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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Important advances have been made in understanding the role of the renin-angiotensin-aldosterone system in the pathogenesis and diagnosis of hypertensive disorders. Measurement of plasma renin activity (PRA) and aldosterone is very important in the assessment of secondary hypertension. Hypertensions with increased PRA include renovascular hypertension, some cases of unilateral and bilateral renal parenchymal disease, malignant hypertension, hypertension associated with oral contraceptive agents, and renin-secreting tumors. Hypertension with decreased PRA is observed in four recognized types of primary aldosteronism: adenoma, bilateral hyperplasia, indeterminate aldosteronism, and glucocorticoid-responsive aldosteronism. Other conditions with hypertension and depressed PRA include ACTH and DOC secreting tumors, primary hyperpituitarism, syndromes of 17-hydroxylase and 11-beta-hydroxylase deficiency. Liddle's syndrome, licorice abuse, exogenous administration of mineralocorticoids, and preeclampsia.
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PMID:The renin-angiotensin-aldosterone system in primary and secondary hypertension. 611 55

To study left ventricular (LV) geometry in secondary hypertension and its evolution following etiologic treatment, echocardiography was performed in a total of 73 patients: 40 patients with renovascular hypertension (RVH), 21 with aldosterone-producing adenoma (APA), and 12 with pheochromocytoma (PH). Repeat echocardiography was possible in 43 of these patients, 3-24 months following curative renal revascularization or adrenal surgery. Age, sex ratio, and initial drug treatment score were comparable in the three etiologic categories, but 24-h ambulatory blood pressure and LV mass index were significantly higher in APA and RVH than in PH. End-diastolic LV volume was significantly smaller in PH than in APA and RVH. After treatment, the greatest reduction in LV mass occurred in APA (-18%, P < .05) and the lowest in PH (-5%, NS). Both patients with APA and those with PH exhibited a significant decrease in LV wall thickness, whereas LV diameter tended to decrease in APA patients and to increase in PH patients. No significant cardiac changes occurred in RVH patients after treatment. Although LV mass index and ambulatory blood pressure were correlated both before and after treatment, LV mass index changes did not correlate with changes in ambulatory blood pressure or with the known duration of hypertension. Systolic function was normal before and following etiologic treatment in the three categories. These findings suggest that, in addition to blood pressure, volume and/or humoral factors influence the pathogenesis of left ventricular hypertrophy and its reversibility.
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PMID:Left ventricular mass and geometry before and after etiologic treatment in renovascular hypertension, aldosterone-producing adenoma, and pheochromocytoma. 830 63

Primary aldosteronism is one of the differential diagnosis of secondary hypertension. This is usually caused by an aldosterone producing adenoma or bilateral adrenal hyperplasia which comprise about 65% and 30% of the cases, respectively. However, less than 1% of primary aldosteronism is caused by unilateral adrenal hyperplasia which is a relatively rare subset of primary aldosteronism. The clinical and biochemical manifestations of the disorder are indistinguishable from aldosterone-producing tumor, and a definitive diagnosis can only be made by pathological finding. A 33-year-old male Chinese patient presented with hypertension, hypokalemia, metabolic alkalosis, and the hypersecretion of aldosterone associated with suppressed plasma renin activity which is a typical hallmark of primary aldosteronism. Image studies including both magnetic resonance imaging (MRI) and 131I NIP-59 scan as well as postural test suggested an aldosterone-producing tumor of the right adrenal gland. Unilateral adrenectomy and pathological examination of the right adrenal gland eventually proved a case of unilateral adrenal hyperplasia. Blood pressure, plasma potassium, aldosterone and renin activity levels returned to normal two weeks after operation and had remained normal at up to one year of follow up. In addition, a saline loading test showed normal suppression of plasma aldosterone level one year after the operation, suggesting that the function of the left adrenal gland remains normal. The etiology of unilateral adrenal hyperplasia is unclear and the future recurrence of the disease is possible. Long-term follow-up is necessary to ensure the cure of this disorder.
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PMID:Primary aldosteronism due to unilateral adrenal hyperplasia: a case report. 917 1

Different types of statistical methods have been used for circadian blood pressure (BP) rhythm analysis in secondary forms of hypertension. In the present study, we used the two-step statistical approach by Fourier analysis with four harmonics for the parametrization of the diurnal BP pattern in secondary hypertension. In 43 essential hypertensives (EH), eight patients with aldosterone producing adenoma (APA), 25 with idiopathic hyperaldosteronism (IHA), four with glucocorticoid remediable hyperaldosteronism (GRH) and seven with renovascular hypertension (RVH), 24-h ambulatory BP was measured. The diurnal BP and heart rate (HR) rhythm was present in more than 70% of patients with secondary hypertension, without significant differences with EH and despite the attenuation in the degree of the nocturnal BP fall. In conclusion, the statement that secondary hypertension is characterized by an abnormal diurnal rhythm of BP is a gross over-simplification. Our findings suggest that the two-step method with four harmonics Fourier analysis may represent a useful method and a more complete statistical approach to providing circadian parametrization of the 24-h profile in secondary hypertension.
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PMID:Fourier analysis of circadian blood pressure profile in secondary hypertension. 920 36

A 36-year-old woman had fibrous dysplasia of the left renal artery and an aldosterone-producing adenoma of the right adrenal gland. The patient was evaluated first for secondary hypertension using a renal angiogram that showed fibrous dysplasia with stenosis of the left renal artery; angioplasty was successful. However, 1 month after angioplasty, hypertension recurred. Initially, it was thought that it had restenosed but after a negative angiography, adrenal computed tomography showed a 0.8-cm x 1-cm tumor of the right adrenal gland. The tumor was removed surgically, markedly improving her hypertension.
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PMID:Fibromuscular dysplasia of the renal artery and adrenal adenoma in a 36-year-old woman with hypertension. 921 43

Patients with primary aldosteronism often present with hypokalemia and hypertension. Primary aldosteronism presenting as sudden death due to ventricular fibrillation is described in an otherwise healthy 37-year-old woman. After successful direct current cardioversion, serum potassium was 1.4 mmol/L. Investigations revealed a suppressed renin level, elevated serum aldosterone and a right adrenal nodule found on imaging. Ventricular fibrillation has not previously been described as a presention of a biochemically and surgically proven aldosterone-producing adenoma. This case highlights the importance of early detection and proper diagnosis of secondary hypertension before serious sequelae occur.
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PMID:Ventricular fibrillation: an extreme presentation of primary hyperaldosteronism. 1020 99

Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. However, with improved screening methodologies, it appears that primary aldosteronism is the most common form of secondary hypertension. Diagnosis of this disorder results in either the cure of hypertension or targeted pharmacotherapy. In addition, recent evidence suggests that aldosterone excess may have specific cardiotoxicity that is reversible with treatment. Patients with hypertension and hypokalemia and most patients with treatment-resistant hypertension should undergo screening for primary aldosteronism. A random and ambulatory ratio of plasma aldosterone concentration (ng/dl) to plasma renin activity (ng/ml per hour) >20 and a plasma aldosterone concentration >15 ng/dl is a positive screen for primary aldosteronism. A plasma aldosterone concentration/plasma renin activity ratio >20 alone is not diagnostic of primary aldosteronism; primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion with either the intravenous saline suppression test or measurement of 24-hour urinary aldosterone while on a high-sodium diet. The 2 major subtypes of primary aldosteronism are unilateral aldosterone-producing adenoma and bilateral idiopathic hyperplasia. Patients with aldosterone-producing adenoma are usually treated with unilateral adrenalectomy, and patients with idiopathic hyperplasia are treated medically. The subtype evaluation may require one or more tests, the first of which is imaging the adrenals with computed tomography (CT). When CT reveals a solitary unilateral macroadenoma (>1 centimeter) and normal contralateral adrenal morphology in a patient with primary aldosteronism, unilateral laparoscopic adrenalectomy is a reasonable therapeutic option. However, in many cases, CT imaging may reveal normal-appearing adrenals or ambiguous findings. Adrenal venous sampling helps solve these clinical dilemmas.
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PMID:Primary aldosteronism: A common and curable form of hypertension. 1042 72

The relationship between arterial hypertension and insulin resistance has long been established. We used primary hyperaldosteronism as a model of the relationship between secondary hypertension and insulin sensitivity. Our group consisted of 9 patients with arterial hypertension caused by primary hyperaldosteronism. Five of these patients with aldosterone producing adenoma were operated on and four patients with idiopathic hyperaldosteronism were treated with spironolactone. Hyperinsulinaemic euglycaemic clamp technique was performed before and at least 6 months following the treatment to evaluate the insulin action. Significantly lower glucose disposal rate (M), insulin sensitivity index (M/I) and decreased metabolic clearance rate of glucose (MCR(G)) were found in patients before treatment as compared to healthy controls. In both treated groups the blood pressure and plasma potassium concentrations returned to normal values, whereas plasma aldosterone levels were normalised only after surgical removal of the adenoma. Significantly improved insulin action (M/I: 30.2 +/- 5.9 vs. 51.4 +/-12.2 micromol.kg(-1).min(-1) per mU.l(-1) x 100, p = 0.017) was observed in patients after operation of aldosterone producing adenoma. In contrast, spironolactone treatment of patients with idiopathic hyperaldosteronism did not significantly influence insulin action (M/I: 24.5 +/- 7.3 vs. 18.7 +/- 7.6 micromol.kg(-1).min(-1) per mU.l(-1) x 100, p = 0.198). Since plasma aldosterone concentrations have been normalised only in patients after removal of the adenoma whereas they remained increased in spironolactone treated group, we suppose that aldosterone itself could play a role in the development of impaired insulin action.
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PMID:Insulin action in primary hyperaldosteronism before and after surgical or pharmacological treatment. 1076 28

Primary aldosterone excess or hyperaldosteronism is an important cause of hypertension which, when associated with an aldosterone secreting adenoma, is amenable to surgical cure. The biochemical hallmarks of the condition are a relative excess of aldosterone production with suppression of plasma levels of renin (a proxy for angiotensin II, the major trophic substance regulating aldosterone secretion). This combination of a high aldosterone and a low renin is however more commonly associated with 'nodular hyperplasia' of the adrenal glands, a condition not improved by surgery and variably responsive to the effects of the mineralocorticoid antagonist, spironolactone. Until recently the prevalence of either form of secondary hypertension has been thought to be low such that few clinicians 'hunted' for it in the absence of hypokalaemia (the traditional clue for the syndrome). This view has been challenged, firstly by the realisation that no more than 50% of such patients will have a low plasma potassium and secondly by the assumption that a 'normal' plasma aldosterone is in fact inappropriately elevated if the renin level is low. A single measurement of the ratio of aldosterone to renin levels is claimed to be highly predictive of patients who will have primary aldosterone excess. This paper examines the logic behind such claims and presents evidence from the literature that an abnormal ratio is simply a different description of the low renin state and that such patients do not necessarily have mineralocorticoid hypertension. Most patients 'discovered' by this test will have what many call low-renin hypertension, a condition not amenable to specific therapy. Claims that they are peculiarly sensitive to the hypotensive effects of spironolactone have not been tested in controlled trials. The test would however be expected to pick up those individuals with true Conn's syndrome but such patients remain too few in number to justify widespread use of an expensive screening test.
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PMID:Primary aldosteronism, a common entity? the myth persists. 1208 Apr 39

Three patients diagnosed with primary hypertension suddenly developed hard-to-treat blood pressure after several years of stable blood pressure. One patient, a man aged 48 years, had developed a renal artery stenosis, which had not been present five years earlier. The other two patients, a man aged 57 years and a woman aged 27 years, were diagnosed with an aldosterone-producing adenoma of the left adrenal gland and a pheochromocytoma, respectively. In patients with previously stable blood pressure, sudden derangement may be due to secondary hypertension on top of the pre-existing primary hypertension. A thorough history and physical examination together with limited laboratory investigations usually leads the way to the correct diagnosis.
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PMID:[Hypertension: once primary, always primary?]. 1191 6


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