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Local secretion of stress hormones increases in alopecia areata lesions after treatment with UVA-1 phototherapy.

PMID: 31997403 (view PubMed database entry)
DOI: 10.1111/exd.14077 (read at publisher's website )

Adrian Cuellar-Barboza, Jesus Alberto Cardenas-de la Garza, Luis Gerardo Cruz-Gómez, Oralia Barboza-Quintana, Juan Pablo Flores-Gutiérrez, Minerva Gómez-Flores, Oliverio Welsh, Jorge Ocampo-Candiani, Maira E Herz-Ruelas,

Alopecia areata (AA) is an autoimmune disease of the hair follicle. Keratinocytes of the hair follicle generate an immunosuppressive environment by the local secretion of hormones of the hypothalamic-pituitary-adrenal axis of the skin (skin HPA analog). Our objective was to measure the local production of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and α-melanocyte-stimulating hormone (α-MSH) in the scalp tissue of patients with AA before and after ultraviolet A1 (UVA-1) phototherapy to determine their role in the pathogenesis of AA and the effect of UVA-1 on the AA hormonal environment. This was a retrospective and descriptive study of skin samples from 22 patients with AA before and after UVA-1 treatment. We compared the changes in the local hormonal environment by measuring CRH, ACTH, type 2 melanocortin receptor (ACTH receptor) and α-MSH with immunohistochemical stains. The positivity of MSH was significantly higher (P = .037) in the post-treatment samples compared with the baseline value. ACTH was significantly higher in intensity (P = .032) in the post-treatment samples compared with the initial value. CRH was significantly higher in intensity (P = .013) in baseline samples compared with the final biopsies. The positivity of the ACTH receptor MC2R was not different between the two groups (P = .626). In AA, an interruption in the signalling of CRH could decrease the local concentration of ACTH and MSH, and consequently, the immunosuppressive effect of these hormones. This phenomenon is normalized in the skin treated with UVA-1. A defective signalling system in the cutaneous HPA axis may be involved in the pathogenesis of AA.

Exp. Dermatol. (Experimental dermatology)
[2020, 29(3):259-264]

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