[Primary hyperaldosteronism syndrome].
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Biomedical subjects
Publications and source records attributed to D Armanini.
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Vena cava and renal veins PRA were measured and their ratios calculated (Ra/Rc and Rc/P) in 15 hypertensive patients before and after diazoside infusion (300 mg i.v.). Among the 4 patients with unilateral renal artery stenosis, 3 had both ratios significant in basal conditions. After diazoxide infusion, the ratios became significant in the 4th case, successfully operated. Surgery induced normalization of blood pressure also in 2 of 3 cases affected by renoparenchimal alterations: of these patients 1 had ratios significant in basal conditions and both after diazoxide. One patient had unilateral renal artery stenosis and controlateral small kidney: his ratios was significant in favour of small kidney both before and after diaxozide infusion. The correction of renal artery stenosis gave no results in blood pressure. In patients with essential hypertension the PRA values in renal veins were not significantly different either before and after diazoxide. In conclusion the acute diazoxide stimulation seems to improve the prognostic value of renal veins PRA and their ratios for the detection of surgically curable forms of renal hypertension.
The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
In 37 patients with coarctation of the aorta, arterial blood pressure and ambulant plasma renin activity (PRA) were determined before and, in 15 patients, after surgical correction. The systolic blood pressure was raised in all the cases and the diastolic pressure was raised in 30 patients. Ambulant PRA was increased in 11 patients when compared with normal subjects of similar age. Twelve of the 15 operated patients had a significant decrease of systolic pressure after operation. Eight had raised PRA, and in 7 of these PRA fell to normal after operation and the blood pressure also fell; in 1 patient the decrease of PRA was unaccompanied by a fall in blood pressure. Though there was no significant correlation between the changes in blood pressure and PRA after operation it seems possible from our results that the renin-angiotensin system may be activated and contribute to the raised arterial pressure which occurs in patients with aortic coarctation.
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Reference is made to 20 cases of pheochromocytoma operated at the surgical clinic of the University of Padua since 1963. Stress is laid on the importance of modern angiographic techniques in diagnosis and their attendant risks and the main aspects of surgical management are examined. The results show that success depends on careful preoperative localisation, choice of a suitable approach route, and correct technique coupled with suitable intraoperative management.
1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), cortisol and adrenocorticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values of 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was significantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.
The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.