Licorice raises urinary cortisol in man.

The finding that urine cortisol excretion was increased in patients with hypokalaemic hypertension induced by licorice addiction led to this study on the effect of licorice in normal subjects. Thirteen normal volunteers ate either 100 or 200 g licorice for 1-4 weeks and assessment of pituitary-adrenal function was made before, during, and 1 week after cessation of licorice ingestion. Urine cortisol excretion more than doubled in 10 of 13 subjects (mean, 33.8 +/- 15.6 SD before and 83.3 +/- 56 SD micrograms/24 h at 1 week after commencing licorice) and excretion rates similar to those observed in Cushing's syndrome were seen in 7 subjects (range, 91-226, compared to normal range of 11-82 micrograms/24 h). Urine cortisol excretion remained significantly elevated (P less than 0.01) above control levels for at least 1 week after licorice was withdrawn. Despite these increases, urinary steroid metabolite (tetrahydrocortisol, tetrahydrocortisone, tetrahydro-11-deoxycortisol, 17-ketogenicsteroids, and 17-ketosteroids) excretion was not affected, plasma cortisol and ACTH values were unchanged, and normal 0800-1600-h diurnal variation of plasma cortisol was maintained. The direct intraadrenal infusion of the active mineralocorticoid component of licorice, glycyrrhetinic acid, in two sheep with autotransplanted adrenal glands failed to stimulate cortisol secretion acutely. It is concluded from these studies that the licorice-induced changes in cortisol excretion are not a result of adrenocoritcal stimulation but more likely represent a change in the renal handling of cortisol.

Response of plasma testosterone, urinary 17-oxosteroids, oestrogens, and androsterone plus aetiocholanolone to human chorionic gonadotrophin in dexamethasone-suppressed men.

The administration of human chorionic gonadotrophin (HCG) to dexamethasone-suppressed men caused parallel changes in the concentration of plasma testosterone and in the urinary output of androsterone+aetiocholanolone, total 17-oxosteroids and oestrogens. Discrepant results occurred in only four of the thirty-seven men tested. With these exceptions, the response to HCG could by followed as well by measuring androsterone+aetiocholanolone, 17-oxosteroid or oestrogen excretion rates as by following plasma testosterone levels. The most sensitive index of response was the rate of appearance of oestrogens in urine, and the next that of androsterone+aetiocholanolone.

The effect of cyproterone acetate on the plasma gonadotrophin response to gonadotrophin releasing hormone.

Cyporterone acetate (100-150 mg daily) was administered to 8 male patients with excessive libido. Within 3 months a significant fall (P less than 0.02) in plasma testosterone was demonstrated. The plasma luteinising hormone (LH) and follicle stimulatin hormone (FSH) responses to gonadotrophin releasing hormone (LH/FSH-RH) were also significantly impaired (P less than 0.05). A direct correlation between the resting plasma testosterone level and the LH response to LH/FSH-RH was demonstrated (r = 0.743). It is concluded that the fall inplasma testosterone levels in patients receiving cyproterone acetate may be attributed to suppression of LH release, rather than an antiandrogen effect on the testis or hypothalamus.