Alopecia areata and Affected Skin CRH Receptor Upregulation Induced by Acute Emotional Stress

Background: Recent evidence indicates that acute stress can precipitate a number of dermatological conditions, including alopecia areata. This effect may be mediated by corticotropin-releasing hormone (CRH) released locally in the skin from dorsal root ganglia or immune cells. CRH typically acts thr...

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Veröffentlicht in:Dermatology (Basel) 2001-01, Vol.203 (2), p.157-161
Hauptverfasser: Katsarou-Katsari, Alexandra, Singh, Leena K., Theoharides, Theoharis C.
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Sprache:eng
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Zusammenfassung:Background: Recent evidence indicates that acute stress can precipitate a number of dermatological conditions, including alopecia areata. This effect may be mediated by corticotropin-releasing hormone (CRH) released locally in the skin from dorsal root ganglia or immune cells. CRH typically acts through activation of specific receptors that are either type 1 or types 2α and 2β. CRH, or related peptides such as urocortin, could have proinflammatory effects directly or through activation of mast cells leading to destruction of the hair root. Objectives: To investigate the expression of CRH receptors on the affected skin of patients who developed alopecia areata following acute emotional stress. Methods: Scalp skin biopsies were obtained from 1 normal volunteer and 3 patients after ring infiltration of the relevant site with lidocaine. The biopsies were frozen and were later processed for in situ hybridization for CRH receptors type 1 or types 2α and 2β. Sections showing positive results were photographed. Results: The skin from the normal volunteer showed weak background expression of all three receptor types. However, skin from the affected sites of all 3 patients studied showed intense expression only on the type 2β receptor around the hair follicles. Conclusion: Acute emotional stress may precipitate alopecia areata by activation of overexpressed type 2β CRH receptors around the hair follicles leading to intense local inflammation.
ISSN:1018-8665
1421-9832
DOI:10.1159/000051732