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PubMed1990

Correctable subsets of primary aldosteronism. Primary adrenal hyperplasia and renin responsive adenoma.

Among 154 cases of primary aldosteronism seen in the General Clinical Research Center at San Francisco General Hospital, twelve patients did not fulfill established characteristics of an aldosterone producing adenoma (APA) or idiopathic hyperaldosteronism (IHA). Eight patients had nodular adrenocortical hyperplasia; plasma and urinary aldosterone were elevated and responses to stimulatory and suppressive maneuvers demonstrated the same autonomy seen in patients with APA. This subset is designated primary adrenal hyperplasia. Four additional patients also had elevated aldosterone levels that were responsive to these maneuvers, similar to IHA, but had unilateral tumors. This group has been designated as aldosterone-producing renin-responsive adenoma. Eleven patients had unilateral adrenalectomy and one preferred prolonged spironolactone therapy, resulting in a sustained cure or amelioration of hypertension, hypokalemia and normalization of aldosterone production.

18-Hydroxycorticosterone↗

PubMed2002

Diagnostic value of the post-captopril test in primary aldosteronism.

Primary aldosteronism is a disorder with hypertension, hypokalemia, increased plasma aldosterone, and suppressed renin activity. A random plasma aldosterone/renin activity (PA/PRA) >65 (conventional units ratio [CUR] >30) has been proposed as a screening test. We have retrospectively determined the value of the post-captopril plasma aldosterone/renin activity (CAPT PA/PRA) test for the diagnosis of patients with primary aldosteronism whose PA/PRA was <65. We considered the CAPT PA/PRA test to be positive for primary aldosteronism if either the plasma aldosterone concentration did not drop below 0.33 nmol/L (12 ng/dL) or the ratio was >26 (CUR >12). We found 6 patients with a random PA/PRA of 21 to 60 (CUR 10 to 28), yet with an abnormal post-captopril test criteria for primary aldosteronism. Five had an abnormal saline suppression test, and all 6 were confirmed by a combination of diagnostic localization with computerized axial tomography, iodocholesterol scan, adrenal venous sampling, and/or surgery. Four had idiopathic adrenal hyperplasia, and 2 had an aldosterone-producing adenoma. One other patient had an abnormal random plasma aldosterone/renin activity ratio of 99 (CUR 46), a negative saline infusion study, and was determined to have essential hypertension. In summary, the CAPT PA/PRA, but not the random PA/PRA, correctly diagnosed 6 patients with primary aldosteronism in our institution. An additional patient with essential hypertension was incorrectly diagnosed as having primary aldosteronism by the PA/PRA test. We conclude that the simple addition of 25 mg of captopril, taken orally 2 hours before sampling, enhances the accuracy for diagnosing patients with primary aldosteronism.

Adult↗

PubMed2003

Recent advances in diagnosis and treatment of primary aldosteronism.

Primary aldosteronism is the most common form of secondary hypertension. The use of aldosterone/plasma renin activity ratio (ARR) as a screening test has elevated its prevalence up to 10% of hypertensive patients. Idiopathic bilateral adrenal hyperplasia and aldosterone-producing adrenal adenoma are the leading causes of primary aldosteronism. Most patients with this conditions are normokalemic and clinically undistinguishable from essential hypertensives. However, they suffer from anticipated and more severe target organ damage than other hypertensives. Thus, being primary aldosteronism a common, specifically treatable and sometimes surgically cured form of hypertension, a prompt diagnosis is necessary and cannot be overlooked. The measurement of ambulatory ARR represents the screening test and should be performed in the majority of hypertensive patients. ARR higher than a set cutoff suggests the need of a confirmatory test for primary aldosteronism, such as intravenous saline load or fludrocortisone suppression test. If inability to suppress aldosterone is demonstrated, the disease is confirmed. The subtype evaluation is based on adrenal imaging (CT scan) and selective adrenal venous sampling. The latter is the gold standard for the diagnosis of a lateralized aldosterone secretion, as typically observed in aldosterone-producing adenomas. Microadenomas are frequently overlooked by adrenal image. If lateralization is confirmed, unilateral adrenalectomy is the reasonable therapeutic option, leading to a significant reduction of blood pressure, if not normotension. If bilateral aldosterone excess is demonstrated, an aldosterone receptor antagonist should be administered. This article reviews and discusses the new data about prevalence, diagnosis and treatment of primary aldosteronism.

Adrenal Cortex Neoplasms↗

PubMed1999

Leptin levels are suppressed in primary aldosteronism.

Primary aldosteronism is associated with hypertension secondary to salt and water retention, hypokalemia and impaired insulin secretion with glucose intolerance in some patients. The secretion of leptin, a hormone produced by adipocytes, may be altered by reduced insulin secretion in primary aldosteronism. We measured plasma leptin approximately 3 months before and 3 months after curing of primary aldosteronism in 18 patients (12 male, 6 female, body mass index 29.1+/-4.4, mean +/- SD). Patients were treated by unilateral laparoscopic adrenalectomy to remove an aldosterone-producing adenoma. There was a 46% postoperative increase in plasma leptin concentrations from 6.65+/-0.81 to 9.68+/-1.50 ng/ml (P=0.004), despite a non-significant fall in body mass index. Plasma leptin was noted to increase after adrenalectomy in 16 of the 18 patients. The patients also had improved blood pressure and a significant increase in plasma potassium post-operatively. It is proposed that increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism. Further studies are indicated to identify the mechanism of plasma leptin suppression in primary aldosteronism.

Adult↗

PubMed2002

Primary aldosteronism.

Primary aldosteronism is a potentially curable form of hypertension. Recent studies using the plasma aldosterone to plasma renin activity ratio as screening test in hypertensive populations have demonstrated a high prevalence of primary aldosteronism close to 10%. This frequency is clearly higher than the classically described when hypokalemia is used as the screening method. The most common subtypes of primary aldosteronism are idiopathic aldosteronism and aldosterone-producing adenoma. Other causes are glucocorticoid-remediable aldosteronism, unilateral or primary adrenal hyperplasia and adrenal carcinoma. The diagnosis of primary aldosteronism is advocated to confirm the autonomy of aldosterone secretion from the renin-angiotensin system and to differentiate the clinical subtypes of the disease. This article reviews the new data about prevalence, diagnosis criteria and describes the clinical, biochemical and genetic characteristics of the different subtypes of the disease. We also discuss the treatment, and the differential diagnosis with other hyper-mineralocorticoid states.

Aldosterone↗

PubMed2002

Drug effects on aldosterone/plasma renin activity ratio in primary aldosteronism.

Primary aldosteronism is a specifically treatable and potentially curable form of secondary hypertension. The aldosterone/plasma renin activity ratio (ARR) is routinely used as a screening test. Antihypertensive therapy can interfere with the interpretation of this parameter, but a correct washout period can be potentially harmful. We have investigated the effects of therapy with atenolol, amlodipine, doxazosin, fosinopril, and irbesartan on the ARR in a group of 230 patients with suspected primary aldosteronism. The percent change from control of ARR in patients taking amlodipine was -17%+/-32; atenolol, 62%+/-82; doxazosin, -5%+/-26; fosinopril, -30%+/-24; and irbesartan, -43%+/-27. The ARR change induced by atenolol was significantly higher compared with that induced by all other drugs (P<0.0001), and the ARR change induced by irbesartan was significantly lower than that induced by doxazosin (P<0.0001). One of 55 patients from the group taking amlodipine (1.8%) and 4/17 of the patients taking irbesartan (23.5%) gave a false-negative ARR (<50). None of the patients of the groups taking fosinopril, doxazosin, and atenolol displayed a false-negative ARR. Doxazosin and fosinopril can be used in hypertensive patients who need to undergo aldosterone and PRA measurement for the diagnosis of primary aldosteronism; amlodipine gave a very small percentage of false-negative diagnoses. beta-Blockers also do not interfere with the diagnosis of primary aldosteronism, but they can be responsible for an increased rate of false-positive ARRs. The high rate of false-negative diagnoses in patients undergoing irbesartan treatment requires confirmation in a higher number of patients.

Aldosterone↗

PubMed2005

[Hypertension due to primary aldosteronism].

Primary aldosteronism is a rare cause of hypertension. However, its incidence seems to be underestimated. It is important to identify this syndrom since the disease is potentially curable. In the present paper, we depict different forms of primary aldosteronism as well as the diagnostic procedures. When the diagnosis is suspected (hypertension associated to spontaneous or diuretic-induced hypokaliemia), the more efficient screening test is the determination of the aldosteron/renin ratio. Saline infusion or posture tests can thereafter confirm the diagnosis. Differential diagnosis between bilateral and unilateral forms of primary aldosteronism can be made by CT-scanner and the response of aldosterone to the posture test. Such a complex assessment leads to the identification of patients who can be surgically treated. This treatment consists in a unilateral adrenalectomy which can be realised by laparoscopy.

Aldosterone↗

PubMed1988

Sodium transport parameters in erythrocytes of patients with primary aldosteronism.

Primary aldosteronism is an uncommon cause of hypertension but one of particular interest because of its distinctive pathophysiological mechanism of blood pressure elevation. Aldosterone has been associated with increased Na+,K+-adenosine triphosphatase (ATPase) activity, but there is controversy over which sodium transport parameters are responsible for this increase. We measured intracellular sodium, ouabain-sensitive and ouabain-insensitive sodium efflux, and the number of Na+,K+-ATPase sites of washed erythrocytes, as well as Na+-Li+ countertransport and the Li+-K+ cotransport rate constant of lithium-loaded red blood cells (RBCs) in six patients with primary aldosteronism and in 50 normal subjects. Ouabain-sensitive sodium efflux was significantly (p less than 0.001) higher for the primary aldosteronism patients than for normal subjects (1.85 +/- 0.29 vs 1.51 +/- 0.21 mmol/L RBC/hr) even though the intracellular sodium concentration (7.2 +/- 1.5 vs 6.7 +/- 1.9 mM) and the number of the Na+,K+-ATPase sites per RBC (331 +/- 52 vs 385 +/- 97) were not increased. The elevated sodium efflux appeared to be due to a significant (p less than 0.001) increase in the rate constant (1.60 +/- 0.12 x 10(-15) vs 1.28 +/- 0.15 x 10(-15) mmol/site/hr) of the ouabain-sensitive sodium efflux. The rate constant decreased significantly (p less than 0.01) after treatment.

Adult↗

PubMed1995

Primary aldosteronism.

Primary aldosteronism occurs much more commonly than generally appreciated. Diagnosis is facilitated by measuring urinary aldosterone excretion in conjunction with determination of the level of plasma aldosterone suppression after infusion of 2,000 mL of normal saline over 4 hours. Multiple diagnostic procedures are required to determine the specific type of primary aldosteronism. Patients with aldosterone-producing tumors, unilateral adrenal hyperplasia, and primary adrenal hyperplasia are treated surgically, whereas those with bilateral zone glomerulosa hyperplasia and glucocorticoid-remediable aldosteronism are treated medically.

Aldosterone↗

PubMed1977

Effect of a spirolactone on plasma and urinary aldosterone in primary aldosteronism.

In primary aldosteronism due to an adrenal adenoma (n=2), treatment with a spirolactone (160 mg Canrenone/day for 7 days) decreased plasma aldosterone and urinary aldosterone-18-glucuronide. However, in the presence of a normalization in urinary aldosterone 18-glucuronide plasma aldosterone remained elevated above normal. Continued therapy with higher doses (320 mg/day for 7 days and 480 mg/day for 28 days) did not significantly alter plasma aldosterone, while urinary aldosterone-18-glucuronide returned to values comparable to those obtained before therapy. Cessation of the drug resulted in a marked increase in plasma aldosterone and urinary aldosterone-18-glucuronide. The results indicate that in primary aldosteronism due to an adrenal adenoma, the spirolactone (Canrenone) inhibits aldosterone biosynthesis and seems to influence aldosterone degradation.

Adenoma↗

PubMed1993

Hypertensive crisis during the resection of an adrenal tumor in primary aldosteronism.

Primary aldosteronism is one of the few causes of hypertension which is subject to total surgical treatment, but a hypertensive crisis can occur during the resection of the adrenal tumor. We undertook this study to evaluate the relationship between hormonal factors and a hypertensive crisis during surgery. Sixteen patients with primary aldosteronism who were scheduled for the resection of an adrenal tumor were participated in this investigation. Hormonal factors and hemodynamic variables were evaluated before induction of anesthesia, after induction of anesthesia, 30 minutes after the incision, during tumor manipulation, during resection, and immediately after surgery. During tumor manipulation, a hypertensive crisis occurred in six patients (hypertensive group; HG) but not in any others (non-hypertensive group; NHG). There were no differences in hormonal levels, except epinephrine, during tumor manipulation between HG and NHG. Hemodynamic evaluations revealed an increase of systemic vascular resistance during the hypertensive crisis. We conclude that the hypertensive crisis during the manipulation of an adrenal tumor is caused by the rapid release of epinephrine from the manipulated adrenal gland.

Journal Article↗

PubMed2004

[A brief history of diagnosis and treatment of primary aldosteronism.].

Primary aldosteronism is a clinical syndrome characterized by hypokalemia, suppressed activities of plasma renin and high urinary and plasma aldosterone levels in hypertensive patients. It was first defined and reported by Jerome W. Conn in 1955. From 1960s to early 1970s, its techniques of diagnosis and treatment were greatly improved by the availability of spironolactone, realization of the renin-angiotensin-aldosterone system, and progress in laboratory tests and adrenal venous sampling. In 1970s, notwithstanding the extensive application of modern imaging modalities, such as CT scanning, adrenal venous sampling and steroid analysis have remained to be the most accurate and reliable localization method. From 1980s, more and more patients with primary aldosteronism were screened out from the hypertensive population by plasma renin activity/plasma aldosterone concentration ratio and cured by surgical interventions; laparoscopic unilateral adrenalectomy has become the generally accepted golden standard of operation.

Adrenalectomy↗

PubMed1998

Diagnosis of glucocorticoid-remediable aldosteronism in primary aldosteronism: aldosterone response to dexamethasone and long polymerase chain reaction for chimeric gene.

Aldosterone suppression by dexamethasone, and high 18-hydroxycortisol and 18-oxocortisol levels are used to differentiate glucocorticoid-remediable aldosteronism (GRA) from other forms of primary aldosteronism. These methods are time consuming, expensive, and impractical for large studies. Moreover, diagnosis of GRA requires a confirmatory genetic test. We evaluated 117 patients with primary aldosteronism referred to our centers by the use of a long PCR technique to reveal the chimeric gene of GRA. In 60 of 117 patients, the response of aldosterone to dexamethasone (2 mg/day for 4 days) was also assessed. None of our patients, including 2 pairs of siblings, was positive for the chimeric gene. The results of long PCR were confirmed by Southern blotting. Despite a negative genetic test, 6 patients (1 with aldosterone-producing adenoma and 5 with idiopathic hyperaldosteronism) had plasma aldosterone suppressed by dexamethasone (i.e. < or = 2 ng/dL). Of 117 patients, 43 were identified as having aldosterone-producing adenoma and 74 as having idiopathic hyperaldosteronism. In our experience, the long PCR technique is a reliable and simple test to at least exclude GRA in patients with primary aldosteronism. A short term dexamethasone suppression test of aldosterone can be misleading in identifying GRA. The prevalence of GRA in primary aldosteronism remains to be established.

Adult↗

PubMedDate not supplied

Screening and diagnosis of primary aldosteronism.

Primary aldosteronism (PA) is the commonest form of secondary hypertension in South Africa with an approximate prevalence of 7.5% in the primary-care setting. Hypokalaemia is a poor screening test with 70% of proven cases having normal serum potassium levels. The aldosterone/rennin ratio is a robust screening test with a high sensitivity and specificity, but in South Africa this should be combined with an absolute aldosterone level because of the high incidence of low-renin hypertension in Blacks. The limitations of the ratio, especially with regard to concomitant drug therapy will be discussed in detail. The fludrocortisone suppression test remains the investigation of choice for confirming the diagnosis, but requires four days of hospitalisation. CT scanning will miss 50% of adenomas and incorrectly lateralise the adenoma in occasional cases, and bilateral adrenal venous sampling is the gold standard for indirectly confirming and adenoma by demonstrating lateralisation of aldosterone secretion, but its use is limited by lack of technical expertise in South Africa. Low-dose spironolactone is the medical therapy of choice for PA.

Aldosterone↗

PubMed1996

Malignant hypertension in association with primary aldosteronism.

Primary aldosteronism is associated with low plasma renin levels, whilst malignant phase hypertension is generally associated with raised renin activity. These two conditions are therefore at opposite ends of the renin spectrum, so in theory their co-existence would be unusual. We describe in detail 3 cases of primary hyperaldosteronism from a disease register of 315 cases of malignant hypertension seen in one medical centre over 29 years.

Adult↗

PubMed1999

Cardiovascular complications in patients with primary aldosteronism.

Primary aldosteronism (PA) is widely believed to be a relatively benign form of hypertension associated with a low incidence of vascular complications. However, several recent studies showed that cardiovascular complications were not rare in PA. PA is known as one of the most typical forms of sodium-sensitive hypertension. Recently, we found that the sodium sensitivity of blood pressure was a marker for greater risk for cardiovascular complications, especially stroke, in patients with essential hypertension. Therefore, we investigated cardiovascular complications in 58 patients with PA confirmed to be Conn's adenoma. Cardiovascular complications were found in 34% of 58 patients. Coronary artery disease was found in only one patient (1.7%), as angina pectoris. Stroke was found in nine patients (15.5%), four patients (6.9%) with cerebral infarctions and five patients (8.6%) with cerebral hemorrhages. Proteinuria and renal insufficiency were found in 14 (24.1%) and 4 (6.9%) patients, respectively. The incidence of cerebral infarction and renal insufficiency was greater in men than women. The prevalence of proteinuria was greater in patients with than without stroke (P = 0.03) among those aged older than 40 years. These results indicated that cardiovascular complications, especially stroke and proteinuria, were common in patients with PA, and proteinuria might be an indicator for stroke as target-organ damage.

Cardiovascular Diseases↗

PubMed1989

Primary aldosteronism.

Primary aldosteronism remains a diagnostic challenge. Despite the availability of sensitive and specific immunoassay techniques, the simplification of diagnostic testing, and the introduction of sensitive imaging techniques, there remain uncertainties about the optimal methods of screening, the sensitivity and specificity of various tests, diagnostic criteria, and differentiation among the growing number of etiologic subgroups of the disorder. The author stresses the differentiation of the surgically correctable lesion (adenoma) from the other etiologic subgroups.

Adenoma↗

PubMed2003

New aspects on primary aldosteronism.

The adrenal cortex synthesizes and releases steroid hormones, mainly mineralocorticoids and glucocorticoids. There is a functional zonation of the adrenal cortex and steroid synthesis is thoroughly regulated. Overproduction of aldosterone, primary aldosteronism, may be much more common than previously known and may be responsible for 10% of essential hypertension. Primary aldosteronism is characterized by autonomous production of aldosterone, suppressed renin activity, hypokalemia, and hypertension. The two most common forms are unilateral adenoma and bilateral hyperplasia. In spite of thorough clinical workup and careful histopathology it is often difficult to differentiate between adenoma and hyperplasia. The gene CYP11B2 encodes the steroid synthesizing enzymes for aldosterone production, while the genes CYP17 and CYP11B1 are needed for cortisol production. Most normal controls show expression of CYP11B2 in zona glomerulosa. Expression of CYP11B1 and CYP17 is seen in zona fasciculata and reticularis, whereas the expression of CYP21 is present in all three cortical layers. Adenomas from patients with primary aldosteronism show considerable variation in the expression of CYP11B2. Adenomas from patients with Cushing's syndrome have a strong expression of CYP11B1 and CYP17. In a patient material of 29 cases of primary aldosteronism, 4 patients had small nodules detected with expression of CYP11B2 gene. These nodules were not visualized on CT, whereas adrenal masses seen on CT in these patients showed CYP11B1 and CYP17 gene expression. This suggests that these small nodules are responsible for the aldosterone production and this is characteristic of nodular hyperplasia in patients with primary aldosteronism. In conclusion, this method to visualize mRNA gene expression of steroidogenic enzymes, and especially expression of CYP11B2, has increased the knowledge of adrenal pathophysiology. The results emphasize the value to include functional studies (venous sampling and/or scintigraphy) in the preoperative work up of patients with primary aldosteronism.

Adrenal Cortex↗