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)

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

Abdominal computed tomography (CT) was performed on nine patients with primary aldosteronism in an attempt to evaluate the utility of this noninvasive procedure in localizing aldosterone-producing adenomas. Confirmation of the diagnosis of primary aldosteronism was made by demonstrating elevated urinary aldosterone excretion, low PRA, and failure of plasma aldosterone to fall after acute saline load. Each patient had diagnostic lateralizing adrenal venous sampling and adrenal venography before unilateral adrenalectomy. The CT scan correctly predicted unilateral adenoma in the four patients whose tumors measured the largest in diameter at surgery. Bilateral tumors measuring 0.8 and 1.2 cm on scan (at or below the resolution capabilities of our scanner) were falsely predicted in two patients. The CT scan failed to identify an adrenal abnormality in three patients whose tumors measured 0.9, 1.0, and 1.0 cm in greatest diameter. It is concluded that at its current state of precision, the CT scan is of diagnostic utility in primary aldosteronism when a large adenoma is present. In our patients, the adrenal venogram and CT scan were equally accurate. The sampling of adrenal venous blood for aldosterone and cortisol remains the gold standard for localization of unilateral adenoma.
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PMID:Localization of aldosterone-producing adenoma by computed tomography. 47 53

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.
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PMID:Plasma renin activity and urinary aldosterone in acromegaly. 48 12

To detect changes in previously unmeasurable low renin activity plasma specimens of 20 patients with primary aldosteronism (12 with an unilateral adenoma and 8 with idiopathic bilateral adrenal hyperplasia), obtained at short term intervals between 20.00 and 8.00, were incubated over a prolonged period of 18 hours. 6 of 12 patients with an aldosterone producing adenoma (APA) and 3 of 8 patients with idiopathic bilateral adrenal hyperplasia (IAH) showed typical night-day variations of PRA with lower values before and higher values after midnight. 7 of these 9 patients with night-day rhythmicity of PRA simultaneously showed secretory episodes. In 2 patients (1 with APA, 1 with IAH) PRA was constantly undetectable (less than 0.2 ng/ml . 18 h) and in 2 patients with APA a fixed secretion of renin was observed. We failed to demonstrate typical night-day variations of PRA in 3 patients with APA and in 4 with IAH, although in 5 of these 7 patients secretory episodes of PRA were found. Our results show that different patterns of PRA curves may be observed both in patients with APA and IAH. Thus, analysis of PRA curves is of no value to differentiate patients with APA from those with IAH.
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PMID:Night-day variations of renin-activity in primary aldosteronism. 57 49

Twenty-eight patients with primary aldosteronism were treated from 1974 to 1990. The serum potassium concentration was higher than normal level in all patients with the exception of one whose serum potassium concentration was normal. All of 14 tested patients had low renin values. The plasma aldosterone concentration was higher than standard value in all of 5 patients, and the A/PRA ratio was more than 400. Spironolactone administered preoperatively could not only normalize serum potassium concentration level and blood pressure, but also predict postoperative prognosis of hypertension. Only 37.5% of adenomas were detected by retroperitoneal pneumography with tomography in the early period. 80.0% of adenomas were found by B-ultrasonography, and 92.8% by CT after 1982. The operation was done through abdominal incision because of indefinite localization of adenoma before 1982, and the operation was performed through lumbar incision because of definite localization of adenoma after 1982.
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PMID:[Diagnosis and treatment of primary aldosteronism]. 130 99

Forty-one patients with aldosterone-producing adenoma (APA) were subjected to a dexamethasone suppression test (DST) before surgery. Serum cortisol and urinary excretion of 17-hydroxycorticosteroids were suppressed by dexamethasone in 39 patients [DST(+)]. In two patients (cases A and B), they were not suppressed [DST(-)]. Clinical manifestations of the two DST(-) patients were similar to those of DST(+) patients. Hypertension, hypokalemia, high serum aldosterone levels, and suppressed PRA were found in all of the patients. The cut surfaces of the adenomas from all of the patients, including cases A and B, were golden yellow, which is typical of APA. However, atrophies of the adjacent normal tissues were evident exclusively in the two DST(-) patients. After removal of the affected adrenals, the serum cortisol level was suppressed by dexamethasone in one of the DST(-) patients (case B). These findings suggested autonomous cortisol production by APA. To evaluate whether cortisol could be produced from the adenoma tissue, the presence of several steroidogenic enzymes was studied by immunohistochemistry and mRNA analysis in the adenomas and the adjacent nonneoplastic adrenals from the 2 DST(-) and 5 DST(+) patients. Immunohistochemical analysis demonstrated that steroidogenic enzymes were expressed in APA tumor tissues from both DST(-) and DST(+) patients. In both groups, mRNAs coding steroidogenic enzymes were present not only in the nonneoplastic but also in the tumor tissues. Quantitative analysis of the mRNA levels revealed that in the adrenals from DST(+) patients, the mRNAs were more abundant in nonneoplastic tissue than in tumor tissue. However, in those from DST(-) cases, the mRNAs were much more abundant in the tumor tissues than in the nonneoplastic tissues. These results indicate that tumor cells of the two DST(-) patients autonomously synthesized not only aldosterone but also cortisol. The diameters of the tumors from the two DST(-) patients exceeded 3 cm, while those from other DST(+) patients were smaller. In patients with large APA, adrenal insufficiency should be anticipated upon removal of the tumor.
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PMID:Dexamethasone-nonsuppressible cortisol in two cases with aldosterone-producing adenoma. 199 11

Since calcium entry blocker drugs can interfere with aldosterone secretion in vitro, a similar effect in vivo, in man, has been suggested and partially confirmed. The data available in primary aldosteronism are more controversial. Therefore, we have studied the acute and chronic effect of nifedipine in 7 patients with idiopathic hyperaldosteronism (IHA) and 8 with aldosterone producing adenoma (APA). On 2 different days, 10 mg of nifedipine or placebo were given sublingually to the patients and blood pressure and heart rate were recorded every 5 min. for 60 min. Plasma aldosterone, cortisol, PRA and serum K+ were measured at 0, 30 and 60 min. 5 patients with IHA and 6 with APA received nifedipine 20 mg per os bid for 3 months; the same parameters were evaluated on days 0, 30, 60 and 90; urinary aldosterone was measured on days 0, 30, 60 and 90. BP decreased in both groups both after acute and chronic administration of nifedipine. Plasma aldosterone showed a similar trend either after acute nifedipine or placebo; however, during chronic treatment it was slightly decreased in IHA patients. Cortisol, PRA, urinary aldosterone and K+ remained unchanged. In conclusion, nifedipine is an effective antihypertensive agent also in primary aldosteronism; its aldosterone inhibiting properties are minimal and seem to be present only during long-term therapy in IHA.
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PMID:Acute and chronic effect of nifedipine in primary aldosteronism. 280 62

Endogenous opioids have been suggested to play a pathogenetic role in idiopathic hyperaldosteronism (IHA). To investigate this issue, the opiate antagonist naloxone was administered to 8 normals and 14 patients with primary aldosteronism, 6 with an aldosterone-producing adenoma (APA) and 8 with IHA. In normals, APA, and IHA, naloxone caused a significant increase in plasma cortisol and no change in ACTH, renin activity (PRA), and aldosterone levels. All subjects were retested after dexamethasone 2 mg. ACTH and cortisol were reduced and PRA was unchanged without modifications after naloxone. Baseline aldosterone was unaltered in all. While normals and APA failed to show any aldosterone response to naloxone under dexamethasone, IHA patients demonstrated a significant decrease. beta-Endorphin concentrations were in the normal range before and after dexamethasone. In normals as well as in APA and IHA, naloxone may act directly on the adrenal cortex increasing zona fasciculata responsiveness to physiological levels of ACTH. The decrease of aldosterone induced by naloxone in IHA under dexamethasone may be due to an intra-adrenal opioid control of zona glomerulosa in this disorder.
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PMID:Effect of naloxone on the adrenal cortex in primary aldosteronism. 283 6

A 23-yr-old male patient with normotensive primary aldosteronism is reported. He complained of muscle weakness, polydipsia, and polyuria. His blood pressure was generally 118/60 to 124/70 mm Hg. Serum sodium, potassium and chloride were 152.2.2, and 108 meq/liter, respectively. Arterial blood pH, glomerular filtration rate, renal plasma flow and circulating plasma and blood volumes were normal, and plasma bicarbonate was normal or elevated. PRA was 0.16 ng/ml.h and did not increase significantly after sodium deprivation, ambulation, and iv furosemide injection. Plasma aldosterone was 64.1 ng/100 ml. He showed pressor responses to infused angiotensin II and norepinephrine which were similar to those in normal men. Adrenal scintiscanning after iv injection of [131I]6 beta-iodomethyl-19-nor-cholesterol during dexamethasone administration showed dense uptake on the right adrenal and minimal uptake on the left. Intravenous infusion of angiotensin III at a rate of 20 ng/kg. min for 30 min did not cause an increase in plasma aldosterone. Serum electrolytes became normal after spironolactone but not after dexamethasone. At surgery, the right adrenal, bearing a benign adenoma, was removed. After surgery, blood pressure was unchanged, but all biochemical abnormalities disappeared. The cause of this normotension remains to be elucidated, but the diagnosis criteria of primary aldosteronism should now be partly modified.
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PMID:Normotensive primary aldosteronism: report of a case. 626 53

Prostacyclin has been implicated as a mediator of renin release, whereas angiotensin II evokes prostaglandin I2 (PGI2) release from both vascular and nonvascular tissues in vitro. The physiological significance of these observations was assessed by measurement of an index of endogenous prostacyclin biosynthesis in human volunteers during varied activation of the renin-angiotensin system secondary to manipulation of dietary sodium. Excretion of the major urinary metabolite of prostacyclin in man, 2,3-dinor-6-keto-PGF1 alpha (PGI-M), fell from 295 +/- 51 to 176 +/- 35 (+/- SEM) ng g creatinine-1 (P less than 0.01) in 10 normal subjects when sodium intake was decreased from 150 to 10 meq/day. In five patients with primary hyperaldosteronism, PGI-M fell from 199 +/- 34 ng g creatinine-1 preoperatively to 120 +/- 26 pg/mg creatinine-1 after removal of the adenoma. In such patients, the reduction in PGI-M was associated with a significant increase in PRA. Thus, in both normal subjects and patients with hyperaldosteronism, PGI-M excretion fell rather than increased with activation of the renin-angiotensin system. This suggests that systemic biosynthesis of PGI2 is unrelated to renin release and that angiotensin II is unlikely to stimulate endogenous prostacyclin biosynthesis under these conditions in man.
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PMID:Endogenous prostacyclin synthesis is decreased during activation of the renin-angiotensin system in man. 636 36


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