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 217 records · Page 12Linked to original sources

PubMed1991

A neonate with idiopathic hyperaldosteronism.

A boy with functional abnormalities of the gastro-intestinal tract, hyponatraemia, hypokalaemia and hypertension is described. All symptoms developed within the first 2 months of life. Increased aldosterone levels were associated with suppressed values in the renin-angiotensin system. The diagnosis of idiopathic hyperaldosteronism was made because of adrenal hyperplasia and the failure to suppress aldosterone to undetectable levels with glucocorticoids. Treatment with spironolactone alone, or in combination with either intravenous dopamine or ibopamine orally, amiloride, enalapril, hydralazine or clonidine corrected serum potassium values but failed to normalize blood pressure and to correct plasma renin activity and plasma aldosterone. However, the combination of spironolactone with nifedipine decreased blood pressure. Abnormal gastro-intestinal motility was corrected by low doses of oral magnesium hydroxide. To assess intracellular calcium homeostasis, the patient's peripheral blood mononuclear cells were incubated with increasing concentrations of calcium. As these cells failed to maintain physiological calcium concentration, a defect in intracellular calcium homeostasis was suspected.

Aldosterone↗

PubMed1978

Differentiation between subtypes of primary hyperaldosteronism by multiple steroid measurement after dexamethasone administration.

In 6 patients with primary hyperaldosteronism (P.H.) and a unilateral adrenal adenoma (A) and in 5 patients with P.H. obviously due to bilateral adrenal hyperplasia (H), multiple serum corticosteroids were measured after different dietary or drug regimens. After administration of dexamethasone on a normal sodium diet, serum levels of 11-deoxycorticosterone (DOC), corticosterone (B) and cortisol (F) were much lower in the H than in the A group. With respect to 11-deoxycorticosterone levels, there was no overlap between the two groups. Multiplication of individual serum DOC, B and F levels allowed a clearer separation of patients with A and H. This non-invasive method may offer an additional means in the differential diagnosis of P.H.

Adenoma↗

PubMed1990

Concurrent hypercortisolism and hyperaldosteronism due to an adrenal adenoma.

The case of a 39-year-old woman with Cushing's syndrome, hypertension and severe hypokalemia, caused by a unilateral adrenal adenoma composed of cells of the zona fasciculata histological type, is described. Plasma renin activity, plasma levels of mineralocorticoids and the aldosterone secretion rate were determined before and after surgical removal of the adenoma. The tumor appeared to produce autonomously cortisol as well as corticosterone, 18-hydroxycorticosterone and aldosterone. This condition has not previously been described in the literature and might be explained by strong expression of the full spectrum of activities of the mitochondrial enzyme P450 C11 by the tumor cells. Interestingly, despite hyperaldosteronism, plasma renin activity was not suppressed.

Adenoma↗

PubMed1987

Dexamethasone-suppressible hyperaldosteronism: pathophysiology, clinical aspects, and new insights into the pathogenesis.

A profile of dexamethasone-suppressible hyperaldosteronism (DSH), a variant of primary aldosteronism, is drawn by reviewing its pathophysiological and clinical aspects. Genetic studies show no HLA linkage and point to an autosomal dominant mode of inheritance, suggesting that the prevalence of this disease has been underestimated in the past. Hypertension, hypokalemia, suppressed renin, and high aldosterone values characterize DSH in the basal state, similar to the other forms of primary aldosteronism, i.e., aldosterone-producing adenoma (APA) or bilateral idiopathic adrenal hyperplasia (IAH). Biochemically DSH and APA can be differentiated from IAH since in both aldosterone does not respond to upright posture, to angiotensin II infusion, and to angiotensin-converting enzyme (ACE) captopril. In contrast, morphologically DSH is similar to IAH, since neither macroscopic nor histologic examinations of the adrenals give evidence of any unilateral abnormality. However, DSH is differentiated from APA and IAH by the hyperresponsiveness of aldosterone to acute ACTH administration as well as by the failure of aldosterone to escape from prolonged ACTH stimulation. The final diagnosis of DSH rests upon the prompt reversal of the features of mineralocorticoid excess by glucocorticoid therapy. In some cases hypertension is unresponsive to dexamethasone and needs alternative treatment. The main pathogenetic hypotheses point to a pituitary and/or an adrenal abnormality, but the intrinsic nature of the disease remains to be elucidated.

Adenoma↗

PubMed1992

A low molecular weight heparin decreases plasma aldosterone in patients with primary hyperaldosteronism.

Four patients with primary hyperaldosteronism were treated with nadroparin 4100 or 6150 antiXa IU daily for 4 days. Plasma and urine sodium and potassium, and plasma aldosterone and renin were monitored before, during and after the study. After four days of treatment, and for the following two days, plasma aldosterone was decreased (by a mean of 49% on Day 6), and urinary Na/K was increased (3.7-fold). The direction of the changes was reversed on Day 8. The study has confirmed the effect of low molecular weight heparin on aldosterone, and makes it unlikely that it is related to inhibition of angiotensin II stimulation in these patients, as renin could not be detected in their plasma.

Aged↗

PubMed2004

A case of insulin edema with inappropriate hyperaldosteronism.

Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.

Adult↗

PubMed1980

The occurrence of hyperaldosteronism in infants with congestive heart failure.

Serum aldosterone and plasma renin were measured in 20 normal infants and 15 infants with congestive cardiac failure. Serum aldosterone was significantly increased (151 +/- 38 ng/dl mean +/- standard error of the mean) in patients before treatment when compared with aldosterone in normal infants (29 +/- 7 ng/dl). Increasing serum aldosterone was related to increasing plasma renin. The response to furosemide appeared to be inversely related to serum aldosterone concentrations. In four infants, administration of an aldosterone antagonist (spironolactone) resulted in improved diuresis and decreased serum aldosterone. Hyperaldosteronism is an important factor contributing to fluid and sodium retention in infants with heart failure.

Aldosterone↗

PubMed1984

Pure primary hyperaldosteronism due to adrenal cortical carcinoma.

A 47-year-old woman is described who had pure primary hyperaldosteronism due to an adrenal cortical carcinoma. This may represent the first such case in which modern laboratory tests allowed specific diagnosis and exclusion of hypersecretion of other adrenal steroids, and also the first reported case in which modern localizing procedures have been utilized. Other interesting facets of the case include calcification of the tumor, visualization with 131l iodomethylnorcholesterol , metaplastic histologic changes, and coexistent bilateral renal artery fibromuscular disease.

Adrenal Cortex Neoplasms↗

PubMed1986

Primary hyperaldosteronism in pregnancy.

A case is reported of a primigravid woman presenting in midgestation with severe hypertension caused by primary hyperaldosteronism. Symptomatic treatment with an aldosterone blocker, a peripheral vasodilator, and a combined alpha beta-blocker allowed pregnancy to continue to 36 weeks' gestation. Cesarean section for fetal distress resulted in delivery of a dysmature female infant who did well. Further postpartum studies confirmed the presumptive diagnosis made during pregnancy. An adenoma, localized in the right adrenal gland, was surgically removed.

Adenoma↗

PubMed1992

The chimeric gene linked to glucocorticoid-suppressible hyperaldosteronism encodes a fused P-450 protein possessing aldosterone synthase activity.

Glucocorticoid-suppressible hyperaldosteronism (GSH) is one variety of primary aldosteronism with hypertension and is inherited in an autosomal dominant mode. A recent report has indicated that GSH is caused by a gene duplication arising from unequal crossing over between the two genes, CYP11B1 and CYP11B2, encoding P-450(11 beta) and P-450C18, respectively (Lifton et al. Nature (1992) 355, 262-265). The nucleotide sequence analysis in the present study has demonstrated that unequal crossing over in the chimeric gene formed by the gene duplication occurs within the region from the 3'-portion of exon 4 through the 5'-portion of intron 4 in Australian GSH patients. Namely, the chimeric gene encodes a fused P-450 protein consisting of the amino-terminal side of P-450(11 beta) (encoded by exons 1-4 of CYP11B1) and the carboxyl-terminal side of P-450C18 (encoded by exons 5-9 of CYP11B2). When a cDNA corresponding to the chimeric gene is transfected into COS-7 cells, the fused P-450 protein expressed in the mitochondria exhibits steroid 18-hydroxylase or aldosterone synthase activity. These results provide the molecular genetic basis for the characteristic biochemical phenotype of GSH patients.

Animals↗

PubMed2005

Induction of 11beta-hydroxysteroid dehydrogenase type 2 and hyperaldosteronism are essential for enhanced sodium absorption after total colectomy in rats.

BACKGROUND: Patients who undergo total colectomy with ileopouch anal reconstruction often have persistent diarrhea and frequent bowel movements. Analysis of the intestinal adaptation after total colectomy may lead to developing novel therapies for postoperative diarrhea. METHODS: Sprague-Dawley rats underwent total colectomy with ileoanal reconstruction and were sacrificed 4 and 8 weeks later. Mucosal response to aldosterone was evaluated with the use of ileal mucosa in an Ussing chamber by measuring short circuit current after in vitro stimulation with aldosterone. We investigated the expression of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD 2) in intestinal epithelial cells. To examine the role of hyperaldosteronism, we also evaluated rats treated with a sodium-deficient diet or subcutaneous aldosterone infusion. RESULTS: Aldosterone levels increased 80-fold after total colectomy. A comparable amount of aldosterone dramatically increased aldosterone-mediated, amiloride-sensitive short circuit current in the mucosa from colectomized rats, but not in control rats. We measured an increase in 11beta-HSD 2 messenger RNA and protein in the distal ileum from colectomized rats. Circulating aldosterone appears to be essential for these functional and molecular changes because similar results were obtained by using the mucosa from both dietary sodium-depleted and aldosterone-infused rats. CONCLUSIONS: Induction of 11beta-HSD 2 is essential for enhanced mineralocorticoid action in the remnant ileum after total colectomy in rats.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

PubMed2006

Adrenal venous sampling in primary hyperaldosteronism: comparison of radiographic with biochemical success and the clinical decision-making with "less than ideal" testing.

BACKGROUND: Adrenal venous sampling (AVS) is used in the workup of primary hyperaldosteronism (PA). The purpose of this study was to determine the success rate of AVS and to examine the decision-making process after "less than ideal" AVS. METHODS: A total of 60 patients underwent 62 AVS for PA. Biochemical evidence of adrenal vein cannulization was analyzed with adrenal-peripheral cortisol ratios. Pathology and clinical outcomes were reviewed in patients undergoing adrenalectomy. RESULTS: Bilateral cannulization was confirmed in only 21% (pre-adrenocorticotropic hormone [ACTH] infusion) and 44% (post-ACTH infusion) AVS. Of 39 patients who underwent adrenalectomy for presumed unilateral disease, only 16 patients had "ideal" AVS, and 18 patients had only unilateral cannulization on AVS. Despite this, 11 appeared to lateralize and 7 had imaging to support unilateral disease. Postoperatively, 15 (82%) had a significant reduction in their blood pressure, and 7 (39%) of these were cured. Surgery failed in 2 patients; both were found to have bilateral hyperplasia. Bilaterally unsuccessful cannulization (n = 5) still lateralized in 3 patients, and 2 patients had nodules on computed tomography scan. All 5 patients had significant reduction in blood pressure, and 2 were cured. CONCLUSIONS: ACTH infusion during AVS enhances the biochemical evidence of adrenal vein cannulization. Following "less than ideal" AVS, clinical decisions can still be made using anatomic and partial AVS data.

Adrenal Glands↗

PubMed1996

Hyperaldosteronism and sudden cardiac death.

From a database of 130 implantable cardiac defibrillator recipients, 2 patients (1.5%) with sudden cardiac death as a presenting symptom, leading to diagnosis of primary hyperaldosteronism, are described. This is a newly described cause of sudden cardiac death, possibly more frequent than suspected, which should be considered in patients with malignant arrhythmias and hypokalemia.

Adult↗

PubMed1979

Hyperreninemia and secondary hyperaldosteronism in pheochromocytomas.

Foremost in the differential diagnosis of hypertension is the identification of surgically correctable lesions. Increased plasma renin activity in a hypertensive patient suggests the presence of a renovascular or renal etiology. We have recently seen two adolescent patients whose hyperreninemia was cuased by a pheochromocytoma. Secondary hyperaldosteronism was an associated finding.

Adolescent↗

PubMed1981

Hyperaldosteronism due to unsuspected adrenal carcinoma: discovery during investigation of hypertension in a young woman.

During investigation for hypertension a 19-year-old black woman was found to have an unsuspected adrenal carcinoma. Hyperaldosteronism was established as the cause of the hypertension by observing suppressed plasma renin activity and nonsuppressible plasma aldosterone concentration. The causal relationship was confirmed by a cure of the hypertension and a return in the responsiveness of the renin-angiotensin-aldosterone axis to normal after removal of the carcinoma. This report emphasizes the value of a comprehensive investigation of hypertension, especially in young patients.

Adrenal Gland Neoplasms↗

PubMed1996

Renal pathology in patients with primary hyperaldosteronism secondary to an adrenal cortical adenoma.

OBJECTIVES: The cause of persistent hypertension following the removal of an aldosterone-producing adrenal adenoma is unknown. The purpose of this study was to determine whether this occurrence is due to existing renal histopathologic damage. METHODS: Thirty-two patients with primary hyperaldosteronism due to an aldosterone-secreting adrenal cortical adenoma underwent open renal biopsy at the time of unilateral adrenalectomy. Biopsy results were correlated with the duration and severity of hypertension before and after surgery. RESULTS: Nineteen patients were cured of their hypertension postoperatively, whereas 13 patients had persistent diastolic hypertension. Statistical analysis of these two groups revealed no difference when renal histopathologic variables, preoperative severity of hypertension, or preoperative duration of hypertension were compared. CONCLUSIONS: Persistent hypertension in these patients does not appear to be due to renal histopathologic changes; coexisting essential hypertension is a more likely cause.

Adolescent↗

PubMed2003

Hyperaldosteronism and pheochromocytoma: new tricks and tests.

Hyperaldosteronism, previously thought to represent only 1% to 2% of cases of hypertension, may cause as much as 25% of hypertension in a primary care setting. The renin/aldosterone ratio is the best test for initial screening, followed by localization if possible. Aldosterone antagonists, such as spironolactone, and surgery are the mainstays of treatment. Pheochromocytomas are rare, but because they are a curable cause of hypertension and potentially fatal if not found, important to diagnose. Clinical presentation is variable; however, if symptoms are present, they usually include hypertension, hyperhydrosis, headaches, or palpitations sometimes occurring in dramatic fashion. Once a diagnosis is entertained, appropriate laboratory confirmation is essential. Positive laboratory confirmation then leads to localization of the tumor for eventual surgical removal. New biochemical tests and imaging procedures are making the difficult job of diagnosing and finding these tumors.

Adrenal Gland Neoplasms↗

PubMed2000

Suppression of surgical hyperaldosteronism by potassium canrenoate during gynecologic surgery under sevoflurane anesthesia.

BACKGROUND: Surgical hyperaldosteronism leads to sodium and water retention during surgery and often causes postoperative edema. This study investigated the effect of potassium canrenoate (PC) on pituitary adrenocortical function in lower abdominal surgery under sevoflurane anesthesia. METHODS: Twenty patients were randomized to receive 400 mg of PC (the PC group, n=10) or saline (the control group, n=10) intravenously. The following parameters were determined: plasma aldosterone, adrenocorticotropic hormone (ACTH), plasma renin activity (PRA), serum sodium and potassium, urinary sodium and potassium, and urine output. RESULTS: The aldosterone and ACTH levels showed significant increases in the control group during surgery. Plasma ACTH also increased significantly in the PC group, but plasma aldosterone levels were unchanged during surgery. The urine Na/K ratio of the PC group was significantly higher than that of the control group. CONCLUSION: The present study suggested that PC suppresses the increase of plasma aldosterone caused by surgical stress. That may prevent sodium retention and potassium excretion during surgery.

Adrenocorticotropic Hormone↗