Aldosterone suppression on contralateral adrenal during adrenal vein sampling does not predict blood pressure response after adrenalectomy.

Context: Adrenal vein sampling (AVS) is the only reliable means to distinguish between aldosterone-producing adenoma and bilateral adrenal hyperplasia, the two most common subtypes of primary aldosteronism (PA). AVS protocols are not standardized and vary widely between centers.

Objective: The objective of the study was to retrospectively investigate whether the presence of contralateral adrenal (CL) suppression of aldosterone secretion was associated with improved postoperative outcomes in patients who underwent unilateral adrenalectomy for PA.

Somatic ATP1A1, ATP2B3, and KCNJ5 mutations in aldosterone-producing adenomas.

Aldosterone-producing adenomas (APAs) cause a sporadic form of primary aldosteronism and somatic mutations in the KCNJ5 gene, which encodes the G-protein-activated inward rectifier K(+) channel 4, GIRK4, account for ≈40% of APAs. Additional somatic APA mutations were identified recently in 2 other genes, ATP1A1 and ATP2B3, encoding Na(+)/K(+)-ATPase 1 and Ca(2+)-ATPase 3, respectively, at a combined prevalence of 6.8%.

Visceral adipose tissue: emerging role of gluco- and mineralocorticoid hormones in the setting of cardiometabolic alterations.

Several clinical and experimental lines of evidence have highlighted the detrimental effects of visceral adipose tissue excess on cardiometabolic parameters. Besides, recent findings have shown the effects of gluco-and mineralocorticoid hormones on adipose tissue and have also underscored the interplay existing between such adrenal steroids and their respective receptors in the modulation of adipose tissue biology. While the fundamental role played by glucocorticoids on adipocyte differentiation and storage was already well known, the relevance of the mineralocorticoids in the physiology of the adipose organ is of recent acquisition.

Aldosterone, mineralocorticoid receptor and the metabolic syndrome: role of the mineralocorticoid receptor antagonists.

Several lines of evidence suggest a detrimental effect of aldosterone excess on the development of metabolic alterations. Glucose metabolism derangements due to aldosterone action are frequently observed not only in patients with primary aldosteronism but also in patients with obesity. A contribution to the hyperaldosteronism observed in obese subjects can be attributed, at least in part, to the action of still unidentified adipocyte-derived factor.

Blood pressure, thyroid-stimulating hormone, and thyroid disease prevalence in primary aldosteronism and essential hypertension.

Background: A positive correlation between thyroid-stimulating hormone (TSH) and blood pressure (BP) has been identified in normotensives and in patients with essential hypertension (EH). This study was designed to evaluate, in primary aldosteronism (PA) and in EH, potential association of BP, TSH, and ultrasonographic changes of the thyroid.

Methods: We studied 188 patients: 92 with PA and 96 matched essential hypertensives.

The functional c.-2G>C variant of the mineralocorticoid receptor modulates blood pressure, renin, and aldosterone levels.

The mineralocorticoid receptor (MR) is essential in the regulation of volemia and blood pressure. Rare mutations in the MR gene cause type 1 pseudohypoaldosteronism and hypertension. In this study we characterized the common MR polymorphism c.

Management of primary aldosteronism: its complications and their outcomes after treatment.

Primary aldosteronism is the most common cause of secondary hypertension, accounting for about 10% of all forms of high blood pressure. Life-time pharmacological therapy is the treatment of choice for primary aldosteronism due to idiopathic adrenal hyperplasia (IHA), while adrenalectomy is effective in curing most patients with an aldosterone producing adenoma (APA). Far from being a benign form of hypertension, primary aldosteronism is characterized by the development of cardiovascular renal and metabolic complications, including left ventricular hypertrophy, myocardial infarction, atrial fibrillation and stroke, microalbuminuria, renal cysts as well as metabolic syndrome, glucose impairment and diabetes mellitus.

MF59 emulsion is an effective delivery system for a synthetic TLR4 agonist (E6020).

Purpose: The effectiveness of vaccines depends on the age and immunocompetence of the vaccinee. Conventional non-adjuvanted influenza vaccines are suboptimal in the elderly and vaccines with improved ability to prevent influenza are required. The TLR4 agonist E6020, either given alone or co-delivered with MF59, was evaluated and compared to MF59 and the TLR9 agonist CpG.

Small tumor size as favorable prognostic factor after adrenalectomy in Conn's adenoma.

Objective: Primary aldosteronism (PA) due to aldosterone-producing adenoma (APA) is the most common curable form of secondary hypertension.

Design: In order to evaluate blood pressure outcome after adrenalectomy for APA and to identify new favorable prognostic factors, data from 42 consecutive APA patients who underwent adrenalectomy were collected from 2005 to 2007.

Methods: Renin-angiotensin-aldosterone system (upright and postsaline infusion test), serum and urinary electrolytes, office and ambulatory blood pressure monitoring were evaluated at baseline and after a follow-up of 2.

Diagnosis and management of primary aldosteronism.

Purpose Of Review: To illustrate the steps for clinical management of primary aldosteronism from screening evaluation to surgical and/or medical treatment.

Recent Findings: It is now widely accepted that primary aldosteronism represents the most common form of endocrine hypertension and its early diagnosis is crucial for hypertensive patients who can be cured by the surgical removal of an aldosterone-secreting adenoma or benefit from a specific medical treatment with mineralocorticoid receptor antagonists. Recent evidence indicates that hyperaldosteronism is indeed associated with detrimental consequences on cardiovascular system, renal function and glucose metabolism.

Primary aldosteronism: cardiovascular, renal and metabolic implications.

For many years primary aldosteronism was considered a relatively benign form of hypertension. This assumption reflects the primacy accorded to elevated levels of angiotensin in terms of deleterious cardiovascular effects, and the fact that in primary aldosteronism renin and angiotensin levels are low. We now know that primary aldosteronism causes a constellation of cardiovascular, renal and metabolic sequelae which make it far from benign and that these are not merely effects of blood pressure elevation.

Adipose cell-adrenal interactions: current knowledge and future perspectives.

The central role of adipose tissue in the development of cardiovascular and metabolic pathology has been highlighted by the discovery of mediators (adipokines) secreted by adipose tissue and their involvement in the regulation of various biological processes. In light of recent experimental data, cross-talk between adipose tissue and the adrenal gland, particularly via the mineralocorticoid aldosterone, has been proposed. Aldosterone can induce adipogenesis, and human white adipose tissue is reported to release as-yet-uncharacterized factors that stimulate adrenocortical steroidogenesis and aldosterone production.

Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study.

Objective: Primary aldosteronism (PA) is characterized by the onset of both cardiac and gluco-metabolic alterations. The aim of this study was to evaluate the impact of aldosterone excess on the development of such complications, and the effects of surgical and pharmacological treatment on their long-term outcome.

Methods: We prospectively re-examined 61 patients: 25 with aldosterone-producing adenoma (APA), after surgery, and 36 patients with idiopathic hyperaldosteronism (IHA) on pharmacological treatment.

Adipose tissue 11beta-hydroxysteroid dehydrogenase type 1 expression in obesity and Cushing's syndrome.

Objective: To evaluate the expression of 11beta-hydrxysteroid dehydrogenase type 1 (11beta-HSD1) in omental adipose tissue of patients with Cushing's syndrome and simple obesity, compared with normal weight controls.

Design And Methods: We have performed a case-control study and studied omental adipose tissue from a total of 24 subjects (eight obese subjects, ten patients with Cushing's syndrome due to adrenal adenoma, and six normal weight controls). Body mass index, blood pressure, plasma glucose, plasma insulin, plasma cortisol, urinary free cortisol and post dexamethasone plasma cortisol were measured with standard methods.

Cytoskeleton rearrangement induced by tetraspanin engagement modulates the activation of T and NK cells.

The hepatitis C virus (HCV) binds to human cells through the interaction of its envelope glycoprotein E2 with the tetraspanin CD81. We have previously reported that engagement of CD81 has opposite effects on T and NK cell function, as it enhances T cell receptor-mediated T cell activation and inhibits CD16- or IL-12-mediated NK cell activation. We further investigated this dichotomy and found that another tetraspanin, CD82, induces the same opposing effects on human primary T and NK cells.

Analysis of screening and confirmatory tests in the diagnosis of primary aldosteronism: need for a standardized protocol.

Background: The upright serum aldosterone/upright plasma renin activity ratio (ARR) has been recommended as a screening tool for the diagnosis of primary aldosteronism.

Objective: We reviewed the data collected from hypertensive patients in order to define retrospectively the cut-off values and evaluate the reliability of the ARR and of the saline infusion test in the diagnosis of primary aldosteronism.

Patients: In 157 patients referred to our unit with a suspicion of primary aldosteronism, 61 of whom had confirmed primary aldosteronism [26 aldosterone-producing adenoma (APA); 35 idiopathic hyperaldosteronism], the supine and upright ARR, and the ARR after the administration of captopril and losartan were calculated, and the results of the saline infusion test were analysed.

Reduced nitric oxide levels in acromegaly: cardiovascular implications.

Acromegaly is characterized by major cardiovascular alterations. Although the underlying mechanisms of these vascular modifications have not been elucidated, recent studies have focused on endothelial dysfunction. Nitric oxide (NO) may contribute to increased vascular resistance, reduced platelet aggregation, inhibition of smooth muscle cell proliferation, and reduction of lipoxygenase activity.

Analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) in human essential hypertension.

Background: The HSD11B2 gene, encoding the kidney isoenzyme 11beta-hydroxysteroid dehydrogenase, is a candidate for essential hypertension. We previously showed that the frequency of shorter alleles of a CA repeat polymorphism in the first intron of 11beta-HSD2 gene was significantly higher among salt-sensitive than salt-resistant individuals with hypertension. The aim of the study was to analyze the HSD11B2 gene to assess whether some of its variants might be involved in hypertension.

[Endocrinology of aldosterone].

Aldosterone is the major mineralocorticoid hormone produced by the zona glomerulosa of the adrenal cortex. Aldosterone secretion is mainly regulated by the renin-angiotensin system, and to a minor extent by serum concentration of potassium, sodium, adrenocorticotropic hormone. and dopamine.

Aldosterone as a cardiovascular risk factor.

Aldosterone exerts cardiovascular effects by influencing epithelial fluid and electrolyte excretion, and thus blood volume and pressure. Mineralocorticoid receptors (MR) are found in epithelial and non-epithelial tissues (vessel walls, heart, brain), with high affinity for aldosterone and physiological glucocorticoids cortisol and corticosterone. MR blockade by spironolactone or eplerenone favorably affects cardiovascular outcomes.

Late-onset apparent mineralocorticoid excess caused by novel compound heterozygous mutations in the HSD11B2 gene.

Mutations in the gene encoding 11beta-hydroxysteroid dehydrogenase type 2, 11beta-HSD2 (HSD11B2), explain the molecular basis for the syndrome of apparent mineralocorticoid excess (AME), characterized by severe hypertension and hypokalemic alkalosis. Cortisol is the offending mineralocorticoid in AME, as the result of a lack of 11beta-HSD2-mediated cortisol to cortisone inactivation. In this study, we describe mutations in the HSD11B2 gene in 3 additional AME kindreds in which probands presented in adult life, with milder phenotypes including the original seminal case reported by Stewart and Edwards.