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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six cases of Cushing's syndrome with adrenocortical tumors which showed a variety of responsiveness to ACTH were investigated in relation to their clinical pictures and laboratory findings. Abnormal responses to ACTH in tumors was analyzed by in vitro experiments with surgically obtained tumor tissues, and the ACTH responsive mechanism of the tumors was discussed. An 8 hour intravenous ACTH infusion test showed that three of these patients were ACTH responsive, and the other three unresponsive. Histological observation of the tumors revealed that ACTH responsive tumors were adenomas and that ACTH unresponsive tumors were "black adenomas" in two and a carcinoma in one. To investigate possible factors which might account for these differences in ACTH responsiveness, tumor specimens of each one of the responsive and unresponsive adenomas, and a carcinoma were subjected to in vitro studies. When incubated with ACTH or cyclic AMP, tissue sections of a responsive adenoma enhanced cortisol secretion, while that of a black adenoma failed to show any change. Steroidogenesis by carcinoma sections were significantly suppressed in the presence of ACTH or cyclic AMP. Cycloheximide abolished a stimulatory effect of ACTH and cyclic AMP on steroidogenesis in a responsive adenoma without affecting its basal secretion of cortisol. Steroidogenesis by unresponsive tumors (an adenoma and a carcinoma) were decreased by cycloheximide. Since the conversion of cholesterol to pregnenolone, the rate limiting step in steroidogenesis, takes place in adrenal mitochondria, the effect of cyclic AMP on pregnenolone formation from 14C-cholesterol by mitochondrial fractions of these tumors was examined. Cyclic AMP stimulated pregnenolone formation by mitochondrial fraction of an ACTH responsive adenoma, while with that of an unresponsive adenoma pregnenolone formation was not affected. Pregnenolone formation by cancer mitochondria was significantly suppressed by cyclic AMP. These results suggest that the unresponsiveness to ACTH of these tumors might be explained by the ineffectiveness of cyclic AMP to stimulate pregnenolone formation by tumor mitochondria, and that the steroidogenic pathway in unresponsive tumors are in an enhanced state even without cyclic AMP. It should be mentioned that all unresponsive adenomas gave a characteristic appearance of a "black adenoma". Histologically, tumors were composed of compact cells with abundant lipofuscin granules. The possible relationship between the ACTH responsiveness of adrenocortical tumors and some clinical pictures caused by them was also noticed. ACTH unresponsive adenomas resulted in shorter duration, severer conditions of the disease and higher 17-ketosteroid excretion than responsive adenomas. The growth of unresponsive tumors seemed faster than that of responsive ones.
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PMID:[Studies on the responsiveness of human adrenocortical tumors to ACTH the clinical and experimental observations (author's transl)]. 18 66

The relationship of plasma aldosterone concentration to its identified stimuli was examined in three patients with hypertension, hyperaldosteronism, and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, sodium, and potassium concentrations and renin activity were measured in blood samples taken at 20 minute intervals from 2 A.M. to 8 A.M. during recumbency and sleep. The tests were performed on all patients following a regular sodium diet both before and after short-term treatment with dexamethasone. Two of the three subjects with adrenal hyperplasia were re-examined after 2 weeks of dexamethasone therapy. All four control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the two hormones (r = +0.76 and +0.77); one did not (r = 0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the four patients with an adenoma and in the two patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the third patient. The first two patients with idiopathic hyperplasia were subsequently retested following 2 weeks of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlated with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The second had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosteerone concentrations. These data indicate that ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.
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PMID:The role of ACTH in the episodic release of aldosterone in patients with idiopathic adrenal hyperplasia, hypertension, and hyperaldosteronism. 18 90

The aim of this study of 101 pre- and postoperatively controlled hypersecreting pituitary adenomas (80 acromegalies, 15 Cushing's diseases, 6 Nelson's syndromes) was to establish in what cases a selective adenoma extirpation by the transnasal route is possible and advisable. In primary operations on acromegalics with small and medium size tumours 92% were postoperatively GH normal. Eighty five per cent of these had intact pituitary function. The results with larger tumours were worse (72%). During a control period of 1.5-5.5 years a renewed elevation of GH levels was observed in three cases, all in the first year, but never after clearly selective adenomectomy. These results, and the anterior lobe biopsies, which showed no GH cell hyperplasia, favour selective adenoma extirpation. In contrast to acromegaly, nodular ACTH cell hyperplasia in the anterior lobe was found in most cases of Cushing's disease, and therefore complete hypophysectomy was performed. The cortisol levels became either normal or, in most cases, lower than normal. A selective operation was performed on 6 Nelson tumors. The ACTH values became normal in about 50% of the patients but there was a tendency towards recurrence. Our experiences with Cushing's disease and Nelson's syndrome lead us to recommend total hypophysectomy.
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PMID:Selective removal of hypersecreting pituitary adenomas? An analysis of endocrine function, operative and microscopical findings in 101 cases. 18 63

A patient with Cushing's disease due to a chromophobe adenoma was studied for 243 days before pituitary surgery and evidence for periodicity in cortisol steroid production was found with cycles occurring every 85.8 days (peak-to-peak length), associated with laboratory remissions and paradoxical response to dexamethasone. The autonomy of ACTH secretion was suggested by the nonresponsiveness to repeated lysine-vasopressin stimulation tests and lack of increase in urinary 170HCS following metyrapone. A distinct response of the hyperplastic glands (as demonstrated by percutaneous adrenal venography) was obtained on several B1-24 corticotropin stimulation. The patient's hypercortisolism disappeared following removal of the chromophobe adenoma through transphenoidal hypophysectomy.
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PMID:Periodic remission in Cushing's disease with paradoxical dexamethasone response: an expression of periodic hormonogenesis. 18 34

Morphological studies of 3 pituitary "chromophobe" adenoma in patients without hypercorticism show positive immunofluorescenct cells with anti alpha, 17-39 ACTH antibody which are not revealed with anti beta, 1-24 ACTH antibody. These cells observed at the ultrastructural level contain secretory granules of 1,000 to 1,500 A in diameter. The existence in these cells of a substance having an immunological relationship with ACTH without biological activity is discussed.
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PMID:[Dissociation of results obtained with an immunofluorescence technique by using anti-ACTH antibodies in three cases of pituitary "chromophobe" adenoma without hypercorticism; ultrastructural study (author's transl)]. 18 73

Plasma levels of the delta5-pregnenes, pregenolone and 17-OH-pregnenolone, were measured in patients with disordered steroidogenesis. While 17-OH-pregnenolone was within the normal range in patients with hypercortisolemia due to Cushing's disease, ectopic ACTH or adrenal adenrenal adenoma, 4 of 6 patients with an adrenal carcinoma had elevated levels of this precursor. Thus, elevated plasma 17-OH-pregnenolone levels in patients with Cushing's syndrome indicate adrenal carcinoma, although a normal value does not exclude this diagnosis. Abnormal resistance of delta5-pregnenes to suppression with dexamethasone proved useful in detecting the presence of residual tumor in the post-operative evaluation of adrenal carcinoma. Basal plasma pregnenolone was within the normal range in 19 of 20 patients with Cushing's disease and was invariably normal in patients with other varieties of hypercortisolism. Since acute administration of ACTH causes marked elevation of delta5-pregnene levels while patients with chronic ACTH excess (Cushing's disease and ectopic ACTH production) have normal levels, it is suggested that ACTH has a chronic influence on the intraadrenal utilization of delta5-pregnenes in addition to stimulating their formation. In pre-menopausal women with idiopathic hirsutism, basal levels of both delta5-pregnenes were elevated (P less than 0.001). Following dexamethasone administration the absolute decrease in delta5-pregnenes levels was greater than that seen in normal subjects. This observation indicates that the metabolism of delta5-pregnenes is abnormal in patients with idiopathic hirsutism.
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PMID:Plasma pregnenolone and 17-OH-pregnenolone in patients with adrenal tumors, ACTH excess, or idiopathic hirsutism. 19 Feb 51

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.
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PMID:[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)]. 19 Dec 34

Elevated plasma testosterone levels were found in 8 women with Cushing's disease and oligo-or amenorrhea and/or hirsutism. In 4 men with Cushing's syndrome either due to adrenal hyperplasia or adenoma, plasma testosterone levels were lowered. Three of these 4 men complained of impotence or loss of libodo. Evidence for a major adrenal origin of the elevated testosterone values in the women with Cushing's disease was derived from the parallel suppression of cortisol and testosterone during dexamethasone administration, the testosterone responsiveness to ACTH and its dramatic fall after adrenalectomy. In the men with Cushing's syndrome the lowered plasma testosterone values were further suppressed by high doses of dexamethasone irrespective of concomitant cortisol suppression. Adrenalectomy or adenotomy restored the decreased plasma testosterone levels to normal. In women with Cushing's syndrome adrenal hyperandrogenism may account for the sexual and gonadal disturbances, in men glucocorticoid induced suppression of Leydig cell function may be responsible.
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PMID:Plasma testosterone profiles in Cushing's syndrome. 19 73

The presenting signs, symptoms, roentgenographic findings, endocrine evaluations, treatment, and results in 68 cases of presumed pituitary adenomas treated over an 18-year period are discussed. The most common symptoms were headache, acromegalic changes, visual symptoms, and amenorrhea. Most common physical findings were obesity, acromegaly, and visual field defects, usually bitemporal hemianopsia. Roentgenographic evidence of sellar erosion was almost universal but angiography and pneumoencephalography were required to evaluate suprasellar extension. Brain scan was not considered a particularly useful diagnostic tool. Endocrine status was best evaluated by a battery of tests including 17-OH, 17-KS, T3, T4, PBI, ACTH stimulation, and FSH and STH levels. (Prolactin levels are currently being obtained, also). Surgical specimens were obtained in 29 patients, with subsequent diagnoses of 22 chromophobe adenomas, five eosinophilie adenomas, one cystic adenoma, and one necrotic tumor. All five eosinophilic tumors came from acromegalic patients. Patients treated by operation alone or operation followed by radiotherapy generally had less "medical morbidity" than did patients who received radiotherapy alone.
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PMID:Review of 18 years' experience with pituitary tumors. 19 48

ACTH sensitive murine adrenocortical adenoma cells (Y-1) were examined by transmission and scanning electron microscopes under non-stimulated and stimulated conditions. They showed the ultrastructural characteristics which were fairly different from those of the original adrenocortical cells of LAF1 mice. The smooth-surfaced endoplasmic reticulum (sER) were poorly developed, and the mitochondrial cristae showed lamellar rather than tubular or tubulo-vesicular type. Administration of ACTH induced rounding-up of the Y-1 cells with slight increase in sER, BUt no mitochondria with vesicular inner structure appeared. The effects of dbcAMP on the morphology of the Y-1 cells were similar to those of ACTH except that the rounding-up occurred more rapidly and uniformly.
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PMID:Transmission and scanning electron microscopic observations of mouse adrenocortical adenoma cells (Y-1) in non-stimulated and stimulated states. 20 54


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