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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Resistant hypertension, defined as uncontrolled hypertension on three medications, is becoming an increasingly common problem. In most cases, blood pressure remains elevated because of persistently high systolic blood pressure levels. Common characteristics of patients with resistant hypertension include older age, obesity, excessive dietary salt ingestion, and presence of sleep apnea. The evaluation of patients with resistant hypertension is focused on identifying contributing and secondary causes of hypertension. Treatment should include both lifestyle changes (weight loss, exercise, dietary salt restriction) and the use of effective multidrug regimens, including a diuretic. Recent data indicate that aldosterone antagonists may be effective when added to existing antihypertensive regimens even in the absence of primary aldosteronism.
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PMID:Resistant or difficult-to-treat hypertension. 1652 95

The purpose of this review is to summarize the current knowledge regarding metabolic syndrome prevalence and features in primary aldosteronism. We will also discuss the link between aldosterone and the different metabolic changes typical of the metabolic syndrome. Hypertensive patients have a high prevalence of obesity, dyslipidemia and hyperglycaemia. These are risk factors for the metabolic syndrome, and are associated with an increased cardiovascular risk profile. In particular, insulin resistance seems to be the major alteration in patients affected by primary aldosteronism. We will then describe the experimental and clinical evidences of the role of aldosterone in the pathogenesis of insulin resistance. Higher rates of cardiovascular events have been recently reported in primary aldosteronism: they could be partly due to the increased prevalence of the metabolic syndrome in this disorder.
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PMID:[Role of aldosterone in the metabolic syndrome]. 1706 41

Blacks have a high prevalence of hypertension and adrenal cortical adenomas/hyperplasia. We evaluated the hypothesis that adrenal steroids are associated with hypertension and the metabolic syndrome in blacks. Ambulatory blood pressures, anthropometric measurements, and measurements of plasma renin activity (PRA), aldosterone, fasting lipids, glucose, and insulin were obtained in 397 subjects (46% hypertensive and 50% female) after discontinuing antihypertensive and lipid-lowering medications. Hypertension was defined as average ambulatory blood pressure >130/85 mm Hg. Late-night and early morning salivary cortisol, 24-hour urine-free cortisol, and cortisone excretion were measured in a consecutive subsample of 97 subjects (40% hypertensive and 52% female). Compared with normotensive subjects, hypertensive subjects had greater waist circumference and unfavorable lipid profiles, were more insulin resistant, and had lower PRA and higher plasma aldosterone and both late-night and early morning salivary cortisol concentrations. Twenty-four-hour urine-free cortisol and cortisone did not differ. Overall, ambulatory blood pressure was positively correlated with plasma aldosterone (r=0.22; P<0.0001) and late-night salivary cortisol (r=0.23; P=0.03) and inversely correlated with PRA (r=-0.21; P<0.001). Plasma aldosterone correlated significantly with waist circumference, total cholesterol, triglycerides, insulin, and the insulin-resistance index. Based on Adult Treatment Panel III criteria, 17% of all of the subjects were classified as having the metabolic syndrome. Plasma aldosterone levels, but not PRA, were elevated in subjects with the metabolic syndrome (P=0.0002). The association of aldosterone with blood pressure, waist circumference, and insulin resistance suggests that aldosterone may contribute to obesity-related hypertension in blacks. In addition, we speculate that relatively high aldosterone and low PRA in these hypertensive individuals may reflect a mild variant of primary aldosteronism.
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PMID:Association of adrenal steroids with hypertension and the metabolic syndrome in blacks. 1715 85

Resistant hypertension is defined as failure to achieve goal blood pressure despite adherence to 3 different antihypertensive medications, one of which must be a diuretic. True resistant hypertension must be distinguished by apparent resistant hypertension, of which an important cause is medication nonadherence, which can be recognized through a variety of monitoring strategies and may be improved through better patient education. A thorough history and examination should focus on evaluating for associated factors such as medication and illicit drug use, alcoholism, obesity, and obstructive sleep apnea. Further evaluation to differentiate apparent resistant hypertension from true resistant hypertension should include consideration of ambulatory blood pressure monitoring to rule out white coat hypertension. Routine laboratory work will reveal chronic kidney disease, which is the most common associated factor in resistant hypertension. Secondary or identifiable causes of resistant hypertension include primary aldosteronism, renovascular disease, and pheochromocytoma. Diagnostic evaluation for identifiable causes should be tailored for each patient and guided by signs and symptoms, as well as risks and benefits.
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PMID:Clinical characteristics of resistant hypertension: the importance of compliance and the role of diagnostic evaluation in delineating pathogenesis. 1721 49

We reported a rare case of simultaneous primary aldosteronism and preclinical Cushing's syndrome due to unilateral double adrenocortical adenomas in a 57 year-old woman who had had hypertension for the last 10 years. Abdominal computed tomography showed double tumors in her right adrenal gland. Physical findings revealed simple obesity and hypertension, but no other abnormal findings were detected. Laboratory findings demonstrated that serum potassium was 3.8 mmol/l; plasma renin activity, 0.3 ng/ml/h; plasma aldosterone, 100 pg/ml, and aldosterone renin ratio (ARR), 33. Serum cortisol was 15.7 microg/dl. There was no circadian rhythm of serum cortisol, and no suppression of serum cortisol in response to exogenous dexamethasone administration. Right adrenalectomy was performed under laparoscopy. Two well-circumscribed tumors, whose sizes were 21 and 19 mm in greatest diameter, were detected. They were macroscopically composed of a golden-yellow portion admixed with a brown portion, which corresponded to clear cells and compact cells, respectively. Immunohistochemical staining for steroidogenic enzymes demonstrated the presence of all the enzymes involved in corticosteroidogenesis in these two adenomas, indicating that the two adenomas produced both cortisol and mineralocorticoid. Specifically, one adenoma mainly caused excessive production of cortisol as compared to the other one. These findings indicate that overproduction of both cortisol and mineralocorticoid was evident in the two adenomas of the right adrenal gland in immunohistochemical study for steroidogenic enzymes, whereas there was less clinical manifestation of primary aldosteronism and Cushing's syndrome in the present patient.
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PMID:Possibly simultaneous primary aldosteronism and preclinical Cushing's syndrome in a patient with double adenomas of right adrenal gland. 1737 61

Patients with hypertension have a high prevalence of concurrent metabolic abnormalities (eg, obesity, dyslipidemia, and hyperglycemia). Clustering of these risk factors, defined as the metabolic syndrome, is associated with a high cardiovascular risk profile. This review summarizes current knowledge about the prevalence and characteristics of the metabolic syndrome in primary aldosteronism, and discusses the possible pathophysiological link between aldosterone and individual components of the metabolic syndrome, other than hypertension. Impaired glucose metabolism due to insulin resistance appears to be the major contributor to metabolic dysfunction in primary aldosteronism. Experimental observations support the possibility that aldosterone could act directly on insulin receptor function. The potential proadipogenic role of aldosterone and its negative effect on insulin sensitivity through production of cytokines remains to be investigated. Higher rates of cardiovascular events reported in primary aldosteronism could be due in part to the increased prevalence of the metabolic syndrome in this disorder.
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PMID:The metabolic syndrome in primary aldosteronism. 1744 20

Resistant hypertension is defined as blood pressure that remains uncontrolled despite using at least three antihypertensive medications in effective doses, ideally including a diuretic. Stricter blood pressure goals, higher obesity rates, older age, and increased use of certain exogenous substances are related to an increasing prevalence of resistant hypertension. The evaluation of patients with resistant hypertension focuses on identifying contributing factors and secondary causes of hypertension including hyperaldosteronism, obstructive sleep apnea, renal artery stenosis, and pheochromocytoma. Hyperaldosteronism is now recognized as the most common secondary cause and all patients with resistant hypertension should be screened with a plasma aldosterone-renin ratio even if the serum potassium level is normal. Treatment includes reversal of contributing factors, appropriate treatment of secondary causes, and use of effective multidrug regimens. Recent studies indicate that the addition of spironolactone to standard treatment regimens induces significant blood pressure reduction in patients with resistant hypertension.
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PMID:Resistant hypertension and aldosteronism. 1817 80

Resistant hypertension is defined as blood pressure (BP) that remains uncontrolled in spite of the use of >/=3 antihypertensive medications. Stricter BP goals, higher obesity rates, older age, and increased use of exogenous BP-elevating substances are related to an increasing prevalence of resistant hypertension. The evaluation of patients with resistant hypertension is focused on identifying contributing and secondary causes of hypertension, including hyperaldosteronism, obstructive sleep apnea, chronic kidney disease, renal artery stenosis, and pheochromocytoma. Hyperaldosteronism is now recognized as the most common cause of resistant hypertension, and all patients with resistant hypertension should be screened with a plasma aldosterone/renin ratio even if the serum potassium level is normal. Treatment includes removal of contributing factors, appropriate management of secondary causes, and use of effective multidrug regimens. Recent studies indicate that the addition of spironolactone to standard treatment induces significant BP reduction in most patients with resistant hypertension.
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PMID:Mechanisms and treatment of resistant hypertension. 1832 68

Patients with hypertension have a high prevalence of concurrent metabolic abnormalities (eg, obesity, dyslipidemia, and hyperglycemia). Clustering of these risk factors, defined as the metabolic syndrome, is associated with a high cardiovascular risk profile. This review summarizes current knowledge about the prevalence and characteristics of the metabolic syndrome in primary aldosteronism, and discusses the possible pathophysiological link between aldosterone and individual components of the metabolic syndrome, other than hypertension. Impaired glucose metabolism due to insulin resistance appears to be the major contributor to metabolic dysfunction in primary aldosteronism. Experimental observations support the possibility that aldosterone could act directly on insulin receptor function. The potential proadipogenic role of aldosterone and its negative effect on insulin sensitivity through production of cytokines remains to be investigated. Higher rates of cardiovascular events reported in primary aldosteronism could be due in part to the increased prevalence of the metabolic syndrome in this disorder.
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PMID:The metabolic syndrome in primary aldosteronism. 1836 98

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome. Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension. Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats. Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress. In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-alpha, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion. Therefore, aldosterone/MR activation plays a key role not only in the development of salt-sensitive hypertension, but also in cardiovascular injury in metabolic syndrome, possibly through its function as a feed-forward system.
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PMID:Aldosterone in salt-sensitive hypertension and metabolic syndrome. 1843 32


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