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Urinary TG and fractionated 17-ketosteroid (Drosdowsky) determinations were performed before and after the intramuscular administration of 15,000 IU of human chorionic gonadotropin (hCG) in 10 sexually immature healthy boys and in 12 bilaterally cryptorchid boys. The same basal determinations were made in 11 gonadless girls. Basal serum FSH and LH were determined (by radioimmunoassay) in controls and also in cryptorchid boys. If 15mug/24 h (three SD's of basal excretion in controls) is considered the smallest adequate response, the TG but not the fractionated 17-KS determination assessed fairly well either the presence or the functional capacity of the Leydig cell-containing tissue. Agonadic girls had significantly higher basal excretion of steroids and this is presumably due to their greater absolute body size and to their more advanced bone age.

Two brothers with Reifenstein syndrome underwent LH-RH and HCG tests at various ages ranging from 13 to 17 years. We found that at age 13 the plasma LH and FSH response to one LH-RH injection was normal. After the age of 14, the basal plasma concentration of LH and FSH and their response to LH-RH became elevated. Concomitantly the plasma testosterone levels rose to abnormal levels. These findings are compatible with progressive development of primary gonadal dysfunction and with peripheral insensitivity to testosterone.

The authors present four cases of operatively confirmed anorchism. The plasma levels of testosterone and 11-deoxy-17-ketosteroids and dehydroisoandrosterone in urine were low in all cases. After stimulation with HCG, plasma testosterone levels increased in two cases and did not change in another two. The levels of 11-deoxy-17-ketosteroids and dehydroisoandrosterone in urine did not increase.

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.

Seven oophorectomized patients were administered a total of 60,000 units of human chorionic gonadotropin over a 3-day period, and plasma testosterone levels were obtained. One of the 7 patients demonstrated a definitive response to the hormone but repeat testing proved to be negative. The potential role of luteinizing hormone in the pathogenesis of polycystic ovarian syndrome is discussed and current evidence linking LH to adrenal androgenesis is reviewed. Modifications that may be employed for future study are suggested.