<jats:title>Abstract.</jats:title> <jats:p>In patients with anorexia nervosa 24-h mean plasma concentration of cortisol were 0.44± 0.09 μmol/l (normal < 0.28 μmol/l). Following stimulation by ACTH (1–24) urinary excretion rates of cortisol were stimulated from 0.22 ± 0.08 to 4.85 ± 2.78 μmol/24 h. Similarly, plasma concentrations of the glucocorticoid metabolite, tetrahydrocortisone, increased from 23.3 ± 9.0 to 47.3 ± 30.2 nmol/l; urinary excretion rates of tetrahydrocortisone increased from 3.61 ± 0.90 to 8.40 ± 1.72 μmol/24 h. The relative share of the sulphate, glucuronide and free fractions of tetrahydrocortisone in the patients' urine did not indicate any defect in metabolization of this steroid metabolite. Excretion rates of the four glucocorticoid tetrahydro-metabolites, tetrahydrocortisone, allotetrahydrocortisone, tetrahydrocortisol, and allo-tetrahydrocortisol, expressed as percent of total steroid excretion, were similar in patients with anorexia and in healthy women under basal conditions (24 ± 6 vs 23 ± 6%) and during stimulation by ACTH (1–24) (36 ± 10 vs 45 ± 6%). The share of the two androgen metabolites, androsterone and etiocholanolone, was 24 ± 5% of total steroid excretion (basal; healthy women: 27 ± 8%) and 13 ± 2% (ACTH stimulation; healthy women: 12 ± 4%) in patients with anorexia nervosa. Thus, analysis of urinary steroid excretion rates did not indicate a shift in adrenocortical function. The results confirmed enhanced secretion of cortisol in patients with anorexia nervosa under basal conditions and during/following stimulation by ACTH. The ACTH-induced increase in the concentrations of the tetrahydro-glucocorticoid metabolites in urine was less pronounced than that of cortisol. The data strongly suggest a rate-limiting step in the transformation of cortisol into its main metabolites, most likely an impaired reduction of the double bond in positions C4/C5.