli Lilly, Kyowa, Mitsubishi Tanabe, Asana Biosciences, and Promius. Dr Krueger has received research support (grants paid to his institution) and/or personal fees from Pfizer, Amgen, Janssen, Lilly, Merck, Novartis, Kadmon, Dermira, Boehringer, Innovaderm, Kyowa, Bristol Myers Squibb, Serono, Biogen Idec, Delenex, AbbVie, Sanofi, Baxter, Paraxel, Xenoport, and Kineta. Authors Glickman and Dubin; Dr Renert-Yuval; Author Dahabreh; Dr Kimmel; Authors Auyeung, Estrada, and Singer; and Dr Pavel have no conflicts of interest to declare. |
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IRB approval status: Reviewed and approved by Department of Dermatology at the Icahn School of Medicine (approval protocol HS# 14-00436). |
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Reprints not available from the authors. |
Vol 84 - N° 2
P. 370-380 - février 2021 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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