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

Hypertension and hypokalemia occur in patients with Cushing's syndrome whereas aldosterone production is normal and plasma renin activity is usually normal or increased. A normal aldosterone level in the face of suppressed plasma renin activity is unusual and suggests excess mineralocorticoid hormone activity. Our patient, who had Cushing's syndrome due to adrenocortical adenoma, can be classified as having low renin hypertension (suppressed renin and normal aldosterone levels). The mineralocorticoid hormone in excess was deoxycorticosterone which suppressed renin. The aldosterone production was normal and was produced solely by the adenoma. Contralateral adrenal gland suppression of both the zona glomerulosa by deoxycorticosterone via renin, and of the fasciculata by cortisol via ACTH was demonstrated after removal of the adenoma. Normal adrenal function was gradually restored.
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PMID:Concurrent hypercortisolism and hypermineralocorticoidism. 87 Nov 29

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 sodium and bicarbonate; while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, and plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing 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. Only negligible side-effects were encountered in the entire series of twenty-four patients.
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PMID:Amiloride in the treatment of primary hyperaldosteronism and essential hypertension. 89 Sep 99

The effect of circadian rhythm and alterations in posture on plasma aldosterone concentration was studied in 13 patients with primary aldosteronism (six adenoma, five idiopathic hyperplasia, two carcinoma) to define the regulatory mechanism in each of these pathologic subtypes. Blood samples for aldosterone, cortisol, renin, and potassium concentrations were obtained every 4 h during prolonged recumbency (32 h) and upright posture (16 h). During recumbency, aldosterone and cortisol followed a normal circadian pattern in patients with adenoma and hyperplasia, with peak values at 0400-0800 h and the nadir at 1600-2400 h. Normalized aldosterone and cortisol values correlated significantly in both groups (adenoma r=+0.66, P less than 0.001; hyperplasia r=+0.42, P less than 0.01). With upright posture, aldosterone levels declined parallel to the normal circadian fall in cortisol in patients with adenoma (r=+0.68, P less than 0.001); whereas aldosterone levels increased in patients with hyperplasia parallel to small increments in renin (r=+0.65, P less than 0.001) and potassium (r=+0.64, P less than 0.001). During the administration of dexamethasone, aldosterone no longer correlated with cortisol in patients with adenoma but continued to correlate with renin during upright studies in patients with hyperplasia (r=+0.77, P less than 0.01). Aldosterone circadian rhythm was abnormal in patients with carcinoma and no effect of posture was noted. Unilateral adrenalectomy restored the normal postural relationship in four patients with adenoma. These studies suggest that aldosterone secretion is under continuous ACTH control regardless of posture in patients with adenoma, whereas persistent adrenal responsiveness to small increments in renin and/or potassium mediate the postural increase in plasma aldosterone in patients with hyperplasia. True adrenal autonomy occurs only in patients with adrenal carcinoma and when ACTH is suppressed in those with adenoma.
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PMID:Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism. 94 31

A close relationship exists between the endocrine system and hypertension. A brief survey is conducted of the endocrine diseases most frequently associated with high blood pressure. The available means for preoperative differentiation of an aldosterone-producing adenoma from idiopathic aldosteronism with bilateral hyperplasia are considered. For cases where high blood pressure is the principal presenting sign in a patient without overt endocrinopathy, the diagnostic resources for the detection of a hormonal cause--particularly renin--are critically examined.
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PMID:[Endocrinology and arterial hypertension]. 100 37

In a prospective study of 7 patients with aldosterone-producing adenoma (APA), long-term (6-72 months) preoperative stimulation of plasma renin activity (PRA) by diuretic therapy (spironolactone plus hydrochlorothiazide) did not prevent selective aldosterone deficiency postoperatively. In all patients aldosterone excretion rate (AER) fell to subnormal values (from a mean of 97 to 2.6 mug/24 h) following removal of APA, although PRA remained elevated. Generalized adrenocortical insufficiency was excluded by the demonstration of normal baseline plasma cortisol and urinary 17-OHCS and the appropriate response to ACTH stimulation. In 6 of 7 patients studied 1-3 months postoperatively, short-term (4 days) sodium deprivation evoked normal increases in PRA, but AER response was blunted (except in 1). Restudy of 3 of 6 patients after 6-12 months revealed that aldosterone production had returned to normal. These results indicate that renin deficiency is not the principal cause of postoperative selective hypoaldosteronism in these patients. On the other hand, they appear to substantiate the possibility raised by in vitro and in vivo studies that spironolactone can directly inhibit aldosterone biosynthesis.
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PMID:Selective hypoaldosteronism despite prolonged pre- and postoperative hyperreninemia in primary aldosteronism. 115 65

A system for discriminating between adrenal adenoma and hyperplasia based on the levels of aldosterone production, plasma renin concentration, severity of electrolyte disturbances, plasma aldosterone patterns during recumbency and after assuming erect posture, and 131I-19-iodocholesterol scan has been developed. Indicated for operation are patients with adenomas whose elevated blood pressure cannot be continuously controlled with usual doses of medication and patients with documented deterioration of target organ function. Adrenalectomy has been performed 83 times in 81 patients with a diagnosis of primary hyperaldosteronism. Results of excision of adrenal adenomas have been excellent with significant lowering of blood pressure in all cases and cure of hypertension in over 60%. Results of total or subtotal adrenalectomy for hyperplasia have been poor with almost all patients still requiring medication for hypertension. Adenomas have always been unilateral, and usually can be localized so that unilateral exploration is curative. Therefore, we have tried to distinguish preoperatively between adenoma and hyperplasia. Anterior transperitoneal adrenalectomy has been effective with few complications, and no postoperative hypercortisolism after unilateral adrenalectomy for adenoma. The unilateral extraperitoneal approach gives shorter morbidity and potentially fewer serious complications.
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PMID:Selection of patients and operative approach in primary aldosteronism. 118 May 75

Plasma aldosterone, plasma renin activity and plasma cortisol were determined in patients with primary aldosteronism in response to posture and at short-time intervals overnight while the patient were supine. In the 5 patients with an aldosterone-producing adenoma postural changes in plasma aldosterone were paralleled by those in cortisol while plasma renin activity was generally undetectable indicating an ACTH-dependent secretion of aldosterone. This concept was supported by the observation that in 3 of these patients who were tested overnight 1. episodic secretion of plasma aldosterone was paralleled by those of cortisol and 2. episodic secretion of plasma aldosterone could be blunted by dexamethasone. In the patient with idiopathic adrenal hyperplasia concomittant changes in plasma aldosterone and plasma renin activity occurred. The assumption that in this patient the fluctuations in plasma aldosterone were mediated through changes in renal renin secretion was supported by the finding that episodic secretion of plasma aldosterone persisted under suppression of ACTH-secretion by dexamethasone. Our results indicate, that the described procedures may all serve as diagnostic criteria to differentiate between aldosterone-producing adenoma and idiopathic adrenal hyperplasia.
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PMID:Regulation of aldosterone secretion in primary aldosteronism. 118 23

In 16 patients with hypokalemic hypertension the combination of abnormally high and unsuppressible plasma aldosterone with low or undetectable renin activity led to the diagnosis of primary aldosteronism. To differentiate between aldosterone producing adenoma and idiopathic bilateral hyperplasia, determination of aldosterone concentration in both adrenal veins was performed in 12 patients. In 4 of these patients the two forms of primary aldosteronism could not be differentiated as in these cases only one of the two adrenal veins simultaneously showing an abnormally high aldosterone concentration could be canulated. Plasma aldosterone and plasma cortisol were determined overnight (20.00-8.00 h) at short time intervals in 8 patients with adenoma, 1 patient with carcinoma of the adrenal cortex and 3 patients with bilateral hyperplasis. In all patients with adenoma a significant correlation between aldosterone and cortisol was observed (p less than 0.05-0.001) whereas no correlation was seen in the patients with hyperplasia and carcinoma. The clinical importance of these findings is that in the presence of ACTH-dependent secretion of aldosterone the site of the adenoma can be predicted even when blood from only one adrenal vein is obtained.
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PMID:[Primary aldosteronism: diagnosis, laterality and regulation of hormone secretion]. 121 58

We used 131I-19-iodocholesterol as an adrenal-imaging agent in 27 hypertensive patients who had biochemical evidence of abnormalities in the renin-angiotensin-aldosterone system. In 10 of 12 patients in whom the biochemical findings suggested the presence of an aldosterone-producing adenoma the adrenal uptake was asymmetric. The adenoma was subsequently confirmed in all eight patients in this group who underwent operation. In contrast, the adrenal uptake was asymmetric in only one of 13 patients with biochemical evidence of iodopathic hyperaldosteronism or low-renin essential hypertension. Two patients with adrenal carcinoma causing primary aldosteronism did not concentrate the isotope in their tumors. When metabolic studies suggest an aldosterone-producing adenoma, adrenal imaging with 131I-19-iodocholesterol may locate the tumor before operation.
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PMID:Location of aldosterone-producing adenomas with 131I-19-iodocholesterol. 124 8

The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.
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PMID:[Primary aldosteronism]. 126 63


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