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PubMedDate not supplied

[Primary hyperaldosteronism: our experience with 34 patients].

Primary aldosteronism (PA) is a relative new endocrine disease that account for almost 1-2% of the hypertensive population. In spite of the large number of reports there is still disagreement around the preoperative diagnosis and surgical treatment. In a nineteen year period from 1970 to 1989, 34 patients came to our Department with a diagnosis of Primary Aldosteronism. 18 patients were female. Mean age at time of diagnosis was 45.5 yrs. (range 27-67 yrs.). Mean follow-up was 71 months (range 1-227 months). Follow-up was achieved in all patient. Hypertension and hypokalemia were discovered in all patients. Three patients had extremely low values of potassium and presented severe metabolic, cardiac and neurologic troubles. Localization procedure techniques improved during this period of time and at this moment CAT scan appears to be the most accurate method. Flank incision was the approach of choice in all but four patients. No postoperative complications were recorded. Histology demonstrated an incidence of adenomas according to the literature. One patient had an adrenal carcinoma with functioning metastases. He was operated on several times in order to remove the functioning node metastases but finally died with widespread disease four years after the first surgical treatment. Another patient in this series died three years after the operation for an unrelated event. In 29 patients hypertension and hypokalemia disappeared while in two patient, one with an adrenal carcinoma hypertension increased. Primary aldosteronism is a rare endocrine disorder whose incidence is increased in the last years because of the improvement in diagnostic procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMedDate not supplied

[Role of ketanserin in the treatment of primary hyperaldosteronism].

Ketanserin (Ket), a 5HT-2 serotoninergic receptor antagonist, is currently used as an antihypertensive agent. In our previous studies, both in vitro and in vivo when administered as bolus i.v. in subjects with primary aldosteronism (IAP), Ket exhibited an inhibitory action on aldosterone secretion. Therefore in the present study we investigated, in IAP patients, the effects of chronic treatment with Ket on blood pressure and mineralocorticoid secretion. Ket was administered at increased doses of 20 and 40 mg twice daily per os for 30 days and the following parameters were evaluated: blood pressure, heart rate, ur. aldosterone, pl. aldosterone both basal and after ACTH and angiotensin II (AII) stimulation, PRA, and atrial natriuretic factor (ANF). Our study demonstrated that Ket is a powerful blood pressure lowering agent with no relevant side effects and no variations of heart rate. Ur and pl aldosterone levels did not change during therapy; correspondingly, Ket did not modify ACTH or AII-induced stimulation. ANF levels, basally elevated in this syndrome, increased during Ket treatment. This new and interesting aspect deserves further evaluation. In conclusion Ket showed an effective antihypertensive effect in this syndrome, even if steroidogenesis inhibition does not seem to be a relevant component of its antihypertensive effect.

Administration, Oral↗
PubMed1989

[Renal response to acute volume expansion in primary hyperaldosteronism].

The exaggerated natriuretic response to extracellular fluid volume expansion (VE) observed in essential hypertension (EH) is related directly to blood pressure (BP) and indirectly to plasma renin activity (PRA). In order to evaluate the precise role of different hormonal parameters, the response to acute VE (isotonic saline, 1,800 ml IV over 3 hours) was assessed in 14 patients with primary aldosteronism (PA, surgically proven adrenal adenoma) and 18 clinically matched EH. At the time of the maneuver, BP and sodium intake were similar in the two groups, but serum potassium (2.89 +/- 0.13 vs 3.69 +/- 0.09 mmol/l), PRA (0.9 +/- 0.2 vs 3.5 +/- 0.9 ng/ml/h) and plasma aldosterone concentration (PAC, 25.9 +/- 3.8 vs 12.6 +/- 1.6 ng/dl) were significantly different. During VE, sodium excretion (UNaV) increased more in PA than in EH (98.1 +/- 15.2 vs 63.5 +/- 7.9 mmol/3 h); moreover, the slope of the regression line relating UNAVVE to UNaVcontrol was significantly steeper in PA. By contrast, the change in BP and indices of VE (hematocrit and plasma protein concentration) as well as the decrease in PRA (-45 +/- 9 vs -43 +/- 5 p. 100) and the increase in ANP (+ 65 +/- 16 vs + 69 +/- 28 p. 100) were similar in the two groups. VE left PAC unchanged in PA, whilst it decreased PAC in EH. We conclude that the natriuretic response to volume expansion is more marked in primary aldosteronism than in essential hypertension, a difference which is not explained by variations in the renin-angiotensin system or atrial natriuretic peptide.

Female↗
PubMed1989

[Iodo-methyl norcholesterol scintigraphy in the localization of primary hyperaldosteronism].

UNLABELLED: The aim of the study was to investigate the accuracy of iodomethyl norcholesterol, a new adrenal isotopic scanning agent, in the strategy of aldosteronism localization. Among 1499 patients examined in the clinic in 1987, 49 presented with primary aldosteronism. Nine were explored by adrenal scintigraphy (SCI). Mean age was 50 +/- 10 ans, blood pressure was 188 +/- 26/110 +/- 17 mmHg. Initial serum kalemia was 3.2 +/- 0.4 mMol/l, urinary potassium 67 +/- 39 mMol/d; standing plasma active renin was 9.9 +/- 5.0 pg/ml (20 less than N less than 50), supine plasma aldosterone was 316 +/- 200 pg/ml (50 less than N less than 150) and aldosterone excretion rate was 49 +/- 27 microgr/day (N less than 17). Adrenal CT-scan correctly predicted unilateral adenoma in 7 patients (size from 5 to 15 mm). CT-scan was negative twice. Adrenal vein aldosterone sampling and phlebography confirmed adenoma in the 8th patient. 7 patients underwent surgery, with pathological confirmation of the diagnosis. The diagnosis of adrenal hyperplasia (AH) was made in the 9th patient. (table; see text) When compared to CT-scan, SCI is unuseful if a tumor (greater than or equal to 10 mm) is detected on CT-scan (2 SCI false-negative/5 CT-scan tumors). At the opposite, when CT-scan is negative, SCI localizes 2 tumors in 4 patients (2 adenomas). CONCLUSION: SCI should not be used as first step diagnosis procedure in the localization of primary aldosteronism.

19-Iodocholesterol↗
PubMed1989

[Effect of a calcium inhibitor, nicardipine, on aldosterone secretion in primary hyperaldosteronism].

The purpose of the study was to evaluate the effects of a dihydropyridine calcium antagonist, nicardipine (N), on blood pressure (BP) and aldosterone secretion in hypertensive patients (pt) with primary aldosteronism. The study concerned 8 pts, mean age 55.6 +/- 7.7 years, 1 pt with aldosterone-producing adenoma (APA) and 7 pts with idiopathic aldosteronism: plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were respectively 0.30 +/- 0.2 ng/ml/h) and 314 +/- 109 pg/ml. Acute administration of 12 mg of nicardipine during 90 mn (three periods of N infusion during 30 mn: 0.4 mg/mn-5 mn; then 0.08 mg/mn-25 mn) significantly decreased BP, with an increase in heart rate (HR); the levels of PAC were significantly reduced with a slight but not significant increase in PRA, 60 mn after N: (table; see text) N decreased also PAC in the pt with APA [600 to 410 pg/ml] but did not improve hypokalemia (3.1 vs 3.3 mmol/l, n = 8 N.S.). In contrast, PAC levels were not modified 2 hours after acute oral administration of captopril (1 mg/kg): 302 +/- 164 pg/ml vs 332 +/- 191 pg/ml (NS). This study demonstrated the antihypertensive efficacy of acute infusion of nicardipine in primary aldosteronism; the decrease of PAC under this calcium antagonist suggested its potential interest in the management of idiopathic aldosteronism.

Aged↗
PubMed1989

Surgery for primary hyperaldosteronism.

The most common underlying disorder in primary aldosteronism is a benign unilateral adenoma. Some cases, termed idiopathic, are secondary to bilateral adrenal hyperplasia, and a few are caused by adrenocortical carcinoma. The therapeutic alternatives are pharmacologic management with an aldosterone antagonist and surgical adrenalectomy. The author reviews patient selection and preparation for surgery, the technical details of adrenalectomy in this setting, and relevant postoperative considerations.

Adrenalectomy↗