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At least 721 records · Page 40Linked to original sources
PubMed1975

[Effect of calcium on steroidogenesis in isolated human adrenal cells (author's transl)].

Isolated adrenal cells were obtained surgically from patients with primary aldosteronism, breast cancer, or Cushing's syndrome. They were prepared by the modification of Sayers method, and incubated at 37 degrees C for 2 hours under 95% O-2-5% CO-2, in the medium of calcium-free Krebs-Ringer bicarbonate buffer containing 0.2% glucose and 0.5% bovine serum albumin, to which various doses of calcium, ACTH, dibutyryl cyclic AMP or cycloheximide were added. Steroid production was measured by the method of Silber et al. In isolated normal adrenocortical cells, 11-OHCS was produced by calcium alone in the absence of ACTH or dibutyryl cyclic AMP, while it was not produced by ACTH alone without calcium. 11-OHCS production by ACTH was decreased in the high concentration of calcium (10.16 mM, 12.70 mM). Cycloheximide partially blocked an increase in 11-OHCS synthesis induced by calcium. These data suggest that adenyl cyclase of human adrenocortical cells may be stimulated by calcium alone, supporting the notion that calcium is a second messenger. The ratio of 11-OHCS production by calcium alone to that by dibutyryl cyclic AMP was higher in adenoma cells than in normal cells. This may account for the character of autonomic steroid production in adrenocortical adenoma cells.

Adenoma↗
PubMed1979

Comparison of two tests for heterozygosity in congenital adrenal hyperplasia (CAH).

The increase of plasma cortisol (F), androstenedione (A), 17 alpha-hydroxy-progesterone (17-OH-P) and testosterone (T) was measured after iv administration of ACTH in heterozygotes for CAH and in controls under two different conditions: Test 1: ACTH stimulation was performed without any particular preparation. Test 2: 1.5 mg of dexamethasone (dex.) was given the evening before the ACTH stimulation. Plasma F, A, 17-OH-P and T were measured by specific radioimmunoassays (RIA). Following ACTH stimulation, the increase of 17-OH-P was significantly higher in CAH-heterozygotes than in controls in both tests (P less than 0.0005). Heterozygotes were characterized by a 17-OH-P increase after ACTH stimulation exceeding the + 2 SD limit of the 17-OH-P increase found in controls. The detection of female heterozygotes was considerably improved by the administration of dex. before testing (test 2). In males, however, a better identification of heterozygotes was obtained without previous administration of dex. (test 1). By these tests, 100% of female (test 2) and 79% of male (test 1) CAH heterozygotes could be correctly identified. There were no significant differences in the levels of F, A and T between heterozygotes and controls except for decreased T levels in test 1 (2P less than 0.01) in most male heterozygotes after ACTH stimulation.

Adrenal Cortex Function Tests↗
PubMed2001

Hyperadrenocorticism associated with excessive sex hormone production by an adrenocortical tumor in two dogs.

An 11-year-old spayed female Labrador Retriever and a 9-year-old castrated male miniature Poodle were evaluated because of clinical signs of hyperadrenocorticism. Cortisol testing did not support a diagnosis of hypercortisolemia in either dog; however, imaging studies revealed unilateral adrenal tumors in both dogs. Serum concentrations of 17-hydroxyprogesterone, progesterone, and estradiol were high in both dogs, and androstenedione concentrations were also high in 1 dog. It is suspected that sex hormone secretion by the adrenal tumors in these dogs resulted in clinical signs of hyperadrenocorticism. Clinical signs and hormonal abnormalities resolved in the male dog after surgical resection of the tumor. There was no improvement in clinical signs after treatment with mitotane in the female dog, which died 2 months after diagnosis. Histologic evaluation confirmed the presence of adrenocortical carcinoma in both dogs.

Adrenal Cortex Neoplasms↗
PubMed1999

Progesterone secreting adrenal mass in a cat with clinical signs of hyperadrenocorticism.

A 7-year-old 7-kg (16-lb) neutered male Himalayan cat had nonpruritic progressive alopecia of 9 months' duration. The cat had hyperglycemia and glucosuria. Physical examination revealed complete alopecia along the abdomen, inguinal area, medial and caudal areas of the thighs, ventral area of the thorax, and axilla. Clinical signs were consistent with endocrine-induced alopecia and hyperadrenocorticism, however, results of diagnostic tests (ACTH stimulation and low-dose dexamethasone suppression) were not supportive of hyperadrenocorticism. Abdominal ultrasonography revealed a mass cranial to the left kidney. Blood samples were obtained before and after ACTH stimulation to measure sex hormone concentrations. Analysis revealed markedly high blood progesterone concentrations before and after ACTH stimulation. An adrenalectomy was performed and histologic examination of the mass revealed a well-differentiated adrenocortical carcinoma. The right adrenal gland could not be viewed during surgery and was assumed to be atrophic. Following surgery, the hyperglycemia and glucosuria resolved. Within 4 months of surgery, the hyperprogesteronemia had resolved, and at 12 months the cat's coat quality appeared normal. Findings suggest that cats with signs of hyperadrenocorticism should be evaluated not only for abnormal cortisol concentrations, but also for sex hormone abnormalities.

Adrenal Cortex Function Tests↗
PubMed2000

[Hyperplasia of chromaffin cells in adrenocortical hyperplasia and adenoma].

OBJECTIVE: To study whether there is chromaffin cells hyperplasia in adrenocortical hyperplasia and adenoma. METHODS: Chromaffin cells with chromogranin A were marked by immunohistochemistry method. RESULTS: In 52 cases of adrenocortical hyperplasia and adenoma 3 were associated with eochromocyte hyperplasia and 5 with micro-pheochromocytoma. Six of the 8 cases were characterized by hypercortiso (or aldostero)-hypercatecholamine clinically. CONCLUSIONS: Few cases of adrenocortical hyperplasia and adenoma may be associated with pheochromocytic hyperplasia and micro-pheochromocytoma, and may be characterized by symptoms of hypercortiso (or aldostero)-hypercatecholamine.

Adrenal Cortex↗
PubMed1956

Aldosteronism associated with adrenal cortical adenoma.

An electrolyte-regulating corticoid has been identified and given the name aldosterone. This hormone may be produced in amounts above normal in adrenal cortical tumors in hyperplastic adrenal glands and in normal appearing adrenal glands. Overproduction of aldosterone is accompanied by certain characteristic clinical manifestations which should suggest the diagnosis. The diagnosis may be supported by examinations available in most well equipped clinical laboratories. Bioassay of aldosterone in the urine and estimation of exchangeable body sodium and potassium, using radioactive salts, are necessary for confirmation of the diagnosis.Since the description of this salt-retaining hormone by Simpson and Tait and the discovery of its chemical structure by Reichstein in 1954, reports of 14 cases have been published. Surgical removal of the offending tissue gives spectacular relief from the very distressing symptoms.

Adrenal Cortex↗
PubMed1986

Evaluation of a six-hour combined dexamethasone suppression/ACTH stimulation test in dogs with hyperadrenocorticism.

Seventeen dogs with hyperadrenocorticism were studied. Three dogs had functioning adrenocortical tumors and 14 had pituitary-dependent hyperadrenocorticism. Each dog was evaluated by determining the endogenous plasma ACTH concentration and by performing 4 tests: ACTH stimulation, dexamethasone screening, dexamethasone suppression, and a 6-hour combined dexamethasone suppression/ACTH stimulation test. The combined test was less reliable as a screening test in diagnosing hyperadrenocorticism than was the dexamethasone screening test or the ACTH stimulation test. Compared with the endogenous plasma ACTH concentration, results of the dexamethasone suppression portion of the combined test were less reliable in distinguishing dogs with adrenocortical tumors from those with pituitary-dependent hyperadrenocorticism. It was concluded that the combined test cannot be recommended for use.

Adrenal Cortex Function Tests↗
PubMedDate not supplied

[Nuclear medicine diagnostic localization in primary aldosteronism and Cushing syndrome].

The main indication for 131J-cholesterol scintigraphy is primary aldosteronism. The preoperative localization of aldosterone - producing adenomas may be obtained with the non-invasive NP-59 - scintigraphy in 75-85% of the patients. Idiopathic bilateral adrenal hyperplasia is diagnosed correctly in 90-100% of the cases. In Cushing's syndrome scintigraphy of the adrenal cortex is indicated only in specific cases such as very small adenomas, primary nodular adrenal hyperplasia and/or for the localization of ectopic adrenal cortex tissue. A false diagnosis may be caused by asymmetric uptake of the radioisotope in idiopathic bilateral hyperplasia or by unspecific absorption in non - adenomatous adrenal cortex tissue with symmetric uptake in patients with unilateral adenomas.

Adenoma↗