pituitrin and Klinefelter-Syndrome

We studied plasma vasopressin concentrations during hypertonic saline infusions in 5 men with hypogonadism and 10 normal men to investigate the effect of gonadal steroid on hypothalamo-neurohypophyseal function. All the subjects received the infusion of 5% saline, and plasma vasopressin concentrations were determined by radioimmunoassay (RIA). Three of the 5 men were patients with isolated hypogonadotropic hypogonadism (IHH) and the other two were patients with Klinefelter's syndrome. None of them had any symptoms of diabetes insipidus. Although there was no difference between basal plasma osmolality in the patients and the normal subjects (287.2 +/- 2.1 vs. 285.3 +/- 1.8 mmol/kg), the basal level of plasma vasopressin in the patients was lower than that in the normal subjects (0.62 +/- 0.17 vs. 1.36 +/- 0.15 pg/ml, P < 0.05). Hypertonic saline infusion revealed varying degrees of subnormal vasopressin responses in the patients except one patient with Klinefelter's syndrome. The mean vasopressin response to osmotic stimuli (delta plasma vasopressin/delta plasma osmolality) in the 5 patients was lower than in the normal subjects (0.04 +/- 0.01 vs. 0.16 +/- 0.02, P < 0.05). Three patients with IHH and one patient with Klinefelter's syndrome were re-examined after pulsatile gonadotropin-releasing hormone (GnRH) infusion or testosterone enanthate i.m. injection. After the treatment with testosterone or GnRH, the response of plasma vasopressin to hypertonic saline infusion was normalized in three patients who had subnormal vasopressin response before treatment (delta plasma vasopressin/delta plasma osmolality: 0.04 +/- 0.01 vs. 0.09 +/- 0.01, P < 0.05). These results suggest that testosterone improves the subnormal vasopressin response to osmotic stimuli in men with hypogonadism.

Topics: Adolescent; Adult; Gonadotropin-Releasing Hormone; Humans; Hypogonadism; Infusions, Intravenous; Injections, Intramuscular; Klinefelter Syndrome; Male; Osmolar Concentration; Saline Solution, Hypertonic; Testosterone; Vasopressins

The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease. TRF administration was associated with a mean increment of 267 pg/ml in plasma ACTH concentrations in patients with Nelson's syndrome, and of 42 pg/ml in patients with Cushing's disease. The increment in plasma cortisol concentrations in the latter group was 12 mug%. No ACTH or cortisol response was observed in normal subjects. Patients with Cushing's disease or Nelson's syndrome exhibited significantly greater increments in plasma ACTH concentrations in response to vasopressin administration (P less than .05, P less than .02 respectively) than did normal subjects; the increment in cortisol concentration was also greater, (P less than .05), in patients with Cushing's disease than in normal subjects. No significant difference was present between patients with Cushing's disease and Nelson's syndrome with regard to the magnitude of the ACTH response to vasopressin administration. In contrast, the increment in plasma cortisol and plasma ACTH concentrations following insulin induced hypoglycemia was significantly less in patients with Cushing's disease than seen in normal subjects, (P less than .001, P less than .05 respectively); while this stimulus was associated with a significantly greater increment in plasma ACTH concentrations in patients with Nelson's syndrome as compared to that seen in normal subjects, (P less than .01) and in patients with Cushing's disease (P less than .01). These findings indicate that pituitary function in patients with Nelson's syndrome is not autonomous and suggest the possibility that altered central nervous regulatory mechanism might play a role in the etiology of the pituitary tumors which are frequently associated with this syndrome. The TRF induced rise in plasm cortisol and ACTH concentrations in patients with Cushing's disease and Nelson's syndrome suggests the possibility of altered hypothalamic or pituitary receptors in such patients.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Female; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Klinefelter Syndrome; Male; Middle Aged; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone; Vasopressins