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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 50-year old female with primary aldosteronism and masked hyperaldosteronemia is reported. Her blood pressure was 176/110 mmHg with no paralysis of hypokalemia. Serum potassium, aldosterone and renin activity were 4.3 mEq/L, 17 ng/dl and 0.6ng/ml/h, respectively. Following a stimulation test by sodium loading and furosemide plus standing, neither aldosterone nor renin activity responded. Adrenal computed tomographic scanning, ultrasonography and cortical scintiscanning failed to reveal the tumor mass. A definite diagnosis of aldosterone producing adenoma was made after adrenal venous sampling in which the concentration of aldosterone was 15-fold greater in the right adrenal vein than in the left. The diagnosis of right adrenal cortical adenoma was confirmed by surgery. Thus, this case indicates the usefulness of the sampling technique in making an accurate diagnosis for primary aldosteronism with normo-kalemia, normo-aldosteronemia and normo-reninemia.
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PMID:A case report of aldosterone producing adenoma with masked hyperaldosteronemia. 355 Nov 99

An adrenocortical carcinoma (15.5 g) secreting excessive amounts of steroids with weak mineralocorticoid activity in a 25-year-old woman was studied with particular reference to its in vivo and in vitro secretions of steroids. Severe hypertension, occasional low serum potassium and suppressed PRA were the major clinical findings, and were improved with removal of the tumor. In the preoperative stage, plasma levels of 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone, corticosterone and 18-hydroxycorticosterone were all increased. However, the plasma level of aldosterone was repeatedly normal. Although plasma levels of pregnenolone, 17-hydroxypregnenolone, progesterone and 17-hydroxyprogesterone were very high, those of other late step steroids, i.e. 11-deoxycortisol, cortisol, dehydroepiandrosterone, androstenedione and testosterone were almost normal. From these findings, a major etiological role of weak mineralocorticoids such as 11-deoxycorticosterone, 18-hydroxycorticosterone and corticosterone in her hypertension was suggested. Pregnenolone and 17-hydroxypregnenolone in tumor tissue were increased, but 11-deoxycorticosterone, corticosterone, aldosterone, cortisol and adrenal androgens such as dehydroepiandrosterone, androstenedione and testosterone were below normal or low normal. In vitro production of 11-deoxycorticosterone, aldosterone or cortisol by the tumor tissue slices was very low and scarcely responded to synthetic ACTH.
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PMID:An adrenocortical tumor secreting weak mineralocorticoids. 360 14

Adrenocortical carcinoma is a rare disorder that can be revealed by an isolated syndrome of mineralocorticoid excess. In a retrospective study of 137 patients referred to our hypertension clinic in the past 10 years for primary aldosteronism, four cases of adrenocortical carcinoma were identified. The clinical presentation of these patients was similar to that of patients with Conn's adenoma, but preoperatively, malignant tumoral primary aldosteronism was suspected because of profound hypokalemia, marked elevation in plasma aldosterone levels, and enlarged size and weight of an heterogenous adrenal tumor with internal calcifications. Malignancy was confirmed by the histologic features. No prognostic criteria could be established and two patients died despite specific surgery, which was performed in all cases. More recent developments in the use of mitotane led to the addition of adrenocorticolytic therapy in the remaining two patients, who are still alive at the time of this report.
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PMID:Isolated clinical syndrome of primary aldosteronism in four patients with adrenocortical carcinoma. 367 52

Operation for tumors responsible for a Conn's syndrome was performed in 16 patients, 11 women and 5 men, over a period of 13 years, the average time before diagnosis being 5 1/2 years. All patients presented hypertension, permanent in 14 and paroxysmal in 2 cases while blood potassium levels were below 3 mmol/l in all patients. Diagnosis was confirmed by elevation of plasma aldosterone and of urine tetrahydroaldosterone, associated with low plasma renin activity not responding to a stimulus. The tumor was demonstrated by imaging in 15 cases before operation and its mean size was 1.7 cm. Investigatory methods for diagnosis and localization are discussed. One patient died during the immediate post-operative period from decompensated cardiac failure. Long-term review showed persistent hypertension in 5 patients but electrolyte disturbances were corrected in all cases. Lack of consistency of results of surgical reduction in case of hyperplasia suggests that only patients with hyperaldosteronism related to an adrenal cortex tumor should be operated upon.
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PMID:[Surgery of Conn's syndrome. Apropos of 16 cases]. 370 May

We evaluated the in vitro steroidogenic potential of a benign Leydig cell tumor of the testis. Tumor tissue was found to secrete deoxycorticosterone, progesterone, 17 alpha-hydroxyprogesterone, estradiol and testosterone into the medium. No corticosterone or aldosterone was detected. The ratio of progesterone to 17 alpha-hydroxyprogesterone was 4:1, consistent with a partial enzymatic block of 17 alpha-hydroxylase. The finding of deoxycorticosterone indicates the presence of 21-hydroxylase activity within the tumor. The high local levels of estrogen produced by Leydig cell tumors may induce this enzyme system and, together with the elevated concentrations of progesterone serving as substrate, may provide a favorable hormonal milieu for extra-adrenal deoxycorticosterone production by these neoplasms.
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PMID:In vitro secretion of deoxycorticosterone by a benign Leydig cell tumor of the testis. 371 95

Among the many potential causes of secondary hypertension are renal parenchymal disease, occlusive renal arterial disease, adrenocortical abnormalities, and pheochromocytoma. Renovascular hypertension can result from either renal parenchymal or occlusive renal arterial disease. Laboratory testing can help in identification and differentiation. Parenchymal diseases usually modify the urine substantially without producing urographic abnormalities, while occlusive arterial lesions produce urographic abnormalities but the urine remains normal. The diagnosis of renal occlusive arterial disease is best defined by arteriography. The only definite criterion for the existence of hypertension of renal origin is cure by either nephrectomy or renal revascularization. Adrenocortical causes of hypertension include enzymatic deficiencies, Cushing's syndrome, and primary aldosteronism. In enzymatic deficiencies, the physical findings provide the most important clues to the type of enzyme deficiency involved. In Cushing's syndrome, accurate determination of the cause of the hypercortisolism is important in terms of choice and success of treatment. The diagnosis of primary aldosteronism rests primarily on the demonstration of nonsuppressible aldosterone excretion rate during salt loading; the presence of inappropriate kaliuresis and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Pheochromocytoma, although rare, is a serious and potentially fatal cause of hypertension. Definitive diagnosis depends on laboratory test results, and the tumor is usually localized by computed tomography.
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PMID:Secondary hypertension. A streamlined approach to diagnosis. 372 9

Unilateral adrenalectomy for benign causes of primary aldosteronism is an established procedure. The established surgical cure for aldosterone-producing adenoma justifies a thorough preoperative evaluation. No single test accurately identifies aldosterone-producing adenomas in patients with primary aldosteronism. However, a useful algorithm combines postural studies, computerized axial tomography, and adrenal vein catheterization for selective hormonal assay, if computerized axial tomography is negative or equivocal and the suspicion of aldosterone-producing adenoma is high. If an adrenal mass is present and biochemical studies suggest a diagnosis of aldosterone-producing adenoma, resection of the affected gland from a limited unilateral approach is indicated. Cure can be expected in 80 percent of cases. In the uncommon circumstance that the adrenal tumor was not an aldosterone-producing adenoma but a hyperplastic nodule, these patients may still be cured or more easily controlled with antihypertensive medications. Thirty-eight patients who underwent unilateral adrenalectomy are presented and discussed.
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PMID:Primary aldosteronism: changing concepts in diagnosis and management. 372 4

Calcium and magnesium metabolism was investigated in 10 hypertensive subjects with primary aldosteronism (seven adenomatous, three idiopathic). Serum levels of total calcium (9.03 +/- 0.2 mg/dl) and ionized calcium (2.06 +/- 0.06 meq/liter) were in the low-normal range, except for two patients who had levels of serum ionized calcium clearly above normal. Furthermore, both serum total (n = 6, p less than 0.01) and ionized calcium levels (n = 3) rose postoperatively in the patients who had an aldosterone-producing tumor removed. Dramatic elevations of parathyroid hormone levels (mean, 645 +/- 109 pgeq/liter; normal, less than 150 to 375 pgeq/liter) were seen in the majority of patients, including those two with frank ionized calcium elevations. Magnesium levels were within normal limits (2.07 +/- 0.07 meq/liter). These results indicate that parathyroid hypersecretion is a common feature of primary aldosteronism and also suggest a physiologic relationship between the activity of the renin-aldosterone system and parathyroid physiology. Sodium-volume expansion and negative calcium balance induced by aldosterone excess may predispose to hyperparathyroidism.
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PMID:Calcium metabolism and parathyroid function in primary aldosteronism. 388 68

A 38-year-old woman is described to have a primary hyperaldosteronism due to an aldosteronoma with foci of lymphocytic infiltration. The finding suggests: a concomitant lymphoid adrenalitis; or, an immunological attack to neoplastic cells. The hypothesis is that there may be a relationship in the association. The lymphocytic infiltrates could have a pathogenic role in the development of the aldosterone-producing adrenocortical neoplasm by interrupting some inhibitory mechanism(s) of the cells that secrete aldosterone.
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PMID:May a lymphocytic infiltration have a pathogenic role in an aldosterone-producing adrenal tumor? 401 May 82

Seventeen patients with adrenal adenoma causing Cushing's syndrome, eight patients with Cushing's disease due to hypersecretion of ACTH, and five patients with primary aldosteronism due to an aldosteronoma were studied for their computed tomographic (CT) patterns, hormonal profiles, and macroscopic and microscopic findings of the adrenal gland. Black (or brown) adrenal adenomas were found in 71% of the patients with Cushing's syndrome, but not in patients with aldosteronoma. The adrenal tissue of patients with Cushing's disease was predominantly yellow. The number of compact cells was larger in black or brown adenomas than in yellow tumors or hyperplastic adrenal tissue. In patients with Cushing's syndrome, urinary excretion of 17-ketosteroids (17-KS) and serum aldosterone concentrations were lower in those with black or brown adenomas than in those with yellow adenomas (P less than 0.05). Patients with Cushing's disease had even higher 17-KS and serum aldosterone levels. No difference was found in serum cortisol concentrations and dexamethasone suppressibility in two types of adenomas causing Cushing's syndrome. Visual estimation of radiological density of the adrenal tissue relative to the kidney on CT scan and quantitative measurement of it by CT number revealed a difference between the two types of adrenal tumors causing Cushing's syndrome. Adrenal tumors with decreased density on CT scan were yellow adenomas with predominantly clear cells, and those with equal or increased density were black or brown adenomas with predominantly compact cells. All aldosteronomas had decreased density and consisted of clear cells. It is suggested that black or brown adenomas of the adrenal gland have higher radiological density and accompanying lower serum aldosterone and urinary 17-KS levels than ordinary yellow tumors. The abundance of compact cells may have some significance for the development of this particular type of adrenal tumor.
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PMID:Black (or brown) adrenal cortical adenoma: its characteristic features on computed tomography and endocrine data. 403 Oct 14


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