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At least 865 records · Page 48Linked to original sources
PubMed1981

Steroid secretion by masculinizing and "feminizing" Hilus cell tumors.

The clinical course, histology, and steroid secretion observed in two patients with hilus cell tumors are presented. One patient had signs of virilism and the other had estrogenic signs only. Steroid secretion was examined by measuring peripheral and ovarian venous gradients and pre- and postoperative levels of hormones to explain the profound differences in the biological effects exerted by the neoplasms. In the patient with virilism, the tumor's major secretory product was testosterone (T), and the dominant biosynthetic pathway was pregnenolone (Pe) leads to 17-hydroxypregnenolone leads to 17-hydroxyprogesterone leads to androstenedione (delta) leads to T. In the patient with estrogenic signs, the major secretory product was delta, derived from a similar pathway of pregnenolone leads to 17-hydroxypregnenolone leads to 17-hydroxyprogesterone leads to delta. Circulating estrone and estradiol levels were elevated, but the tumor showed limited aromatase activity, as reflected by 60- to 1500-fold larger peripheral-ovarian venous gradients of delta and T than estrone and estradiol. The high circulating estrogen levels mainly arose from the peripheral aromatization of the increased secretion of delta by the tumor. It was concluded that a similar steroidogenic pathway was employed by both tumors. The predominant secretion by the neoplasm of either T of delta was determined by the presence and the oxidation reduction equilibrium of the 17 beta-dehydrogenase enzyme. The action of this enzyme resulted in profound differences in the biological effects exerted by these tumors.

Aged↗
PubMed1984

Morphometry and histology of gonads from twelve children and adolescents with the androgen insensitivity (testicular feminization) syndrome.

Gonadal histology was investigated by means of stereology and Conventional microscopy in 12 patients, aged 2 months to 19 yr, with the androgen insensitivity syndrome (AIS). Eight patients had the incomplete variant of the syndrome and 4 patients had the complete form. Testicular tissue was removed as a prophylactic measure in all patients. In 6 patients less than 5 yr of age testicular histology was normal, except for slightly decreased mean tubular diameters, and, in 1 of the patients, abnormal morphology of the germ cells including a carcinoma-in-situ pattern. The number of germ cells was within the normal range in these 6 patients. In contrast, in older patients (greater than 7 yr of age), germ cells were absent or present only in small foci. In patients with the complete AIS the testicular histology also was immature after puberty, whereas some maturation and subsequent degeneration was found in adolescent patients with the incomplete form of the syndrome. In addition, 2 of these latter patients had a carcinoma-in-situ germ cell pattern. Although patients with the AIS have no reduction of the number of germ cells during the first years of life, this syndrome is associated with abnormal morphology of the germ cells, including patterns of carcinoma-in-situ and impaired pubertal maturation of the seminiferous tubules and the germ cells, in older patients.

Adult↗
PubMed1987

Feminizing testicular Leydig cell tumor: hormonal profile before and after unilateral orchidectomy.

The effect of chronic hyperestrogenism on gonadal function was studied in three men who had estrogen-secreting Leydig cell tumors before unilateral orchidectomy and for 11-43 months after surgery. All three men had low plasma gonadotropin and testosterone levels and increased estradiol levels. Impairment of testicular steroidogenesis was also suggested by increased progesterone to 17-hydroxyprogesterone and 17-hydroxyprogesterone to androstenedione ratios in both spermatic venous plasma and the medium of Leydig tumor cells from one patient incubated in vitro. Before surgery, spermatogenesis was abnormal in two men. Testicular endocrine function and spermatogenesis did not return to normal after surgery. During the follow-up period, plasma gonadotropin levels were high in all three men, and testosterone was low normal. Estradiol levels decreased to normal immediately after surgery and then returned to the upper normal limit. The response to hCG stimulation in one man was subnormal. We conclude that chronic hyperestrogenism produced hypothalamo-pituitary inhibition as well as direct steroidogenic blockade at the testicular level. Long term impairment of both endocrine and exocrine testicular functions may be secondary to slowly reversible (or irreversible) estrogen-induced damage to tubular and Leydig cells.

Adult↗
PubMed1990

Feminizing adrenocortical tumor: steroid hormone response to ketoconazole.

A 58-yr-old man presented with gynecomastia and elevated serum estrogens. The diagnosis of an estrogen-secreting adrenal tumor was made based upon the finding of a 4-cm left adrenal mass, elevated levels of estradiol in peripheral and left adrenal venous blood, and increased urinary 17-ketosteroids. In addition to marked elevations in estradiol and 17-ketosteroids there was an increased baseline level of 11-deoxycorticosterone and a slightly decreased level of 18-hydroxycorticosterone, suggesting the possibility of impaired P450c11 activity. The effect of ketoconazole administration (600 mg/day) for 4 weeks was studied. Urinary free cortisol and 17-ketosteroid excretion and serum testosterone levels fell acutely (1 week). Serum estradiol levels decreased gradually over the 4-week course. Plasma aldosterone levels were essentially unaltered and 18-hydroxcorticosterone levels fell gradually, but there were marked increases in 11-deoxycorticosterone and corticosterone. Coincident with the increase in 11-deoxycorticosterone there was an increase in blood pressure and a transient fall in serum potassium. We conclude that ketoconazole administration may result in a hypermineralocorticoid state. Therefore, the usefulness of ketoconazole therapy for steroid hormone-producing neoplasms will depend upon the individual tumor's steroidogenic profile.

17-Ketosteroids↗