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Results for “Adrenocortical Hyperfunction”

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At least 289 records · Page 16Linked to original sources
PubMed1996

Persistent and recurrent hypercortisolism after transsphenoidal surgery for Cushing's disease.

After transnasal operations in Cushing's syndrome persisting hypercortisolism either due to negative pituitary exploration or due to subtotal tumor removal, and recurrence of the disease after successful surgery still are challenging. We report on the therapeutic failures among 310 consecutive patients who underwent primary transsphenoidal microsurgery for Cushing's disease. In 287 patients an ACTH-producing pituitary adenoma could be detected (finding rate: 92.6%). In 264 cases remission of hypercortisolism could be attained (remission rate with adenoma 92.0%, for the whole series of primary operations 85.2%). In 23 patients no adenoma could be found despite extensive pituitary exploration (7.4%). Here, we will focus on the management of the 23/287 patients with persistent hypercortisolism after transnasal tumor operation (8.0%) and those 29 cases of the 264 patients with a remission who developed a recurrence of hypercortisolism (11.0%). In recurrent hypercortisolism we recommend transsphenoidal reoperation even when no tumor is visible in MRI. Seventeen of 24 reoperations in recurrent Cushing's disease were successful (70.8%). In persistent hypercortisolism we perform a reoperation during the same hospital stay. Nine of 16 early reoperations led to remission of hypercortisolism (56.3%). If transsphenoidal reoperation fails we indicate radiation therapy of different modalities depending on the extension and location of the tumor remnants. Bilateral adrenalectomy is proposed by us only if all other therapeutic measures failed.

Adrenalectomy↗
PubMed1983

Morphometric investigations into the mechanism of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy.

Compensatory hypertrophy of the remaining gland in unilaterally adrenalectomized rats was investigated by morphometric techniques. It was observed that compensatory adrenal growth occurred in both dexamethasone-treated and hypophysectomized rats, receiving maintenance doses of ACTH. However, it was only half that found in intact animals. These results support the view that activation of the hypothalamo-hypophyseal axis is not the unique mechanism underlying adrenal compensatory hypertrophy in the rat.

Adrenal Glands↗
PubMed1977

Use of 131I-19-cholesterol in functional dynamic studies of the adrenals in vivo. II. Clinical application.

Functional dynamic studies of the adrenal in vivo employing 131I-19-cholesterol were carried out as a further screening test, according to the method previously described (Pavonia and Magrini, 1977), on seven patients in whom hyperadrenocorticism was suspected on the basis of clinical symptoms. The data obtained in basal conditions, under ACTH stimulation, and under dexamethasone suppression, compared with each other and supported by the results of conventional examinations, demonstrate that the quantitative information provided by this radioisotope test is correlated with the functional state of each adrenal, thus confirming the potential value of the method for diagnostic purposes. The functional dynamic test proposed does not require a higher dose of tracer than morphologic studies and the radiation risk (approximately 2.5 rad to the ovaries or gonads) seems acceptable in adult subjects.

Adenoma↗
PubMedDate not supplied

Point mutations of ras genes in human adrenal cortical tumors: absence in adrenocortical hyperplasia.

Point mutations of ras genes (K-, H-, and N-ras) at codons 12, 13, and 61 and of the Gi2 alpha gene at codons 179 and 205, were studied in 56 primary adrenal cortical tumors and 6 adrenal cortical hyperplasias. Of 56 tumors, 24 were carcinomas and 32 were benign. The 24 carcinomas and 20 of the benign tumors were from American patients; the 12 remaining adenomas were from Japanese patients. Of the benign tumors 12 were cortisol-producing adenomas, 15 were aldosterone-producing adenomas, 3 were nonfunctioning adenomas, and 2 were adenomas that produced a virilizing syndrome. Tumor DNA obtained from archival formalin-fixed, paraffin-embedded tissue or fresh frozen tissue was amplified by polymerase chain reaction; and point mutations were detected by sequence-specific oligonucleotide hybridization. Activating ras mutations were found in 7 of 56 (12.5%) of all tumors: 3 of 24 (12.5%) carcinomas and 4 of 32 (12.5%) adenomas. Of adenomas from an American population, 4 of 20 (20%) exhibited positive ras mutations, whereas none was present in the Japanese tumors. All mutations detected were adenine to guanine transitions at the second position of N-ras codon 61, resulting in a conversion from glutamine to arginine. No mutations were found in K-ras or H-ras genes. Furthermore, no mutations of the Gi2 alpha gene were identified. These findings demonstrate that N-ras mutations at codon 61 may contribute to the genesis of both benign and malignant human adrenal cortical tumors. Finally, no mutations of the ras or Gi2 alpha genes were identified in hyperplastic adrenocortical tissues.

Adenoma↗
PubMed1977

Congenital adrenal hyperplasia: renin and steroid values during treatment.

Plasma renin activity (PRA), aldosterone (Aldo), 17alpha-hydroxyprogesterone (17-OHP) and testosterone (T), together with urine sodium, pregnanetriol, 17-oxosteroids and the 11-oxygenation index (11-OH) were estimated in 23 patients (age 5.7--18 yrs.) with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency during glucocorticoid treatment. Elevated PRA levels (1400--17200 ng Al/l/hr) were found in 13 out of 15 patients with a history of salt loss. Three non-salt losers showed high PRA levels and in the remaining 5 the levels were in the upper normal range (540--900 ng Al/l/hr). Plasma Aldo levels were normal (25--620 pmol/l) in 18 patients and slightly elevated (690--2360 pmol/l) in 5. While these results indicate persistent impairment of sodium homeostasis in CAH patients, no significant correlations between log. PRA, log. Aldo and urinary sodium excretion were found. Mid-day 17-OHP levels ranged from 9 to 117 nmol/l and T from 0.3 to 18.0 nmol/l. Neither the 17-OHP nor the T results correlated well with the clinical assessment of therapeutic control. The results of the urinary steroid determinations showed better agreement with the clinical assessment of treatment and the 17-oxosteroid, pregnanetriol and 11-OH index results appeared to be better discriminants between good and poor control. Twelve of the patients with a history of early salt loss were reinvestigated after one month's treatment with oral 9 alpha-flurohydrocortisone (0.05 mg/day). PRA was reduced in 7 patients and 17-OHP fell in 10 patients. No consistent changes were found in Aldo, T, or urinary sodium and steroid excretion during this low-dose mineralocorticoid treatment.

17-Ketosteroids↗
PubMed1976

A test for heterozygocity of 21-hydroxylase deficiency: preliminary report.

The urinary excretion of steroids was studied in 8 parents of children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency of the simple virilizing and of the salt-losing type. Eight parents of normal children served as controls. 24-hour urines before and after the injection of 40 IU of ACTH were fractionated using gas liquid chromatography on glass capillary columns. Before stimulation no excretion of pregnanetriolone was detected in heterozygous and in normal parents. Following ACTH only heterozygotes showed an excretion of pregnanetriolone in the urine. This averaged 289 mug per 24 h. Employing gas liquid chromatography on glass capillary columns heterozygous carriers of congenital adrenal hyperplasia due to 21-hydroxylase deficiency may reliably be detected by their increased urinary excretion of pregnanetriolone following ACTH.

Adrenocortical Hyperfunction↗
PubMed1979

Sex hormones and female homosexuality: a critical examination.

To ascertain the validity of hormonal theories of human homosexuality, which are based on animal research, this article reviews psychoendocrine data on lesbian and transsexual women. Sex hormone levels were found to be normal in the majority of homosexual women, but about a third of the subjects studied had elevated androgen levels. In women with prenatal androgen excess, heterosexuality appears to be more frequent than bisexuality, and exclusive homosexuality is rare. Two recent reports suggest abnormalities of the neuroendocrine regulation of LH secretion in female transsexuals. Clearly, prenatal or postpubertal hormone levels do not determine the development of sexual orientation, but a facilitating neuroendocrine predisposition cannot be ruled out at present.

Adrenal Hyperplasia, Congenital↗
PubMed1990

Concurrent hypercortisolism and hyperaldosteronism due to an adrenal adenoma.

The case of a 39-year-old woman with Cushing's syndrome, hypertension and severe hypokalemia, caused by a unilateral adrenal adenoma composed of cells of the zona fasciculata histological type, is described. Plasma renin activity, plasma levels of mineralocorticoids and the aldosterone secretion rate were determined before and after surgical removal of the adenoma. The tumor appeared to produce autonomously cortisol as well as corticosterone, 18-hydroxycorticosterone and aldosterone. This condition has not previously been described in the literature and might be explained by strong expression of the full spectrum of activities of the mitochondrial enzyme P450 C11 by the tumor cells. Interestingly, despite hyperaldosteronism, plasma renin activity was not suppressed.

Adenoma↗
PubMed1990

Isolated dehydroepiandrosterone sulphate hypersecretion: a case report.

The case of a 17-year-old male with isolated hypersecretion of dehydroepiandrosterone sulphate (DHEAS) is described. Cushing syndrome, congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase deficiency, an androgen producing adrenal tumour, and elevated plasma DHEAS due to an increased renal threshold were excluded. Selective renal vein catheterization confirmed bilateral, isolated adrenal DHEAS hypersecretion. The dexamethasone suppression suggests a functional nature of this alteration. This condition has to be considered in the differential diagnosis of excessive adrenal androgen production in males, or of hirsutism in females.

Adolescent↗