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PubMed1993

[Primary hyperaldosteronism--4 clinical cases].

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate hypertension. Serum potassium and plasmatic aldosterone values were high although plasmatic renin levels were normal. The captopril test (Lyons version), abdominal CT and iodocholesterol (NP-59) scan proved useful to exclude essential hypertension. A good therapeutical results was achieved in all cases by unilateral adrenalectomy. After surgery, diagnosis was confirmed in all cases by histological studies. At one year follow-up, all patients were asymptomatic, with no hypertension without therapeutic and the serum potassium and plasmatic aldosterone and renin values were normal.

Adenoma↗
PubMed1994

[Primary hyperaldosteronism caused by small adenoma not visible with CAT using typical postural studies for hyperplasia. Report of a case].

The paper describes a case of primary hyperaldosteronism using typical postural tests for hyperplasia and negative CAT, elements which in the majority of cases allow an adrenal gland hyperplasia to be confirmed, but which should not overlook the rare but documented possibility of a small adenoma not visible with CAT, responding to angiotensin II and which can be treated with surgery.

Adenoma↗
PubMed1993

Primary hyperaldosteronism--diagnostic approach and management.

Primary hyperaldosteronism was detected in 1% of patients evaluated for secondary hypertension in a referral hospital in Southern India. The presence of hypokalemia with inappropriate kaliuresis (24 hr. urine K > 20mEq) was an important diagnostic clue. High resolution CT scans were found to be useful for localising the tumour. Preoperatively nifedipine and spironolactone were employed to correct hypertension and hypokalemia. The same drugs were also found to be excellent for long-term control of hypertension and hypokalemia in patients who had bilateral adrenal hyperplasia and aldosteronism.

Adult↗
PubMed1993

[A case of idiopathic hyperaldosteronism diagnosed by adrenal imaging].

We report a case of idiopathic hyperaldosteronism (IHA) which was differentiated from an aldosterone producing adenoma by the adrenal imaging techniques with computed tomography (CT) and scintigraphy. In this patient, the high basal aldosterone level with the suppressed plasma renin activity typically indicated the diagnosis of primary aldosteronism. However, the differentiation from an aldosterone producing adenoma by responses of plasma aldosterone levels to upright posture, captopril or adrenocorticotropic hormone (ACTH) administration was not definitive. Abdominal CT revealed bilateral adrenal swelling. Adrenal scintillation scanning with 131I-iodocholesterol showed bilateral uptake even after the administration of dexamethasone. Blood sampling from the right adrenal vein was unsuccessful. Blood pressure and serum potassium levels remained unchanged during dexamethasone administration (2 mg/day) over ten days. After the administration of spironolactone and nisoldipine blood pressure and serum potassium levels were normalized. Adrenal imaging is considered to be very useful for the diagnosis of IHA.

Adrenal Glands↗
PubMed1993

[Primary hyperaldosteronism. A report of 2 clinical cases].

We describe two clinical cases of primary hyperaldosteronism caused by adrenal adenoma (Conn's syndrome) with very different forms of clinical presentation. Some theoretical considerations about diagnosis and treatment of the disease are made.

Adenoma↗
PubMedDate not supplied

Primary hyperaldosteronism. Analysis of risk factors associated with persistent postoperative hypertension.

Between 1983 and 1992, 24 patients with primary hyperaldosteronism were operated at our division. Among these, 21 had adrenal adenoma and constituted the subjects of our study. The aim of this retrospective study was to determine risk factors that could potentially lead to persistent arterial hypertension (5 cases or 23.9%). The variables of the univariate and the multivariate analyses were: sex, age, diameter of the neoplasm, preoperative duration of the hypertension, and familial hypertension. The analysis demonstrated no statistically significant difference between the resolution of hypertension and the variables. Though not statistically significant, the only variable that approached statistical significance (p < 0.11) was familial hypertension.

Adenoma↗
PubMed1998

[Primary hyperaldosteronism: report of 2 clinical cases].

The authors report two cases of primary hyperaldosteronism (Conn's adenoma and hyperplasia). Based on available data, the authors discuss clinical laboratory and imagiologic evaluation, the factors influencing prognosis, strategy and the results of the proposed therapies.

Female↗
PubMed1998

[Idiopathic primary hyperaldosteronism: significance of functional diagnosis].

Primary aldosteronism is a rare cause of hypertension caused by increased aldosterone secretion. The two essential stimuli for aldosterone production, potassium and angiotensin II, tend to be low. At a time when imaging procedures are becoming more common, more patients are being found with adrenal masses, and patients with incidentalomas and low renin hypertension could be considered as candidates for surgery. Apart from an appropriate work-up for the diagnosis of primary aldosteronism, the differential diagnosis between unilateral adenoma and idiopathic ("hyperplasia") hyperaldosteronism is relevant for the choice of therapy. Based on data from the literature and four patients we observed as outpatients in 1997, we suggest that a properly conducted and carefully interpreted postural stimulation test can be useful in identifying patients who are successfully treated by drugs.

Adenoma↗
PubMedDate not supplied

[Acute intermittent porphyria associated with hyperaldosteronism and inappropriate antidiuretic hormone secretion syndrome].

Acute intermittent porphyria, the most commun acute porphyria in France, is an autosomal dominant disorder of heme biosynthesis. The basic biochemical defect is reduced activity of the enzyme porphobilinogen deaminase. Clinical evolution is characterized by acute attacks, with a severe prognosis due to acute abdominal pain and risk of neurological complications, induced by drug intake, infection, alcohol intake or unknown factors. We report the case of a patient with an inappropriate antidiuretic secretion syndrome and secondary hyperaldosteronism associated with acute intermittent porphyria and polyradiculoneuritis syndrome. This syndrome was found to be induced a delayed reaction to thiopental. A favorable response was achieved with heme-arginate treatment.

Adult↗
PubMed1977

[Hyperreninism without hyperaldosteronism in diuretic abuse: a report of a case with identification of mefruside and ethacrynic acid in urine (author's transl)].

A 46-year-old nurse had been hospitalized 16 times during the preceding five years because of episodes of excessive hypokalaemia. On admission to hospital there was hypokalaemia, polyuria, excessive plasma renin activity but no increased aldosterone secretion rate. Diuretic abuse was confirmed by gas-chromatography and mass spectrometry of mefruside and ethacrynic acid in the patient's urine. Apart from other interesting aspects of this case there was the demonstration of hyperreninism without hyperaldo-steronism. The stimulating effect of renin on aldosterone secretion was obviously lower than the inhibiting effect of hypokalaemia. The general term "renin-angiotensin-aldosterone system" is, therefore, misleading because it mentions only one pathway of aldosterone regulation. The combination of hypokalaemia, polyuria, hyperreninism without hyperaldosteronism is apparently the principal but not widely recognised feature of diuretic abuse.

Aldosterone↗
PubMed1979

Hyperaldosteronism in the sodium depleted rat: effect of a low sodium diet or diuretic treatment on steroid output by the superfused adrenal zona glomerulosa.

The effect of chronic and acute sodium depletion on the function of the adrenal zona glomerulosa was examined by means of superfusion of adrenal capsular glands. The glands were removed from rats kept on a low sodium diet for 7 days or from dexamethasone-pretreated rats 30 min after administration of the diuretic drug furosemide. Chronic sodium depletion brought about a high initial output of aldosterone followed by a rapid fall in output. The initial rate of corticosterone output did not differ significantly from that by control glands but exhibited a more rapid decline with time. Aldosterone: corticosterone ratio, an indicator of the rate of conversion of corticosterone to aldosterone, was much higher in the sodium depleted group throughout the whole superfusion period. Acute sodium depletion was followed by high initial and rapidly falling aldosterone and corticosterone output, without any significant change in the ratio of aldosterone to corticosterone output rate. The above dynamic patterns of steroid output indicate that a sodium deficient diet evokes hyperaldosteronism by increasing the formation of aldosterone from corticosterone (not excluding the possibility of increasing the formation of corticosterone as well) while diuretic treatment stimulates aldosterone secretion by acting on the formation of corticosterone only.

Adrenal Cortex↗