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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Hyperaldosteronism (Conn's disease) presenting as depression. 46 62

During a protocol study for the evaluation of patients with primary aldosteronism, a variety of diagnostic studies were employed in an attempt to identify patients with primary aldosteronism and to differentiate patients with adrenal adenoma from patients with idiopathic adrenal hyperplasia. In this study, we are able to demonstrate the utility of (1) absent postural increase in plasma aldosterone concentration, (2) adrenal scanning and (3) normalization of blood pressure with spironolactone therapy in identifying patients with primary aldosterone excess who have an adrenal adenoma, surgical removal of which results in eliminating their hypertension.
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PMID:Identification and differentiation of surgically correctable hypertension due to primary aldosteronism. 47 85

A 56-year-old woman had a 22-year history of hypertension. Investigation showed hypokalemia and kaliuresis without pronounced suppression of plasma renin activity or elevation of urinary aldosterone excretion. There was biochemical evidence of catecholamine metabolite excess but the usual clinical features of pheochromocytoma were absent. Laparotomy revealed a pheochromocytoma and adrenal adenoma in the right adrenal gland. Excision of the tumours was followed by resolution of the hypertension and metabolic abnormalities.
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PMID:Coexistence of pheochromocytoma, adrenal adenoma and hypokalemia. 84 17

Among the atypical pictures of primary aldosteronism, sometimes, normal blood and urine concentration of aldosterone have been observed in association with an adrenal aldosterone-producing adenoma. Here we report a case of atypical primary aldosteronism so characterized: -- the patient had the typical clinical findings of aldosteronism (hypertension, hypokalemic alkalosis, polyuria, etc). -- the patient exhibted all the biochemical abnormalities of primary aldosteronism: increase of exchangeable Na and of plasma volume, decrease of exchangeable K, etc. -- the patient had normal blood and urine levels of aldosterone. -- the patient's blood and urine aldosterone concentration increased following sodium depletion and K administration. Such increase was comparable with that obtained in normal subjects after the same tests. However, at the end of these tests, the patient was still in potassium depletion and sodium repletion. Therefore, it was concluded that the secretion of aldosterone, although normal in absolute values, was inappropriate to the metabolic status of the patient, since such "normal" values were found in association with conditions that should have produced an inhibition of aldosterone production. The catheterization of adrenal veins demonstrated the existence of a right adrenal adenoma. The blood pressure and the biochemical parameters of the patients have been normalized by right adrenalectomy.
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PMID:[Physiopathological and functional semeiologic considerations in a case of primary normoaldosteronemic hyperaldosteronism]. 88 97

Primary hyperaldosteronism is a potentially curable cause of hypertension, and much interest has been shown in methods of diagnosing the associated hypokalaemic hypertension and localising the adrenal adenoma. In two patients the diagnosis of primary aldosteronism was confirmed by colonic potential measurement and the adenoma localised by a new subtraction technique for early adrenal imaging applied to the use of 131I-19-iodocholesterol. Both patients underwent adrenalectomy and in each case an adenoma was removed. Blood pressure and electrolyte levels returned to normal after operation. In one patient bilateral adrenal phlebography had failed to show the tumour, and sampling of aldosterone concentrations in the adrenal veins had been unsatisfactory.
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PMID:Adrenal aldosterone-producing adenoma: use of colonic potential in diagnosis and subtraction scanning technique for localisation. 93 76

Mineralocorticoids are out of the causes of secondary hypertension. Excess production of mineralocorticoids induces sodium and fluid retention, loss of potassium and metabolic alcalosis. The diagnosis of mineralocorticoid syndromes depends on the interpretation of the functional status of the renin-mineralocorticoid-system, which is in part responsible for the maintenance of normal blood pressure. The classical representative of this group is the syndrome of primary aldosteronism. Causes of mineralocorticoid syndromes associated with hypertension are: 1. autonomous production of mineralo-corticoids by an adrenal adenoma or by idiopathic bilateral adrenal hyperplasia; 2. deficiency of adrenal 17-alpha-hydroxylase or of 11-beta-hydroxylase; 3. secondary aldosteronism associated with primary reninism, or renal arterial stenosis; and 4. pseudo aldosteronism due to excessive ingestion of licorice. Malign or essential hypertension may also often be followed by secondary aldosteronism.
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PMID:[Mineralocorticoid syndromes and hypertension]. 96 85

Steroid production, plasma renin activity (PRA) and plasma renin substrate (PRS) were measured in eight patients with hypertension due to Cushing's syndrome of benign origin. Despite elevation of cortisol secretion in all patients, hypokalemia and suppressed PRA was noted in the one subject with a functioning adrenal adenoma. PRA was normal in six patients on an unrestricted sodium intake but was markedly increased in the two patients on low salt diets. PRS was significantly increased during active disease, but decreased substantially with treatment. The absence of uniform hypokalemia and of suppression of renin indicates that mineralocorticoid production could not account for the increase in arterial pressure. It is suggested that glucocorticoid-induced hypertension may be initiated by alterations in vascular responsiveness to pressor agents and that elevated PRS levels may contribute to increase angiotensin formation.
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PMID:Pathogenesis of hypertension in Cushing's syndrome. 111 68

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.
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PMID:Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension. 117 11

A system for discriminating between adrenal adenoma and hyperplasia based on the levels of aldosterone production, plasma renin concentration, severity of electrolyte disturbances, plasma aldosterone patterns during recumbency and after assuming erect posture, and 131I-19-iodocholesterol scan has been developed. Indicated for operation are patients with adenomas whose elevated blood pressure cannot be continuously controlled with usual doses of medication and patients with documented deterioration of target organ function. Adrenalectomy has been performed 83 times in 81 patients with a diagnosis of primary hyperaldosteronism. Results of excision of adrenal adenomas have been excellent with significant lowering of blood pressure in all cases and cure of hypertension in over 60%. Results of total or subtotal adrenalectomy for hyperplasia have been poor with almost all patients still requiring medication for hypertension. Adenomas have always been unilateral, and usually can be localized so that unilateral exploration is curative. Therefore, we have tried to distinguish preoperatively between adenoma and hyperplasia. Anterior transperitoneal adrenalectomy has been effective with few complications, and no postoperative hypercortisolism after unilateral adrenalectomy for adenoma. The unilateral extraperitoneal approach gives shorter morbidity and potentially fewer serious complications.
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PMID:Selection of patients and operative approach in primary aldosteronism. 118 May 75

1. In 7 patients with hypertension, aldosteronism, and low plasma renin (6 patients with a solitary adrenal adenoma, 1 patient with bilateral adrenal hyperplasia) circulatory reflexes (Valsalva's maneuver, head-up tilt and cold pressure test) were examined. Furthermore, the reactivity to the pressor action of tyramine and norepinephrine was determined. For comparison 10 patients with essential hypertension were studied. 2. In 4 of the 7 patients with primary aldosteronism no overshoot following Valsalva's maneuver could be observed. Compared to the patients with essential hypertension the mean overshoot in the patients with primary aldosteronism was significantly reduced. The decrease in blood pressure during head-up tilt was significantly more pronounced in the patients with primary aldosteronism. However, both groups did not differ in their reaction to the cold pressure test. In the patients with primary aldosteronism responsiveness to tyramine was significantly reduced compared to the patients with essential hypertension. No significant difference was observed in the reactivity to norepinephrine between both groups studied. 3. The results point towards a disturbance of the sympathetic nervous system in patients with primary aldosteronism.
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PMID:[Circulatory reflexes in primary aldosteronism (author's transl)]. 121 78


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