Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to elucidate renal uric acid metabolism in patients with primary aldosteronism (PA;16 cases) as compared with normotensive subjects (NT;25 cases) and essential hypertensives (EHT;51 cases). All subjects were hospitalized and received a regular diet(Na;120 mEq,K;75 mEq,daily) for more than two weeks, after which renal clearance tests were performed, and serum uric acid(SUA), fractional excretions of uric acid(FEUA), sodium(FENa), and inorganic phosphorus(FEP) were evaluated. Plasma aldosterone concentration(PAC) was measured in 16 patients with PA before treatment and in 8 patients after adrenalectomy. SUA was lower in PA than in either NT or EHT, and this lowering was more obvious in male subjects. In NT, PA and EHT, FEUA, an index of renal excretion of uric acid, correlated negatively with SUA and positively with FENa and FEP, which reflected sodium reabsorption at the renal total tubules and proximal tubules, respectively. Although FENa was nearly the same in all the three groups, FEUA and FEP were significantly higher in PA than in EHT or NT. However, no significant correlation was found between PAC and SUA or FEUA in PA. In PA a significant increase of SUA, and decreases of FEUA and FEP were observed after the removal of adenoma compared to before the surgery. These results suggest that uric acid transport might be closely related to sodium transport in the renal tubules, particularly at the proximal site, and also lead to the conclusion that the lower SUA in PA resulted from the suppression of reabsorption and/or an enhancement of secretion of uric acid in the proximal tubules, being related to the so-called escape phenomenon.
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PMID:[Study on uric acid metabolism in patients with primary aldosteronism]. 154 67

Urinary excretion of 18-hydroxycortisol (18-OHF), 18-hydroxycorticosterone (18-OHB) and aldosterone 18-glucuronide (Aldo-18-glu) was measured in 10 patients with primary aldosteronism; 5 with aldosterone-producing adenoma (APA) and 5 with idiopathic hyperaldosteronism (IHA), 10 patients with essential hypertension (EHT) and 11 normotensive subjects. In EHT patients, urinary 18-OHF (172 +/- 15 micrograms/24h) and 18-OHB (3.1 +/- 0.6 micrograms/24h) values were not significantly different from 18-OHF (142 +/- 35 micrograms/24h) and 18-OHB (3.6 +/- 0.5 micrograms/24h) in the controls. Urinary 18-OHF values were significantly higher in APA (640 +/- 213 micrograms/24h) when compared with controls and EHT, whereas 18-OHB (11.3 +/- 1.5 micrograms/24h) values were only slightly elevated. Both 18-OHF and 18-OHB were significantly increased in APA compared with 18-OHF (232 +/- 56 micrograms/24h) and 18-OHB (4.6 +/- 0.3 micrograms/24h) in IHA. The two urinary steroids, especially 18-OHF proved to be a useful marker for the diagnosis of APA, confirming the previous findings. Aldo-18-glu was not significantly different between APA and IHA. In normal subjects when sodium intake was restricted to 48meq/day for four days the urinary 18-OHF was increased two fold to 383 +/- 59 micrograms/24h (p less than 0.01 vs control period) associated with comparable rise in plasma renin activity. This suggests that the biosynthesis of 18-OHF is partly under control of renin-angiotensin axis in normal subjects.
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PMID:Determination of urinary 18-hydroxycortisol in the diagnosis of primary aldosteronism. 156 Jan 87

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

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

Adrenal venous sampling of blood was performed for nine patients with aldosterone-producing adenoma (APA). Measurement of adrenal venous aldosterone is useful for localization of APA but difficult, because catheterization of the right adrenal vein is not easy, and the blood is diluted by nonadrenal flow. To solve these problems, levels of aldosterone (A; ng/dl) and cortisol (C; micrograms/dl) were measured in samples from the left adrenal vein (LAV) and the inferior vena cava (IVC), and the LAV A/C and (LAV A/C)/(IVC A/C) ratios were calculated. These ratios were also obtained for 16 patients with essential hypertension. The adenoma could be localized in three of the nine cases by the measurement of aldosterone alone, but the use of a LAV A/C ratio greater than 5 x 10(-3) and a (LAV A/C)/(IVA A/C) ratio less than 1.0 as criteria separated the patients into those with a left APA, right APA, or essential hypertension. Consequently, adrenal venous sampling and the calculation of these ratios enables preoperative localization of APA with more accuracy, especially when the tumor is small or the result of CT and adrenal scintigraphy is not consistent.
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PMID:Localization of aldosterone-producing adenoma: venous sampling in primary aldosteronism. 238 50

Serotonin is known to have aldosterone-stimulating properties in humans, which are counteracted by the serotonin-antagonist metergoline. Suppression of aldosterone levels by cyproheptadine in patients with idiopathic aldosteronism has also been shown. Since ketanserin, a more specific 5-HT2-serotoninergic (5-HT2) antagonist, has been shown to affect aldosterone secretion in essential hypertension, we have further investigated this mechanism by injecting ketanserin (10 mg i.v.) in 10 patients with primary aldosteronism (four adenoma, six idiopathic aldosteronism). A transient decrease (20% when compared with the basal levels) of plasma aldosterone was seen at 30 min. A concomitant decrease of plasma cortisol was also noticed, whereas plasma renin activity and potassium did not change. Blood pressure decreased in all cases. These observations suggest that ketanserin acts directly at the adrenal level by interfering with a possible modulatory activity of serotonin. However, an adrenocorticotropic hormone-mediated effect cannot be completely ruled out at the present time.
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PMID:Effect of ketanserin in primary aldosteronism. 241 45

Plasma concentrations of atrial natriuretic factor and some vasoactive substances were determined in 8 patients with aldosterone-producing adenoma, 10 with idiopathic adrenal hyperplasia, 10 normotensive subjects and 12 patients with essential hypertension. Plasma atrial natriuretic factor concentration in patients with aldosterone-producing adenoma was the highest among the examined groups. Adrenal surgery reduced plasma concentrations of atrial natriuretic factor and aldosterone concomitant with the elevation in urinary sodium excretion, plasma renin activity and urinary sodium-to-potassium ratio. Withdrawal of trilostane (3 beta-hydroxysteroid dehydrogenase inhibitor) in patients with idiopathic adrenal hyperplasia increased plasma concentrations of atrial natriuretic factor and aldosterone, and decreased the urinary sodium-to-potassium ratio, plasma renin activity and urinary sodium excretion. However, reduced urinary sodium excretion following trilostane treatment returned to the control level successively despite the high levels of plasma atrial natriuretic factor and aldosterone. Acute infusion of saline remarkably increased plasma atrial natriuretic factor concentration in patients with idiopathic adrenal hyperplasia and aldosterone-producing adenoma. These results suggest that a high level of atrial natriuretic factor is a characteristic feature in patients with aldosterone-producing adenoma caused chiefly by the expansion of extracellular fluid volume, and circulating atrial natriuretic factor may contribute to regulation of the sodium escape phenomenon in patients with aldosterone-producing adenoma or idiopathic adrenal hyperplasia.
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PMID:The effect of adrenal surgery on plasma atrial natriuretic factor and sodium escape phenomenon in patients with primary aldosteronism. 252 99

Plasma 18-hydroxycorticosterone (18-OHB) and aldosterone responses to angiotensin II (AII) and ACTH were examined in 2 patients with a 18-OHB-producing tumor (18-OHBPT) versus those in 8 patients with a aldosterone-producing adenoma (APA), 7 patients with low renin essential hypertension (LREH) and 10 normal subjects. Plasma 18-OHB and aldosterone levels and the 18-OHB: aldosterone ratio were high in patients with an APA and normal in patients with LREH. In patients with a 18-OHBPT, plasma 18-OHB and aldosterone levels were high and normal, respectively, resulting in a 2-fold greater 18-OHB: aldosterone ratio than that in patients with an APA. Patients with an APA had a blunted response of plasma 18-OHB and aldosterone to AII and a supranormal response of these corticoids to ACTH. Patients with LREH had a supranormal response of plasma 18-OHB and aldosterone to AII and a normal response of these corticoids to ACTH. In patients with a 18-OHBPT the responses of both plasma 18-OHB and aldosterone to AII and ACTH closely resembled those in patients with an APA but not in patients with LREH. These data suggest that 18-OHBPT may be a variant of aldosteronomas, producing a large amount of 18-OHB and a small amount of aldosterone.
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PMID:Altered responses of plasma 18-hydroxycorticosterone and aldosterone to angiotensin II and adrenocorticotropin in patients with a 18-hydroxycorticosterone-producing tumor. 255 39

Red cell sodium (RBC-Na+) concentrations were measured using 23Na nuclear magnetic resonance (NMR), without the destruction of erythrocyte membranes. Subjects were categorized into four groups: 20 normotensive subjects (NT group), 20 age-matched essential hypertensive patients (EHT group), 10 patients with primary aldosteronism (PA group), and 18 patients treated with digoxin (DIG group). Although RBC-Na+ concentrations were similar between the NT group (6.14 +/- 0.80 (Mean +/- SD) mmol/l) and the EHT group (5.92 +/- 0.99), they were significantly higher in both the PA group (7.55 +/- 0.88, p less than 0.001) and the DIG group (8.43 +/- 3.81, p less than 0.02). In the PA group, RBC-Na+ concentrations decreased significantly after resection of the adenoma, and there was an inverse relationship between serum potassium and RBC-Na+ concentrations (r = -0.65, p less than 0.01). In the DIG group, RBC-Na+ concentrations tended to increase in proportion to serum digoxin levels (r = 0.53, p less than 0.05). These results support the view that RBC-Na+ concentrations are determined primarily by Na+/K+-pump activity of red cell membranes. This study showed also that Na+ NMR is an useful method determining intracellular Na+ concentrations.
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PMID:Clinical application of sodium-23 nuclear magnetic resonance for measurement of red cell sodium concentrations. 259 44

Authors report here an interesting case of a woman who has been treated for essential hypertension for 12 years. Beside the hypertension, an extreme virilization appeared. A large adenoma, originated from the left adrenal gland have been explored behind the clinical picture. After surgical removal of the adenoma, adrenocortical hormones decreased to the normal levels. Systemic blood pressure decreased considerably the virilisation showed gradual involution. The correct treatment of the patient was a decade late, resulting in the development of encephalopathic syndromes.
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PMID:[Essential hypertension caused by a virilizing adrenal tumor]. 272 34


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