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

Plasma concentrations of renin and aldosterone were measured before and 60 min after taking 25 mg captopril in 242 patients with arterial hypertension (124 men, 118 women, aged 51.9 +/- 12.7 years; unilateral aldosterone-producing adrenal adenoma in 8, idiopathic hyperaldosteronism in 16 and essential hypertension in 189). Basal plasma aldosterone levels were twice as high in those with adenoma or hyperaldosteronism (216.9 +/- 99.1 pg/ml and 256 +/- 123 pg/ml, respectively) as in those with essential hypertension (117.7 +/- 115 pg/ml). Basal renin levels in adenoma and idiopathic hyperaldosteronism (1 +/- 0.8 microU/ml and 2.6 +/- 1.9 microU/ml, respectively) were decreased compared with those in essential hypertension (13.1 +/- 14.2 microU/ml). The basal aldosterone/renin ratio was higher in adenoma (436 +/- 370 pg/microU) and idiopathic hyperaldosteronism (615 +/- 950 pg/microU) than in essential hypertension (52.9 +/- 151.3 pg/microU). The sensitivity of this ratio in combination with the aldosterone concentration was 100% for recognizing an adrenal adenoma, its specificity 92.7%. The mean plasma aldosterone level after captopril administration did not change in adenoma patients, but fell to 162 +/- 85 pg/ml (P less than 0.001) in those with idiopathic hyperaldosteronism. These data indicate that the captopril test contributes to distinguishing primary from idiopathic hyperaldosteronism.
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PMID:[Does the captopril test improve the diagnosis of primary hyperaldosteronism?]. 164 14

We report the case of a 38-year-old patient with primary hyperaldosteronism. The diagnosis was made by the demonstration of a non-suppressible high aldosterone level in association with a hypokalemia, an inappropriate kaliuresis and low plasma renin activity. As the choice of the therapeutic approach is dictated by the subtype, further investigation was needed. Using a number of hormonal studies and noninvasive imaging techniques, we could establish the diagnosis of adrenocortical adenoma. Histological examination confirmed our diagnosis. We further discuss briefly the characteristics of the four subtypes of primary hyperaldosteronism and show that the used biochemical markers and imaging techniques are able to differentiate them.
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PMID:Diagnostic approach to patients with primary hyperaldosteronism. 164 27

A 25-year-old female was admitted for evaluation of hypertension and hypokalemia. Plasma renin activity was suppressed and plasma aldosterone level was higher than normal. The CT scan of adrenal gland revealed a 2.5cm in size low density tumor mass over right adrenal area, and NP-59 adrenal scan showed early and persistent uptake of radioactivity in the right adrenal gland. Interestingly, the plasma aldosterone level was elevated, decreased and unchanged to postural change on three different occasions. After right adrenalectomy, the plasma aldosterone level decreased to 4.77ng/dl, blood pressure, serum potassium, and plasma aldosterone returned to normal response to postural change. Histologically, it was compatible with the picture of cortical adenoma. However, the tumor cell may not have reached autonomous function yet, since different responses of plasma aldosterone to postural change were observed clinically.
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PMID:Aldosterone-producing adenoma--variable serum aldosterone response to postural change: a case report. 165 41

This paper documents an unexpected rise in plasma aldosterone concentration (PAC) to the furosemide-upright test despite a decrease in adrenocorticotropin (ACTH) by dexamethasone, and an unresponsiveness in plasma renin activity to this stimulus in a patient with aldosterone producing adenoma. Furthermore, this patient showed an appropriate response in PAC to a rapid ACTH test, and an insensitivity in PAC to angiotensin-II (Ang-II) infusion. Other factor(s) besides ACTH or Ang-II may play a role in the plasma aldosterone response to ambulation after intravenous furosemide administration in patients with primary aldosteronism.
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PMID:An unexpected rise in plasma aldosterone to furosemide-upright test in primary aldosteronism due to aldosterone producing adenoma. 166 49

Twelve patients (7 men and 5 women) with an average age of 53 years (range 37-69) were hospitalized for renal stones and found to have primary hyperparathyroidism. Five were hypertensive and 7 normotensive. The systemic hemodynamics, plasma renin activity and glomerular filtration rate were evaluated before and at least 6 months after removal of a parathyroid adenoma. After surgery the mean intra-arterial blood pressure fell in almost all patients, due to some reduction in the peripheral vascular resistance index with no change in the cardiac index. However, the hemodynamic variations were not uniform in all patients. No change was seen in plasma renin activity and glomerular filtration rate. A positive correlation between the percent change in mean arterial pressure and percent decrease in total serum calcium was found. The results obtained indicate that it is likely that hypercalcemia plays some role both in patients with high and those with normal blood pressure. The systemic hemodynamic changes after parathyroidectomy indicate that the fall in peripheral vascular resistance could have a certain influence.
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PMID:Systemic hemodynamic pattern in primary hyperparathyroidism and its changes after parathyroidectomy. 177 35

The effect of captopril on the aldosterone response to potassium was studied in 6 patients with idiopathic adrenal hyperplasia (IAH) and in 4 patients with an aldosterone-producing adenoma (APA), who all have suppressed activity of circulating renin-angiotensin system (RAS). Precaptopril, KCl infusion induced a significant increase in aldosterone in both groups. This increment was significantly blunted by captopril in IAH, but not in APA. Decreased potassium-stimulated aldosterone secretion after captopril in IAH supports the hypothesis that adrenal RAS plays a role in aldosterone production under potassium stimulation.
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PMID:Effect of captopril on aldosterone response to potassium infusion in primary aldosteronism. 177 41

Plasma levels of atrial natriuretic peptide (ANP) were measured in patients with normal renin essential hypertension (n = 12), low renin essential hypertension (n = 11) and primary aldosteronism due to aldosterone producing adenoma (APA, n = 8) and idiopathic hyperaldosteronism (IHA, n = 3) after overnight rest in the supine position and after 4 h upright posture and furosemide administration. Plasma renin activity (PRA) and aldosterone (Aldo) levels were also determined. Compared to normal renin essential hypertension (33.6 +/- 2.2 pg/ml), basal plasma ANP was significantly higher in low renin essential hypertension (66.8 +/- 6 pg/ml), IHA (54.1 +/- 6.3 pg/ml) and APA before (62.4 +/- 4.9 pg/ml) but not after adrenal surgery (22 +/- 3 pg/ml). After upright posture and furosemide administration plasma ANP was decreased (p less than 0.01) in patients with low renin and, less markedly, with normal renin essential hypertension, however not in IHA and APA. In about half of the patients with low renin essential hypertension, unchanged PRA after upright posture and furosemide administration was associated with increased plasma Aldo and decreased ANP levels. We conclude that (i) the relatively high basal plasma ANP levels in low renin essential hypertension, IHA and APA may reflect the presence of volume expansion in these patients; (ii) the hormonal responses to upright posture and furosemide administration in patients with normal and low renin essential hypertension may indicate a counterregulatory role of ANP during activation of the renin-angiotensin-aldosterone system; (iii) the high plasma ANP, which is unresponsive to upright posture and furosemide administration, in patients with APA and IHA may be a potentially interesting new finding whose pathophysiological significance remains to be established.
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PMID:Dissociation of plasma atrial natriuretic peptide responses to upright posture and furosemide administration in patients with normal-, low renin essential hypertension and primary aldosteronism. 183 96

Isotonic-isooncotic central volume expansion by head-out water immersion was induced in six aldosterone-producing adenoma subjects and in six patients with idiopathic hyperaldosteronism. Plasma renin activity and plasma aldosterone levels did not significantly change during water immersion while serum cortisol was significantly suppressed (P less than .001) and the aldosterone-cortisol ratio increased (P less than .02) in aldosterone-producing adenoma patients. Water immersion also revealed the failure of plasma aldosterone levels to decrease below 10 ng/dL in these subjects, thus confirming previous results obtained during isotonic saline infusion. Otherwise, plasma renin activity and plasma aldosterone were significantly reduced (P less than .05 and P less than .01 respectively) by water immersion and plasma aldosterone invariably fell below 10 ng/dL in patients with idiopathic aldosteronism. In view of the diagnostic reliability of such a suppression test we conclude that water immersion is suitable for discriminating between the two forms of primary aldosteronism. We therefore suggest its use for assessing renin-aldosterone responsiveness in primary aldosteronism.
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PMID:A new diagnostic test for primary aldosteronism. 193 Aug 52

Postural stimulation tests (PST) from 146 patients with primary aldosteronism were reviewed: 83 had an aldosterone-producing adenoma (APA), 48 idiopathic hyperaldosteronism (IHA), nine primary adrenal hyperplasia (PAH), and six aldosterone-producing renin-responsive adenoma (AP-RA). Plasma aldosterone and cortisol levels were measured after overnight recumbency and in response to upright posture for 2 to 4 h. The test was considered invalid in 32% of the patients because cortisol levels increased during the maneuver. As both cortisol and aldosterone are responsive to ACTH in subjects with primary aldosteronism, as well as in normal subjects, we examined their percent variation instead of the absolute values. In order to validate those tests in which cortisol increased, we subtracted the percent cortisol change from the percent aldosterone response. An aldosterone increase of less than 30% (considered a positive response for the presence of an adenoma) identified 76 of the 89 patients with an adenoma (APA and AP-RA) (sensitivity of 85%). Among the 13 false-negative tests, six were proven cases of AP-RA. In each and every case an adenoma was detected by CT/MRI scanning (or bilateral adrenal vein catheterization). Hypertension was ameliorated or cured by surgery. A postural response of less than 30% was also present in 11 of the 57 patients who did not have a discrete adenoma confirmed by imaging techniques (specificity of 81%). Among these false-positive results there were the nine cases of PAH where the hypertension could be ameliorated or cured by partial removal of hyperplastic adrenal tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reassessment of the predictive value of the postural stimulation test in primary aldosteronism. 193 Aug 62

A case of left adrenal adenoma with bilateral testicular Leydig cell tumor in a 38-year-old man is reported. He had received bilateral orchiectomy for testicular Leydig cell tumor at the age of 37. After operation computed tomography revealed left adrenal mass and aldosterone-secreting adrenal tumor was suspected. Left adrenalectomy was performed and histopathological diagnosis was adrenocortical adenoma. Serum ACTH, aldosterone and plasma renin activity were still high after operation. The adrenal cortex and gonads are of common embryologic origin and the histologic pattern may overlap. Examination of the adrenal gland is necessary for the patient with a testicular Leydig cell tumor.
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PMID:[Adrenal adenoma with bilateral testicular Leydig cell tumor: a case report]. 195 32


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