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PubMedDate not supplied

[Endocrine arterial hypertension. Primary hyperaldosteronism].

The authors emphasize some adrenal embryologic features, mainly the cortex and medulla relationships. After brief considerations both on the biosynthesis and physiologic actions of aldosterone, the Primary Hyperaldosteronism physiopathology is described. The clinical, biochemical and anatomic evidences are presented as a basis for both the Syndrome diagnosis and its subtypes. The theoretical and practical aspects of the diagnostic tests are also referred as a basis for the rationale of the medical and surgical therapeutic approach. Some clinical and biochemical similar aspects between the Syndrome of Hyperaldosteronism and Essential Hypertension with low renin, are put forward as a possible physiopathologic link that could eventually contribute for a better understanding of the pathogenesis of Essential Hypertension.

Aldosterone↗
PubMed1989

[Clinico-morphologic characteristics of 2 tumor forms of primary hyperaldosteronism].

Unilateral adrenalectomy was performed in 32 patients with primary hyperaldosteronism due to tumour of the adrenal gland and with arterial hypertension (AH) of various degree of severity. Stable normalization of AH occurred in 14 patients and in 18 its course improved. The results of a retrospective analysis of a hypotensive effect, the morphological picture of the removed adrenal and the findings of clinico-biochemical and instrumental study made it possible to establish preoperatively the diagnostic criteria for the identification of two tumorous forms of primary hyperaldosteronism: aldosterone-producing adenoma proper and the tumorous form of adrenocortical hyperplasia. They have different pathogenesis and postadrenalectomy hypotensive effect.

Adenoma↗
PubMed1985

Idiopathic hyperaldosteronism in a dog.

Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.

Adrenal Glands↗
PubMed1985

The therapeutic effect of a new angiotensin-converting enzyme inhibitor, enalapril maleate, in idiopathic hyperaldosteronism.

Patients with idiopathic hyperaldosteronism (IHA) manifest hypertension, hypokalemia, and renin suppression. IHA is thought to have one of three possible etiologies: zona glomerulosa autonomy, an aldosterone secretory factor, or angiotensin-II (A-II) adrenal hypersensitivity. To determine the contribution of A-II adrenal hypersensitivity in IHA, four patients with IHA were treated with a new angiotensin-converting enzyme inhibitor, enalapril, on a controlled diet (sodium [128 mEq/day] and potassium [80 mEq/day]) in a metabolic unit. The results of this study demonstrate that enalapril therapy in three of four patients normalized blood pressure, improved potassium balance, elevated PRA, reversed the postural increment in plasma aldosterone concentration (PAC), and reduced aldosterone secretion to normal. The fourth patient with bilateral macronodular disease, on the other hand, had no improvement in any of the above indices, despite maximal doses of enalapril (80 mg/day). This patient, however, may have had bilateral adrenal adenomas, based on extremely elevated 18-OH-corticosterone levels (greater than 100 ng/dl), and because of a lack of adrenal A-II hypersensitivity, demonstrated by a fall in pre-enalapril, postural-, and lasix-induced PAC. In conclusion, enalapril improved the hypertension, hypokalemia, renin suppression, and hyperaldosteronism in three patients with IHA over 28 days of therapy. The results of this study suggest an etiologic role of A-II adrenal hypersensitivity in IHA.

Adult↗
PubMed1986

Mineralocorticoid hypertension due to hyperaldosteronism and hyperdeoxycorticosteronism.

Hypermineralocorticoid hypertension is usually due either to aldosterone or deoxycorticosterone excess. Only in hyperaldosteronism due to adenoma or primary adrenocortical hyperplasia is cure achieved by surgery. Idiopathic hyperaldosteronism may be due to different aldosterone stimulators not related to hypertension. Rare adrenocortical tumours (benign or malignant) producing hyperdeoxycorticosteronism have suppressed aldosterone and in malignancy, cortisol. They provide evidence for a separate non-adrenocorticotrophic regulator of the deoxycorticosterone pathway. The dissociation of normal or reduced cortisol from elevated deoxycorticosterone levels suggests either an adrenal enzymatic disorder or tumour.

Desoxycorticosterone↗
PubMed1979

[Secondary hyperaldosteronism in patients with liver cirrhosis, frequently caused by therapy].

Plasma angiotensin II and plasma aldosterone was measured by radioimmunoassay in 78 patients with cirrhosis of the liver (group I: untreated, without ascites, n = 21; group II:untreated, with ascites, n = 25; group III: with ascites, during saluretic therapy, n = 32). From the obtained results it was concluded: (1) Excluding any pretreatment on the outpatient basis in most cirrhotics with or without ascites unaltered plasma levels of angiotensin II and aldosterone were found. (2) In contrast to previous suggestion secondary aldosteronism seems to be a minor determinant of hepatic ascites formation. (3) In untreated patients the 24-h-urinary excretion of electrolytes (Na+/K+ less than 1) represents an insufficient index of hyperaldosteronism. Obviously the kidney retains considerable amounts of sodium independent of circulating aldosterone levels. (4) Far above other mechanism hyperaldosteronism is most often induced by saluretic treatment of ascites and edema. The increased aldosterone secretion might indicate an adaptation phenomenon to restore total body sodium content. Certainly, the established concept of ascites therapy remains unimpaired by this physiological reaction.

Aldosterone↗
PubMed1980

The acute effect of angiotensin II on adrenal and anterior pituitary function in normal subjects and subjects with primary hyperaldosteronism.

Previous studies have shown that infused angiotensin II acutely suppresses ACTH release. In normal human subjects, the response to angiotensin II infused alone is specific to aldosterone and 18-hydroxycorticosterone. Other compounds such as cortisol, corticosterone and DOC do not respond. This is transformed into a general adrenocortical response by infusing small, constant quantities of ACTH. In patients with primary hyperaldosteronism, a poor response of plasma aldosterone to angiotensin II infused alone was altered to a response comparable with that in normal subjects by supplying ACTH during the infusion. Aldosterone secretion is more sensitive to ACTH in cases of primary hyperaldosteronism than in normal subjects. The poor response to angiotensin infusion may have been caused by inhibition of ACTH release, a phenomenon shown to occur in normal human subjects.

Adrenal Glands↗
PubMed1984

[Pseudohypoparathyroidism associated with hyperaldosteronism and polyglobulia].

A new case of familial PHP, associated with polyglobulia and biochemical parameters of hyperaldosteronism has been described. This association represents a very rare entity. PHP has been documented by the common tests and the unresponsiveness of AMPc to PTH. The poliglobulia , which appears after a period of severe anaemia, needs now periodical blood subtraction; nevertheless a cerebral thrombosis with conseguent hemiparesis has recently occurred. The hyperaldosteronism has been documented by hypopotassiemia , a raised level of plasma aldosterone as well as suppressed plasma renin activity even after adequate stimulus.

Aldosterone↗
PubMed1984

[Clinical aspects, diagnosis and treatment of idiopathic hyperaldosteronism].

Fifteen patients with idiopathic hyperaldosteronism were examined. Ten patients were subjected to surgery with 9 of them having an operation of the "portalization" of the renal and adrenal venous blood flow in combination with contralateral adrenalectomy aimed at inactivating the hormone of the adrenal cortex in the liver. One patient had unilateral adrenalectomy in combination with the incision of the celiac ganglions. There were no lethal outcomes following surgery. Postoperationally, all patients were followed up from 3 months to 2.5 years. In 78% of the cases the results of surgery were assessed as good, in 22% the arterial pressure decreased insignificantly although it became more sensitive to hypotensive therapy. The results obtained indicate the efficacy of surgery for the "portalization" of the renal and adrenal venous blood flow in conjunction with contralateral adrenalectomy in patients with idiopathic hyperaldosteronism.

Adrenalectomy↗
PubMed1983

[Malignant adrenal cortex tumors responsible for primary hyperaldosteronism and biological hypercorticism. Remarks apropos of 2 surgically-treated cases].

Two cases of malignant adrenal cortex tumors revealed by primary hyperaldosteronism with hypertension, and associated with a biological hypercortisonism, are reported. Diagnosis of this very rare affection depends on the finding of marked biological hyperaldosteronism associated with a large adrenal tumor. The outcome appears to be rapidly fatal for tumors exceeding 5 cm in diameter and associated with lymph node invasion. This raises the problem of the utility of surgery in these cases, operative intervention apparently accelerating progression of the lesion. In practice, however, a laparotomy is always justifiable, the most rational biopsy being excision of the tumor.

Adrenal Cortex Neoplasms↗
PubMed1995

[Primary hyperaldosteronism].

The diagnosis of primary aldosteronism (PA) is based on the finding of the combination of elevated urinary and/or plasma aldosterone and suppressed renin activity in patients with hypertension and hypokalemia. However, PA consists in a number of subsets, and diagnostic criteria for a correct identification of surgically remediable forms are of great interest. The methods and the results concerning our series of 113 patients with primary aldosteronism are presented in this review. Aldosterone producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were the most frequent forms, 51% and 44% respectively. They had similar BP levels, but hypokalemia was most frequently found in APA. Urinary and upright plasma aldosterone were similar, but supine plasma aldosterone was lower in IHA. Plasma aldosterone response to upright posture and angiotensin II infusion was absent in most cases of APA and present in IHA, but occasionally renin-responsive adenoma were found. Captopril failed to decrease plasma aldosterone in most patients with APA, and in a subgroup of patients with IHA. Patients with adenoma had also higher values of the aldosterone precursor 18-OH-B, and of atrial natriuretic peptide (ANP), probably as a consequence of a greater degree of volume expansion. Among morphological studies, CT scan and adrenal radio-cholesterol scintiscan provided similar results (85% accuracy): adrenal vein catheterization clarified almost all the remaining cases. Among the subsets of PA, 3 familiar cases of dex-suppressible hyperaldosteronism were recognized, with characteristically high levels of aldo, 18-OH-B, 18-OH-cortisol and 18-oxo-cortisol, due to the genetic abnormalities of the 11-18 hydroxylase system.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1993

Primary hyperaldosteronism--evaluation of procedures for diagnosis and localization.

We have reviewed the clinical, investigative and pathological findings in 16 patients with primary hyperaldosteronism, 6 with idiopathic adrenal hyperplasia and 10 with an aldosterone-producing adenoma. The ratio of serum aldosterone to plasma renin activity was > 1400 pmol/micrograms/l/h in all patients when measured supine on a normal salt diet, negating the need for salt loading to confirm primary hyperaldosteronism. Postural changes in serum aldosterone confirmed the presence of an aldosterone-producing adenoma in all but one patient when results on normal and high salt intakes were reviewed together. Nevertheless, the need for salt loading for discrimination is questioned, as the combination of postural changes in serum aldosterone on normal salt intake combined with CT confirmed and localized all aldosterone-producing adenomas. Urinary aldosterone measurements were of little value. Localizing procedures consisting of CT and isotopic scanning using 75Se-seleno-methyl-cholesterol proved most useful; adrenal venous sampling yielded less useful information. The latter may be due to the high predominance of patients (8) showing a background of micronodular hyperplasia with a dominant aldosterone-producing tumour. Only three of these patients have remained normotensive and normokalaemic on no medication. The presence of micronodular background suggests the need for life-long monitoring of such patients.

Adenoma↗
PubMed1976

[Primary and idiopathic hyperaldosteronism. Course 1 year after operation. Apropos of 28 cases].

The course of mean arterial pressure was compared in two series concerning 18 primary or tumoral hyperaldosteronism and 8 idiopathic ones. Identification of the nature of the hyperaldosteronism should not yet motivate a decision on principle, surgical in case of tumor, medical in an idiopathic case. In the latter case cooperation and tolerance of medical treatment, severity of hypertension also come into consideration. A positive spirolactone test, a hypertension course of less than six years were in our experience a good indication of successful surgery, as opposed to a normal unilateral renal biopsy. In case of operation, the removal protocol should adapt to the peroperative findings; 80% adrenalectomy is the most common procedure, except in the case of isolated adenoma of more than 10 mm diameter.

Adrenal Cortex Neoplasms↗
PubMed1993

[Radiographic endovascular correction of hyperaldosteronism in patients with arterial hypertension].

The authors describe a new method of X-ray endovascular destruction of the adrenal in patients with arterial hypertension and hyperaldosteronism. Destruction of the adrenal is accomplished by acute occlusion of its venous channel by introduction of a 3% thrombovar solution through a catheter installed in the central vein of the suprarenal gland. This method was applied in 22 patients with arterial hypertension; essential hypertension with secondary hyperaldosteronism was found in 18 of them, renoparenchymatous hypertension in 2, aldosteroma of the left adrenal in one, and Itsenko-Cushing's disease in one patient. Acute occlusion of the adrenal venous channel was achieved in 20 patients. The intervention normalized blood pressure in 16 and reduced it significantly in 4 patients.

Adrenal Glands↗
PubMed1996

[Adrenal adenoma or hyperplasia? Problems of differential diagnosis in an unusual case of primary hyperaldosteronism].

Although primary hyperaldosteronism is an uncommon cause of hypertension, it is the most common form of renin-independent hypermineralocorticoidism. The plasma aldosterone concentration and PRA with orthostatic test and saline infusion test are very useful aids to make a diagnosis. In this case the inconsistency between hormonal data and morphologic images (TC and NMR) led us to a dilemma: it was a question of adrenal adenoma or hyperplasia? Because it was impossible to dose the 18-OH-corticosterone, we had to perform a iodocholesterol scintigraphy NP 59. To distinguish an hyperplasia as cause of this kind of hyperaldosteronism made us able to define a therapeutic program useful to hypertension control.

18-Hydroxycorticosterone↗
PubMed1977

[The renin-angiotensin-aldosterone system in hypertensive patients. II. Diagnosis of primary hyperaldosteronism].

Twenty patients suffering from primary hyperaldosteronism were studied. Sixteen had a single adenoma of the adrenal and four had bilateral hyperplasia affecting both adrenals. Cases of primary hyperaldosteronism due to a tumour were characterised by a higher degree of hypermineralocorticism than was seen in the patients with hyperplasia. Plasma aldosterone, after acute volaemic expansion, did not fall below 13 ng/100 ml in the adenoma patients whilst it was lower in the case of hyperplasia. Adrenal phlebography is a useful tool in preoperative diagnosis.

Adenoma↗
PubMed2001

In situ demonstration of angiotensin-dependent and independent pathways for hyperaldosteronism during chronic extracellular fluid volume depletion.

In wild-type mice, 2-wk administration of losartan, an angiotensin (Ang) II type 1 (AT1) receptor antagonist, along with dietary sodium restriction, resulted in an elevation of plasma aldosterone greater than that seen with sodium restriction alone (2.75 +/- 0.35 vs. 1.38 +/- 0.16 ng/ml, P < 0.01). Plasma potassium increased in sodium-restricted, losartan-treated mice (6.0 +/- 0.2 mEq/liter), while potassium remained unchanged in mice with sodium restriction alone. To study the effect of Ang II on glomerulosa cells that may operate independently of plasma potassium in situ, we used chimeric mice made of cells with or without the intact AT1A gene (Agtr1a). When animals were fed a normal diet or chronically infused with Ang II, the aldosterone synthase mRNA was detectable only in Agtr1a+/+ but not Agtr1a-/- zona glomerulosa cells. After 2 wk of sodium restriction, plasma aldosterone increased (1.51 +/- 0.27 ng/ml) and potassium remained on average at 4.5 +/- 0.2 mEq/liter, with aldosterone synthase mRNA expressed intensively in Agtr1a+/+, but not detectable in Agtr1a-/- cells. Simultaneous sodium restriction and losartan treatment caused increases in plasma potassium (5.5 +/- 0.1 mEq/liter) and aldosterone (1.84 +/- 0.38 ng/ml), with both Agtr1a-/- and Agtr1a+/+ cells intensively expressing aldosterone synthase mRNA. Thus, aldosterone production is regulated by Ang II in the adrenal gland during chronic alterations in extracellular fluid volume when plasma potassium is maintained within the normal range. In the light of a previous observation that dietary potassium restriction superimposed on sodium restriction abolished secondary hyperaldosteronism in angiotensinogen null-mutant mice, the present findings demonstrate that when the renin-Ang system is compromised, plasma potassium acts as an effective alternative mechanism for the volume homeostasis through its capacity to induce hyperaldosteronism.

Adrenal Glands↗
PubMed1985

Morphological changes in the adrenal cortex in different variants of low-renin hyperaldosteronism. Comparison with the functional state of certain hormonal systems.

On the basis of morphological and histochemical examination of adrenal tissue of 45 patients with arterial hypertension and low-renin hyperaldosteronism, the following five morphological variants of this disease were differentiated: 1) with adenoma of the adrenal cortex and atrophy of surrounding cortical tissue; 2) with adenoma and hyperplasia of elements of the zona glomerulosa and(or) the zona fasciculata and the zona reticularis; 3) with multiple adenomatosis of the adrenal cortex; 4) with isolated diffuse or focal hyperplasia of the zona glomerulosa; 5) with nodal, diffuse-nodal or diffuse hyperplasia of all cortical zones. In tumours, three structural variants, corresponding to their histogenesis, were identified. A correlation was found between morphological variants and hormonal diagnosis of different forms of low-renin hyperaldosteronism.

Adenoma↗