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PubMed1988

Mild adrenal 3 beta-hydroxysteroid dehydrogenase deficiency with hyperaldosteronism.

The patient was admitted to our hospital at 19 and again at 22-yr of age for hirsutism and hypertension. Her baseline and ACTH-stimulated plasma 17-hydroxy pregnenolone, dehydroepiandrosterone and dehydroepiandrosterone sulfate were increased whereas plasma 17-hydroxy progesterone and androstenedione were normal and responded poorly to ACTH. Plasma deoxycorticosterone, corticosterone and cortisol baseline levels were normal, and they responded normally to ACTH. The plasma aldosterone concentration (PAC) was always high and responded well to ACTH, angiotensin III and furosemide-upright stimulation. However, plasma renin activity (PRA) was normal or slightly high, and responded normally to furosemide-upright stimulation and fluorohydrocortisone suppression. Dexamethasone (2 mg/day) for 1-2 weeks suppressed the androgens, cortisol and corticosterone levels. PRA and PAC were suppressed temporally, but PRA returned to normal and PAC to be a high level after 2 weeks of dexamethasone administration. Blood pressure was also reduced temporally but returned to a high level after 2 weeks of dexamethasone. These results indicate that primary aldosteronism and dexamethasone-suppressible hyperaldosteronism were not likely to be present, and unknown aldosterone stimulating factors which potentiated the action of endogenous angiotensin II or ACTH might be responsible for the hyperaldosteronism in this patient. We conclude that this patient had a mild and non-salt losing 3 beta-HSD deficiency in the zona reticularis with normal fasciculata and high glomerulosa function.

3-Hydroxysteroid Dehydrogenases↗

PubMed1989

Normotensive glucocorticoid-suppressible hyperaldosteronism in adult.

A 40 year-old man was admitted to our hospital for detailed examination of hypokalemia (2.7 mEq/l). His blood pressure was normal. Metabolic alkalosis, ACTH dependent hyperaldosteronism (18 ng/dl) and over-response to synthetic ACTH were observed. Plasma renin activity, on the other hand, was within the normal range (1.7 ng/ml/hr). Serum potassium was normalized to 4.1 mEq/l and the responsiveness of the renin-angiotensin-aldosterone system was recovered after the administration of dexamethasone. These results led us to suggest that this case might be normotensive glucocorticoid-suppressible hyperaldosteronism. The etiology which was not associated with hypertension and low plasma renin activity has not been clarified but may be related to the shortness of duration of this disease. Our case was also afflicted with mild hypercortisolemia and excessive excretion of urinary 17-hydroxycorticosteroid and 17-ketosteroid which was suppressed by the administration of dexamethasone (2 mg/day). These findings may be related to hypersensitivity of the fascicular zone of the adrenal gland to ACTH.

17-Hydroxycorticosteroids↗

PubMed2005

Primary hyperaldosteronism with normokalaemia secondary to an adrenal adenoma (Conn's syndrome) in a 12 year-old boy.

A 12-1/2 year-old boy presented to the Accident Department following an episode of dizziness and was found to be hypertensive. Investigations revealed primary hyperaldosteronism secondary to an adrenal adenoma (Conn's syndrome). He had normal electrolytes during the period of investigation and potassium concentrations were > or = 4.2 mmol/l on all but one occasion. The hypertension resolved following excision of the adrenal tumour. Normokalaemia with potassium >4.0 mmol/l is very unusual in patients with Conn's syndrome and has not been described in childhood before. Primary hyperaldosteronism needs to be considered in hypertensive children even when potassium concentrations are well within the laboratory reference range.

Adolescent↗

PubMed1986

The value of scintigraphy and computed tomography for the differential diagnosis of primary hyperaldosteronism.

Adrenocortical adenoma is the most common cause of primary hyperaldosteronism. Most tumours are small, less than 2 cm in diameter and, therefore, their localization may be difficult. We have compared two different methods, adrenal scintigraphy (AS) and computed tomography (CT) in the differential diagnosis of 12 patients with primary hyperaldosteronism. AS was performed using either [131I]cholesterol or 6-iodomethyl-19-norcholesterol during dexamethasone suppression. Of the patients, five showed a normal CT and symmetrical uptake of the isotope as AS. They were considered representative of bilateral hyperplasia. All showed good therapeutic response to spironolactone. Seven patients had an adrenocortical adenoma verified at operation. The CT finding indicated a tumour in five patients. This was correct in four, but in one patient the adenoma was found in the contralateral adrenal gland. In two patients with an adenoma, CT was considered normal. AS correctly indicated the tumour in all seven patients. The uptake was unilateral in six, and bilateral but clearly asymmetrical in one patient. The results indicate that AS is superior to CT in the pre-operative localization of aldosteroma. Although CT remains the primary method for the investigation of these patients, AS should be applied always when CT does not unequivocally indicate the presence and localization of an adrenal tumour.

Adenoma↗

PubMed1979

Hyperaldosteronism in the sodium-depleted rat: mode of aldosterone-stimulating action of frusemide.

The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin-angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.

Adrenal Glands↗

PubMed1976

Radiology in primary hyperaldosteronism.

Autonomous hypersecretion of aldosterone (primary hyperaldosteronism) is caused by either hyperplasia (usually bilateral) or an adenoma (frequently unilateral) of the adrenal cortex. Systemic hypertension due to an aldosteronoma is a potentially curable condition through surgical extirpation of the offending organ. In our experience with 37 patients clinically suspected to have primary hyperaldosteronism, radiological methods contributed significantly in preoperative diagnosis. These included (1) selective bilateral adrenal vein catheterization and blood sample collection, (2) adrenal venography, and (3) radioisotope adrenal scan. Unilateral hyperfunction could be accurately detected by the aldosterone assays from the collected samples. When adrenal venography was technically satisfactory, a nodule or aggregate of nodules measuring at least 7 mm and located on the margin of the gland or 1.5 cm or more in diameter when located in the center of the gland were readily identified. Enlarged adrenal gland on venography, in itself, was not a dependable index of a hyperfunctioning gland. Presence of a higher uptake on one side on the radioisotope adrenal scan did not always indicate the hyperfunctioning gland, but lack of lateralization of adrenal hyperfunction was more accurately predicted on the radioisotope scan than by venography. Four histopathological patterns were recognized in the surgically removed adrenal glands, but no correlation between these patterns and clinical behavior or postoperative course was found.

Adenoma↗

PubMed2000

Effect of serotonin4 (5-HT4) receptor agonists on aldosterone secretion in idiopathic hyperaldosteronism.

Serotonin (5-HT) stimulates aldosterone secretion in man through 5-HT4 receptors positively coupled to adenylyl cyclase. In particular, it has been shown that oral administration of a single dose of the 5-HT4 receptor agonist cisapride induces a significant increase in plasma aldosterone levels (PAL) in healthy volunteers. Idiopathic hyperaldosteronism (IH) is a rare disorder characterized by hypertension, hypokalemia and bilateral adrenal hypersecretion of aldosterone. In patients with IH, administration of the 5-HT precursor 5-hydroxytryptophan (5-HTP) is followed by a significant increase in PAL. 5-HTP-induced aldosterone secretion has been attributed to the activation of central serotonergic pathways. The aim of the present study was to evaluate the effect of the oral administration of a single dose of cisapride (10 mg) on aldosterone secretion in 15 patients with IH, in a simple blind fashion versus placebo. Cisapride induced a significant increase in PAL but did not affect renin, cortisol and potassium levels. The present study demonstrates that 5-HT4 receptor agonists are able to stimulate aldosterone secretion in patients with IH. These data also indicate that hyperplastic glomerulosa tissue, like normal glomerulosa cells, expresses a functional 5-HT4 receptor. Therefore, 5-HT4 receptor antagonists may represent a new approach in the treatment of primary hyperaldosteronism.

Aldosterone↗

PubMedDate not supplied

Aldosterone synthase gene in patients suffering from hyperaldosteronism.

In this study the known promoter region of P450aldo gene (CYP11B2) was investigated in patients with idiopathic hyperaldosteronism, a disease characterised by hypertension due to aldosterone oversecretion. We amplified the 2.2 kb promoter region of 6 patients and 7 controls from the same ethnic population by PCR and sequenced the product. Thirteen polymorphic sites were found. Of the most significant, one was within a predicted CRE and another previously described polymorphic site was located in a putative SF-1 binding site. To elucidate the allelic distribution of the polymorphisms, the PCR products were cloned and both alleles for each patient were sequenced. As the same alleles and allele combinations were found in hypertensive patients as well as in normal subjects, it was concluded that none of the polymorphisms was responsible for hyperaldosteronism.

Alleles↗

PubMed1999

[Incidence of primary hyperaldosteronism in hospitalized patients with hypertension].

AIMS: To detect the incidence of primary hyperaldosteronism (PH) in hospitalized hypertensive patients. METHODS: Authors assessed plasma renin activity (PRA) and plasma aldosterone (PA) in 100 patients with arterial hypertension hospitalized at the II. department of Internal medicine in Kosice because of resistance to ambulatory treatment, eventually with the aim of differential diagnosis of arterial hypertension. RESULTS: From 100 hypertensive patients 90 (90%) have had essential hypertension (EH), 8 (8%) PH, 2 (2%) renovascular hypertension and 1 patient (1%) pheochromocytoma. Aldosterone-renin ratio was in PH patients 10-fold higher comparing with EH patients. From the 8 patients with PH 4 have had adenoma and in 3 patients hyperplasia was diagnosed with the use of CT or histology, 1 case was idiopathic hyperaldosteronism without CT hyperplasia evidence. In all PH patients the level of kalemia was less than 4 mmol/l, i.e. kalemia 4.0 mmol/l has 100% sensitivity for PH detection. CONCLUSION: Introduction of PRA and PA examinations in the diagnostic process of arterial hypertension led to more frequent diagnosis of PH, which may probably represent the most frequent form of endocrine hypertension. Although ARR is a reliable test for PH screening, routine ARR examinations in ambulatory practice are technically complicated and connected with high costs. Increasing the threshold level of kalemia for PH detection led to higher sensitivity and that is why the authors consider ARR examination rational in every patient with kalemia level less than 4 mmol/l. (Tab. 4, Ref. 18.)

Adult↗

PubMed2000

[Isolated primary hyperaldosteronism caused by adrenocortical carcinoma].

OBJECTIVE: To report a case of adrenocortical carcinoma and primary aldosteronism as the sole endocrine manifestation. METHODS/RESULTS: A 39-year-old male with adrenocortical carcinoma and primary aldosteronism is presented. Following complete hormonal and radiological evaluation, right adrenalectomy and nephrectomy were performed (pT2pN0M0, stage II). Blood pressure, serum potassium and aldosterone levels returned to normal. The patient received adjuvant therapy with carboplatin and etoposide. After 15 months' disease-free interval, lung metastasis was diagnosed, without evidence of local recurrence until 5 months later, when hypertension and primary hyperaldosteronism reappeared. There were no other endocrine disorders. Treatment with spironolactone, 5-FU and adriamycin was instituted with no tumor response and the patient died 3 years later from complications of endobronchial metastasis. CONCLUSION: Adrenocortical carcinoma with isolated primary hyperaldosteronism is uncommon and consequently there is no wide experience in regard to its diagnosis and treatment. Although randomized studies are not available, adjuvant therapy using other agents instead of mitotane (o,p-DDD), such as the combination of cisplatin and etoposide (VP-16), seems reasonable in the locally advanced stages. Mitotane may be useful when hypercortisolism is present, but its efficacy as an antitumor agent has been controversial.

Adrenal Cortex Neoplasms↗

PubMed2001

[Adrenal ACE and type II glucocorticoid receptors in primary hyperaldosteronism].

Adrenal tissue from 6 patients with primary hyperaldosteronism has been examined for the presence of angiotensin-converting enzyme (ACE). Its activity and amount of glucocorticoid receptors of type II (GR-II) were measured. ACE and GR-II were detected in adrenal tissue. GR-II induce ACE activity in interaction with plasma hydrocortisone. The glucocorticoid-receptor mechanism is an essential element in regulation of ACE activity determining a vasopressor effect. Disclosed is one of the aspects of tissue renin-angiotensin system function in primary hyperaldosteronism.

Adrenal Cortex↗

PubMed2002

[Diagnosis and surgical treatment of primary hyperaldosteronism].

Primary hyperaldosteroneism (PHA) is one of the main causes of secondary arterial hypertension (AH). Medical histories of 62 patients with PHA were analyzed. aldosterone-produced adenoma (APA) was diagnosed in 37 (59.7%) patients (all of them were operated), idiopathic hyperaldosteroneism (IHA)--in 25 (40.3%) patients, 11 of them were operated. Complex clinical and instrumental examination (hormonal analysis, USI, CT, MRT, in difficult cases in 35 patients--selective phlebography with blood sampling) was carried out in all the patients. Clinical picture in the majority patients with PHA was unclear. Hypokaliemia is not obligatory symptom of PHA. AH is often the only symptom of PHA, therefore all the patients with AH require complex laboratory examination including repeated detection of potassium blood level, examination of serum aldosterone concentration and renin activity, diurnal urinary excretion of aldosterone. In difficult differential diagnosis between APA and IHA it is necessary to perform selective phlebography with blood sampling from inferior cava and adrenal veins with obligatory detection of aldosterone and hydrocortisone concentration. Diagnostic and curative algorithm are developed. Surgical treatment is indicated for patients with APA, and also for ones with IHA who had functionally dominant adrenal gland (based on selective blood sampling analysis) and resistant for drug therapy AH.

Adrenal Glands↗

PubMed2003

Does the treatment of primary hyperaldosteronism influence glucose tolerance?

Primary hyperaldosteronism (PH) is frequently considered to be a secondary form of diabetes mellitus (DM). In our previous study we attempted to evaluate the prevalence of DM among patients with PH compared to control subjects with essential hypertension (EH). We have noted a relatively high prevalence of DM and impaired glucose tolerance in PH, but the differences between the PH and EH groups did not reach statistical significance. We performed this study to assess whether the effective treatment of PH (surgical and conservative) would improve the glucose tolerance. We have studied 24 patients with PH of the following two subtypes: aldosterone-producing adenoma (APA) treated with adrenalectomy and idiopathic hyperaldosteronism (IHA) treated with spironolactone. No significant changes of glucose levels were found in the 60th and 120th min of the oral glucose tolerance test (OGTT) in the APA group. On the other hand, fasting glucose levels were decreased significantly after adrenalectomy. Plasma glucose levels were significantly increased in the 60th min, but no differences were found in fasting values and in the 120th min in the IHA group. There was a significantly higher incidence of impaired glucose tolerance (36 per cent before, 45 per cent after treatment) and DM (9 per cent, 18 per cent) in the IHA group compared to the APA group (8 per cent, 32 per cent; DM 0 per cent, 0 per cent). In conclusion, the treatment of PH does not improve glucose tolerance. Mild worsening of glucose tolerance after treatment could be explained by an increase of the body mass index. These data, in accordance with our previous study, do not support the idea that PH is a secondary form of diabetes mellitus.

Adrenalectomy↗

PubMedDate not supplied

[Primary dexamethasone-suppressible hyperaldosteronism and hyperprolactinemia].

This report describes a clinical case with rare association: dexamethasone-suppressible hyperaldosteronism (DSH) and hyperprolactinemia. Previous studies reported that endogenous dopaminergic activity would be increased in both primary aldosteronism and in hyperprolactinemic syndromes. By manipulating dopamine tone with metoclopramide, bromocriptine, ACTH and amineptine, the aldosterone and prolactin responsiveness was evaluated. Our results showed a lack of dopamine inhibiting aldosterone secretion, despite dopaminergic tone is known to be increased in hyperprolactinemia. Thus it seems unlikely that dopaminergic control of aldosterone secretion could be account for this type of hyperaldosteronism associated to hyperprolactinemia, where the suggestion is that ACTH represents the principal regulator of aldosterone secretion.

Adrenocorticotropic Hormone↗

PubMed2003

[Primary hyperaldosteronism: report of two cases (normalization of hypertension after adrenalectomy)].

Two cases of Conn Syndrome with high hypertension, who were successful operated, have been prescribed. Retrospective evaluation of both cases suggests that severe and hypocalemic hypertension should motivate the researchers towards primary hyperaldosteronism. Etiology of the disease remains to be an important diagnostic challenge, optimal treatment will vary for each case of primary hyperaldosteronism. For individuals with aldosterone producing tumours the recommended type of treatment will be surgical as in most cases; it results in stabile normalization of RR level and abatement of metabolic dysfunction.

Adolescent↗

PubMed1976

The role of ACTH in the episodic release of aldosterone in patients with idiopathic adrenal hyperplasia, hypertension, and hyperaldosteronism.

The relationship of plasma aldosterone concentration to its identified stimuli was examined in three patients with hypertension, hyperaldosteronism, and idiopathic adrenal hyperplasia. Four patients with hyperaldosteronism due to adrenal adenomas served as controls. Plasma aldosterone, cortisol, sodium, and potassium concentrations and renin activity were measured in blood samples taken at 20 minute intervals from 2 A.M. to 8 A.M. during recumbency and sleep. The tests were performed on all patients following a regular sodium diet both before and after short-term treatment with dexamethasone. Two of the three subjects with adrenal hyperplasia were re-examined after 2 weeks of dexamethasone therapy. All four control patients with adenomas had episodic increases of plasma aldosterone which were significantly correlated with those of plasma cortisol (r = +0.48 to +0.90). This confirms the previously reported relationship between aldosterone and ACTH in such patients. Two patients with idiopathic adrenal hyperplasia had a similar secretion pattern and a highly significant correlation of the two hormones (r = +0.76 and +0.77); one did not (r = 0.13). Short-term dexamethasone pretreatment attenuated the episodic release pattern and partially suppressed the mean plasma concentrations of aldosterone in the four patients with an adenoma and in the two patients with idiopathic hyperplasia whose plasma aldosterone and cortisol concentrations were positively correlated. There was no such effect in the third patient. The first two patients with idiopathic hyperplasia were subsequently retested following 2 weeks of dexamethasone treatment to determine if the episodic secretion pattern of plasma aldosterone would correlated with other stimuli following this period of ACTH suppression. One showed little change from the pattern observed after short-term glucocorticoid treatment. The second had a similarly blunted aldosterone response until ACTH secretion led to a resumption of episodic changes in plasma aldosteerone concentrations. These data indicate that ACTH frequently is the dominant stimulus of the episodic secretion of aldosterone in patients with either adrenal adenomas or hyperplasia. When ACTH is suppressed, the hypersecretion of aldosterone is presumably sustained by an intrinsic adrenal abnormality or by an as yet unidentified stimulus.

Adenoma↗

PubMed1991

Diagnosis of hyperaldosteronism.

Hyperaldosteronism is associated with hypertension, potassium depletion, and suppressed plasma renin activity. It may involve one or both adrenal glands. This article reviews the different types of hyperaldosteronism and the diagnosis and management of each.

Adenoma↗

PubMed1990

[Significance of the captopril test in the diagnosis of primary hyperaldosteronism --apropos of 4 clinical cases].

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate to severe hypertension. In three patients an adrenal adenoma was found; in another patient was due to unilateral adrenal hyperplasia. A good therapeutic response was achieved in all cases by unilateral adrenalectomy. The captopril test (Lyons version) proved useful to exclude essential hypertension and, may be, in distinguishing the new sub-types of primary hyperaldosteronism recently described. Indeed, only in the case of unilateral adrenal hyperplasia a fall in plasma aldosterone levels was observed. However, we feel that further investigation is needed to clarify this point.

Adult↗