Androsterone, urinary excretion

Overall, other adrenal androgens also show a progressive decrease in urinary excretion in both men and women. Thus, the mean 17-ketosteroid urine levels of elderly people are about 50% of those in young adults. This is primarily secondary to decreased dehydroepiandrosterone (DHEA) and androsterone production. In men, about one-third of the daily 17-ketosteroids are of testicular origen, the remainder being mainly from the adrenals. Androstenedione is a prehormone for testosterone. 

Cll. Cleary, R. E., and Pion, R. J., Urinary excretion of 16a-hydroxydehydroepi-androsterone and 16-keto-androstenediol during the early neonatal period. J. Clin. Endocrinol. Metab. 28, 372-378 (1968). 

Urinary ll-deoxy-17-ketosteroids (dehydroeplandrosterone (D), etiocholanolone (E), androsterone (A) excretion after treatment with combination FSH and LH fractions (HMG)... 

An estimate of the maximum daily production of testosterone of a normal adult male was made by the slow intravenous infusion of 11 mg. of testosterone-D and the isolation of labeled androsterone and etiocholano-lone from the urine during the period of administration, Calculations based on this conversion and this subject s normal urinary excretion of androsterone give a daily testosterone secretion of approximately 15 mg. as a maximal value. 

The elimination of the side chain, which here leads to the synthesis of a hormone, is on the other hand a catabolic reaction for the adrenal cortical hormone 17-hydroxy-l 1-deoxycorticosterone. As we have mentioned, the hormones are inactivated by reduction in ring A. The urinary excretion product androsterone is formed by the oxidative loss of the side chain at C-17 and reduction of ring A. 

In a study in which individual urinary components were determined and repeated samples from the same individuals analyzed, Dobriner and co-workers23 found that the androsterone excretion in twenty normal males 21 to 76 years of age varied from 0.2 to 7.0 mg. per day, a 35-fold range. Age was a factor in contributing to the wideness of this range, since older individuals tended to excrete less, but each individual s androsterone excretion was distinctive, and large differences which were truly inter-individual were observed. One man of 72 excreted, for example, more than twice as much as one who was 21 years old. This study will be referred to further in a later discussion (p. 101). 

Patients with a complete block have almost undetectable excretions of cortisol metabolites. The major urinary steroids are androsterone, etiocholanolone, tetrahydro-... 

The composition of the excreted urinary 17-ketosleroids also reveals a close similarity between the hormones of different origin the testis accounts for 30% while the adrenal cortex contributes the remaining 70% of the total urinary 17-ketosteroids [383]. Androsterone, ep a-androsterone, and 5/8-androsterone (etiocholanolone) are the main urinary metabolities of testosterone, and dehydroepiandrosterone is the major urinary 17-ketosteroid derived from the adrenal cortex. 

Fia. 7. Urinary steroid spectrum in Cushing s syndrome. Upper curve attenuation 10 X 4. Lower curve attenuation 10 X 16 K = 17-ketosteroid excretion (mg/24 hours) H = ketogenic steroid excretion (mg/24 hours) Peaks 1, oxyandrostane 2, eticholanolone S, androsterone and dehydroisoandrosterone 4, ll-oxy-17-keto-steroids S, /3-cortol compounds 6, cholesterol. Reproduced from Hoek and van Kampen (H8) with permission. 

There seems to be a correlation between the absence of progestational activity and the increased excretion of urinary 11-deoxy-17-ketosteroids (dehydroepiandrosterone, etiocholanolone, androsterone) in the absence of ovulation. 

It has been known for quite some time that the administration of testosterone resulted in increased urinary a-ketosteroid (3a-hydroxy-17-ketosteroids) excretion and only a very small increase in the /8-keto-steroid (3/3-hydroxy-17-ketosteroids) and nonketonic steroid fractions. Careful chemical separation and characterization have shown that after the administration of testosterone (L) to normal and diseased human subjects and other mammals, increased amounts of androsterone (XLVIII)... 

Adrenocortical Tumors. Virilization, hypercortisolism, feminization, abdominal pain, palpable abdominal tumor, or combinations of these features are clinical symptoms of adrenocortical tumors. Both types of adrenocortical tumors (carcinoma and adenoma) can produce a wide variety of steroid hormones. This is a consequence of multiple enzyme deficiencies in tumor tissues. The tumor cells are capable of synthesizing large amounts of steroid hormone precursors independent of ACTFI stimulation. Excessively high amounts of DHEA and other 3p hydroxy-5-ene steroids characterize the urinary steroid profile in children with adrenocortical carcinoma, but similar profiles can also be produced by adrenal adenomas. Elevated lip hydroxy-androsterone excretion alone or combined with high excretion of cortisol metabolites or 3p hydroxy-5-ene steroids are characteristic of the urinary steroid profile for adrenocortical adenomas [36,37]. 

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