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

Since its initial description in 1955, primary aldosteronism was thought to be a rare cause of hypertension. However, improved screening methods show that primary aldosteronism is a common form of secondary hypertension. Diagnosis of this disorder results in improved or cured hypertension or targeted pharmacotherapy. 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 (PAC) to plasma renin activity (PRA) that is elevated and a PAC higher than a set cutoff is a positive screen for primary aldosteronism. An increased PAC/PRA ratio 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-hr urinary aldosterone while the patient is on a high-sodium diet. The two major subtypes of primary aldosteronism are unilateral aldosterone-producing adenoma (APA) and bilateral idiopathic hyperplasia (IHA). Patients with APA are usually treated with unilateral adrenalectomy, and patients with IHA are treated medically. The subtype evaluation may require one or more tests, the first of which is imaging the adrenals with computerized tomography (CT). When a solitary unilateral macroadenoma (> 1 cm) and normal contralateral adrenal morphologic pattern are found on CT in a young 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 to resolve these clinical dilemmas.
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PMID:Primary aldosteronism: management issues. 1238 42

Primary aldosteronism (PA) is the commonest form of secondary hypertension in South Africa with an approximate prevalence of 7.5% in the primary-care setting. Hypokalaemia is a poor screening test with 70% of proven cases having normal serum potassium levels. The aldosterone/rennin ratio is a robust screening test with a high sensitivity and specificity, but in South Africa this should be combined with an absolute aldosterone level because of the high incidence of low-renin hypertension in Blacks. The limitations of the ratio, especially with regard to concomitant drug therapy will be discussed in detail. The fludrocortisone suppression test remains the investigation of choice for confirming the diagnosis, but requires four days of hospitalisation. CT scanning will miss 50% of adenomas and incorrectly lateralise the adenoma in occasional cases, and bilateral adrenal venous sampling is the gold standard for indirectly confirming and adenoma by demonstrating lateralisation of aldosterone secretion, but its use is limited by lack of technical expertise in South Africa. Low-dose spironolactone is the medical therapy of choice for PA.
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PMID:Screening and diagnosis of primary aldosteronism. 1238 57

Recently published studies from different parts of the world report significantly higher prevalence of primary hyperaldosteronism (PH) in hypertensives (ranging from 5 to 25%) than the previously accepted figures. There have been no data so far about the prevalence of PH in Central Europe. Therefore, we have undertaken this study to evaluate the prevalence of PH in patients with moderate to severe hypertension referred to a hypertension unit in the Czech Republic, together with the determination of the percentage of different subtypes of PH including familial forms. In addition to that, we have evaluated the prevalence of other types of secondary forms of hypertension.A total of 402 consecutive patients (230 females and 172 males) with hypertension, referred to our hypertension unit, were studied. Positive aldosterone/renin ratio (ARR, (ng/100 ml)/(ng/ml/h)) >/=50 as a more strict marker of PH was found in 87 patients (21.6%), 30% of them were normokalaemic. The diagnosis of PH was later confirmed in 77 cases (89%); the total prevalence of PH was thus 19%. PH consisted of the following forms: idiopathic hyperaldosteronism 42%, unilateral aldosterone-producing adenoma 36%, unilateral hyperplasia 7%, nonclassifiable PH (refused operation/adrenal venous sampling) 13%, familial hyperaldosteronism type 1.2%. The prevalence of other types of secondary hypertension was as follows: pheochromocytoma 5%, renovascular 4.5%, hypercortisolism 2%, renal 0.75%. In conclusion, we have noted that PH in the Central Europe region (Czech Republic) is the most frequent form of endocrine hypertension with a considerably high prevalence in moderate to severe hypertension. Application of more strict criteria raises the probability of correct diagnosis of PH including the early normokalaemic stages of PH.
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PMID:Prevalence of primary hyperaldosteronism in moderate to severe hypertension in the Central Europe region. 1275 8

1. Only limited information is available concerning the changes in the electrocardiogram in primary aldosteronism. The aim of the present study was to determine factors influencing the QTc interval in patients with primary aldosteronism. 2. Nineteen patients with primary aldosteronism caused by a Conn's adenoma and 69 patients with essential hypertension, in whom all possible causes of secondary hypertension had been excluded, were included in the present study. Before and 10-20 days after adrenalectomy, blood and electrocardiographic examinations were conducted. 3. Systolic and diastolic blood pressures in primary aldosteronism were found to be comparable to those in essential hypertension. However, the QTc interval was significantly prolonged and serum potassium concentrations were significantly decreased in patients with primary aldosteronism compared with patients with essential hypertension (492.7+/-20.3 vs 428.5+/-3.1 msec for QTc interval, respectively (P<0.01); 3.07+/-0.12 vs 4.07+/-0.05 mEq/L for serum potassium concentrations, respectively (P<0.01)). The QTc interval was significantly correlated with serum potassium concentrations in primary aldosteronism (P=0.0011; r=-0.6902), but not in patients with essential hypertension. 4. Blood pressure significantly decreased after adrenalectomy. Furthermore, serum potassium concentrations increased significantly and did not correlate with the QTc interval after adrenalectomy (P=0.54; r=-0.1500). 5. Our results indicate that the QTc interval is prolonged in patients with primary aldosteronism, probably owing to hypokalaemia.
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PMID:Prolongation of the QT interval in primary aldosteronism. 1573 Apr 37

Normokalaemic manifestation of primary aldosteronism is a frequent cause of secondary hypertension. It occurs in approximately 5-12% of all patients with hypertension, primarily patients with severe and uncontrolled blood pressure. Main causes are bilateral adrenal hyperplasia (2/3 of cases) and aldosterone-producing adenoma (1/3 of cases). Screening is performed by measurement of the aldosterone/renin ratio, which is raised in affected patients. Suspicion of primary aldosteronism due to a pathological ratio requires confirmatory testing e.g. by saline infusion test or fludrocortisone suppression test. If the diagnosis is confirmed, the underlying cause of aldosterone excess needs to be identified because therapy differs. First, adrenal imaging (CT/MRI) is performed, which is followed by postural testing in cases with a unilateral lesion. Concordant results confirm the diagnosis of an aldosterone-producing adenoma and allow treatment to proceed to adrenalectomy. In cases of equivocal results or normal/bilaterally enlarged adrenal glands on imaging, adrenal venous sampling must be performed for subtype differentiation.
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PMID:Screening for primary aldosteronism. 1698 Feb

We describe a case of secondary hypertension in which aldosterone-producing adenoma (APA) and renal artery stenosis (RAS) coexisted. RAS caused a significant pressure gradient, and successful angioplasty of it improved the affected renal function but did not reduce the systemic blood pressure (SBP). Surgical resection of APA performed several months later reduced SBP. In cases of suspected secondary hypertension, other cause(s) of hypertension should be considered, if hypertension persists after correction of one possible cause.
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PMID:Aldosterone-producing adenoma accompanied with renal artery stenosis. 1704 16

Primary aldosteronism is defined as secondary hypertension accompanied by aldosterone hypersecretion that leads to suppressed plasma renin, hypokaremia and hypertension. Primary aldosteronism occurs in 3-15% of hypertensive patients and is commonly caused by aldosterone-producing adenoma (APA) or bilateral idiopathic hyperaldosteronism (IHA). APA is usually treated by adrenalectomy, whereas IHA is best managed medically. Therefore, it is important to distinguish between unilateral and bilateral disease. Computed tomography (CT) is used to differentiate the subtypes. Even when multidetector CT is used, the detection rate of APAs of 1 cm or less is lower than 60% for the following reasons: (a) aldosterone secretion does not depend on tumor size, (b) a tumor may exist without lipid-rich cells, and (c) non-functioning unilateral adenomas are not uncommon, especially in older patients. Adrenal venous sampling is the gold standard for the differentiation of unilateral from bilateral disease in patients with primary aldosteronism. It is important to compare the laterality of aldosterone secretion by performing simultaneous bilateral blood collection 15 min following adrenocorticotropic hormone stimulation. The value of (aldosterone/cortisol)(side)/(aldosterone/cortisol)(contralateral side) provides the best discrimination between patients with and without APA.
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PMID:Primary aldosteronism: a pictorial essay. 1715 4

Primary aldosteronism (PA) due to aldosterone-producing adenoma (APA) is a form of surgically curable secondary hypertension, and distinguishing APA from idiopathic hyperaldosteronism (IHA) is important for treatment. We made a differential diagnosis between APA and IHA using imaging tests such as adrenal CT and MRI as well as adrenal venous sampling (AVS) in all 93 cases of PA presenting at our institutions over the last decade. We identified 27 patients with aldosterone-producing microadenoma (APmicroA), all of whom could be diagnosed by AVS but not by the imaging tests. Then, we compared the clinical and roent-genological findings of these 27 patients with those of 42 patients with aldosterone-producing macroadenoma (APmacroA) and of 24 patients with IHA. Using surgically removed adrenal tissues, histopathological examinations and immunohistochemical analyses of steroidogenic enzymes were conducted. The findings for APmicroA were similar to those for APmacroA, except with respect to the diameter of the adrenal adenomas. Endocrinological and roentgenological findings for APmicroA were similar to those for IHA, but not to those for APmacroA. The rate of cure of hypertension was much greater in patients with APmicroA than in patients with APmacroA after the unilateral adrenalectomy (odds ratio, 4.0; p=0.028). In conclusion, it is important to accurately diagnose APmicroA, in which the laterality of the hyperproduction of aldosterone is only detectable by AVS, and to treat these patients by unilateral adrenalectomy in order to avoid long-term medical treatment and prevent hypertensive vascular complications.
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PMID:Clinical characteristics of aldosterone-producing microadenoma, macroadenoma, and idiopathic hyperaldosteronism in 93 patients with primary aldosteronism. 1734 88

Great strides have been made in our understanding of the pathophysiology of primary aldosteronism syndrome since Conn's description of the clinical presentation of a patient with an aldosterone-producing adenoma (APA) more than 50 years ago. It is now recognized that the APA is just one of the seven subtypes of primary aldosteronism. APA and bilateral idiopathic hyperaldosteronism (IHA) are the most common subtypes of primary aldosteronism. Although most clinicians had thought primary aldosteronism to be a rare form of hypertension for more than three decades, it is now recognized to be the most common form of secondary hypertension. Using the plasma aldosterone to plasma renin activity ratio as a case-finding test, followed by aldosterone suppression confirmatory testing, has resulted in much higher prevalence estimates of 5-13% of all patients with hypertension. In addition, there has been a new recognition of the aldosterone-specific cardiovascular morbidity and mortality associated with aldosterone excess. Although thought to be daunting and complex in the past, the diagnostic approach to primary aldosteronism is straightforward and can be considered in three phases: case-finding tests, confirmatory tests and subtype evaluation tests. Patients with hypertension and hypokalaemia (regardless of presumed cause), treatment-resistant hypertension (three antihypertensive drugs and poor control), severe hypertension (>or= 160 mmHg systolic or >or= 100 mmHg diastolic), hypertension and an incidental adrenal mass, onset of hypertension at a young age or patients being evaluated for other forms of secondary hypertension should undergo screening for primary aldosteronism. In patients with suspected primary aldosteronism, screening can be accomplished by measuring a morning (preferably between 0800 and 1000 h) ambulatory paired random plasma aldosterone concentration (PAC) and plasma renin activity (PRA). An increased PAC:PRA ratio is not diagnostic by itself, and primary aldosteronism must be confirmed by demonstrating inappropriate aldosterone secretion. Aldosterone suppression testing can be performed with orally administered sodium chloride and measurement of urinary aldosterone or with intravenous sodium chloride loading and measurement of PAC. Unilateral adrenalectomy in patients with APA or unilateral adrenal hyperplasia results in normalization of hypokalaemia in all these patients; hypertension is improved in all and is cured in approximately 30-60% of them. In bilateral adrenal forms of primary aldosteronism, unilateral or bilateral adrenalectomy seldom corrects the hypertension and they should be treated medically with a mineralocorticoid receptor antagonist.
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PMID:Primary aldosteronism: renaissance of a syndrome. 1749 46

The diagnosis of primary aldosteronism, the most common form of secondary hypertension, is based on clinical and biochemical features. Although radiology plays no role in the initial diagnosis, it has an important role in differentiating between the two main causes of primary aldosteronism: aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH). This distinction is important because APAs are generally managed surgically and BAH medically. Adrenal venous sampling is considered the standard of reference for determining the cause of primary aldosteronism but is technically demanding, operator dependent, costly, and time consuming, with a low but significant complication rate. Other imaging modalities, including computed tomography, magnetic resonance imaging, and adrenal scintigraphy, have also been used to determine the cause of primary aldosteronism. Cross-sectional imaging has traditionally focused on establishing the diagnosis of an APA, with that of BAH being one of exclusion. A high specificity for detecting an APA is desirable, since it will avert unnecessary surgery in patients with BAH. However, an overreliance on cross-sectional imaging can lead to the incorrect treatment of affected patients, mainly due to the wide variation in the reported diagnostic performance of these modalities. A combination of modalities is usually required to confidently determine the cause of primary aldosteronism. The quest for optimal radiologic management of primary aldosteronism continues just over a half century since this disease entity was first described.
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PMID:Role of radiology in the management of primary aldosteronism. 1762 Apr 72


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