Contribution of Plasma Androstenedione to 5α-Androstanediol Glucuronide in Women with Idiopathic Hirsutism

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Abstract
To confirm that plasma Δ4 androstenedione (Δ4) is the main precursor for 5α-androstane-3α, 17β-diol glucuronide (Adiol G) in patients with idiopathic hirsutism (IH), Δ4 was cutaneously applied to five normal women and five women with IH. Several parameters of androgen metabolism were assayed basally and throughout the studies. Those included plasma Δ4, testosterone, and dihydrotestosterone as well as urinary Adiol G and testosterone glucuronide excretion. Under basal conditions plasma testosterone, Δ4, and dihydrotestosterone did not differ significantly between the two groups of subjects. Urinary Adiol G excretion was significantly higher (P < 0.01) in IH patients [123 ± 36 (SE) µg/24 h] than in the normal women group (45 ± 20 µg/24 h). After percutaneous administration of Δ4, plasma Δ4 increased in both groups by nearly 600% and there was a 300% increase in Adiol G excretion in IH patients (336 ± 57 µg/24 h), whereas only a 50% increase occurred in normal women (65 ± 17 µg/24 h). We postulate that plasma Δ4 may be the main precursor accounting for the increased production of urinary Adiol G in women with IH, in whom hirsutism may be due to a high 5αreductase activity. Indeed, 5α-reductase as measured in vitro in pubic skin was significantly higher in hirsute patients (224 ± 66 fmol/mg skin · h) than in normal women (45 ± 15 fmol/mg skin · h).

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