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At least 847 records · Page 47Linked to original sources
PubMed1983

Surgical treatment of primary aldosteronism.

An aldosterone-producing adenoma is the cause of primary aldosteronism in about 85%. Unilateral adrenalectomy cures the potassium wasting and normalizes the blood-pressure in more than 70%, independently of the severity or duration of the hypertension. The location of an aldosteronoma is best obtained by computerized tomography and selective venous catheterization with determination of the aldosterone/cortisol ratio. When the biochemical studies suggest hyperplasia, medical treatment is recommended. It is, however, our policy to remove an adrenal gland with hyperplasia, when catheterization demonstrates unilateral hyperfunction. At operation a posterior or a flank approach is preferably used.

Adenoma↗
PubMed1981

Spironolactone bodies in aldosteronomas and in the attached adrenals. Enzyme histochemical study of 19 cases of primary aldosteronism and a case of aldosteronism due to bilateral diffuse hyperplasia of the zona glomerulosa.

The formation of spironolactone (S) bodies, eosinophilic laminated cytoplasmic inclusions, is induced in the aldosterone-producing cells of the human adrenal cortex after the administration of spironolactone. The aim of this study was to define the enzyme histochemical characteristics of S bodies, S-body-containing cells, and the apparently hyperplastic zona glomerulosa (zG) of adrenal tissues attached to aldosteronomas. S bodies were found in 14 of 19 aldosteronomas, in 10 of 19 adrenal tissues attached to aldosteronomas, and in the adrenal tissues in a patient with aldosteronism due to bilateral diffuse zG hyperplasia. The S bodies themselves exhibited most intense 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) activity but did not exhibit glucose-6-phosphate dehydrogenase (G6PD), NADP-dependent isocitrate dehydrogenase (NADP-ICDH), or succinate dehydrogenase (SDH) activity, confirming histochemically the origin of S bodies in the smooth endoplasmic reticulum. In two adenomas, S bodies were found to be surrounded by reaction products of acid hydrolase but were not found in the other adenomas and the remaining adrenal tissues. S-body-containing cells, irrespective of being neoplastic or not, showed enhanced 3 beta HSD, G6PD, and NADP-ICDH activity and weak SDH activity (Type I pattern of enzyme activity). Though zG was hyperplastic in most of the adrenal tissues attached to the adenomas, zG cells that did not contain S bodies showed the opposite pattern (Type II pattern) of enzyme activity (ie, weak 3 beta HSD, G6PD, and NADP-ICDH activity and intense SDH activity), in contrast to those in the adrenal tissues in a patient with aldosteronism due to bilateral diffuse zG hyperplasia (which showed the Type I pattern). The results are consistent with the view that hyperplastic zG cells, except S-body-containing cells, in the case of aldosteronoma are not hyperfunctioning. The latter cells may have enhanced but possibly abortive steroidogenic activity.

Adenoma↗
PubMed1995

[Critical study of the characterization of hyperandrogenism in a group of obese women].

The authors report the hormonologic characteristics of 20 obese and hirsute women meeting the criteria for adrenaltype hyperandrogenism, suppressible by dexamethasone, without hyperprolactinemia and without any late developing partial enzyme block appearance. The laboratory profile of these women differed from that of a group of women with type 1 polycystic ovaries syndrome. In this same group obese women in whom LH/FSH ratio was below 1, there was evidence under baseline conditions of a moderate increase in testosterone and delta 4-androstenedione in relation to increased plasma levels of DHA and SDHA, plasma delta 4 and delta 5-androgen levels falling precipitalely during the dexamethasone suppression test. The ACTH stimulation test revealed greater reactivity for 17 hydroxy-pregnenolone (p < 0.001) and less for 21-deoxycortisol than in the control group of normal women (p < 0.01). The essentially adrenal origin of plasma hyperandrogenism in certain cases of obesity is discussed. Insulin could increase adrenal sensitivity to ACTH and its possible action in vivo on the activity of adrenal enzymes requires clarification. The accumulation of certain androgens in the adrenal cortex could also be responsible for dysregulation of 3 beta ol-dehydrogenase and 11-hydroxylase.

Adolescent↗
PubMedDate not supplied

Studies of the reproduction function in hyper- and hypoadrenocorticism.

The investigation was carried out on 66 patients with hypo- or hyperfunctional syndromes of adrenocorticism, hospitalized and treated by our team. The patients were grouped into 5 lots according to their diseases. Lot one consisted of 34 female patients with Cushing's syndrome, lot two of 10 males with Cushing's syndrome, lot three of 10 males with Addison's disease and lot four, of 6 females with androgenic hypercorticism. The morphofunctional disorders of reproduction were followed up clinically and by complex hormone assays, before and after treatment. The incidence of these disorders is very high, and the results of clinical observations and of laboratory data demonstrate that both the excess of adrenocortical hormones and the decrease in their circulating level have a negative influence on the reproduction function or represent a risk factor in cases of pregnancy. By the curative treatment of the adrenal cortex a preventive treatment of abortion and/or sterility is achieved.

Adrenal Insufficiency↗
PubMed1975

131I-19-iodocholesterol scintigraphy of the adrenal cortex.

131-I-19-iodocholesterol scintigraphy of the adrenal cortex has been carried out in 26 patients. In 4 patients with normal adrenocortical function the tracer was equally accumulated on the two sides. In 7 patients with untreated Cushing's syndrome, bilateral uptake was found in 4 patients with bilateral hyperplasia whereas unilateral visualization was obtained in three cases of cortisol producing adenomas. The side localization was confirmed at operation. Eight patients had been operated for Cushings syndrome prior to the scintigraphy. Remnant adrenocortical tissue with negligible or subnormal function (4 patients) could not be visualized. Normo- or hyperfunctioning remnant tissue was visualized in 3 patients. One patient had recurrent hypercorticism due to metastases from a previously removed adrenocortical carcinoma; a single pelvic accumulation was seen, whereas several metastases in the abdomen and thorax were not visualized. Four patients with aldosteronism were investigated. Three had primary aldosteronism due to an adrenocortical adenoma. In two of these, the site of the adrenal lesion was localized pre-operatively. In the third patient, equal bilateral accumulation of iodocholesterol was seen even after suppression with dexamethasone. At operation a small tumour was found. In 1 patient with indeterminate aldosteronism both glands were visualized and at a second examination the uptake was equally suppressed by dexamethasone.

Adrenal Cortex↗
PubMed1996

Oncogenic role of heterotrimeric G proteins.

Mutations that constitutively activate the alpha chains of Gs and Gi2 by inhibiting their intrinsic GTPase activity are present in human endocrine tumours. The gsp oncogene is mainly found in pituitary GH secreting tumours and thyroid hyperfunctioning adenomas, where it induces a constitutive activation of the adenylyl cyclase-cAMP pathway. In pituitary and thyroid cells, this signal leads to abnormal proliferation and a persistent activation of differentiated functions. The gip2 oncogene has been identified in tumours of the ovary and adrenal cortex. Although the mechanisms of the oncogenic action of mutationally activated alpha i2 are less clear than those of alpha s, the protein can induce transformation of certain cell types. At least five other alpha chains, which share with alpha s and alpha i2 common structural and functional mechanisms of GTP hydrolysis, activate mitogenic pathways leading to transformation. In addition, the G protein beta gamma subunits clearly control signals involved in cell growth. So far, there is no evidence for mutations of these molecules in human tumours. Further studies will tell us whether at present we know of only two members of a much larger family of G protein oncogenes.

Adenylyl Cyclases↗
PubMed1988

Hypercortisolism and the resistance to dexamethasone suppression during gestation.

Maternal adrenocortical function was studied by measuring plasma cortisol and urinary free cortisol during gestation. Changes in suppressibility of pituitary-adrenocortical function were determined by dexamethasone administration. Urinary free cortisol as well as plasma cortisol increased during the course of gestation. The suppressibility by dexamethasone became less effective as pregnancy advanced. These results suggest that pregnant women have pituitary-adrenocortical hyperfunction and tissue refractoriness to glucocorticoid which increases during the course of gestation.

Adrenal Cortex↗
PubMed1988

DNA polymerase beta in human thyroid of Graves' disease and thyroid tumors.

We have shown that the level of DNA polymerase beta of rat adrenal cortex is regulated by pituitary trophic hormones and may correlate with their endocrine function. Here we measured DNA polymerase beta activity in human thyroid tissues of various benign and malignant thyroid disorders in order to verify the correlation between DNA polymerase beta activity and endocrine function. In Graves' disease (hyperfunction), the level of DNA polymerase beta per cell was three times higher than in normal thyroid, while in undifferentiated thyroid carcinomas this enzyme level was lower than normal. Furthermore, DNA polymerase beta in the crude extracts of cancer cells showed larger molecular forms, ranging from five to 12S, upon sucrose gradient sedimentation. These observations further support the hypothesis that the activity of DNA polymerase beta correlates, in part, with the functional level of the endocrine organ and with cell differentiation.

Adenoma↗
PubMed1988

[Functions of the sympathetic-adrenomedullar system and adrenocortex in patients with vibration syndrome. Investigations of plasma and urine catecholamine and plasma cortisol during cold exposure].

Much discussion has been made as to whether vibration syndrome is a peripheral or systemic disorder. We studied plasma and urine norepinephrine and epinephrine, and plasma cortisol under resting and cold exposure conditions (7 degrees C cold room for 30 min). The subjects were 20 patients with vibration syndrome and with a history of Raynaud's phenomenon, 20 patients with vibration syndrome without a history of Raynaud's phenomenon, and 20 healthy controls. They were all males and the three groups were matched by age. The following results were obtained. 1. Mean temperatures of finger skin in the patient groups under resting and cold exposure conditions were lower than in the control group. Mean systolic and diastolic blood pressures in the patient groups under both conditions were higher than in the control group. Mean values of blood pressure change produced by cold exposure in the patient groups were lower than in the control group. Some of these differences were statistically significant (p less than 0.05 or p less than 0.01). 2. Mean levels of plasma norepinephrine in the patient groups under resting and cold exposure conditions were significantly higher (p less than 0.01 or p less than 0.05) than in the control group. This finding indicates that the patients with vibration syndrome had hyperfunction of the sympathetic nervous system. Mean levels of urine norepinephrine in the patient groups were not significantly different from the control group. 3. Mean levels of plasma epinephrine in the patient groups under resting and cold exposure conditions were lower than in the control group. The differences between the patient groups and the control group were significant (p less than 0.05 or p less than 0.01) in the cold exposure condition. This finding suggests that the patients with vibration syndrome had hypofunction of the adrenomedullar system. Urine epinephrine in the patient groups was not significantly different from the control group. 4. Mean levels of cortisol in the patient groups were higher than in the control group. The difference in cortisol level between the group of patients without Raynaud's phenomenon and the control group was significant (p less than 0.01) in the resting condition. This finding may suggest that the patients with vibration syndrome had hyperfunction of the adrenocortex. The foregoing data support the hypothesis that vibration syndrome is a systemic dysfunction, which includes disorders of the sympathetic-adrenomedullar system and adrenocortex.

Adrenal Cortex↗
PubMed1976

Cushing's disease in a child with lymphosarcoma and acute leukemia.

A 6-year-old girl with lymphosarcoma developed Cushing's syndrome. Suppression-stimulation studies verified adrenal hyperfunction secondary to bilateral adrenocortical hyperplasia, and the course suggested the possibility of "ectopic ACTH" production by the neoplasm as the etiology.

Adrenal Cortex↗
PubMed1987

Congenital 17 alpha-hydroxylase deficiency: a clinicopathologic study.

The histopathologic features of the adrenal glands in three cases of congenital 17 alpha-hydroxylase deficiency are described in relation to clinical and endocrine findings. Diffuse or nodular adrenocortical hyperplasia, particularly in the zonae fasciculata and reticularis, was observed in all cases examined. The hyperplastic adrenal cortices were composed of cells with morphologic features of hypercorticism and hyperstimulation. Myelolipomatous lesions were detected in two cases. These morphologic findings were consistent with excessive adrenocorticotropic hormone secretion in this disorder. In all the cases examined, the plasma aldosterone concentration was within normal limits, and plasma renin activity was suppressed prior to dexamethasone treatment. Morphologically, however, hyperplasia of the cells with abundant mitochondria and smooth endoplasmic reticulum seemed to involve the zona glomerulosa. Nonencapsulated nests of hypertrophied cortical cells in periadrenal tissue were remarkable in one case. From these morphologic findings, we postulated hyperfunction of the zona glomerulosa as well as involvement of corticosteroids from the zona glomerulosa in the pathophysiology of this disorder.

Adrenal Cortex Hormones↗
PubMed1990

Effect of hypertonic saline on the corticotropin-releasing hormone and arginine vasopressin content of the rat pituitary neurointermediate lobe.

The changes in the levels of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in the neurointermediate lobe of the pituitary (NIL) following hypertonic saline administration were examined in rats. The plasma osmotic pressure in rats receiving 2% NaCl for 8 days was greatly increased. Plasma AVP concentration in rats receiving 2% NaCl for 8 days were significantly higher than in control rats (566% of the control level). Plasma corticosterone was significantly higher in the saline-treated rats than in controls, whereas plasma ACTH was not significantly different. The pituitary ACTH concentration was much higher in the saline-treated rats than in controls. CRH in the NIL was increased significantly by saline treatment (419% of the control concentration), whereas the CRH in the paraventricular nucleus and median eminence of control and saline-treated rats did not differ significantly. The AVP in the NIL fell greatly in saline treated rats. The extract from both control and saline-treated rats showed a major peak for immunoreactive CRH, with a retention time identical to that of rat CRH. However, the peak was much higher in the extract from saline-treated rats. The immunoreactive AVP peak was greatly reduced in saline-treated rats. These results suggest that hypertonic saline administration increases the CRH in the NIL and causes AVP hypersecretion and/or hyperfunction of magnocellular-NIL CRH might be responsible for pituitary-adrenal stimulation in saline-treated rats.

Adrenal Cortex Hormones↗