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PubMed1983

10. Hypertension. A comparison of the effects of angiotensin II infusion and variations in salt intake on plasma aldosterone levels in normal subjects, patients with essential hypertension and patients with hyperaldosteronism.

Infusion of angiotensin II into a patient with dexamethasone-suppressible hyperaldosteronism caused a brisk increase in plasma aldosterone concentration. In this behaviour, the patient resembled those patients with idiopathic hyperaldosteronism rather than those with tumorous primary hyperaldosteronism. Sodium depletion of a small group of patients with mild essential hypertension elicited a spectrum of increases in plasma aldosterone levels ranging from zero to normal. Angiotensin II infusion in both sodium replete and deplete states also caused variable aldosterone responses. These results suggest that the derangement of adrenal function in this condition varies continuously in severity.

Adrenocorticotropic Hormone↗
PubMed1983

Adrenal cortical carcinoma: an unusual cause of hyperaldosteronism.

Although secondary hyperaldosteronism due to renal vein thrombosis may occur as a result of renal cell carcinoma or adrenal cortical carcinoma, primary hyperaldosteronism is rarely associated with the latter. This paper describes a patient with adrenal cortical carcinoma who presented with the clinical features of primary hyperaldosteronism 1 year after hypertension had been diagnosed; intravenous pyelography had not been done then. Drug therapy was ineffective, and the patient died 10 weeks after presentation.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Primary hyperaldosteronism. Diagnostic procedure useful in hospital routine].

Personal experience in the management of three cases of primary hyperaldosteronism, in which a cure was obtained by surgical removal of an adrenocortical adenoma, is was used in the elaboration of a diagnostic procedure requiring hospitalisation for 12 days. During 6 days, the patient is kept on a diet containing 100 mEq Na and K, and blood potassium values are repeatedly determined. Other causes of hypertension are ruled out. On the 6th day, baselines for blood renin and urinary aldosterone are calculated. Next, a hyposodic diet is given for 4 days, and a diuretic is administered on the last of these days, after which renin is determined "in response to stimulation". Lastly, two days of i.v. NaCl loading are followed by the determination of urinary aldosterone "during inhibition". If the picture is positive for hyperaldosteronism, the patient is discharged and followed during treatment with spironolactone, and eventually subjected to renal and adrenal arteriography to determine the site of the adenoma. Division of the procedure into increasingly complex steps enables the examination to be halted at any point when evidence in support of the suspected diagnosis fails to appear. This feature, coupled with the simplicity of the procedures adopted, enables all young subjects admitted for unexplained hypertension to be screened for hyperaldosteronism, with the assurance of obtaining certain diagnosis without an excessively long stay in hospital.

Adenoma↗
PubMed1994

[Results of unilateral adrenalectomy for primary hyperaldosteronism].

From 1970 to 1992, 57 patients underwent unilateral adrenalectomy for primary hyperaldosteronism. All were hypertensive and the biochemical profile was diagnosed in all cases but two. 44 out of 57 were operated on using to the posterior Young Mayor approach. The present series included 44 macroadenomas > or = 1 cm in diameter (21 > 2 cm; 23 < or = 2 cm), 7 microadenomas (< 1 cm), 3 associations of macro and microadenomas and 3 cases of unilateral hyperplasia. All were biochemically cured. 4/57 patients remained hypertensive postoperatively (3/44 macroadenomas and 1/3 unilateral hyperplasia). There were two late recurrences, which were both clinical and biochemical (2 macroadenomas < or = 2 cm), and one of these was reoperated on for contralateral multiple "adenomas". Pathological background was defined by preoperative imaging studies with a sensitivity of 100% for MRI (23 cases), 96% for CT-scan (52 cases), 73% for NP 59 scanning (15 cases), 38% for sonography (16 cases) and 85% for venous sampling (7 cases). Cure of hyperaldosteronism or hypertension after unilateral adrenalectomy was therefore not predictable by the pathological background. If a firm diagnosis of primary hyperaldosteronism has been made and the unilaterality of the disease has been established, the patient should be operated. Even adrenalectomy for unilateral hyperplasia can lead to cure, and the syndrome can recur after removal of a solitary macroadenoma.

Adrenalectomy↗
PubMed1995

[Hyperaldosteronism suppressible by glucocorticoids. An unusual cause of familial hypertension].

The glucocorticoid suppressible hyperaldosteronism (GSH) is a rare form of systemic hypertension. We report a family--a father and his two children--with this disease. GSH represents a peculiar form of primary hyperaldosteronism, with usually an absence of increase of aldosterone in response to upright posture, a sustained responsiveness of aldosterone to prolonged ACTH stimulation and high levels of two steroids, the 18-hydroxy- and the 18-oxocortisol. But the two main features of GSH which distinguish it from other causes of hyperaldosteronism are the prompt reversal of the features of mineralocorticoids excess by glucocorticoid therapy and the autosomal dominant mode of inheritance. Recent studies demonstrate that this disorder is caused by an abnormal structure of the aldosterone synthase gene. Treatment by glucocorticoid (usually 0.30 to 0.75 mg dexamethasone daily) can reverse hypertension and hypokaliemia.

Adult↗
PubMed1994

[Which screening tests should be chosen in 1994 in the cascade of primary hyperaldosteronism (Conn's syndrome)? Apropos of 3 personnel cases].

On the occasion of three cases of primary hyperaldosteronism the author expresses disapproval of the recently published recommendation of a general screening for aldosterone, plasma renin activity and their respective quotient in all hypertensive patients. Compared with the rareness of the disease, this screening seems extremely expensive and mostly useless. Even in view of the possibility of delaying diagnosis of extremely rare cases of normokalemic primary hyperaldosteronism by three to five years--an occurrence without negative consequences--the author recommends as a first step to follow clinical parameters by repeated determination of potassium and to engage highly specific and expensive tests not before strong suspicion for hyperaldosteronism arises. In 1994 costs of public medicine have increased to intolerable levels; therefore the consideration of a price/quality ratio is mandatory.

Adenoma↗
PubMed1996

Primary hyperaldosteronism in pregnancy. A case report.

BACKGROUND: Primary hyperaldosteronism is an uncommon disorder, and there are few reports of its occurrence and management in pregnancy. CASE: Primary hyperaldosteronism was suspected before pregnancy in a 31-year-old women with refractory hypertension and hypokalemia. Pregnancy evaluation revealed suppressed renin levels and high aldosterone levels; computed tomography revealed a 1-cm mass in the left adrenal gland. The patient became pregnant before completion of evaluation and treatment. On high doses of nifedipine and nadolol, the first-trimester blood pressure was 130/98 mm Hg and remained high in the early second trimester. In view of the risks of poorly controlled hypertension, adrenalectomy was performed at 15 weeks' gestation, with rapid improvement in blood pressure and elimination of the patient's requirement for large doses of potassium daily. Antihypertensive medication was withdrawn, with maintenance of normal blood pressure until 36 weeks' gestation. At that time the blood pressure rose slightly but responded to bed rest. A healthy female infant was delivered at term by cesarean section. CONCLUSION: Previous reports of emergency preterm delivery and a case of neonatal mortality in the setting of hyperaldosteronism in pregnancy confirm the significant risks associated with this condition. In our patient, adrenalectomy in the early second trimester resulted in a rapid and sustained improvement in hypertension, reversal of hypokalemia and a good pregnancy outcome.

Adrenal Glands↗
PubMed1997

[Primary hyperaldosteronism. Apropos of 2 cases].

Primary hyperaldosteronism (PHA) represents less than 1 to 2% of all causes of hypertension (HT). We report 2 cases of primary hyperaldosteronism which emphasize the difficulty of distinguishing neoplastic PHA from idiopathic PHA, observed in a 60-year-old woman and a 42-year old woman, respectively. In both cases, the diagnosis of PHA was suggested by marked hypokalaemia with inappropriate potassium excretion and was confirmed by hyperaldosteronaemia and low and poorly stimulated renin activity. In the first case, computed tomography showed nodular hyperplasia of the 2 adrenal glands. The patient was treated with spironolactone and calcium channel blockers which controlled blood pressure and serum potassium. In the second case, computed tomography and magnetic resonance imaging revealed an adrenocortical adenoma confirmed by pathological examination after the operation. The diagnosis of primary hyperaldosteronism is based on three steps: detection, positive diagnosis and aetiological diagnosis. Detection is essentially based on demonstration of hypokalaemia. Positive diagnosis is based on demonstration of elevated aldosterone secretion with inhibited renin secretion. The aetiological diagnosis is dominated by the differentiation between Conn's adenoma and bilateral adrenal hyperplasia, which has therapeutic implications.

Adenoma↗
PubMed2005

Life-threatening hypokalaemia on a low-carbohydrate diet associated with previously undiagnosed primary hyperaldosteronism [corrected].

BACKGROUND: Low-carbohydrate diets are popular and fashionable for weight loss despite lack of evidence about long-term effects. Many individuals attempting to lose weight have hypertension, especially those with diabetes, and the prevalence of hyperaldosteronism among hypertensive patients is higher than previously recognized. We present a patient with Type 2 diabetes and previously undiagnosed hyperaldosteronism who developed life-threatening hypokalaemia while following a low-carbohydrate diet. CASE REPORT: A 60-year-old man with diet-treated Type 2 diabetes and hypertension presented with generalized muscle weakness and serum potassium of 1.9 mmol/l. He had succeeded in losing three and a half stones during the previous 4 months by adhering strictly to a low-carbohydrate diet. HbA(1c) was 4.8% and plasma aldosterone:renin ratios were elevated suggestive of increased aldosterone secretion. On a low-calorie mixed diet serum potassium levels were maintained in the low-normal range over the following 165 days. The adrenals were normal on CT scanning and blood pressure responded dramatically to the addition of spironolactone on day 212 (125/83 mmHg). CONCLUSIONS: The prevalence of primary hyperaldosteronism in the hypertensive population, based on elevation of plasma renin:aldosterone ratio, is approximately 6%. The majority of these people are normokalaemic and remain undiagnosed. However, when carbohydrate intake is restricted such individuals are at increased risk of potentially life-threatening metabolic derangements.

Aldosterone↗
PubMedDate not supplied

[Histochemical characteristics of aldosteromas and adrenal tissue of patients with primary hyperaldosteronism].

The authors analyze the data of histochemical examinations of 30 patients with tumorous and nontumorous forms of low-renin hyperaldosteronism, as well as the findings of clinical and hormonal examinations of these patients. The activities of enzymes involved in steroidogenesis (3-beta OSD, NAD and NADP tetrazolium reductases, G-6-PD) were measured, as were levels and distribution patterns of lipids involved in steroidogenesis (free and bound cholesterol, etc.). A high functional activity of aldosteromas of any structure was proved, and a trend to increase of steroidogenic activity of malignant aldosteromas demonstrated. Atrophic changes in the cortex adjacent to aldosteroma were found to involve no reduction of adrenal tissue functional activity. In contrast to this, hyperplastic changes in the cortex adjacent to adenoma were characterized by a lower level of functional activity as against adrenal tissue activity in nontumorous hyperaldosteronism. The authors come to a conclusion that adrenocortical elements hyperplasia associated with some aldosteromas does not participate in aldosterone hyperproduction whereas hyperaldosteronism in nontumorous variants is caused by cortical cell hyperplasia and hormone hyperproduction.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

Carcinoma of the adrenal cortex causing primary hyperaldosteronism. A case report and review of the literature.

A male patient presenting with primary hyperaldosteronism after a three-year delay, was found to have an aldosterone producing adrenocortical carcinoma. Evidence is presented that aldosterone was the only steroid produced in excess. Only six other patients with adrenocortical carcinoma and isolated primary hyperaldosteronism could be traced in the literature. The relation between histology and endocrine functions of the tumor cells is discussed.

Adrenal Cortex Neoplasms↗
PubMed1992

Influence of serum potassium on the electrocardiographic pattern of left ventricular hypertrophy in primary hyperaldosteronism.

Only a few studies deal with electrocardiographic (ECG) signs of left ventricular hypertrophy (LVH) in patients with primary hyperaldosteronism, although it may be presumed that many factors such as arterial hypertension, hypokalemia, increased blood volume, and decreased activity of the renin-angiotensin system can modify LVH pattern in this entity. For that reason, we evaluated ECG signs of LVH in 55 patients with primary hyperaldosteronism hospitalized in our department from 1971 to 1990. These data were compared with age, serum potassium level, plasma renin activity (PRA) and-in 14 patients-with left ventricular mass, measured echocardiographically. We found inverse correlation between serum potassium concentration and the Sokolow-Lyon index: SV1 + RV5/6 (r = -0.47, p < 0.001). Among 24 patients with only abnormal QRS voltage, without ST-T changes suggestive of LVH, 19 (79.2%) had hypokalemia. In multivariate analysis, potassium concentration was the single independent predictor of an abnormal QRS voltage: -0.743, p = 0.01 vs. 0.153 (age), -0.337 (PRA) and 0.454 (LV mass). Our observations suggest that hypokalemia is an important factor influencing an amplitude of QRS complexes and may be responsible for false-positive LVH diagnosis.

Adult↗
PubMed1995

A new genetic test for familial hyperaldosteronism type I aids in the detection of curable hypertension.

In Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-suppressible hyperaldosteronism), a curable form of hypertension inherited in an autosomal dominant fashion, the underlying genetic defect is a "hybrid gene" in which 11 beta-hydroxylase gene regulatory elements are fused to the coding region of the aldosterone synthase gene. The detection of this hybrid gene by Southern blotting is time consuming and involves the use of radioactive isotopes. We describe a new, long polymerase chain reaction-based method for detecting the hybrid gene which greatly reduces the time required to obtain a result, avoids exposure of laboratory workers to radioactive materials, and will thereby facilitate the screening of patients for the presence of FH-I.

Bartter Syndrome↗
PubMed1984

Effect of chronic hyperaldosteronism on the electrophysiology of rat distal colon.

Microelectrodes have been used to study the effects of aldosterone on the barriers and forces controlling sodium and potassium transport in rat distal colon. Compared to control tissues, hyperaldosteronism induced by dietary sodium depletion resulted in a 7-fold increase in transepithelial voltage (VT) and a 52% decrease in total resistance (RT). Increased VT reflected both a rise in the basolateral membrane voltage (Vbl) and a fall in the apical membrane voltage (VA). RT was resolved into its separate membrane components using nystatin (585 U X ml-1), and the decrease in RT produced by aldosterone was found to be due entirely to a 66% decrease in the apical membrane resistance (RA). Amiloride had no effect on the control tissues, but restored VT, Vbl and VA in tissues from sodium deprived animals to control values. Amiloride also increased RT in the experimental tissue, but the post-amiloride values remained significantly lower than those in controls. These results indicate, therefore, that hyperaldosteronism results in an increase in VT by hyperpolarizing the basolateral membrane, as well as depolarizing apical membrane in rat distal colon. The fall in RT, however, is due only to a fall in RA since Rbl and junctional resistance (Rj) were unaffected. The data are consistent with the concept that aldosterone acts to stimulate sodium absorption by increasing the rate of cell entry of sodium, through the induction of amiloride-sensitive sodium channels in the apical membrane, and enhances the rate of potassium secretion by increasing the electrical driving force towards the mucosal solution.

Amiloride↗
PubMed1989

Therapeutic value of calcium antagonists in autonomous hyperaldosteronism.

The chronic effect of the calcium antagonist nitrendipine was investigated on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA; n = 3; age, 44 +/- 4 years; PAC, 312 +/- 96 pg/ml; PRA, less than 0.1 ng/l.h; serum potassium, 2.8 +/- 0.3 mmol/l) or to bilateral idiopathic hyperaldosteronism (IHA; n = 3; age, 49 +/- 1 years; PAC, 212 +/- 32 pg/ml; PRA, 0.1 +/- 0.1 ng/l.h; serum potassium, 3.3 +/- 0.2 mmol/l). After withdrawal of antihypertensive medications at least 3 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40 to 60 mg. BP, PAC, PRA, and serum potassium were determined before (see data above) and after 4 weeks of nitrendipine therapy. After 4 weeks, BP was significantly reduced (178 +/- 10 to 165 +/- 6 mmHg systolic, 109 +/- 7 to 101 +/- 6 mmHg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings we conclude that calcium antagonists may be helpful in lowering BP in those patients with primary aldosteronism who develop intolerable side effects under treatment with spironolactone or trilostane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed2005

Idiopathic primary hyperaldosteronism: normalization of plasma aldosterone after one month withdrawal of long-term therapy with aldosterone-receptor antagonist potassium canrenoate.

We have re-evaluated 15 patients with idiopathic primary aldosteronism one month after withdrawal of therapy with aldosterone-receptor antagonist potassium canrenoate. Therapy had lasted for 3 to 24 yr. Median blood pressure (BP) in the sitting position at the time of diagnosis was 160/100 (ranges 150-200/95-110 mmHg); while 1 month after withdrawal of therapy median BP was 145/90 (ranges 125-160/80-100 mmHg). One month after withdrawal, the ratio aldosterone (ng/dl)/plasma renin activity (ng/ml/h) in the upright position was increased only in 3 cases (median 18, range 6.1-125). We found a significant inverse correlation between the upright aldosterone/plasma renin activity (aldo/PRA) ratio, 1 month after withdrawal, and the number of years of therapy with potassium canrenoate. We conclude that long-term therapy with the aldosterone-receptor blocker, potassium canrenoate, can normalize the aldo/PRA ratio in many cases of idiopathic primary hyperaldosteronism after one-month withdrawal of the drug. These data are consistent with possible regression of idiopathic primary hyperaldosteronism after long-term therapy with potassium canrenoate, or in alternative to a persistent effect of potassium canrenoate, on aldosterone synthesis.

Adult↗
PubMed2003

[Hyperaldosteronism persisting after subtotal adrenalectomy].

BACKGROUND: Primary aldosteronism is known to be caused by aldosterone-producing adenoma (APA). Total adrenalectomy is the standard procedure. In contrast to bilateral adrenal diseases (e.g., MEN II pheochromocytomas), there is no consensus about the effect of subtotal adrenalectomy. CASE REPORT: A 44-year-old patient with primary aldosteronism caused by APA underwent subtotal adrenalectomy including removal of one adenoma. Because hypertension and hypokalemia did not disappear and hyperaldosteronism persisted, the patient had to undergo reoperation in which the adrenalectomy was completed. DISCUSSION: Subtotal adrenalectomy in patients with Conn's syndrome is an interesting therapeutic option,whereas its effect is much higher in hereditary diseases of the adrenal gland. The benefit of preserved adrenal tissue has to be weighed against a possible persistence of hyperaldosteronism, especially in cases with normal opposite adrenal glands.

Adrenal Cortex Neoplasms↗
PubMed2007

Primary hyperaldosteronism secondary to unilateral adrenal hyperplasia: an unusual cause of surgically correctable hypertension. A review of 30 cases.

INTRODUCTION: Unilateral adrenal hyperplasia (UAH) is a rare, surgically correctable cause of primary hyperaldosteronism (PH). We report 2 cases and review the literature for cases of PH secondary to UAH successfully treated via surgery. METHODS: Two cases of UAH treated at our institution were retrospectively reviewed. In addition, we reviewed 28 cases of UAH previously reported in the English literature. RESULTS: Median patient age was 49 (range: 10-62) years, with a male to female ratio of 1.7:1. All patients were hypertensive, with a median preoperative systolic and diastolic blood pressure of 170 (range: 135-250) mmHg and 110 (range: 75-140) mmHg, respectively. Most patients were hypokalemic, with a median serum potassium level of 2.8 (range: 1.4-3.9) mmol/l. Ten out of 13 patients (77%) who underwent postural studies had a decrease or no change in the plasma aldosterone level, suggesting a unilateral source of hyperaldosteronism, and 9/17 patients (53%) who underwent a computed tomography (CT) scan were correctly localized. Twelve patients underwent adrenal scintigraphy with or without dexamethasone suppression, of whom 6 (50%) were correctly localized. In 1 patient, adrenal scintigraphy demonstrated localization to the opposite gland. Adrenal venous sampling (AVS) was performed in 22 patients and successfully localized the lesion in all the patients. At a median follow-up of 12 (range: 3-96) months postsurgery, 47% of patients (14/30) were completely cured of their hypertension and 50% (15/30) had improved control. All 30 patients were cured of hypokalemia. CONCLUSION: Although the existence of UAH remains controversial, it is increasingly accepted as a unique pathologic entity and has an excellent outcome after unilateral adrenalectomy.

Adrenal Glands↗