Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADENOMA, VIRILIZING”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Virilization due to a Leydig cell adrenal adenoma.

Virilizing adrenal adenomas are rare, and Leydig cell adenomas of the adrenal rarer still. Our patient, a 60-year-old virilized woman, was found to have a Leydig cell adenoma. Virilization associated with normal 17-ketosteroid and elevated testosterone levels necessitates excluding an adrenal cause. Although one might expect high testosterone levels to suppress gonadotropins, this is not the case. In addition to other studies recommended for assessing the incidentally discovered adrenal mass, we would add a testosterone assay.

17-Ketosteroids↗

Virilizing adrenocortical adenoma responsive to gonadotrophin.

A virilizing adrenocortical adenoma was demonstrated in a yound female. Urinary 17-ketosteroid excretion and subfractions, plasma testosterone level and urinary 17-ketogenic steroid excretion were markedly increased. Dehydroepiandrosterone was the main constituent of the androgen excess. Otherwise the adrenocortical function was found to be normal as evaluated from measurements of cortisol, corticosterone and their metabolites under basal conditions and during dynamic tests. The androgen excess showed an unexpected response to trophic hormones. Human chorionic gonadotrophin stimulation resulted in a pronounced increase in androgen production, whereas no gonadotrophin-dependency could be demonstrated by means of the oestrogen suppression test. Similarly, no corticotrophin-dependency could be demonstrated by corticotrophin stimulation and suppression tests. Removal of the tumour resulted in normalization of the androgen production and no abnormal response upon human chorionic gonadotrophin administration could now be found. The inappropriate response of tumours to trophic hormones is discussed. It is concluded that the reliability of stimulation and suppression tests in determining the site of excessive androgen production should be accepted with reservation.

11-Hydroxycorticosteroids↗

Enzyme histochemical and electron microscopic study of a virilizing adrenocortical adenoma.

Enzyme histochemical and ultrastructural studies of a "dexamethasone-suppressed" virilizing adrenocortical adenoma and the attached cortex revealed that tumor cells showed little activities of some lysosomal enzymes and scarcity of lipofuscins and dense bodies of lysosomal type, forming a marked contrast to the cells of zona reticularis and the virilizing adenomas previously reported. The other findings of tumor cells, such as a pattern of activities of dehydrogenases including 3beta-hydroxysteroid dehydrogenase and the morphology of mitochondria, were those of reticularis cells. The findings showed that scantiness of lipofuscins did not rule out the possibility of adenoma producing adrenal androgen, dehydroepiandrosterone. Most of the tumor cells as well as reticularis cells were positive for alkaline phosphatase, the activity of which was interpreted as the effect of ACTH stimulation.

3-Hydroxysteroid Dehydrogenases↗

Virilizing adrenal adenoma stimulated by dexamethasone in a middle-aged woman.

In a middle-aged woman with virilizing adenoma, 2 mg dexamethasone increased urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids, whereas 8 mg dexamethasone increased urinary excretion only of 17-KS. With discontinuation of dexamethasone, 17-KS excretion returned to the predexamethasone level. Dexamethasone depressed the basal level of cAMP synthesis and basal testosterone production by the normal adrenal tissue in vitro. Dexamethasone also depressed the increase of cAMP produced by ACTH in the normal tissue. In contrast, dexamethasone increased basal cAMP synthesis and stimulated testosterone secretion in the tumor tissue. ACTH and dexamethasone were additive in their effects on cAMP and testosterone in the tumor tissue. It is suggested that dexamethasone acted directly on the adrenal tumor to stimulate steroid secretion in this patients.

11-Hydroxycorticosteroids↗

Peripheral steroid levels in a patient with virilizing adrenal adenoma.

The peripheral levels of pregnenolone (delta5-P), 17-hydroxypregnenolone (17-delta5-P), progesterone (P), 17-hydroxyprogesterone (17-P), testosterone (T), 5alpha-dihydrotestosterone (DHT), androstenedione (A), dehydroepiandrosterone (DHEA), its sulfate (DHEA-S), estrone (E1), estradiol-17beta (E2), and cortisol (F) were measured prior to and 1 1/2 and 9 months after removal of a right adrenal "compact cell" adenoma in an amenorrheic patient with a virilizing adrenal adenoma, under the following conditions: 1) control for 2 days, 2) dexamethasone, 0.5 mg, every 6 hours for 2 days, and 3) dexamethasone, 2 mg, every 6 hours for 2 days. Except for E1, E2, and F, the control levels of all steroids measured were elevated, markedly so for delta5-P, 17-delta5-P, DHEA, A, and DHEA-S. Dexamethasone treatment had no detectable effect on the steroid levels. Following removal of the adrenal adenoma, the levels of all steroids returned to normal. The patient became eumenorrheic, with marked improvement of her hirsutism and virilization.

17-alpha-Hydroxypregnenolone↗

Adrenal and sex steroid hormone production by a virilizing adrenal adenoma and its diagnosis with computerized tomography.

The presence of an androgen-secreting tumor in a 29-year-old woman was confirmed and its location was determined by computerized axial tomographic (CAT) scanning. The hormone production from this virilizing adrenal adenoma was studied in vivo and in vitro. The major secretory products of the tumor (as compared to normal adrenal tissue) were testosterone (24-fold) and 17 beta-estradiol (five-fold). Although the adenoma produced lesser amounts of dehydroepiandrosterone sulfate (DHEAS), the demonstration of elevated serum testosterone and DHEAS in serial samples was a better marker for an androgen-secreting adrenal tumor than were the urinary 17-ketosteroids, which remained in the upper limit of normal. The hormone production from the tumor depended neither on adrenocorticotropic hormone nor on human chorionic gonadotropin. The conclusions were that: (1) on the basis of serial measurements of serum testosterone and DHEAS, virilizing adrenal adenomas may be suspected when the concentrations of these hormones reach or exceed 200 ng/dl and 6,600 ng/ml, respectively; (2) the high-resolution CAT scanner can accurately localize these tumors; (3) cosmetic and menstrual dysfunction regressed after resection of the tumor; and (4) virilizing adrenal adenomas may produce both androgens and estrogens.

17-Ketosteroids↗

Virilizing adrenocortical adenoma with Cushing's syndrome, thyroid papillary carcinoma and hypergastrinemia in a middle-aged woman.

We report a rare case of virilizing adrenocortical adenoma complicated with Cushing's syndrome, thyroid papillary carcinoma and hypergastrinemia. A 45-year-old woman had a history of amenorrhea for 10 years, hypertension for 8 years, and diabetes mellitus for 3 years. Physical examination showed a masculinized woman with severe hirsutism, male-like baldness, deep voice, acne in the precordia, and clitorism. Plasma testosterone, DHEA-S and urinary 17-KS were high, and plasma cortisol level was it at the upper limit of the normal range, but it did not show a diurnal rhythm nor was suppressed by 2 and 8 mg of dexamethasone. Abdominal CT scan showed a left adrenal tumor (4.5 cm in size). Adrenal scintigram revealed uptake of the tracer on the left side, and plasma cortisol concentration was high in a blood sample from the left adrenal vein. Left adrenalectomy was performed. Histopathological features of resected adrenal tumor were consistent with those of adrenocortical adenoma, consisting of tumor cells with eosinophilic compact cytoplasm. Immunohistochemical staining for steroidogenic enzymes showed reactivity for P450sec, 3 beta-HSD, P450c17, P450c21 and P450c11. Plasma testosterone and cortisol levels decreased to the normal range postoperatively. The patient was also found to have a papillary thyroid carcinoma and hypergastrinemia. Our patient is a rare case of virilizing adrenocortical adenoma associated with Cushing's syndrome, thyroid papillary carcinoma, and hypergastrinemia.

Adrenal Cortex Neoplasms↗

Virilizing adrenocortical adenoma: in vitro steroidogenesis, immunohistochemical studies of steroidogenic enzymes, and gene expression of corticotropin receptor.

BACKGROUND: No reports have yet precisely determined corticotropin (ACTH) responsiveness in virilizing adrenocortical adenoma. METHODS: Five women with an androgen-secreting adrenal adenoma were reviewed. Three of them were examined by in vitro steroidogenesis. Two of these 3 patients were studied by immunohistochemistry of steroidogenic enzymes and for the gene expression of ACTH receptor by Northern blot analysis. RESULTS: In preoperative hormonal determinations plasma and urine androgens had increased. Dexamethasone did not suppress plasma and urinary androgens, nor did ACTH increase them. In vitro steroidogenesis revealed that the adenoma cells produced mainly dehydroepiandrosterone and a small amount of testosterone. ACTH did not increase the in vitro production of androgens. In immunohistochemical staining 5 enzymes involved in adrenal steroidogenesis were all expressed, especially 17 alpha-hydroxylase, which was strongly expressed in tumor cells. ACTH receptor messenger RNA was not detected in virilizing tumor tissues, whereas it was expressed in attached adrenal tissues. CONCLUSIONS: The lack of response to ACTH is the result of a deficiency of ACTH receptor expression in the virilizing tumor cells. Androgens were autonomously produced in adrenal adenoma cells without ACTH regulation.

17-alpha-Hydroxypregnenolone↗