Hirsutism pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
It is speculated that insulin, at high enough concentration, stimulates the ovarian theca cells to produce androgens. There may also be an effect of high levels of insulin to activate the insulin-like growth factor-I (IGF-1) receptor in those same cells. Again, the result is increased androgen production. | It is speculated that [[insulin]], at high enough concentration, stimulates the [[ovarian]] [[Thecal cells|theca]] cells to produce [[androgens]]. There may also be an effect of high levels of [[insulin]] to activate the [[insulin-like growth factor-I]] (IGF-1) receptor in those same cells. Again, the result is increased [[androgen]] production. | ||
Androgens are essential for terminal hair and sebaceous gland development. Androgens transform the vellus hair into a terminal hair. In androgen-sensitive areas before puberty, the hair is vellus and the sebaceous glands are small. In response to increasing levels of androgens , pilosebaceous units become large terminal hair follicles in sexual hair areas or they become sebaceous follicles (sebaceous glands) in sebaceous areas. Androgens promote growth of sexual hair by recruiting a population of pilosebaceous units to switch from producing vellus hairs to initiating terminal hair growth.<ref name="pmid10950157">{{cite journal |vauthors=Deplewski D, Rosenfield RL |title=Role of hormones in pilosebaceous unit development |journal=Endocr. Rev. |volume=21 |issue=4 |pages=363–92 |year=2000 |pmid=10950157 |doi=10.1210/edrv.21.4.0404 |url=}}</ref> | [[Androgens]] are essential for terminal hair and [[sebaceous gland]] development. Androgens transform the [[vellus hair]] into a [[terminal hair]]. In androgen-sensitive areas before [[puberty]], the hair is [[vellus]] and the [[sebaceous glands]] are small. In response to increasing levels of androgens , pilosebaceous units become large terminal [[Hair follicle|hair follicles]] in sexual hair areas or they become sebaceous follicles [[Sebaceous glands|(sebaceous glands]]) in sebaceous areas. [[Androgens]] promote growth of sexual hair by recruiting a population of pilosebaceous units to switch from producing vellus hairs to initiating terminal hair growth.<ref name="pmid10950157">{{cite journal |vauthors=Deplewski D, Rosenfield RL |title=Role of hormones in pilosebaceous unit development |journal=Endocr. Rev. |volume=21 |issue=4 |pages=363–92 |year=2000 |pmid=10950157 |doi=10.1210/edrv.21.4.0404 |url=}}</ref> | ||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Hirsutism is a common disorder of the endocrine system, which affects about 10% of women approximately in the United States. It may indicate a serious or unserious medical condition seen as a serious cosmetic problem. Androgens are required for sexual hair development. Hirsutism can arise from increased androgen production or from increased sensitivity of the hair follicles to circulating androgens. [1]
Pathophysiology
It is speculated that insulin, at high enough concentration, stimulates the ovarian theca cells to produce androgens. There may also be an effect of high levels of insulin to activate the insulin-like growth factor-I (IGF-1) receptor in those same cells. Again, the result is increased androgen production.
Androgens are essential for terminal hair and sebaceous gland development. Androgens transform the vellus hair into a terminal hair. In androgen-sensitive areas before puberty, the hair is vellus and the sebaceous glands are small. In response to increasing levels of androgens , pilosebaceous units become large terminal hair follicles in sexual hair areas or they become sebaceous follicles (sebaceous glands) in sebaceous areas. Androgens promote growth of sexual hair by recruiting a population of pilosebaceous units to switch from producing vellus hairs to initiating terminal hair growth.[2]
References
- ↑ Breckwoldt M, Zahradnik HP, Wieacker P (1989). "Hirsutism, its pathogenesis". Hum Reprod. 4 (6): 601–4. PMID 2674189.
- ↑ Deplewski D, Rosenfield RL (2000). "Role of hormones in pilosebaceous unit development". Endocr. Rev. 21 (4): 363–92. doi:10.1210/edrv.21.4.0404. PMID 10950157.