We investigated the developmental patterns of 5 alpha-androstane-3 alpha, 17 beta-diol (AD) and 5 alpha-androstane-3 alpha, 17 beta-diol-glucuronide (ADG) in plasma of normal children and adults of both sexes and in patients with idiopathic hirsutism using a physicochemical method: high-resolution gas chromatography/mass spectrometry (HRGC/MS). In children below the age of 11 years, AD and ADG increased with age showing no differences between sexes (mean +/- SD, nmol/l): normal subjects 3-6 years: AD in females 0.08 +/- 0.03, in males 0.07 +/- 0.03; ADG in females 0.15 +/- 0.05, in males 0.14 +/- 0.04; normal subjects 7-10 years; AD in females 0.17 +/- 0.03, in males 0.17 +/- 0.07; ADG in females 0.59 +/- 0.12, in males 0.47 +/- 0.14. Thereafter, AD and ADG showed a greater increase in males (normal subjects 11-15 years: AD in females 0.24 +/- 0.06, in males 0.41 +/- 0.14; ADG in females 1.47 +/- 0.36, in males 3.36 +/- 1.22). In adults, plasma levels did not overlap between females and males (AD in females 0.24 +/- 0.07, in males 0.99 +/- 0.31; ADG in females 2.32 +/- 0.68, in males 13.01 +/- 3.05). 5 alpha-Androstane-3 alpha, 17 beta-diol-glucuronide discriminated better between sexes than AD. In idiopathic hirsutism, mean plasma concentrations of AD and ADG were higher than those of healthy females (ages 11-15 years: AD 0.31 +/- 0.10, ADG 3.48 +/- 2.00; ages > 16 years: AD 0.44 +/- 0.27, ADG 6.46 +/- 3.11), but 54% of patients had normal plasma concentrations of AD and 29% had normal ADG values. Thus, ADG reflected androgenicity better than AD. However, both metabolites were imperfect markers of androgenicity in idiopathic hirsutism. Therefore, our findings do not support the concept of increased 5 alpha-reductase activity in all patients with idiopathic hirsutism.