Secretion of Unconjugated Androgens and Estrogens by the Normal and Abnormal Human Testis before and after Human Chorionic Gonadotropin

Abstract

A B S T R A C T The secretion of androgens and estrogens by normal and abnormal testes was compared by determining the concentrations of dehydroepiandrosterone (DHEA), androstenedione (A4A), testosterone (T), estrone (El), and 17f-estradiol (E2) in peripheral and spermatic venous plasma samples from 14 normal men and 5 men with unilateral testicular atrophy. Four normal men and one patient with unilateral atrophy of the testis were given human chorionic gonadotropin (HCG) before surgery. Plasma estrogens were determined by radioimmunoassay; plasma androgens were measured by the double-isotope dilution derivative technique. Peripheral concentrations of these steroids before and after HCG were similar in both the normal men and the patients with unilateral testicular atrophy. In normal men, the mean +SE spermatic venous concentrations were DHEA, 73.1±+11.7 ng/ml; A4A, 30.7±7.9 ng/ml; T, 751±114 ng/ml; Ei, 306±55 pg/ml; and Ea, 1298±216 pg/ml. Three of four subjects with unilateral testicular atrophy had greatly diminished spermatic venous levels of androgens and estrogens. HCG treatment increased In the single subject with an atrophic testis who received HCG, the spermatic venous concentrations of androgens and estrogens were much less than in normal men similarly treated. We conclude that: (a) El is secreted by the human testis, but testicular secretion of El accounts for less than 5% of El production in normal men; (b) HCG stimulation produces increases in spermatic venous estrogens equal to or greater than the changes in androgens, including testosterone; and (c) strikingly decreased secretion of androgen and estrogen by unilateral atrophic human testes cannot be appreciated by analyses of peripheral steroid concentrations.

Testosterone and estradiol are co-secreted episodically by the human testis.

“…Although mean gonadal vein T levels are 200 times the E2 concentrations, the use ofa highly specific antiserum after complete chromatographic separation excluded radioimmunoassay crossreactivity as an explanation for these concordant secretory episodes. Mean gonadal vein T and E2 concentrations in this study are similar to values reported in previous studies in which single blood samples were taken (16)(17)(18). The variation in gonadal vein T and E2 levels among the men studied may represent, in part, dilution of gonadal vein blood by the circulation of small collateral veins.…”

Familial gynecomastia with increased extraglandular aromatization of plasma carbon19-steroids.

“…The plasma E2 levels were disproportionately elevated compared with those of plasma T in both the base-line and the post hCG-treatment samples (17). In addition, there was no abnormal accumulation of plasma DHA, P, 17 Io-L I200 10o 1800 2100 24000300 0600 0900 1200 1500 1800 2100 2400 0300 0600 0900 24-HOUR CLOCK TIME (6). A number of similarities exist between the subjects of the present study and the subject described by Hemsell et al The five affected family members in our study developed gynecomastia at an early age (10-1 1 yr), starting concomitantly with the sexual maturational processes of male puberty.…”

“…The results of the hCG stimulation tests conducted in subjects 111-1 and 111-3 are given in Table IV. The plasma E2 levels were disproportionately elevated compared with those of plasma T in both the base-line and the post hCG-treatment samples (17). In addition, there was no abnormal accumulation of plasma DHA, P, 17 Io-L I200 10o 1800 2100 24000300 0600 0900 1200 1500 1800 2100 2400 0300 0600 0900 24-HOUR CLOCK TIME (6).…”

“…Gynecomastia is a common finding among pubertal boys; usually, it is limited to a nodule of subareolar tissue, and ordinarily the breast enlargement begins during the early stages of the pubertal process and thereafter regresses within [6][7][8][9][10][11][12][13][14][15][16][17][18] mo. Levels of plasma testosterone (T),' estradiol-17# (E2), serum luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in boys with pubertal gynecomastia are not significantly different from those in unaffected boys (1), although a relative increase in the level of plasma E2 compared with that of T during certain times of the day has been found (2).…”

Endocrinology of gynaecomastia

“…Human chorionic gonadotrophin (hCG) produced by germ cell tumours stimulates testicular steroids by uninvolved testicular tissue but oestradiol is produced in dispropor-tionate amounts compared with testosterone. 47 Leydig and Sertoli cell tumours are unusual forms of testicular tumours (< 5%) which oestrogenize by secreting oestradiol. 48,49 The oestrogen/androgen ratio in these patients is enhanced by oestradiol inhibition of the activity of 17,20-lyase and 17a -hydroxylase, both of which are critical for the synthesis of testosterone.…”