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PubMed1989

A new variant of 17 alpha-hydroxylase deficiency with hyperaldosteronism in two Japanese sisters.

We present a report on two sisters who have 17 alpha-hydroxylase deficiency with hyperaldosteronism. They have hypertension and hypergonadotropic hypogonadism. The steroid profiles suggest that they have 17 alpha-hydroxylase deficiency. In contrast to the classical biochemical findings in 17 alpha-hydroxylase deficiency, both of these patients have hyperaldosteronism. Thus this report describes a new variant of 17 alpha-hydroxylase deficiency with hyperaldosteronism. Dexamethasone suppressed the mineralocorticoid excess, including aldosterone, and improved their hypertension. In the untreated state, ACTH, instead of the renin-angiotensin system, regulated plasma aldosterone levels, but during dexamethasone treatment the renin-angiotensin system regulated these levels.

Adolescent↗
PubMed1981

Mineralocorticoid and metabolic response to metyrapone on normotensive children and children with dexamethasone-suppressible and primary hyperaldosteronism.

UNLABELLED: The effect of 5 to 9 days of metyrapone administration (400 mg/m2 every 4 h) on aldosterone, deoxycorticosterone, plasma renin activity, electrolyte balance, and blood pressure was investigated in 2 normotensive siblings (one of whom showed limited ACTH reserve), in 3 patients with hypertension and dexamethasone-suppressible hyperaldosteronism, and in a hypertensive patient with primary hyperaldosteronism due to bilateral adrenal hyperplasia. RESULTS: 1. Plasma and urinary aldosterone levels were steadily suppressed by metyrapone in all cases, except in the oldest patient studied who had dexamethasone-suppressible hyperaldosteronism and in whom, after a few days, aldosterone gradually rose to normal levels. 2. Mild mineralocorticoid effect occurred only in the normal subject. In all other patients there was no apparent mineralocorticoid effect despite deoxycorticosterone hypersecretion. 3. There was no significant change in blood pressure with metyrapone administration in any patient.

Aldosterone↗
PubMed1982

Effect of standard oral glucose loading on aldosterone secretion in primary hyperaldosteronism.

The effects of mild acute decreases in plasma potassium induced by standard oral glucose loading (100 g) on plasma aldosterone and renin levels were assessed in 10 patients with primary hyperaldosteronism as compared with 10 normal subjects. Following overnight fast, mean plasma glucose was identical in both groups; plasma insulin, potassium and renin levels were lower and plasma aldosterone higher in patients than in controls. Glucose loading significantly increased plasma glucose and insulin concentrations and decreased plasma potassium and aldosterone levels in both groups. The increases in plasma insulin and the decreases in plasma potassium or aldosterone tended to be blunted in primary hyperaldosteronism. glucose-induced changes in plasma aldosterone correlated significantly (P less than 0.025) with those in plasma potassium in the patients and with variations in plasma renin activity in the normal subjects. These findings suggest that the metabolic changes induced by glucose ingestion are capable of modifying aldosterone secretion in primary hyperaldosteronism. However, the glucose-induced decreases in plasma aldosterone are blunted in this disorder; this could be related to the impaired insulin response to glucose loading.

Adult↗
PubMed1983

Primary hyperparathyroidism associated with primary hyperaldosteronism.

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.

Adult↗
PubMed1986

Long-term treatment of idiopathic hyperaldosteronism using trilostane.

Three patients with idiopathic hyperaldosteronism were continuously treated with trilostane, a competitive inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) (3 to 4 2/3 years). Trilostane, in conjunction with antihypertensive drugs, effectively decreased plasma aldosterone levels and improved hyperaldosteronism symptoms without undesirable side effects. Trilostane continued to be effective even when treatment was continuous. Rapid ACTH testing (iv bolus of 0.25 mg alpha 1-24 ACTH) was done on the day without trilostane after long-term treatment, and plasma levels of aldosterone and cortisol were compared to those obtained during a pre-treatment period. Results suggest that the inhibitory effect of trilostane on steroid biosynthesis rapidly disappears following discontinuance of trilostane administration even after long-term treatment, and that continuous treatment causes no significant or irreversible change in steroid biosynthesis. These results suggest that trilostane is a safe, feasible therapeutic agent for long-term treatment of idiopathic hyperaldosteronism.

Adrenocorticotropic Hormone↗
PubMed2004

Comparison of active renin concentration and plasma renin activity for the diagnosis of primary hyperaldosteronism in patients with an adrenal mass.

OBJECTIVE: Plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio is an established screening test for primary hyperaldosteronism. Due to the increased recognition of adrenal incidentalomas, reliable parameters are required. Determination of active renin concentration (ARC) in contrast to PRA offers advantages with regard to processing and standardization. The present study compared PRA and ARC under random conditions to establish thresholds for the diagnosis of primary hyperaldosteronism. DESIGN AND METHODS: Fifty patients with various adrenal tumors, including ten patients with aldosterone-secreting adrenal adenomas, as well as ten hypertensive patients and 23 normotensive volunteers were studied. PAC and PRA were measured by radioimmunoassay. ARC was determined by an immunoluminometric assay. RESULTS: Receiver operating curve (ROC) analysis suggested a PAC to ARC ratio threshold of 90 ((ng/l)/(ng/l)) (sensitivity 100%, specificity 98.6%) and a ratio threshold of 62 by additional consideration of PAC > or =200 ng/l (sensitivity 100%, specificity 100%) for the diagnosis of aldosterone-secreting adrenal adenomas. CONCLUSIONS: A PAC to ARC ratio of > or =62 in patients with PAC levels > or =200 ng/l is a reliable screening method for primary hyperaldosteronism in patients with an aldosterone-producing adenoma under random conditions. Because of its advantages with regard to probe processing and its independence from endogenous angiotensinogen levels, ARC may be preferred to PRA.

Adenoma↗
PubMed2000

Familial hyperaldosteronism.

Aldosterone, the major circulating mineralocorticoid, participates in blood volume and serum potassium homeostasis. Primary aldosteronism is a disorder characterised by hypertension and hypokalaemia due to autonomous aldosterone secretion from the adrenocortical zona glomerulosa. Improved screening techniques, particularly application of the plasma aldosterone:plasma renin activity ratio, have led to a suggestion that primary aldosteronism may be more common than previously appreciated among adults with hypertension. Glucocorticoid-remediable aldosteronism (GRA) was the first described familial form of hyperaldosteronism. The disorder is characterised by aldosterone secretory function regulated chronically by ACTH. Hence, aldosterone hypersecretion can be suppressed, on a sustained basis, by exogenous glucocorticoids such as dexamethasone in physiologic range doses. This autosomal dominant disorder has been shown to be caused by a hybrid gene mutation formed by a crossover of genetic material between the ACTH-responsive regulatory portion of the 11ss-hydroxylase (CYP11B1) gene and the coding region of the aldosterone synthase (CYP11B2) gene. Familial hyperaldosteronism type II (FH-II), so named to distinguish the disorder from GRA or familial hyperaldosteronism type I (FH-I), is characterised by autosomal dominant inheritance of autonomous aldosterone hypersecretion which is not suppressible by dexamethasone. Linkage analysis in a single large kindred, and direct mutation screening, has shown that this disorder is unrelated to mutations in the genes for aldosterone synthase or the angiotensin II receptor. The precise genetic cause of FH-II remains to be elucidated.

Cytochrome P-450 CYP11B2↗
PubMed2000

Role of dietary potassium in the hyperaldosteronism and hypertension of the remnant kidney model.

The remnant kidney model of progressive renal disease is marked by arterial hypertension, especially when produced by nephrectomy and partial infarction. Hyperaldosteronism sustains much of the hypertension, but the stimuli to the increased aldosterone levels are uncertain. It is hypothesized that the hyperaldosteronism attending this model stems from the combination of fixed dietary potassium load in the face of reduced filtration on the one hand, and persistent renin secretion from the scarred remnant kidney on the other. This hypothesis predicted that dietary potassium restriction would lower aldosterone and BP in this model. To test this prediction, two groups of rats with a remnant kidney were studied. Group 1 consumed 0.4 +/- 0.06 mEq (mean +/- SD) of potassium chloride daily, and group 2 ate 4.8 +/- 1.0 mEq daily. Two sham-operated groups with intact kidneys also were studied. Group 3 consumed 1.7 +/- 0.2 mEq daily and group 4 ate 15.2 +/- 1.4 mEq daily. These levels of intake were designed to provide at least as much potassium per liter of GFR in the sham groups as in the remnant kidney rats. Systolic BP (SBP), 24-h protein excretion, plasma aldosterone levels, 24-h urinary aldosterone excretion, and plasma renin activity (PRA) were determined in all groups at 2 wk. At 4 wk, after SBP and protein excretion measurements, remnant kidneys were perfusion-fixed for morphometric analysis. SBP was normal in both sham-operated groups and was not different between the groups (113 +/- 13 versus 117 +/- 2 mmHg, group 3 versus group 4). In the remnant animals, SBP at 2 wk followed potassium intake: Group 1 had a lower SBP than group 2 (140 +/- 26 versus 170 +/- 34 mmHg, P = 0.005). The same SBP pattern persisted at 4 wk (153 +/- 25 versus 197 +/- 27 mmHg, group 1 versus group 2, P = 0.0006). However, 24-h urinary protein excretion was not different between the two groups with remnant kidneys at either 2 or 4 wk. Both plasma and 24-h urinary aldosterone excretion at 2 wk followed potassium intake (120 +/- 124 versus 580 +/- 442 pg/ml for plasma aldosterone, group 1 versus group 2, P = 0.03, and 2.6 +/- 1.8 versus 23.2 +/-9.8 ng/d for urinary aldosterone, group 1 versus group 2, P = 0.0001). PRA, however, followed a reverse pattern in which dietary potassium restriction resulted in higher levels (16 +/- 6 versus 6 +/- 3 ng angiotensin I/ml per h, group 1 versus group 2, P = 0.01). A similar pattern for PRA and aldosterone excretion was also observed in the sham groups, in which lower potassium intake also resulted in a significantly higher PRA and lower aldosterone excretion. The constancy of BP in the sham groups likely reflects their lack of nephron reduction and greater sodium excretory capacity. Morphometric analysis in remnant animals revealed no significant difference between the two dietary groups in the prevalence of glomerular sclerosis, glomerular volume, or interstitial volume. It is concluded that dietary potassium is a potent determinant of hypertension in the remnant kidney model probably through the actions of aldosterone and that the high aldosterone secretion in this model is a function of the dietary potassium load. In this model, reduction in nephron number is also critical in promoting hypertension in conjunction with hyperaldosteronism.

Aldosterone↗
PubMedDate not supplied

[Primary hyperaldosteronism. Update on a topic of physiopathology and clinical features].

The authors examine the various forms of primary hyperaldosteronism, outlining the most recent acquisitions in terms of etiopathogenesis and physiopathology. While Conn's original description of primary hyperaldosteronism is a syndrome based on corticoadrenal aldosteronesecreting adenoma, it was later seen that this condition could recognise other anatomic substrates, such as carcinoma and in particular bilateral corticoadrenal hyperplasia. A peculiar form of the latter can be suppressed with glucocorticoids sustained by an anomalous recombination of aldosterone-synthase and 11-beta-hydroxylase. The main focus in this paper is on clinical management, in particular the current diagnostic criteria which show that primary hyperaldosteronism affects a higher percentage of the hypertense population that was estimated in the past. Above all, the significance of the aldosterone/PRA (ARR) ratio in screening for this condition is discussed, above all in normokalemic forms, together with the role of molecular biology in identifying glucocorticoid-suppressible forms. Lastly, the principles of medical and surgical management are outlined, emphasising the role of laparoscopic surgery.

Humans↗
PubMedDate not supplied

Renal calculi in primary hyperaldosteronism.

Increased urinary calcium (Ca++) excretion and the presence of negative Ca++ balance is well documented in primary hyperaldosteronism. However, renal calculi as a major manifestation of this disorder is not previously described. This report describes probably the first patient who presented with renal calculi in association with primary hyperaldosteronism. We believe that primary hyperaldosteronism was a major pathogenetic factor in formation of renal calculi since increased urinary excretion of Ca++ and uric acid noted at the onset declined following short-term spironolactone administration and remission from renal calculi has persisted following initial nephrolithotomy and continued spironolactone therapy which also corrected hypertension and hyperkalemia, a hallmark of this disorder.

Calcium↗
PubMed1975

[An ultrastructural study of the adrenal cortex in Cushing's syndrome without and with hyperaldosteronism].

This paper reports ultrastructural comparision of the adrenal gland zones of a rare case of a combination from Cushing's syndrome and hyperaldosteronism with a pure Cushing's syndrom and with a normal human adrenal gland. Whilst between the zona glomerulosa of the normal adrenal gland and of the Cushing's syndrom there are no differences, the morphological state of the glomerulosa cells of the Cushing's syndrom in combination with hyperaldosteronism is interpreted as an inhibition of the activity of these cells. In the cells of the hyperplastic zona fasciculata of Cushing's syndrom in combination with hyperaldosteronism, there are no electronmicroscopical characteristics, who are morphological equivalent of the production of aldosterone. The abundant quantity of steroid producing organells in these cells point to a high function. The cells of the adenoma of Cushing's syndrom contain abundant vacuols of lipids, in which presumable are stored steroid hormones.

Adrenal Cortex↗
PubMed2002

Primary hyperaldosteronism in the era of laparoscopic adrenalectomy.

Laparoscopic adrenalectomy has been recommended as the standard method for removing an aldosteronoma. To assess our surgical experience with primary hyperaldosteronism in the era of laparoscopic adrenalectomy a 6-year retrospective review of 30 consecutive patients was done. The 20 men and 10 women ranged in age from 35 to 78 with a mean of 51.2 years. All patients were hypertensive and hypokalemic with a mean serum potassium of 2.9 +/- 0.32 (standard deviation) mmol/L. Serum aldosterone was elevated in 28 of 30 (94%) patients and normal in the remaining two. Serum renin was suppressed in all patients. CT correctly localized the tumor in all 30 patients. Twenty-eight patients had histologically documented adenomas and two had associated cortical hyperplasia on pathology. Mean adenoma size was 2.0 +/- 1.12 cm. Twenty-four patients underwent left laparoscopic adrenalectomies, whereas right laparoscopic adrenalectomies were performed in five. One was converted to an open left adrenalectomy. Mean operative time was 183 minutes. The mean hospital stay for laparoscopic adrenalectomy was 2.2 days. The patients were followed from one to 63 months (mean 26.1 months). Twenty-nine of 30 (95%) patients were rendered normokalemic. The remaining patient takes a potassium-wasting diuretic. Persistent hypertension was present in 10 of 30 (33%) patients. Blood pressure in nine of 10 patients was controlled with less medical therapy. The other patient's blood pressure remained difficult to control despite multiple medications. Duration of hypertension before surgery was a significant risk factor for persistent hypertension (P < 0.05). Gender (P > 0.05) and age (P > 0.05) at the time of surgery were not statistically significant predicators for persistent hypertension. There were two reported trocar site hernias. We conclude that primary hyperaldosteronism due to aldosterone-producing tumors can be diagnosed and accurately localized with preoperative measurements of serum aldosterone, renin, and CT scanning. Laparoscopic adrenalectomy is safe and effective for the treatment of primary hyperaldosteronism with minimal associated morbidity and a short hospital stay. Hypokalemia may be cured by surgical treatment, although persistent hypertension still occurs. Duration of hypertension before surgery is a risk factor for persistent hypertension whereas age and sex are not.

Adrenalectomy↗
PubMedDate not supplied

[Hyperaldosteronism and simultaneous pheocromocytoma: a puzzle case].

Pheochromocytoma and primary hyperaldosteronism are well-known causes of hypertension. It was recently reported that their frequency in the hypertensive population is 0.1-0.2% and 3-15%, respectively. We describe the case study of a patient with severe hypertension (200/100 mmHg) and the coexistence of pheochromocytoma and primary hyperaldosteronism attributable to adrenal hyperplasia. The originality of this clinical report is that the patient presented a pheochromocytoma in the left adrenal gland and hyperplasia of the contralateral adrenal gland. The simultaneous presence of pheochromocytoma and primary hyperaldosteronism in the same patient is probably due to either genetic predisposition or to specific environmental risk factors for these adrenal diseases.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Outcome of patients undergoing laparoscopic adrenalectomy for primary hyperaldosteronism.

OBJECTIVES: To study the long-term outcome of patients with primary hyperaldosteronism who underwent laparoscopic adrenalectomy and to determine the preoperative predictive factors of persistent hypertension. METHODS: Between 1996 and 2002, 47 patients with primary hyperaldosteronism underwent transperitoneal laparoscopic adrenalectomy at our institution. Their clinical and biochemical parameters were reviewed retrospectively, and the outcome of 46 patients with complete follow-up notes were determined. RESULTS: The study comprised 16 male and 30 female patients with a mean age of 45.6 years (range, 18 to 63 years). Almost all patients had hypertension and hypokalemia at presentation, requiring medication. The average operating time was 127 minutes (range, 70 to 240 min), and the mean postoperative stay was 2.6 days (range, 1 to 5 days). No mortalities occurred, and perioperative morbidity was minimal. Forty-two (91%) patients had adrenal cortical adenoma (including 1 with both adenoma and hyperplasia), and 4 (9%) had adrenal hyperplasia on histology. The average follow-up time was 21 months (range, 1 to 60 months), and at the end of follow-up, all patients had normal serum potassium levels without potassium supplements. Twenty-three (50%) patients were cured of hypertension, and 13 (28%) patients had better control of their hypertension as evidenced by the decrease in the number of antihypertensive medications used. On multivariate analysis, the age of the patient at surgery was shown to be an independent predictive factor of persistent hypertension after successful surgery. CONCLUSION: Laparoscopic adrenalectomy is a safe and effective way to treat primary hyperaldosteronism, especially in controlling hypokalemia and in the management of hypertension. The age of a patient at surgery is an independent preoperative risk factor of persistent hypertension.

Adolescent↗
PubMed2006

[Successful percutaneous angioplasty of renal artery in a patient with severe arterial hypertension and symptoms of hyperaldosteronism: a case report].

Arterial hypertension may result from renal artery stenosis. In this type of hypertension renin-angiotensin-aldosterone system is activated and patients often produce signs of hyperaldosteronism. It must be distinguished from primary hyperaldosteronism in order to chose a proper therapy. In this paper we describe a case of a 65-years-old man with severe arterial hypertension, which was difficult to control pharmacologically. The patient revealed symptoms which suggested primary hyperaldosteronism (except normal plasma renin activity). Only imaging techniques allowed diagnose of renal artery stenosis and carry out successful percutaneous angioplasty of renal artery.

Aged↗
PubMedDate not supplied

[Post-operative hyperaldosteronism and related endocrine perturbations (author's transl)].

Electrolytes disturbances during operative period are believed to be related to an hyperaldosteronism produced by anaesthetic management and surgery. Effects of ethrane anaesthesia and surgery on hydroelectrolytic metabolism and endocrin function were investigated in 11 patients submitted to an abdominal surgery. Plasma and urinary levels of aldosterone were increased (x3) significantly (p less than or equal to 0.001) during operation, then decreased gradually in post-operative period, and return to normal values when Na/K ratio is reversed in urines. Relationship between hyperaldosteronism and other changes in endocrine function are established by determination of following hormones: A.C.T.H., cortisol, plasma renin activity (P.R.A.) catecholamines in plasma and urinary levels of 17-ceto, 17-hydroxysteroids and catecholamines. Ethrane anesthesia give a good neurovegetative stability since plasma catecholamines levels are not affected significatively. Plasma aldosterone level is correlated with urinary aldosterone and plasma renin activity. Plasma A.C.T.H. is much more increased at the operative time and decreases rapidly instead of plasma cortisol which decreases more slowly. Relationship of this hyperaldosteronism with anesthetic management, surgical stress intestinal transit disturbances, other endocrine function changes is discussed.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

[Value of localizing examinations used in the diagnosis of primary hyperaldosteronism].

Localizing examinations were performed in 115 patients with the clinical and biochemical signs of the primary hyperaldosteronism between 1975 and 1978. Adenoma of the adrenal cortex was diagnosed in 52 examined patients out of whom 42 underwent surgery, and 12 were classified for the operation. The remaining patients, in whom a cause of hyperaldosteronism was not found, are treated conservatively and followed-up. It was shown that CT-scanning and scintigraphy of the suprarenal cortex are the most convenient techniques in the localization of tumours in patients with the primary hyperaldosteronism. Ultrasound is less valuable diagnostically but may help in tumour localization in about 50% of patients.

Adenoma↗
PubMed1985

[Concentration of adrenocorticotrophic hormone and aldosterone secretion in essential hypertension and hyperaldosteronism].

The authors studied the effect of adrenocorticotropic hormone (ACTH), potassium and plasma renin activity on blood aldosterone in normal subjects as well as in patients with essential hypertension (of a labile and stable course) and hyperaldosteronism (primary and idiopathic). It was demonstrated that in normal subjects and patients with labile essential hypertension, the secretion of aldosterone was simultaneously stimulated by the renin-angiotensin system (RAS) and the hypothalamus-adenopituitary. The RAS dominated in normal conditions whereas in labile hypertension the hypothalamus-adenopituitary system was predominant. In stable hypertension, the RAS and hypothalamus-pituitary influenced aldosterone secretion in an equal degree. Hyperaldosteronism was associated with the most pronounced deviations in the relationship between stimulants and aldosterone. In addition to decreased plasma levels of renin activity and potassium, the corticotropic activity of the hypothalamus-adenopituitary was increased during the first 10 years of the disease, while later on the function of this system became inhibited. The highest ACTH levels were recorded in idiopathic hyperaldosteronism.

Adrenocorticotropic Hormone↗