Androgen metabolism by isolated hairs from women with idiopathic hirsutism is usually normal.

We have tested the hypothesis that idiopathic hirsutism (IH) may be due to abnormality of androgen-responsive hair follicles. Because androgen metabolism within target cells is an important determinant of androgen action, we have analyzed the rates of formation and disposition of the major mediators of androgen action, testosterone (T) and dihydrotestosterone (DHT). In normal women, the pattern of androgen metabolism by growing hairs favors T predominance over DHT and inactivation of both these 17 beta-hydroxysteroids to 17-ketosteroids. This pattern results greatly from predominance of 17 beta-hydroxysteroid dehydrogenation. For example, in normal women's scalp hair, DHT disposition to 5 alpha-androstanedione proceeded at the rate of 8.6 +/- 2.0 (SEM) %/micrograms DNA/min, whereas DHT was formed from T at a rate of 0.14 +/- 0.02, and T was formed from androstenedione at a rate of 0.60 +/- 0.12, all significantly different from one another. Both the formation of 17-ketosteroids and the apparent 5 alpha-reductase activity were exaggerated in the pubic hair of men; whether these differences are site-, sex-, or androgen-related, remains to be determined. Pubic hairs tended to metabolize androgens at a greater rate than did scalp hair. This was related to the significantly greater DNA content of plucked pubic hairs, a difference unrelated to sex or androgen levels. Women with IH had heterogeneous pubic hair abnormalities. Only 1 of the 4 IH patients studied had abnormal pubic hair follicle androgen metabolism, with the greatest abnormality being an exaggerated rate of 17 beta-hydroxysteroid inactivation to 17-ketosteroids. Two of the other 3 IH cases had increased DNA content of plucked pubic hairs, a different kind of exaggeration of normal, which suggests an abnormality of hair follicle growth unrelated to androgen sensitivity. We favor the concept that IH is related to various distinct types of sexual hair abnormalities which reflect fundamental defects in the regulation of hair growth.