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

Adrenocortical scintigraphy with iodine 131-19-iodocholesterol or selenium 75-6-selenomethylcholesterol was performed in 94 patients with proven or suspected adrenal disease. According to the final diagnosis, 36 patients suffered from primary aldosteronism, 33 from Cushing's syndrome, 8 from low renin hypertension, 6 from nonfunctioning adrenal tumour, 4 from simple obesity, 3 from adrenal metastases, 1 from congenital adrenal hyperplasia, 1 from virilizing adrenal adenoma, 1 from extraadrenal phaeochromocytoma, 1 from ganglioneuroma. Surgical confirmation of the diagnosis was obtained in most cases. With a few exceptions, the scintigraphy results were consistent with the final diagnosis. The two tracers were equally effective adrenal scanning agents. Tracer concentration was measured in a number of surgical specimens, mostly from patients given selenocholesterol. This measurement in surgical samples has not been reported in previous studies with this agent. The results provided a direct validation of uptake measurements in vivo. The data, collected over a 17-year period, demonstrate that despite the advent of new imaging techniques, adrenal scintigraphy that gives both functional and morphologic information still has an important role in the diagnosis of adrenal disease.
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PMID:Clinical experience with the adrenal scanning agents iodine 131-19-iodocholesterol and selenium 75-6-selenomethylcholesterol. 174 5

This is the first published report describing the association between primary aldosteronism and chronic idiopathic orthostatic hypotension. The clinical history of a 57 year old man with incapacitating postural hypotension and severely symptomatic supine hypertension, is described. A possible occupational etiology of postural hypotension, with regard to a prolonged exposure to cutting oils, is considered. The intriguing pathophysiologic aspects of this unique association are discussed. The Authors suggest that, although supine hypertension is common in chronic idiopathic orthostatic hypotension, a careful examination of the adrenal glands is advisable in these patients, to rule out the presence of an associated adrenal adenoma.
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PMID:Aldosterone-secreting adenoma and dysautonomic failure: the challenging association of 2 extreme conditions. 179 2

Forty five patients (35 women and 10 men) who underwent adrenalectomy for aldosterone-producing adrenal adenoma were followed up for 5.7 +/- 4.7 years (1-17 years). Stable normalization of blood pressure was noted in 27 (60%) patients. In 16 patients the primary hypertension and in 1 patient the second adrenal adenoma were diagnosed after surgery. Statistically significant decrease in daily excretion of adrenaline and noradrenaline with the urine, reduced adrenaline/noradrenaline ratio and reduced catecholamines and their metabolites ratio were noted in the operated patients in comparison to healthy volunteers indicating catecholamines metabolism disorders. Surgical treatment of adrenal adenoma besides normalization of blood pressure diminishes biochemical abnormalities. Development of the primary blood hypertension may be expected in some patients.
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PMID:[Blood pressure in patients after unilateral adrenalectomy for aldosterone producing adrenal adenoma]. 184 86

The recent advances in the diagnosis of adrenal diseases owe much to the rapid progress in radiological and endocrinological areas. The former is ascribed to the progress of medical electronics. The latter has been realized by the development, improvement and spread of the measurement of a very small amount of hormones or hormone-like substances in blood, urine or tissues, supported by the improvement of measurement instruments as well as the immunoassay or chemical assay techniques. This paper reviews approaches to diagnosis of adrenal diseases causing hypertension and asymptomatic, incidentally discovered adrenal tumors. Incidentally discovered adrenal tumors have increased owing to the spread of medical electronic instruments such as abdominal ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI). Discrimination of malignancy is an important clinical concern. More than 90% of the tumors reported in the Japanese were larger than 3 cm in diameter. The diagnosis of primary aldosteronism has been made by the measurement of plasma renin and aldosterone, CT and 131I-cholesterol scintigraphy. However the differential diagnosis of adrenal adenoma from bilateral adrenal hyperplasia has remained as a problem. There were a few patients in whom adrenal adenomas appeared after 2-3 years' follow-up period. In Cushing's syndrome, tumors are found with ease by US, CT and MRI. The diagnosis of pheochromocytoma is made mainly by urinary catecholamines and metabolites including metanephrine, normetanephrine and VMA. US, CT and MRI are very useful. Diagnosis and discovery of metastasis will be more reliably made when 131I-MIBG comes to the clinical stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnosis of adrenal diseases focusing on morphological and endocrinological viewpoints]. 194 68

We describe four cases of primary hyperaldosteronism whose initial presentation was a moderate to severe hypertension. In three patients an adrenal adenoma was found; in another patient was due to unilateral adrenal hyperplasia. A good therapeutic response was achieved in all cases by unilateral adrenalectomy. The captopril test (Lyons version) proved useful to exclude essential hypertension and, may be, in distinguishing the new sub-types of primary hyperaldosteronism recently described. Indeed, only in the case of unilateral adrenal hyperplasia a fall in plasma aldosterone levels was observed. However, we feel that further investigation is needed to clarify this point.
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PMID:[Significance of the captopril test in the diagnosis of primary hyperaldosteronism --apropos of 4 clinical cases]. 220 22

The case of a 39-year-old woman with Cushing's syndrome, hypertension and severe hypokalemia, caused by a unilateral adrenal adenoma composed of cells of the zona fasciculata histological type, is described. Plasma renin activity, plasma levels of mineralocorticoids and the aldosterone secretion rate were determined before and after surgical removal of the adenoma. The tumor appeared to produce autonomously cortisol as well as corticosterone, 18-hydroxycorticosterone and aldosterone. This condition has not previously been described in the literature and might be explained by strong expression of the full spectrum of activities of the mitochondrial enzyme P450 C11 by the tumor cells. Interestingly, despite hyperaldosteronism, plasma renin activity was not suppressed.
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PMID:Concurrent hypercortisolism and hyperaldosteronism due to an adrenal adenoma. 223 30

The syndrome of primary aldosteronism produces few signs or symptoms. The diagnosis should be suspected when either spontaneous hypokalemia or easily provoked hypokalemia is found in a patient with hypertension. Hypokalemia in association with inappropriate kaliuresis, low plasma renin activity, and a high plasma aldosterone concentration/plasma renin activity ratio are the findings on initial screening tests that should suggest primary aldosteronism. The diagnosis must be confirmed by demonstrating nonsuppressible aldosterone excretion in conjunction with normal cortisol excretion. The choice of therapy is based on distinguishing unilateral from bilateral adrenal disease. With a unilateral adrenal adenoma, surgical removal reverses the hypokalemia and frequently cures the hypertension. In most patients with bilateral adrenal hyperplasia who are treated surgically, however, hypertension persists; thus, the initial treatment in these patients should be pharmacologic.
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PMID:Primary aldosteronism: diagnosis and treatment. 240 67

A 31 year old woman presented with resistant hypertension. Investigations revealed that she had Conn's syndrome. Computed tomography showed both adrenals to be normal but an ectopic adenoma was identified posterior to the stomach. Surgical excision of the tumor confirmed benign aldosteronoma and cured her hypertension. We believe this to be the first report of Conn's syndrome caused by an ectopic adrenal adenoma.
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PMID:Conn's syndrome due to an ectopic adrenal adenoma. 261 23

Corticosteroid-dependent hypertension can be cured by surgical removal of steroid-producing adrenocortical adenomas or, in case of other etiopathologic factors, specific drug therapy may be introduced for preventing irreversible complications of the hypertension process. In most cases, corticosteroid-dependent hypertension fails to manifest itself with clearcut endocrine symptoms. Therefore, an endocrine evaluation is strongly recommended in all patients with hypertension who are susceptible to hypokalaemia and whose blood pressure is poorly controlled with conventional antihypertensive drugs. The increased blood pressure in corticosteroid-producing adrenocortical adenomas may be attributed not only to the main glucocorticoid, cortisol, and the main mineralocorticoid, aldosterone, but also to the actions of weak mineralocorticoids which may be occasionally predominant. Adrenocortical adenomas including incidentalomas produce in different quantities at least 6 corticosteroids which play direct or indirect roles in hypertension. These adenomas are lacking autonomous hormone secretion and they respond to different regulatory impacts (i.e. stress and, by analogy, CRF or ACTH administration) with markedly-increased hormone secretion. Consequently, hypertension and hypokalaemia develop, often in the absence of other endocrine symptoms. The weak mineralocorticoids may not entirely account for the hypertension, although they may be useful indicators or may serve as precursors for the generation of more potent hypertensinogen steroids and steroid metabolites. This is patently indicated by the disappearance of hypertension, hypokalemia and mineralocorticoid-excess induced suppression of the renin-angiotensin system after the surgical removal of adrenocortical adenomas which produce only weakly-hypertensinogen corticosteroids.
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PMID:[The hypertensive role of corticosteroids in the light of adenoma of the adrenal cortex]. 266 40

The adrenal glands produce glucocorticoids (approximately 25 mg cortisol/day), mineralocorticoids (approximately 100 micrograms aldosterone/day) and androgens (e.g. dehydroepiandrosterone = DHEA approximately 10 mg/day) in their cortex and catecholamines in their medulla. Excessive cortisol production leads to Cushing's syndrome. In approximately 2/3 of the cases this is due to ACTH oversecretion most often from a pituitary adenoma and can be cured by removal of this adenoma. Cushing's syndrome caused by an adrenal adenoma, carcinoma or bilateral nodular adrenal hyperplasia is treated by adrenal surgery. Nelson's syndrome consists of hyperpigmentation of the skin and an often aggressively growing pituitary adenoma which secretes excessive amounts of ACTH. Treatment is surgical. Conn's syndrome (primary hyperaldosteronism) is due to aldosterone hypersecretion most often from an adrenal adenoma (therapy: unilateral adrenalectomy), more seldom from bilaterally hyperplastic adrenals (therapy: spironolactone). Excessive adrenal androgen secretion is found in the adrenogenital syndrome in which defective cortisol biosynthesis leads to ACTH oversecretion and ACTH-stimulated overproduction of cortisol precursors, some of which are androgens. Treatment consists of glucocorticoids which suppress the ACTH oversecretion. Pheochromocytomas produce excessive amounts of catecholamines and cause hypertension which can be persistent as well as episodic. Therapy consists of adrenalectomy. Malignant tumors of the adrenals have a poor prognosis. Incidentally found adrenal masses ("incidentalomas") are observed at regular intervals if they are small and should be surgically removed if they have a tendency to grow or are large (greater than or equal to 5 cm phi).
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PMID:[Normal and pathologic endocrinology of the adrenal glands]. 268 Oct 84


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