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

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

1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), cortisol and adrenocorticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values of 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was significantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.
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PMID:Aldosterone regulation in primary aldosteronism: differences between adenoma and bilateral hyperplasia. 19 15

The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
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PMID:Plasma renin activity and urinary aldosterone in Cushing's syndrome. 20 67

Primary hyperaldosteronism usually causes moderate hypertension. It is rare to note as in our two patients intermittent attacks of paroxysmal hypertension. The diagnosis of aldosteronism will be suspected on the finding of persistent hypokalemia with acidosis. It will be confirmed by laboratory examinations severe fall in plasma renin activity and rise in aldosterone in the adrenal veins. To determine the affected side, one may carry out adrenal phlebography which is a difficult technic, and/or a scan using iodine cholesterol which is benign and precise. Surgery with removal of the adenomatous hyperplasia in one case and of an adenoma in the other, gave one very good result.
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PMID:[Primary hyperaldosteronism with paroxysmal arterial hypertension. Apropos of 2 operated cases]. 20 43

In 31 patients with primary aldosteronism routine clinical and laboratory data, the effect of orthostasis on plasma aldosterone (PA), plasma renin activity (PRA) and cortisol (PC), effect of fludrocortisone or high sodium intake on basal PA and night-day fluctuations of basal PA and PC with and without suppression of pituitary ACTH by dexamethasone were determined to differentiate patients with a unilateral aldosterone producing tumour (adenoma, APA, n=20; carcinoma, CA, n=1) from those with idiopathic bilateral adrenal hyperplasia (IAH, n=10). Mean systolic and diastolic blood pressure, age, serum potassium and urinary excretion of sodium and potassium were not significantly different in both groups of patients. Normokalaemic primary aldosteronism occurred both in patients with APA (n=2) and in patients with IAH (n=1). Mean basal PA and mean urinary excretion rate of aldosterone-18-glucuronide were higher though not significantly different in patients with APA or CA than in those with IAH. A substantial number of the patients with APA (n=5) and with IAH (n=3) showed urinary excretion rates of aldosterone-18-glucuronide less than 13 microgram/24 h. Mean PA and PRA significantly increased (P less than 0.025) in patients with IAH in response to posture. However, these changes also occurred at times in some patients with APA. Both fludrocortisone and high sodium intake produced a variable and no group-specific effect on basal PA. Night-day variations in PA were positively correlated with those in PC in all patients with APA (n=12) and in 5 of 8 patients with IAH. A dissociation of PA and PC, however, was only observed in patients with IAH. Finally, the effect of dexamethasone on plasma aldosterone curves was variable in both groups of patients. Our results indicate that under the described conditions analysis of routine clinical and laboratory data and of peripheral PA, PRA and PC are of limited value in differentiating patients with APA or CA from those with IAH.
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PMID:Primary aldosteronism: inability to differentiate unilateral from bilateral adrenal lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone. 21 20

Measurement of plasma aldosterone concentrations (PAC) at 8 a.m. and after 4 h in the upright posture can further assist in identifying the adrenal pathologic lesion in patients with primary aldosteronism. Increases in PAC are associated with hyperplasia, and decreases with adenoma. Normal increases in response to upright posture are observed in patients with essential hypertension with normal or reduced renin concentration.
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PMID:Effect of posture on the plasma concentrations of aldosterone in hypertension and primary hyperaldosteronism. 22 May 44

Fifty patients with hypertension, aldosterone excess, and low plasma renin concentration underwent adrenal surgery. There was a highly significant fall in mean systolic and diastolic pressures after the operation. The mean postoperative diastolic pressure fell to strictly normal levels, however, in only 19 out of 38 patients from whom an adrenocortical adenoma was removed and in only two out of 10 non-tumour patients. There was a significant correlation between the fall in blood pressure during spironolactone treatment and after adrenal surgery though levels were generally slightly lower during the former therapy. It is suggested that removal of an aldosterone-producing adenoma is the treatment of choice provided a good preoperative hypotensive response to spironolactone occurs, while the treatment of choice for non-tumour patients is often long-term spironolactone.
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PMID:Results of adrenal surgery in patients with hypertension, aldosterone excess, and low plasma renin concentration. 23 68

1. Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium and in serum sodium and bicarbonate, while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing the blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. 2. Only negligible side effects were encountered in the entire series of 24 patients.
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PMID:Amiloride in the treatment of primary hyperaldosteronism and essential hypertension. 35 30

In mice having a high renin content in the submaxillary glands allo- and autotransplantation of the gland showed identical histological changes of the tissue, comprising disappearance of acini and intercalated ducts as well as a reduction in the number and size of granules in the granulated ducts. No structural signs of rejection were found. Adenomas, possibly originating in the granulated ducts, were frequently present in the transplanted glands. The renin content of autotransplanted glands was invariably much higher than in allotransplants, and after noradrenaline injection renin was released only from autotransplants, never from allotransplants. Blockade of the renin system was accordingly followed by a decrease in blood pressure only in mice with autotransplants.
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PMID:Structural changes and ability to release renin in auto- and allo-transplants of mouse submaxillary glands. 46 67

Thirty-eight hypertensive, hypokalemic patients underwent adrenalectomy for primary aldosteronism. Thirty-one patients were found to have an adenoma and seven patients "idiopathic" hyperplasia. The diagnosis was made by finding low plasma renin activity, which could not be stimulated, and unsuppressable elevated plasma or urine aldosterone. The distinction between adenoma and hyperplasia and the localization of an adenoma were accomplished by adrenal venography, adrenal vein blood analysis, and iodocholesterol scanning. Venography was accurate in 87%; adrenal vein blood analysis in 91%; and iodocholesterol scanning in 72%. Dexamethazone suppressed scanning heightened discrimination to 91%. The adenomas were equally distributed between the right and left adrenal gland, with one patient having bilateral adenomas. All but two patients underwent adrenalectomy from a posterior lumbar incision. Postoperative recovery was uncomplicated. Eighteen months after operation 77% of patients with an adenoma were normotensive.
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PMID:Primary aldosteronism: experience with thirty-eight patients. 47 33


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