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A case or primary hyperaldosteronism due to unilateral macronodular adrenal hyperplasia is presented. This entity is exceptional: a review of the literature has yielded only three similar cases. The significance of these adrenal nodules is discussed; in particular, they are compared with the nodules found in hypertensive subjects. Their course after surgery is similar to that of Conn's adenoma.
Dexamethasone-suppressible hyperaldosteronism (DSH) is a rare familial variety of primary aldosteronism in which the biochemical features of mineralocorticoid excess are corrected by treatment with glucocorticoids. We report a large new kindred with this syndrome, the second such family described in the British Isles and the first in Ireland. The family has a dramatic history of premature cardiovascular death. We have documented DSH in four members and found evidence of aldosterone excess in two others. The kindred is unique in that we have documented DSH in distant relatives (fourth cousins). All patients described are well controlled on potassium-sparing diuretics. Our report underlines the importance of a detailed family history in the assessment of hypertension due to primary aldosteronism.
We describe a case of advanced chronic renal failure with persisting hypokalemia. The clinical study revealed the simultaneous presence of a salt and potassium loosing nephropathy associated with aldosterone-producing adenoma. This late pathology was revealed as electrolytic changes characteristic of primary hyperaldosteronism became evident as the renal function progressively deteriorated.
We have identified a subgroup of patients with aldosterone-producing adenoma (APA) who are responsive to angiotensin. Thus, a fall in plasma aldosterone (PA) during saline infusion may cause confusion with low-renin essential hypertension. Responsiveness of PA to angiotensin infusion and to upright posture may cause confusion with bilateral hyperplasia. Renin levels were not as completely suppressed in this angiotensin-responsive subgroup, leading to speculation that non-tumorous adrenal glomerulosa might also be less suppressed and might respond to angiotensin. This is unlikely, since angiotensin infusion soon after removal of the adenoma produced aldosterone levels of less than 10% of those achieved preoperatively. A biosynthetic peculiarity of the tumours is more likely, since urinary 18-oxo-cortisol levels were normal in this subgroup (as in bilateral hyperplasia) and raised in the more typical angiotensin-unresponsive subgroup (as in glucocorticoid-suppressible hyperaldosteronism). Since angiotensin-responsive tumours respond just as well to surgery as angiotensin-unresponsive tumours, it is important not to misdiagnose this subgroup as bilateral hyperplasia or low-renin essential hypertension.
The electrocardiograms (ECGs) of a series of 34 patients with primary hyperaldosteronism (PHA), 17 treated surgically (group I) nine treated medically (group II) and eight treated with/by both surgery and drug therapy (group III) were analysed to determine whether the treatment of PHA resulted in an improvement in the ECG changes of left ventricular hypertrophy (LVH) and also whether there was a difference in this improvement between medically and surgically treated patients. There was a significant reduction of blood pressure in the group as a whole (186/111 to 141/95 mmHg, P less than 0.001) and within each of the treatment groups (group I 183/108 to 137/98 mmHg, group II 188/112 to 147/93 mmHg, group III 193/115 to 144/92 mmHg). This reduction within each group was of a similar magnitude. There were reductions in both precordial voltages (SV1 + RV5) from 3.68 mV to 2.79 mV (P less than 0.01) and in the number of patients with ECG LVH from 15 to 8 (P less than 0.05). Again the reductions were of similar magnitude in each of the groups: group I 3.78 to 2.77 mV, group II 3.78 to 2.84 mV, group III 3.39 to 2.77 mV. Thus the improvement in blood pressure achieved by the treatment of PHA is accompanied by a reduction in precordial voltages and the number of patients with ECG-LVH. This improvement is independent of the type of treatment used.
A comparative assessment of the results of differential-diagnosis load tests and morphologic changes in adrenal tissue removed at surgery has been carried out in patients with arterial hypertension and low-renin hyperaldosteronism. Assessment of plasma aldosterone variations in response to load tests has shown this parameter to be unrelated to the structure of aldosteroma, either before or after the test. Different patterns of aldosterone production control were demonstrated in cases of diffuse-nodular and adenomatous adrenal changes. The study has provided additional information on the pathogenesis of this condition.
The antihypertensive effect of unilateral adrenalectomy was analyzed in 19 patients with arterial hypertension and primary hyperaldosteronism diagnosed by way comparing clinical findings, a degree of hypokalemia, activity of plasma renin and aldosterone concentration and CT data. A follow-up period after operation was 8-14 mos. Clinical and biochemical findings were compared with the results of morphological investigation of the adrenal glands and kidneys. An antihypertensive postoperative effect was observed in 12 patients: good in 6, moderate in 6, the absence of an antihypertensive effect in 7. Different forms of adrenocortical hyperplasia revealed during histomorphological investigation, endocrine nephropathy of various degree and vascular changes of hypertensive genesis in the renal parenchyma were discussed as causes of residual hypertension.
Primary hyperaldosteronism (HA1) represent a rare etiology of arterial hypertension (less than 1%). It concerns, most of the time, aldosterone-producing adenomas or bilateral adrenal hyperplasias although intermediate forms have been reported. The diagnosis of HA1 is based on simple examinations, especially systematic measurement of kaliemia in every hypertensive patient with a normal sodium diet before treatment. The elevation of aldosterone blood levels associated with a low plasma renin activity confirms the autonomous nature of the hormonal secretion which is dissociated from the renin-angiotensin system. Study of the ratio aldosterone blood level/ARP and the captopril test are particularly useful in borderline cases. Once the diagnosis of HA1 is made, a topographic analysis may be undertaken; tomodensitometry and adrenal scintigraphy are currently the examinations of choice in the diagnosis of adrenal tumors. Due to biological, morphological and topographic factors, aldosterone-producing adenomas may be identified with a great deal of certainty: surgical excision ensures a cure in a large majority of cases. The treatment of bilateral hyperplasias remains medical.
1. Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium and in serum sodium and bicarbonate, while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing the blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. 2. Only negligible side effects were encountered in the entire series of 24 patients.
Fifty consecutive Chinese patients with primary hyperaldosteronism were studied. All were considered to have an adrenal cortical adenoma, this being proven by surgery in 46 cases. In contrast to other reports, periodic paralysis was a presenting feature in 42 per cent of patients. Other notable symptoms were palpitations (30 per cent) and syncope (12 per cent). Vascular complications were present in 20 per cent of cases. Mean serum potassium level at presentation was 2.1 +/- 0.1 (mean +/- SEM) and sodium 145.0 +/- 0.1 mmol/l. Serum potassium was significantly lower and plasma aldosterone higher in patients with periodic paralysis. Adrenal venography in order to localise the tumour was unreliable and was misleading in two cases. Adrenal venous sampling for steroid analysis was much more helpful, despite the difficulty of obtaining right adrenal venous blood. The side of the adenoma could be predicted in 97 per cent of cases from measurements of left adrenal venous and vena caval aldosterone levels. The use of high resolution CT gave 100 per cent accuracy in all 18 patients who underwent surgery, the smallest detected tumour being 0.8 cm in diameter. Surgery corrected hypokalaemia in all cases, and 37 of the 46 patients required no further antihypertensive treatment.
The authors report the case of a 41-year-old man suffering from primary hyperaldosteronism due to bilateral adrenal hyperplasia, predominantly on the left. This condition is somewhat less common than Conn's adenoma and differs distinctly on the basis of a very poor response to surgical treatment. It can generally be diagnosed by non-invasive techniques, the most reliable of which are the postural test and adrenal isotope scan under inhibition with dexamethasone. These methods are nevertheless not always valuable in the presence of certain forms of hyperplasia which are less distinct from an anatomical standpoint, and must then be complemented by adrenal phlebography and estimation of aldosterone in adrenal venous blood or, if this proves impossible, in the inferior vena cava and renal veins.
A rare case of primary hyperaldosteronism due to corticosuprarenal carcinoma is presented. The case was treated by suprarenalectomy and is currently under antiblastic treatment with mitotane (o-p'DDD). The clinical and endocrinological elements for differential diagnosis from the much more common suprarenal adenomas are examined in particular detail.
We describe a patient who developed persistant hypokalemia after renal transplantation that was initially attributed to diuretics and/or steroids. However after stopping the diuretic, the patient continued to have urinary losses of potassium (less than 30 mEq/day) at a time when the serum potassium was only 2.4 mEq/l and high urinary chloride (33 mEq/day) suggesting that the diuretics were not responsible for the hypokalemia and the metabolic alkalosis. The results of these simple laboratory tests and the presence of persistent severe hypokalemia prompted additional studies (peripheral renin activity; plasma aldosterone levels; and CT scan) that led to the diagnosis of left adrenal gland adenoma. Surgical removal of the adrenal adenoma led to the normalization of the serum potassium and a fall in the total CO2 content in plasma. To our knowledge this is the first report of a case of hypokalemia secondary to primary hyperaldosteronism in a renal transplant recipient.
Multiple intracranial aneurysms have been reported in association with polycystic disease of the kidney, brain tumor, pituitary adenoma and coarctation of the aorta. We report the association of multiple aneurysms with primary hyperaldosteronism due to bilateral adrenal hyperplasia in an 18 year old left-handed man who presented with subarachnoid hemorrhage and arterial hypertension. We report the excellent outcome of this patient in spite of a difficult and surgical management. Ligation of all three intracranial aneurysms was performed after an extra-intracranial arterial bypass was done as a protective measure.
Aminoglutethimide (AG: 750 mg/day) was administered to a patient with idiopathic hyperaldosteronism (IHA) and circadian rhythms in urinary excretion of sodium (UNaV), potassium (UKV), aldosterone (AER) and 17-OHCS were analyzed by the single cosinor method. Urine was collected every 4h for 24h on the day before and on the 1st, 3rd and 7th day of AG administration, and above variables in each sample were determined. Circadian rhythms of 14 patients with primary aldosteronism (PA) who served as controls were also analyzed. In the present case, circadian acrophases in UNaV and AER studied before AG administration occurred at 22(19) and 07(05), respectively. They were similar to those of preoperative PA-patients. Circadian acrophase in UNaV occurred earlier with AG administration and on the 7th day it was at 14(05), a value similar to that of postoperative PA-patients. Circadian mesor in AER decreased remarkably from 4.1 to 0.6 micrograms/4h with AG administration, as did circadian mesor in UKV, whereas circadian mesor and acrophase in 17-OHCS did not change. Thus, the circadian characteristics in urinary variables in the present IHA-case were pathophysiologically similar to those of PA.
A review was made of the CT findings in a series of 15 patients with a clinical diagnosis of primary hyperaldosteronism. An adrenal tumour (diameter 11-68 mm) was observed in 13 cases. No adrenal involvement was noted in the other two. The initial diagnosis was confirmed either histologically or by means of a thorough clinical and instrumental follow-up in all 15 cases. High-resolution CT may thus be proposed as an initial examination in the diagnosis of primary aldosteronism. Its efficiency is such that venous sampling can be restricted to doubtful or negative cases.
Plasma aldosterone levels before and after walking were compared in a series of 10 controls and 41 patients with cirrhosis of the liver. The latter were distributed in the following way: 8 had compensated cirrhosis, the remaining 33 were in a situación of hydropic decompensation, 10 with associated renal insufficiency, and 23 without. Basal aldosterone levels in compensated cirrhotics were similar to those of the controls, but these values increased significantly more than the controls following postural stimulation. Decompensated cirrhotics without renal insufficiency had significantly higher values than the controls, both in basal conditions and after stimulation. The highest values corresponded to the decompensated cirrhotic patients with renal insufficiency who were in advanced stages of liver disease. On the basis of the present findings and those of other authors, it is suggested that a certain reduction in the metabolic clearance of aldosterone appears to exist in hepatic cirrhosis. However, hormonal hyperproduction is the dominant factor in the pathogenic mechanism of secondary hyperaldosteronism. The pathogenesis of the excessive production of hormone is discussed. In conclusion, it appears that the scant affluence of sodium to the macula densa may be the primary factor in explaining this common situation in patients with cirrhosis of the liver.
A case of muscle weakness with hypertension is presented. The patient had symptoms of depression. Diagnosis of hyperaldosteronism was suspected because of a low serum potassium and confirmed by discovery of an adrenal adenoma. The role of hypokalemia in mental disturbances is reviewed. Emphasis is placed on possible metabolic etiologies when mood changes, muscle paresis and hypertension coexist.