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Abstract. In a 60 year old virilized woman the plasma testosterone concentration was markedly elevated, whereas the plasma cortisol and ACTH as well as urinary 17-ketosteroids, 17-hydroxycorticoids, pregnanetriol and dehydroepiandrosterone were normal. The plasma levels of LH and FSH were in the post-menopausal range. Dexamethasone suppressed the urinary 17-ketosteroids, 17-hydroxycorticoids and pregnanetriol normally, but had no effect upon the plasma testosterone. These findings led to the tentative diagnosis of an ovarian hilus cell tumour. However, bilateral oophorectomy revealed bilateral hyperthecosis without a tumour and did not result in any decrease of the plasma testosterone level. An attempt of adrenal vein catheterization succeeded only on the left side. The lack of a gradient in the testosterone concentration between blood from the left adrenal vein and a peripheral vein prompted a surgical exploration of the right adrenal gland, which led to the discovery and removal of an encapsulated Leydig cell type adenoma, characterized by Reinke's crystalloids. A testosterone concentration gradient between right adrenal and peripheral venous blood obtained intra-operatively, rapid normalization of the plasma testosterone concentration post-operatively, results of a tumour incubation study as well as the clinical outcome proved that this adenoma had been the source of the excessive androgen. A history of a late menarche and persistent menstrual irregularities together with elevated gonadotrophins in spite of excessive testosterone pointed to the possibility of a longstanding gonadotrophin-dependent gonadal cell population in the adrenal, which was fully activated only by the menopausal gonadotrophin rise.

An 18-year-old male patient was referred because of galactorrhea and delayed puberty. There was no gynecomastia, but a white milky secretion could easily be expressed from each breast. The chest and skull X-rays were normal. The plasma prolactin was increased to 58 ng/ml and rose to 97 ng/ml after 200 microgram TRF iv. The patient was treated for one year with testosterone; his voice deepened, body hair developed, libido and sexual function became overt, and bone age advanced from 14 1/2 to 17 years, but the galactorrhea increased. After a satisfactory stage of pubertal development was reached, the testosterone was stopped. tthe galactorrhea then decreased to its pretreatment intensity; however, sexual potency diminished, sexual hair growth decreased, and the plasma prolactin levels rose to 246 ng/ml. After a 5-month interval without treatment, bromocriptine was given and brought about an impressive improvement. Virilization and general well being were superior to that during testosterone treatment, the galactorrhea vanished, plasma prolactin decreased, testosterone rose to normal values, and a normal semen analysis was recorded.

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