Hirsutism, its pathogenesis

Hirsutism can be regarded as a virilizing symptom and may be defined as a male type of body hair distribution in the female. The pathogenesis of hirsutism may be due to an increased androgen production or to an enhanced sensitivity of the hair follicles in sexual areas. The androgen production in th...

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Bibliographic Details
Published in:Human reproduction (Oxford) 1989-08, Vol.4 (6), p.601-604
Main Authors: Breckwoldt, M., Zahradnik, H.P., Wieacker, P.
Format: Article
Language:English
Subjects:
5α-reductase
androgen metabolism
Female
hirsutism
Hirsutism - etiology
Hirsutism - physiopathology
Humans
hypertrichosis
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Summary:Hirsutism can be regarded as a virilizing symptom and may be defined as a male type of body hair distribution in the female. The pathogenesis of hirsutism may be due to an increased androgen production or to an enhanced sensitivity of the hair follicles in sexual areas. The androgen production in the female depends upon direct secretion by the ovaries and the adrenals and upon peripheral conversion of androgen precursors and finally on the metabolic clearance rate which may be regarded as a function of androgen production. More than 98% of the androgens circulating in the blood are bound to specific plasma proteins such as steroid hormone binding globulin (SHBG), cortisol binding globulin (CBG) and albumin. The synthesis of SHBG is controlled by the ratio of oestradiol to testosterone (T). Elevation of oestrogens results in an increase of SHBG. In hirsutism the plasma concentrations are decreased, resulting in elevated levels of free androgens. The intracellular reduction of T to 5α-DHT (dihydrotestosterone) has to be considered as a basic requirement for the androgen-mediated growth of the hair follicle in sexual skin areas. The sensitivity of these areas for androgen depends upon the activity of the local 5α-reductase. In patients suffering from hirsutism, the conversion rate of T to 5α-DHT is significantly increased, almost reaching male levels. DHT is further metabolized by the target cells to 3α–and 3β–androstanediol and the corresponding glucuronides. The elucidation of its complex pathogenesis is still incomplete; however, the information available so far provides a reasonable basis for further diagnostic and therapeutic approaches
ISSN:0268-1161
1460-2350
DOI:10.1093/oxfordjournals.humrep.a136950