SEARCH · Search PubMed

Results for “hyperaldosteronism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1982

Effect of oral glucose loading on plasma insulin, potassium, renin and aldosterone in normal subjects and patients with primary hyperaldosteronism.

The effects of standard oral glucose loading (100 g) on plasma aldosterone and some regulatory factors were assessed in patients with primary hyperaldosteronism and normal subjects. Following overnight fast, mean plasma glucose was identical (10 patients and normal subjects approximately matched per age and sex); plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in the patients. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups; plasma renin activity was significantly increased only in normal subjects. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. Relationships among glucose-induced changes in plasma aldosterone and other factors were assessed by multiple regression analysis in these patients and normal subjects as well as an additional group of 21 normal subjects; in the latter, plasma cortisol was also measured and found to decrease significantly after glucose loading. Changes in plasma aldosterone correlated (P less than 0.025) more closely with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that complex metabolic changes occur following glucose ingestion which are capable of modifying aldosterone secretion in normal subjects and primary hyperaldosteronism. The aldosterone-inhibitory effect of glucose tends to be blunted in the latter disorder. This could be related at least in part to an impaired insulin response in primary hyperaldosteronism.

Administration, Oral↗

PubMed1976

[Rectal electrical potential difference and plasma aldosterone in hyperaldosteronism and low-, normal- and high-renin hypertension].

Rectal electrical potential difference (P.D.), plasma aldosterone and plasma renin activity were measured in 25 normal subjects, 80 patients with untreated essential hypertension, 4 patients with primary and 9 patients with secondary hyperaldosteronism. In normal subjects the rectal P.D. was 26 +/- 10 mV (+/- S.D.); in patients with hyperaldosteronism it was 51 +/- 7 mV. Plasma aldosterone and rectal P.D. were correlated significantly (r = 0.84, p less than 0.001) in these two groups combined. In 29% of patients with low-renin hypertension, in 9% of patients with normal-renin hypertension and in 3 out of 8 patients with high-renin hypertension, rectal P.D. was found to be elevated in the presence of normal plasma and urinary aldosterone and no correlation was observed between plasma aldosterone and rectal P.D. (r = --0.09, n.s.). In 3 out of 7 patients with low-renin hypertension and high rectal P.D., plasma and urinary aldosterone were consistently suppressed. Since patients with low renin and high rectal P.D. responded favourably to spironolactone therapy it is suggested that mineralocorticoids other than aldosterone may contribute to the pathogenesis of the hypertension in these cases. The aetiology of raised rectal P.D. in normal and high-renin hypertension is not clear, but both catecholamines and angiotensin II may be involved. The measurement of rectal P.D. alone is of limited value as a screening test for primary hyperaldosteronism in hypertensive patients, but combined with renin measurements it is a valuable tool for further investigation of patients with suspected mineralocorticoid excess syndromes, as well as for adjusting therapy with competitive aldosterone antagonists in patients with proven primary or secondary hyperaldosteronism.

Action Potentials↗

PubMed1999

[Primary hyperaldosteronism--12 clinical cases].

STUDY OBJECTIVES: To show clinical, biochemical, and morphological data of 12 patients with primary hyperaldosteronism: eight with an aldosterone-producing adenoma and four with adrenal hyperplasia. To compare clinical and biochemical parameters of the patients with adenoma and hyperplasia. For those with adenoma, to verify clinical and biochemical modifications after adrenalectomy. PATIENTS AND METHODS: In the 12 patients with hyperaldosteronism, retrospective analysis of clinical (age, sex, blood pressure), biochemical (plasmatic and urinary potassium, plasmatic aldosterone, plasma renin activity, and plasmatic aldosterone/renin activity ratio), and morphological (computed tomography, magnetic resonance, and norcholesterol scintigraphy) data was performed. RESULTS: 1--In the 12 patients with hyperaldosteronism (seven female), the age was 51.0 +/- 10.2 years (mean +/- standard deviation), the systolic pressure 200.9 +/- 34.5 mm Hg and the diastolic pressure 120.0 +/- 12.3 mm Hg. Hypertension was diagnosed 12.0 +/- 10.1 years before. As biochemical evidence, we found kalaemia of 3.06 +/- 0.28 and urinary potassium of 63.4 +/- 16.5 mEq/l, renin activity 0.98 +/- 1.02 ng/ml/h, plasmatic aldosterone of 49.4 +/- 36.0 ng/dl, aldosterone/renin activity > 30 in 83% of the cases. As morphological evidence, computed tomography allowed diagnosis in nine patients, suggested it in two, being doubtful in one. Performed on four patients, resonance confirmed the tomography in three and was not contributive in one. The scintigraphy performed in four patients visualized two adenomas, was negative in one adenoma and in one hyperplasia. 2--In the eight patients with adenoma (six female), the youngest age and the highest diastolic pressure compared with patients with hyperplasia were statistically significant (p < 0.01 and 0.05). In the adenomas, the biochemical changes were more pronounced, but not statistically significant. The plasmatic aldosterone/renin activity ratio was also higher in the adenoma cases. 3--After the adrenalectomy, blood pressure became normal in five patients and was more easily therapeutically controlled in three. The average systolic and diastolic pressures decreased and the biochemical parameters became normal in all patients. The pre/post surgical modification of these parameters had statistical significance (systolic pressure decrease, p < 0.01; diastolic pressure decrease, p < 0.01; kalaemia increase, p < 0.001; renin activity increase, p < 0.01; aldosterone decrease, p < 0.02). The plasmatic aldosterone/renine activity ratio normalized in all patients. CONCLUSIONS: In diagnosing primary hyperaldosteronism, biochemical (kalaemia, urinary potassium, plasmatic aldosterone, renin activity, aldosterone plasmatic/renin activity) and tomography studies were important. On comparing the patients with hyperplasia with those with adenoma, we found that the latter are younger and exhibit higher diastolic pressure, both findings with statistical significance. After adenoma surgery, blood pressure became normal in five patients and improved in three, these findings, and the improvement of the kalaemia, plasmatic aldosterone, and renin activity parameters were statistically significant.

Adenoma↗

PubMed2000

Impaired insulin action in primary hyperaldosteronism.

The presence of insulin resistance is frequently found in essential hypertension. There are, however, only sparse data with respect to the potential presence of insulin resistance in patients with secondary hypertension. We have therefore undertaken a study to reveal the potential occurrence of insulin resistance in primary hyperaldosteronism (PH). The hyperinsulinemic euglycemic clamp technique together with the evaluation of insulin receptor characteristics were used to study insulin resistance in 12 patients with PH. The measured parameters were compared to normal values in control subjects. We have found a significantly lower glucose disposal rate (M, micromol/kg/min) (18.7+/-6 vs. 29.3+/-4), decreased tissue insulin sensitivity index (M/I, micromol/kg/min per mU/l x100) (23.7+/-9.8 vs. 37.5+/-11.6) and also lower metabolic clearance rate of glucose (MCRg, ml/kg/min) (3.8+/-1.5 vs. 7.0+/-1.1) in patients with primary hyperaldosteronism. The insulin receptor characteristics on erythrocytes did not differ in primary hyperaldosteronism as compared to control healthy subjects. We thus conclude that insulin resistance is also present in secondary forms of hypertension (primary hyperaldosteronism) which indicates the heterogeneity of impaired insulin action in patients with arterial hypertension.

Adult↗

PubMed2001

Can primary hyperaldosteronism be considered as a specific form of diabetes mellitus?

Aldosterone-producing adenoma (aldosteronoma)--the most frequent form of primary hyperaldosteronism (PH)--is considered a specific form of diabetes mellitus (DM). In a previous study we demonstrated insulin resistance in patients with PH. We have therefore undertaken a study to evaluate the incidence of abnormalities of glucose metabolism in patients with PH (36 subjects) compared to control subjects with essential hypertension (EH) (21 patients). The following parameters were measured in all studied subjects: office blood pressure (by mercury sphygmomanometer in the sitting position), body mass index (BMI), plasma potassium, plasma glucose and insulin levels during oral glucose tolerance test (OGTT) (0, 60, 120 min), plasma renin activity and plasma aldosterone. Although patients with PH tended to have higher stimulated plasma glucose levels after 60 and 120 min compared to EH, these differences did not attain statistical significance. Patients with EH tended to have higher insulin levels at each measured interval, but due to a high variability these differences were again not significant. There were no significant differences between PH and EH in the proportion of diabetics (20% vs. 14%) or patients with impaired glucose tolerance (18% vs. 10%). In conclusion, we have found the absence of significant differences in the frequency of diabetes mellitus, impaired glucose tolerance and insulin resistance in patients with EH and PH. Our data thus do not support the idea of primary hyperaldosteronism as a specific type of diabetes mellitus. Furthermore, our results indicate that glucose metabolic characteristics in essential hypertension and primary hyperaldosteronism tend to be similar. The definitive conclusion with respect to the possible causal relationship between DM and PH, however, can be obtained only on larger groups of subjects, in particular after the evaluation of the effect of surgical/pharmacological treatment of primary hyperaldosteronism.

Adenoma↗

PubMed1991

[2 cases of primary hyperaldosteronism].

Two clinical cases of women with primary hyperaldosteronism are reported. The patients presented with arterial hypertension, muscular weakness and paresthesia. Severe hypokalemia was found which was resistant to intravenous infusions of potassium but was successfully treated with low daily doses (100-200 mg) of spironolacton, an aldacton antagonist, in the course of 3-4 days. In one of the patients the primary hyperaldosteronism was related to aldosterone secretion by the cells of a malignant corticosteroma, proved histologically. A successful operation led to full recovery of the patient. In the other patient there was an idiopathic form of primary hyper aldosteronism caused by bilateral hyperplasia of the suprarenal cortex. Contemporary diagnostic and therapeutic possibilities in primary hyperaldosteronism as well as the importance of the examination of potassium serum level and kaliuria in the patients with arterial hypertension for the timely and successful diagnosis and treatment of primary hyperaldosteronism are pointed out.

Adrenal Cortex↗

PubMed1983

[Primary hyperaldosteronism: diagnostic value of the administration of a single dose of captopril].

The diagnosis of primary tumoral hyperaldosteronism is based on a series of hormonal parameters, measured under resting conditions and after stimulation. The results of the administration of a single dose of a converting enzyme inhibitor, Captopril (1 mg/kg body weight per os), can support this diagnosis. In contrast to essential hypertension and hyperaldosteronism due to bilateral adrenal hyperplasia, plasma aldosterone levels remain unchanged in tumoral hyperaldosteronism after administrating Captopril. This is a simple test which can be performed in a morning which clearly differentiated 8 cases of primary tumoral hyperaldosteronism from 6 cases of adrenal hyperplasia.

Adenoma↗

PubMed1981

Hyperaldosteronism after heart surgery in children. Part I: Treatment with aldosterone antagonists.

The course of postoperative hyperaldosteronism and its effect on fluid and electrolyte metabolism were studied in children undergoing open and closed heart surgery. Serum sodium was transiently depressed and red cell sodium concentration remained unchanged. Serum and red cell potassium concentrations were low. Hematocrit did not change significantly during the postoperative period ruling out overhydration. Therefore, the electrolyte changes are interpreted to indicate body potassium loss. That hyperaldosteronism caused potassium loss is suggested by an inverse relationship between plasma aldosterone and red cell potassium concentration. No significant differences were observed between patients undergoing open and those undergoing closed heart surgery. An additional, alternately selected group of patients undergoing open heart surgery was treated with aldosterone antagonists beginning 48 hours before surgery. Treatment did not change the course or extent of hyperaldosteronism. Specifically, potassium loss was not diminished and there was no difference in urine volume postoperatively. We conclude that aldosterone antagonists in the dosage used had no effect on the course of postoperative hyperaldosteronism.

Adolescent↗

PubMed1998

Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy.

OBJECTIVE: To determine the frequency of nonfunctioning adrenal masses in patients with primary hyperaldosteronism. DESIGN: A case series. SETTING: A tertiary care hypertension clinic. PATIENTS: Twenty-seven consecutive patients with primary hyperaldosteronism. MEASUREMENTS: Blood pressure, serum electrolytes, supine and upright plasma renin, cortisol and aldosterone levels, selective adrenal vein aldosterone and cortisol levels, adrenal computed tomography (CT) scans and pathology reports. RESULTS: There was considerable overlap in the clinical features and laboratory investigations for patients with unilateral aldosteronoma and those with bilateral adrenal hyperplasia. Of the 27 patients who had confirmed primary hyperaldosteronism investigated at this centre, 25 had a definitive diagnosis assigned on the basis of postural stimulation tests, adrenal CT scans, and bilateral adrenal vein sampling, surgery or a combination of test results. Of this group, 18 had adrenal masses visualized on CT. However, only 13 of these 18 patients had an adrenal aldosteronoma subsequently proven by selective adrenal vein sampling or surgery, or both; the other 5 patients were found to have bilateral adrenal hyperplasia with nonfunctioning adrenal masses. CT had a sensitivity of 100% for the diagnosis of aldosteronoma, but the specificity was only 58% and the positive predictive value was only 72%. The likelihood ratio for the diagnosis of aldosteronoma in patients with primary hyperaldosteronism and an adrenal mass on CT was only 2.4. CONCLUSION: Given the poor specificity of CT in patients with primary aldosteronism, full biochemical and physiologic testing should be done before adrenalectomy in patients with suspected adrenal aldosteronoma.

Adenoma↗

PubMed2006

Primary hyperaldosteronism: effect of adrenal vein sampling on surgical outcome.

HYPOTHESIS: Adrenal vein sampling is superior to computed tomography for subtype differentiation of primary hyperaldosteronism. DESIGN: Retrospective review. SETTING: University medical center. PATIENTS: Forty-eight patients (32 men and 16 women) with biochemically confirmed primary hyperaldosteronism. MAIN OUTCOME MEASURES: We compared demographic factors, results of biochemical and imaging studies (computed tomography and adrenal vein sampling), therapy, and patient outcomes. RESULTS: Mean +/- SEM adrenal nodule size was 1.54 +/- 0.2 cm. Adrenal vein sampling was performed in 41 (85%) of 48 patients, and it was successful in 39 (95%) of those 41 patients. Concordance between computed tomography and adrenal vein sampling was observed in 22 (54%) of the 41 patients. Thirty-two patients underwent successful laparoscopic adrenalectomy. There was 1 complication and no deaths. All 32 patients were cured of hypokalemia. CONCLUSION: Adrenal vein sampling is superior to image-based techniques for subtype differentiation of primary hyperaldosteronism.

Adrenal Glands↗

PubMed1990

Secondary hyperaldosteronism stimulates acidification in rat distal colon.

Recent studies from this laboratory have determined that colonic K+ absorption is altered by the PCO2 and by secondary hyperaldosteronism. Partial inhibition by vanadate and mucosal ouabain suggested the operation of an H+/K+ exchange pump. To determine the mechanism of acidification in rat distal colon, we measured in vitro acidification using the pH-stat technique by voltage-clamped segments of colonic epithelium in controls and in the presence of secondary hyperaldosteronism, induced by a sodium-deficient diet. Chronic stimulation with aldosterone resulted in increased mucosal acidification in vitro for at least 2 h. This effect could not be accounted for by lactate production and was not altered by elimination of the aldosterone-induced increase in voltage and short-circuit current with 10 microM amiloride. Studies with inhibitors and ion substitution revealed that mucosal acidification resulted from both Na-dependent and Na-independent mechanisms. Na-dependent acidification was inhibited by ATPase inhibitors and was mediated in part by a luminal Na+/H+ exchanger in the presence of secondary hyperaldosteronism. Na-independent acidification was mediated by a pathway dependent on luminal K+ that was inhibited by vanadate and mucosal ouabain, consistent with the operation of an H+/K+ exchange pump.

Adenosine Triphosphatases↗

PubMed2001

Laparoscopic adrenal-sparing surgery for primary hyperaldosteronism due to aldosterone-producing adenoma.

BACKGROUND: Laparoscopic adrenalectomy has been shown to be safe and effective in the treatment of patients with primary hyperaldosteronism due to aldosterone-producing adenoma. Most laparoscopic adrenalectomies for aldosterone-producing adenomas involve total removal of the adrenal gland, and there have been few reports of laparoscopic adrenal-sparing surgery or partial adrenalectomies. METHODS: A prospective review is performed on eight patients with primary hyperaldosteronism due to aldosterone-producing adenoma who underwent laparoscopic transperitoneal adrenal-sparing surgery in our institution over a 2-year period. RESULTS: There were 1 male and 7 females with a mean age of 43.1 years. The mean diameter of the adenoma was 2 cm; there were six right-sided lesions and two left-sided lesions. The adenoma was located in the anterior margin of the adrenal gland in seven cases and was removed by laparoscopic enucleation. One patient had a partial adrenalectomy using the vascular stapler for an adenoma that was located posteriorly in the adrenal gland. Hemostasis was excellent in all cases. All patients were able to tolerate liquid orally on the day of operation and were on diet on the second postoperative day. Postoperative analgesic requirement was minimal. The mean hospital stay was 3.8 days. At a mean follow-up of 25 months, seven patients were cured of their hypertension and one patient had her antihypertensive medications significantly reduced. CONCLUSION: Laparoscopic transperitoneal adrenal-sparing surgery is safe and effective in the treatment of patients with primary hyperaldosteronism due to aldosterone-producing adenoma.

Adenoma↗

PubMed1984

Evaluation of a test using saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism.

We evaluated a new method utilizing saralasin to differentiate primary aldosteronism due to an aldosterone-producing adenoma from idiopathic hyperaldosteronism. The test is based on the marked difference in sensitivity to angiotensin II of aldosterone-producing adenomas and hyperplastic adrenal glands and the partial angiotensin II agonist property of saralasin in low-renin states. Saralasin was infused into 14 patients with primary aldosteronism and the plasma aldosterone responses determined. Plasma aldosterone concentration increased in all eight patients with idiopathic hyperaldosteronism, whereas there was no increase in plasma aldosterone in six patients who had a solitary adenoma. We concluded that saralasin may be a clinically useful, noninvasive tool to distinguish patients with an aldosterone-producing adenoma from those who have idiopathic hyperaldosteronism.

Adenoma↗

PubMed2004

[Renal impact of primary hyperaldosteronism].

The impact of hyperaldosteronism on target organs, and particularly kidney function, is greater than that of essential hypertension. Hyperaldosteronism provokes a glomerular hyperfiltration and hypertension that may cause renal alterations. Those may explain why elevated blood pressure may persist, even after radical treatment of the cause of hyperaldosteronism.

Humans↗

PubMed1976

Elevation of serum creatine kinase in severe hypokalemic hyperaldosteronism.

The association between hypokalemia and increased serum creatine kinase has been investigated. Two patients were found who had severe hypokalemic hyperaldosteronism who had elevation of serum creatine kinase activity. The CPK activity returned to normal values after fluid and potassium replacement. In a prospective study of 129 patients with hypokalemia which did not include any patients with hyperaldosteronism, 12 were found to have increased CPK activity but each of these had some other severe disease process which could account for the increased CPK. Three other patients with K+ (2.2 MEq/1 did not have increased CPK. It is concluded that patients with severe hypokalemia such as that occurring in hyperaldosteronism with muscle weakness may have elevated CPK directly related to their hypokalemia. In other patients with hypokalemia, 10% may have increased CPK but this is related to other disease processes.

Adult↗

PubMed2003

Laparoscopic management of primary hyperaldosteronism: clinical experience with 212 cases.

PURPOSE: Laparoscopy is now widely used to remove benign adrenal tumors. We assessed the value of transperitoneal partial or total adrenalectomy for primary hyperaldosteronism. MATERIALS AND METHODS: From September 1994 to October 2001, 212 consecutive patients with a mean age of 48 years who presented with primary hyperaldosteronism and related arterial hypertension underwent transperitoneal laparoscopic adrenalectomy (193) or tumor enucleation (20) performed by a single surgeon, including 1 who underwent bilateral adrenalectomy. In all cases preoperatively high plasma and urine aldosterone was associated with low plasma renin and hypokalemia. RESULTS: Mean followup was 44 months. Conversion to open surgery was necessary in 30 patients (14%) due to bleeding or adhesion and a procedure duration of greater than 3 hours. Mean operative time was 102 minutes (range 30 to 260). Six patients (2.8%) required blood transfusion. No deaths occurred. Postoperatively complications were observed in 10% of patients and the most frequent one was electrical myocardial ischemia without infarction. Mean postoperative pain medication was 17 mg. morphine sulfate equivalents (range 0 to 60). Mean and median hospital stay was 3.6 and 2.9 days, respectively (range 2 to 20). Postoperatively blood pressure was normal in 58% of patients without any drug, while treatment was decreased in the remainder. Kalemia was normalized in all cases. CONCLUSIONS: Although some complications can occur, mostly at the beginning of the learning curve, laparoscopic transperitoneal adrenalectomy is effective treatment for primary hyperaldosteronism.

Adrenal Gland Neoplasms↗

PubMed1998

Primary hyperaldosteronism causing posttransplantation hypertension: localization by adrenal vein sampling.

A 58 year-old man with end-stage renal disease who had received a cadaveric renal transplant presented with persistent hypertension and hypokalemia. Allograft renal artery stenosis, rejection, and cyclosporine effects were excluded. Hypokalemia persisted despite potassium supplementation and antihypertensive medications with hyperkalemic effects. The biochemical findings of primary hyperaldosteronism with a normal adrenal anatomy imaged by magnetic resonance imaging (MRI) necessitated adrenal vein sampling to lateralize a left adrenal adenoma. His hypokalemia was cured by the removal of the adenoma, and his blood pressure (BP) control was easily achieved with a less complex regimen of antihypertensives. We suggest that the concomitant existence of resistant hypokalemia and posttransplantation hypertension, especially in the cyclosporine era, should stimulate a search for hyperaldosteronism; once transplant renal artery stenosis has been excluded, the patient should be investigated for primary hyperaldosteronism. When imaging studies fail to show adrenal pathology, adrenal vein sampling will likely do so.

Adrenocortical Adenoma↗

PubMed2000

Idiopathic hyperaldosteronism: analysis of aldosterone synthase gene.

We analyzed the CYP11B2, the gene encoding aldosterone synthase, in mononuclear leukocytes in eight patients with primary aldosteronism due to zona glomerulosa hyperplasia (idiopathic hyperaldosteronism) and compared the results with aldosterone-producing adenomas. In idiopathic hyperaldosteronism, aldosterone synthase activity was significantly increased in accordance with gene expression (P < 0.05), compared with aldosterone-producing adenomas. No genetic mutations were found in coding regions of DNA. The T (-344) C allele polymorphism was present in a similar frequency in the general population. In one patient with idiopathic hyperaldosteronism. de novo homozygous mutation in upstream of the 5' flanking region C (-463) T was detected, which cannot be explained by polymorphism. The pathophysiological significance of this mutation for aldosterone hypersecretion is not known. There were no mutations in the known promoter sequences for angiotensin II related cis-segments. Possible contribution of co-regulators for angiotensin 11-induced signalling pathway is discussed.

Adenoma↗