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Immunoreactivity of corticotropin‐releasing hormone, adrenocorticotropic hormone and α ‐melanocyte‐stimulating hormone in alopecia areata
Author(s) -
Kim Hei Sung,
Cho Dae Ho,
Kim Hee Jung,
Lee Jun Young,
Cho Baik Kee,
Park Hyun Jeong
Publication year - 2006
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2006.00001.x
Subject(s) - medicine , adrenocorticotropic hormone , endocrinology , alopecia areata , pathogenesis , melanocyte stimulating hormone , hormone , proopiomelanocortin , corticosterone , scalp , corticotropin releasing hormone , immunology , dermatology
Psychological factors are believed to play a role in the pathogenesis of alopecia areata (AA), a frequently encountered hair disorder. In our study, statistically significant elevation of psychological stress was felt by AA patients prior hair loss compared with control, which was strongly believed contributory to hair loss ( t ‐test, P < 0.01). The corticotropin‐releasing hormone (CRH) and proopiomelanocortin (POMC) mRNA have been identified in the basal layer of the epidermis and pilosebaceous units of the normal scalp. And with the recent discovery of melanocytes and dermal fibroblasts capable of corticosterone production, the presence of a local stress response system resembling the hypothalamic–pituitary–adrenal (HPA) axis has been suggested. The local stress response system is involved in regulation of the normal hair cycle, but its precise role in AA is unknown. The influence of a local HPA axis or rather, CRH–POMC axis in AA was investigated by analysing immunohistochemically the expression levels of CRH and POMC peptides, including the adrenocorticotropic hormone (ACTH) and α ‐melanocyte‐stimulating hormone ( α ‐MSH), in a number of AA lesions and normal scalp (as control). The epidermis and pilosebaceous units of normal scalp stained weakly with CRH, ACTH and α ‐MSH, whereas those from the affected sites of the AA group showed intense expression of the peptides (chi‐square test, P < 0.01). The meaning of this enhanced expression and their role in the pathogenesis of AA should be further evaluated in future.