Plasma Testosterone in Normal Subjects and in Patients with Various Endocrine Disorders

Abstract

Plasma testosterone levels were measured by radioimmunoassay in 43 normal subjects and in 108 patients with various endocrine disorders. They consist of patients with panhypopituitarism, Kallmann's syndrome, Fröhlich's syndrome, idiopathic hypogonadotropic hypogonadism, Sheehan's syndrome, pituitary dwarfism, Klinefelter's syndrome, ovarian dysgenesis, Cushing's syndrome, Addison's disease, primary aldosteronism, congenital adrenal hyperplasia, 17α-hydroxylase deficiency, hyperthyroidism, primary hypothyroidism, idiopathic diabetes insipidus, acromegaly, precocious puberty, anorexia nervosa, simple obesity and idiopathic hirsutism. Base line plasma testosterone levels ranged from 273 to 1131 ng/100 ml with a mean of 568±208 (SD) in 25 normal males aged from 14 to 67, and from 20 to 56 ng/100 ml with a mean of 33±14 (SD) in 18 normal females aged from 17 to 53.
In patients with secondary hypogonadism due to panhypopituitarism, Kallmann's syndrome, Fröhlich's syndrome, idiopathic hypogonadotropic hypogonadism, Sheehan's syndrome and pituitary dwarfism, plasma testosterone levels were lower than normal or low normal in both males and females. In patients with primary hypogonadism, plasma testosterone levels were lower than normal or low normal in Klinefelter's syndrome, and normal or low normal in ovarian dysgenesis.
In female patients with Cushing's syndrome due to adrenocortical hyperplasia, plasma testosterone levels were higher than normal. They were suppressed by 8 mg of dexamethasone and increased slightly by 1 mg of ACTH-Z. On the contrary, plasma testosterone levels in female Cushing's syndrome due to adrenal tumor were normal or lower than normal. They results suggest that the estimation of peripheral plasma testosterone could be helpful in determining the etiology of Cushing's syndrome in female patients.
In patients with Addison's disease, plasma testosterone levels were normal in males and were significantly low in females.
The mean plasma testosterone level in female patients with anorexia nervosa was higher than the normal mean in contrast with significant low levels of plasma testosterone in patients with Sheehan's syndrome.
In female patients with simple obesity, plasma testosterone levels were higher than normal and were suppressed to the normal range by l mg of dexamethasone.
Plasma testosterone levels were increased significantly after administration of HCG, 4,000 units daily for 3 days intramuscularly, in normal males. They were not increased in male patients with hypogonadism of any etiology. It was possible to differentiate more clearly the patients with hypogonadism with border-line testosterone levels from normal subjects by a response of plasma testosterone to HCG administration. However, it was impossible to differentiate the secondary hypogonadism from the primary hypogonadism by present way of administration of HCG.
Clomiphene citrate, 150 mg daily for 3 days administered orally, stimulated the pituitary-Leydig cell axis in normal male subjects. On the 2nd day after cessation of administration of clomiphene, plasma testosterone levels were increased by 50% while plasma LH levels were increased by 110%. In a male patient with Frohlich's syndrome clomiphene stimulated neither plasma LH nor testosterone secretion.
Intravenous injection of 100 μg of synthetic LH-RH induced a significant rise in plasma LH by 350% and plasma testosterone by 120% in normal males. The peaks of plasma LH were observed between 20 and 45 min. after i.v. injection of LH-RH while the peaks of testosterone were observed between 20 to 60 min. In a male patient with Frohlich's syndrome, plasma testosterone level was not increased after injection of LH-RH, although plasma LH was increased significantly. In patients with Klinefelter's syndrome,