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PubMed1998

[Primary hyperaldosteronism].

Any hypertension with hypokaliemia or resistant to the therapeutic requires the investigation of a primary hyperaldosteronism. The first step is to eliminate the absorption of liquorice, alkaline compounds or diuretics. The next step is to verify that the therapeutics are compatible with hormonal measurements and that urinary sodium and potassium are normal. The diagnosis is confirmed by the elevation of plasma or urinary aldosterone and a low renin concentration. Conn adenoma is present in 2/3 of the cases and is treated by surgery, whereas bilateral adrenal hyperplasies require distal diuretics. The 2 aetiological forms are distinguished by CT scan and dynamic hormonal measurements.

Adenoma↗
PubMed2002

[Adrenal insufficiency after unilateral adrenalectomy for primary hyperaldosteronism].

A case of unexpected insufficiency of the remaining adrenal gland after unilateral adrenalectomy for primary hyperaldosteronism is described. The patient recovered from the initial disease, but postoperative tests repeatedly showed insufficient response to injection of ACTH. This case raises the question of interaction between the renin-angiotensin system and the hypothalamic-pituitary-adrenal-axis. Furthermore, it stresses the importance of testing the function of the remaining adrenal gland after unilateral adrenalectomy.

Adrenal Insufficiency↗
PubMed1975

Diagnosis and therapy of primary hyperaldosteronism in general practice.

Taking into consideration an own observation of Conn's syndrome the diagnostics and therapy of the primary hyperaldosteronism is described. The recognition of Conn's syndrome is important for that account as it coincides with an operatively curable hypertension. Therefore, a diagnostic step programme is proposed. Thus, the first tentative diagnosis shall be made already by a general practitioner. Other specialised and highly specialised investigations have the task to ascertain the diagnosis and to find the right way in therapy.

Antihypertensive Agents↗
PubMed2001

[Diagnosis of subtypes and lateralization for primary hyperaldosteronism].

OBJECTIVE: To evaluate the value of CT and posture stimulation test (PST) in the differential diagnosis and lateralization of primary hyperaldosteronism(PA). METHOD: Retrospective study was done based on the clinical data and pathological examinations of 22 patients with PA. RESULTS: The baseline plasma aldosterone concentration (PAC) of most aldosterone-producing adenomas (APAs) was over 250 pg.ml-1. In the diagnosis of APA, the sensitivity of CT was 75% and the specificity of CT was 100%; the sensitivity and specificity of PST were 87% and 100%, respectively. The examination results of CT and PST had no statistical significant correlativity (P > 0.05) and had bad consistency (P > 0.05), and the diagnostic efficiency of them had no significant difference (P > 0.05). CONCLUSIONS: The baseline PAC and the result of PST suggest as the best diagnostic index and methods of APA. Both CT and PST have high value in the differential diagnosis. Both CT and PST cannot be substituted for each other.

Adenoma↗
PubMed2003

[Primary hyperaldosteronism].

Primary hyperaldosteronism (PHA), autonomic secretion of aldosterone by the adrenal gland, is rare. PHA usually results in therapy-resistant hypertension and is often but not always accompanied by hypokalaemia. Common causes of PHA are an aldosterone-producing adenoma, idiopathic aldosterone hypersecretion, unilateral hyperplasia or a genetic variant: glucocorticoid-remediable aldosteronism (GRA). The diagnosis should be phased and first of all requires a biochemical confirmation of the presence of PHA. In PHA patients, plasma renin is invariably suppressed. Blood should be collected under standardised conditions while the patient is not using beta-blockers or centrally-acting antihypertensive medication. Patients with a suppressed plasma renin and an elevated plasma aldosterone concentration have PHA. In patients with a suppressed plasma renin and a high-normal plasma aldosterone concentration a confirming test should be performed in which PHA is diagnosed if aldosterone is not suppressed following volume expansion with sodium chloride. The cause of PHA is determined by means of a CT scan or MRI of the adrenal glands to find a unilateral adenoma. If the CT scan or MRI is normal, adrenal vein aldosterone sampling may be considered as a next step in order to demonstrate lateralisation of aldosterone production. The hypertension and hypokalaemia of all forms of PHA respond well to spironolactone therapy. In the case of a unilateral adenoma or unilateral hyperplasia, adrenalectomy is the treatment of choice. For GRA, dexamethasone in doses that reduce the corticotropin (ACTH) level is indicated.

Adenoma↗
PubMed1992

[Chronic fatigue syndrome, a case of high anti-HHV-6 antibody titer and one associated with primary hyperaldosteronism].

Two cases of chronic fatigue syndrome (CFS) were reported which were suggestive for the study of the etiology and a cure for CFS. Case 1: A 31-year-old woman was admitted for chronic fatigue syndrome. Examination revealed a high titer of anti HHV-6 antigen of x2560 and an increased percentage of suppressor T lymphocytes in the peripheral blood. HHV-6 was speculated to be reactivated and stimulating the immune system in CFS. Case 2: A 46-year-old woman suffering from CFS had been in remission for 6 years. She was admitted for hypertension associated with right adrenal adenoma and hyperaldosteronism. After right adrenalectomy, there was a recurrence of high fever and other CFS symptoms. It was suggested that CFS symptoms may be ameliorated by aldosterone.

Adrenalectomy↗
PubMed1992

[The behavior of serum angiotensin-converting enzyme in normotensive subjects, in subjects with essential hypertension and in subjects with primary hyperaldosteronism on the orthostatic test].

The results of this study demonstrate that only in healthy normotensive subjects during extended orthostatism that the renin-angiotensin-aldosterone system remains integral and is characterized by a significant increase in serum angiotensin-converting enzyme (SACE), plasma renin activity (PRA) and plasma aldosterone (PA). SACE modification do not seems to directly follow that of PRA (as shown by the absence of a direct correlation between SACE and PRA). In essential hypertension, the behavior of SACE seems to change, without demonstrating a significant increase in the mean levels of this enzyme. Finally in hypertension of known origin, such as primary hyperaldosteronism, the low levels of SACE in the recumbent position (not stimulated by orthostatism) seem to depend (by mechanism of negative biofeedback) on the increased serum levels of PA, which is moreover verified in the same group for PRA.

Adult↗
PubMed1992

[Primary hyperaldosteronism suppressed after glucocorticoid administration].

Authors present a case of glucocorticoid suppressible hyperaldosteronism in 18 year old female. Unmeasurable low plasma renin activity and marked increase in aldosterone concentration was established. After administration of dexamethasone, normalization of aldosterone concentration and blood pressure has been observed.

Adolescent↗
PubMed2004

[New potentialities in the treatment of idiopathic hyperaldosteronism].

The study was undertaken to examine whether the drugs affecting the renin-angiotensin system may be used in the combined treatment of patients with idiopathic hyperaldosteronism (IHA). The study covered 20 patients (mean age 46.6 +/- 7.3 years). The diagnosis in all the patients was verified by a complex of instrumental studies, including the determination of plasma aldosterone concentrations (PAC) and plasma renin activity (PRA), and topical diagnostic studies (ultrasonography, computed tomography (CT)/magnetic resonance imaging (MRI), and angiography). The patients were given spironolactone, dihydropyridine calcium blockers, and beta-adrenoblockers, then with the cross-over method, this combination was added by the angiotensin-I receptor blocker (ATRB) losartane or the angiotensin-converting enzyme inhibitor (ACEI) lisinopril for 4 weeks. 24-hour blood pressure (BP) monitoring was used to evaluate the efficiency of therapy. In the combined therapy losartane, 50-100 mg/day, reduced systolic BP (SBP) by 8.4%, diastolic BP (DBP) by 11.1% while lisinopril, 10-20 mg/day lowered SBP and DBP by 7.6 and 9.9%, respectively. Both drugs improved the daily BP profile. When losartane or lisinopril added to the combined treatment, a therapeutic response was achieved in 15 (79%) and 14 (73.7%) patients, respectively. ARB and ACEI exert an antihypertensive effect in patients with IHA and they may be used in the combined treatment of this disease. The use of the above drugs may reduce the dose of spironolactone to the mean therapeutic one. The pathophysiological rationale for the use of ATRB for IHA is that the sensitivity of aldosterone secretion to the stimulating effect of angiotensin II is preserved despite the fact that the PAC is higher and PRA is lower.

Adrenal Glands↗
PubMed2004

Primary hyperaldosteronism treated by radiofrequency ablation.

This is a report of a 57-year-old Jordanian man who had uncontrolled hypertension and hypokalemia. He was diagnosed to have primary hyperaldosteronism with left adrenal adenoma. Traditionally, surgical resection of the adrenal gland whether by laparotomy or laparoscopic procedures would have been considered at this point. However, the treating team elected radiofrequency ablation of the left adrenal in view of the fact that this facility and the expertise was available in the hospital; in addition, this procedure required a shorter duration of hospitalization, was less expensive, and was less invasive. Subsequently, the patients blood pressure improved to 120/75 mm Hg and his anti-hypertensive medications were reduced. Serum aldosterone and computed tomography scan of adrenals improved. We are reporting this case as it is the first time such modalities in the treatment of adrenal adenoma was used.

Adrenal Hyperplasia, Congenital↗
PubMed1992

[Primary hyperaldosteronism, problems in diagnosis and therapy in clinical practice].

The paper summarizes data from the recent literature on pathogenetic variants of primary hyperaldosteronism, screening, diagnosis and therapy of this secondary form of arterial hypertension. On examples from their own practice the authors draw attention to the that the diagnosis and treatment of this disease is not always as straightforward as might appear from the literature. The solution is simple, effective screening in every hypertensive patient by examination of the kalaemia before treatment of arterial hypertension is started. In case of hypokalaemia the subsequent procedure should be the concern of specialized departments.

Aged↗
PubMed2006

[Moot and unsolved problems in diagnosis and surgical treatment of primary hyperaldosteronism (50 years since Conn's syndrome description)].

Personal and fifty-year world experience in diagnosis and treatment of primary hyperaldosteronism (PHA) is analyzed. The following problems are discussed: 1) possibility to use simplified diagnostic algorithm for diagnosis of PHA; 2) possibility to exclude march test from diagnostic algorithm; 3) role of selective venous blood sampling in PHA; 4) Indications for surgical treatment in PHA; 5) validity of surgical procedures for "portalization" of adrenal blood flow.

Adenoma↗
PubMed1991

[Panarteritis nodosa with secondary hyperaldosteronism involving renal arterioles].

A case of a 6 year old girl with angiographically and bioptically verified systemic polyarteritis nodosa is reported. Secondary hyperaldosteronism due to involvement of small and medium-sized renal arteries caused severe hypertension and left ventricular hypertrophy, and together with abdominal complaints, loss of weight, livedo reticularis and elevated titers of streptococcal antibodies formed the clinical pattern of the disease. It may be assumed, that there is a correlation between the recurrent streptococcal infections and the development of systemic polyarteritis nodosa by hypersensitivity or disordered immunologic reactivity. Therapy and short time follow up is reported. For treatment of hypertension an angiotensin converting encyme inhibitor was used, which immediately slowed down the maximal stimulated plasmarenin-angiotensin system.

Aldosterone↗
PubMed1991

[Primary hyperaldosteronism with angina and arrhythmia].

Case report of primary hyperaldosteronism in a 43 year-old man, with 2 years history of hypertension and cardiovascular involvement manifested by "angina pectoris", ventricular arrhythmia and hypokalemia. The CT scan showed a left adrenal gland adenoma. The patient underwent a surgery for tumor removal, and became asymptomatic during a follow-up period of 11 months.

Adenoma↗
PubMed1978

[Primary hyperaldosteronism with paroxysmal arterial hypertension. Apropos of 2 operated cases].

Primary hyperaldosteronism usually causes moderate hypertension. It is rare to note as in our two patients intermittent attacks of paroxysmal hypertension. The diagnosis of aldosteronism will be suspected on the finding of persistent hypokalemia with acidosis. It will be confirmed by laboratory examinations severe fall in plasma renin activity and rise in aldosterone in the adrenal veins. To determine the affected side, one may carry out adrenal phlebography which is a difficult technic, and/or a scan using iodine cholesterol which is benign and precise. Surgery with removal of the adenomatous hyperplasia in one case and of an adenoma in the other, gave one very good result.

Adrenal Glands↗
PubMed1990

[Pseudo-hyperaldosteronism caused by licorice. Pathogenetic considerations and presentation of a clinical case].

A case of pseudo-hyperaldosteronism secondary to prolonged daily ingestion of liquorice is reported. Extreme severity of hypokalemia and of the ensuing neuro-muscular impairment characterized this case. The pathogenetic features leading to the glycyrrhizic acid dependent sodium retention are thoroughly discussed, on the basis of the latest literature. The authors stress the fact that public opinion is to a large extent unaware of risks due to prolonged ingestion of liquorice derivatives.

Glycyrrhetinic Acid↗