Evaluation of a short home blood pressure measurement in an outpatient population of hypertensives.

Current guidelines suggest the use of home blood pressure monitoring (HBPM) as a method complementary to ambulatory blood pressure monitoring (ABPM) for the identification of arterial hypertension. A cross-sectional study was conducted to evaluate the accuracy of a short HBPM schedule compared with ABPM, and to evaluate to what extent HBPM can replace ABPM. A total of 310 patients who performed ABPM in our hypertension clinic were enrolled between November 2011 and June 2015. They performed a 4-day HBPM schedule, with two readings in the morning and two readings at night. Results showed a moderate correlation between HBPM and ABPM (r = 0.59 for systolic blood pressure (SBP) and r = 0.72 for diastolic blood pressure (DBP)) and moderate diagnostic agreement (area under curve: 0.791 for SBP and 0.857 for DBP). No significant difference was found between first-day average and those of days 2-4. Diagnostic agreement between the two techniques was moderate, supporting the notion that HBPM cannot replace ABPM in the general population. However, we identified two HBPM thresholds, 123/75 and 144/87 mm Hg, through which subjects who may not require further ABPM can be identified.

Approach to the Patient on Antihypertensive Therapy: Screen for Primary Aldosteronism.

Primary aldosteronism (PA) is a condition that is still largely overlooked, resulting in a considerable burden of mortality and morbidity. This is despite decades of clinical and translational research on the deleterious effects of aldosterone on the cardiovascular system and the publication of several guidelines and consensuses on its diagnosis and treatment. One of the main reasons for the low rate of testing is the difficulty of screening patients on antihypertensive therapy that potentially interferes with aldosterone and renin levels and thus confound the interpretation of the aldosterone to renin ratio, the accepted and conventionally used screening test. To avoid interference, usually the therapies that affect the renin-angiotensin aldosterone system are withdrawn and substituted with noninterfering medications. However, in many cases the screening test can be confidently interpreted even when such therapies are not discontinued. In this review, we will evaluate the effects of antihypertensive therapies on the screening test for PA and suggest a practical approach for its interpretation.

Comparison of nurse attended and unattended automated office blood pressure with conventional measurement techniques in clinical practice.

Accuracy in blood pressure measurement is critical for proper hypertension diagnosis and treatment in clinical practice. Automated office blood pressure (AOBP) can simplify the measurement process, reducing human error and minimizing the white-coat effect in the unattended mode. The aim of this study was to compare AOBP, both unattended and nurse attended, with conventional office and out-of-office blood pressure measurement techniques. Four different methods of blood pressure measurement were performed in a cohort of hypertensive patients: conventional office blood pressure (OBP), unattended automated office blood pressure (uAOBP), nurse attended automated office blood pressure (nAOBP), and home blood pressure monitoring (HBPM). uAOBP and nAOBP were conducted with the same rigorous standardized procedure. We enrolled 118 consecutive patients. nAOBP values were slightly higher than uAOBP ones (respectively 132.8/73.3 ± 19.4/12.9 and 129.2/71.1 ± 19.0/12.3 mmHg), even if the difference was influenced by order of execution of AOBP measurement. nAOBP was significantly lower than HBPM and OBP (mean values 135.2/80.9 ± 16.6/8.1 and 140.9/84.6 ± 18.7/10.8 mmHg, respectively). AOBP, either attended or unattended, provides lower values than conventional OBP. uAOBP and nAOBP values showed small differences, even if they are not completely interchangeable. This evidence reflects a lower white-coat effect, even in nurse attended technique, but is also due to a lower measurement error through the application of a rigorous standardized protocol.

Mineralocorticoid Receptor Antagonist Effect on Aldosterone to Renin Ratio in Patients With Primary Aldosteronism.

CONTEXT: Although current international guidelines recommend to avoid mineralocortcoid receptor antagonists in patients undergoing screening test for primary aldosteronism, a recent report suggested that mineralocorticoid receptor antagonist treatment can be continued without significant influence on screening results. OBJECTIVE: We aimed to evaluate the effect of mineralocorticoid receptor antagonists on the aldosterone to renin ratio in patients with primary aldosteronism. METHODS: We prospectively enrolled 121 patients with confirmed primary aldosteronism who started mineralocorticoid receptor antagonist (canrenone) treatment. Eighteen patients (11 with unilateral and 7 with bilateral primary aldosteronism) constituted the short-term study cohort and underwent aldosterone, renin, and potassium measurement after 2 and 8 weeks of canrenone therapy. The long-term cohort comprised 102 patients (16 with unilateral and 67 with bilateral primary aldosteronism, and 19 with undetermined subtype) who underwent hormonal and biochemical re-assessment after 2 to 12 months of canrenone therapy. RESULTS: Renin and potassium levels showed a significant increase, and the aldosterone to renin ratio displayed a significant reduction compared with baseline after both a short- and long-term treatment. These effects were progressively more evident with higher doses of canrenone and after longer periods of treatment. We demonstrated that canrenone exerted a deep impact on the diagnostic accuracy of the screening test for primary aldosteronism: the rate of false negative tests was raised to 16.7%, 38.9%, 54.5%, and 72.5% after 2 weeks, 8 weeks, 2 to 6 months, and 7 to 12 months of mineralocorticoid receptor antagonist treatment, respectively. CONCLUSION: Mineralocorticoid receptor antagonists should be avoided in patients with hypertension before measurement of renin and aldosterone for screening of primary aldosteronism.

Differential diagnosis of primary aldosteronism subtypes.

Primary aldosteronism (PA) is the most frequent endocrine form of secondary hypertension. The recognition of this disease has dramatically increased with the widespread use of a screening test in most hypertensive patients, including those who are normokalemic. Interest in PA has grown since the demonstration that aldosterone has deleterious effects that are, at least in part, independent from its effects on blood pressure. The identification of the subtype of PA is fundamental to distinguish between subtypes that benefit from surgery and subtypes that should be treated pharmacologically with mineralocorticoid receptor antagonists. This article reviews the strategies to correctly identify PA subtypes, underlining the central role of adrenal vein sampling.

Roles of clinical criteria, computed tomography scan, and adrenal vein sampling in differential diagnosis of primary aldosteronism subtypes.

CONTEXT: In patients with primary aldosteronism (PA), it is fundamental to distinguish between subtypes that benefit from different therapies. Computed tomography (CT) scans lack sensitivity and specificity and must be followed by adrenal venous sampling (AVS). Because AVS is not widely available, a list of clinical criteria that indicate the presence of an aldosterone-producing adenoma (APA) has been suggested. OBJECTIVE AND DESIGN: The objective of the study was to test the sensitivity and specificity of the last generation CT scans, test prospectively the usefulness of clinical criteria in the diagnosis of APA, and develop a flow chart to be used when AVS is not easily available. SETTING: Hypertensive patients referred to our hypertension unit were included in our study. PATIENTS: Seventy-one patients with confirmed PA participated in our study. INTERVENTION: All patients had a CT scan and underwent AVS. MAIN OUTCOME MEASURE: Final diagnosis of APA was the main measure. RESULTS: A total of 44 and 56% of patients were diagnosed as having an APA and a bilateral adrenal hyperplasia (BAH), respectively. Twenty percent of patients with PA displayed hypokalemia. CT scans displayed a sensitivity of 0.87 and a specificity of 0.71. The posture test displayed a lower sensitivity and specificity (0.64 and 0.70, respectively). The distribution grades of hypertension were not significantly different between APA and BAH. Biochemical criteria of high probability of APA displayed a sensitivity of 0.32 and a specificity of 0.95. CONCLUSIONS: This study underlines the central role of AVS in the subtype diagnosis of PA. The use of the clinical criteria to distinguish between APA and BAH did not display a satisfactory diagnostic power.

Further evidence for linkage of familial hyperaldosteronism type II at chromosome 7p22 in Italian as well as Australian and South American families.

BACKGROUND: Familial hyperaldosteronism type II is a hereditary form of primary aldosteronism not attributable to the hybrid CYP11B1/CYP11B2 mutation that causes glucocorticoid remediable aldosteronism (or familial hyperaldosteronism type I). Although genetic defect(s) underlying familial hyperaldosteronism type II have not yet been elucidated, linkage to chromosome 7p22 was previously reported in two Australian families and a South American family with familial hyperaldosteronism type II. OBJECTIVE: To seek evidence of linkage to chromosome 7p22 in two Italian families with familial hyperaldosteronism type II based on markers that have already yielded evidence of linkage in one South American and two Australian familial hyperaldosteronism type II families and to assess the combined multipoint logarithm of odds score in these five families (two Australian, two Italian, and one South American). METHODS: Primary aldosteronism was diagnosed or excluded using widely accepted clinical and biochemical criteria. Genotypes of affected and unaffected Italian patients from two families were analysed using seven closely spaced microsatellite markers at 7p22, and multipoint logarithm of odds scores were calculated to assess linkage with familial hyperaldosteronism type II. RESULTS: All known affected individuals (four and two, respectively) from each of two Italian families shared identical haplotypes for the seven markers, consistent with linkage of the disease locus with the 7p22 region. The combined multipoint logarithm of odds score for five families showing linkage at 7p22 was highly significant at 5.22 (theta = 0) for markers D7S462 and D7S517. CONCLUSION: Linkage in two Italian families makes this the third geographical area to show linkage of familial hyperaldosteronism type II at 7p22, emphasizing the likely importance of this locus in identifying the causative mutation.

Hypertension and cognitive function.

Arterial hypertension, cerebrovascular disease, and dementia are related pathologies. This paper has reviewed comparatively the incidence of arterial hypertension and adult-onset dementia disorders. Hypertension is associated with cerebrovascular disease, which is in turn associated with dementia. It is the most important modifiable risk factor for stroke, which is a recognized cause of vascular dementia. In terms of pathophysiology of hypertensive brain damage, several hypotheses were developed, such as that vascular alterations induced by hypertension can induce lacunar or cortical infarcts and leucoaraiosis, that hypertension is responsible for cerebrovascular disease and acts into the contest of a pre-existing subclinic Alzheimer's disease (AD), that hypertension determines neurobiologic alterations (such as beta-amyloid accumulation) resulting in neuropathologic damage, and that aging and cerebrovascular risk factors act together to cause cerebral capillary degeneration, mitochondrial disruption, reduced glucose oxidation, and reduced ATP synthesis. The consequence of these alterations are neuronal death and dementia. Macroscopic results of these mechanisms are the so-called white matter lesions (WML), the significance of which is analyzed. Increasing clinical evidence suggests a close relationship between the reduction of elevated blood pressure and countering of both vascular dementia and AD. Antihypertensive treatment probably influences cognitive performances and prevents cognitive function alterations and the development of dementia. It is therefore important to evaluate as soon as possible cognitive functions of hypertensive patients.

Aldosterone as an independent factor in cerebrovascular damage.

Aldosterone is produced not only in the adrenal gland but also in other tissues, including the brain, where it plays an important role in the control of blood pressure and water and electrolyte homeostasis. Aldosterone has also been demonstrated to be a major factor in target organ damage independent of its effects on blood pressure. Herein we review the pathophysiology of aldosterone action in the brain and the clinical and experimental studies on the detrimental effects of aldosterone in the brain.

Adiponectin and insulin sensitivity in primary aldosteronism.

BACKGROUND: A high prevalence of metabolic syndrome has been reported in primary aldosteronism. Low levels of adiponectin, an adipokine with insulin-sensitizing properties, are considered a hallmark of the metabolic syndrome. We evaluated the relationship between adiponectin and insulin sensitivity in primary aldosteronism, with and without metabolic syndrome, compared with essential hypertension. METHODS: Forty patients with primary aldosteronism and 40 matched patients with low-renin essential hypertension (LREH) were studied. Patients with type 2 diabetes were excluded. Each group was divided into two subsets: one including patients with metabolic syndrome and one including patients without metabolic syndrome (ie, hypertension alone or associated with another component of the syndrome). RESULTS: Insulin resistance, defined by increased homeostasis model assessment (HOMA index), was higher in patients with primary aldosteronism than in those with LREH only in the absence of metabolic syndrome (P<.01), whereas in the subsets bearing the syndrome it was similar. Adiponectin levels were lower in primary aldosteronism than in patients with LREH (P<.01). Like HOMA index, the difference was maintained (P<.01) only in the subsets without metabolic syndrome. Adiponectin levels were inversely correlated with HOMA index and positively correlated with potassium levels both in primary aldosteronism (P<.001) or in LREH (P<.05) groups. CONCLUSIONS: Lower adiponectin as well as lower insulin sensitivity in primary aldosteronism compared with LREH seem to result from both direct (aldosterone excess) and indirect (hypokalemia) mechanisms. Therapeutic interventions aimed at correcting both potassium and adiponectin levels by specific antihypertensive agents might improve insulin sensitivity, providing better cardiovascular protection in primary aldosteronism.

Prevalence and Clinical Manifestations of Primary Aldosteronism Encountered in Primary Care Practice.

BACKGROUND: Despite being widely recognized as the most common form of secondary hypertension, among the general hypertensive population the true prevalence of primary aldosteronism (PA) and its main subtypes, aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH), remains a matter of debate. OBJECTIVES: This study sought to determine the prevalence and clinical phenotype of PA in a large cohort of unselected patients with hypertension, consecutively referred to our hypertension unit, by 19 general practitioners from Torino, Italy. METHODS: Following withdrawal from all interfering medications, patients were screened for PA using the ratio of serum aldosterone to plasma renin activity. PA was diagnosed according to Endocrine Society guidelines. The diagnosis was confirmed or excluded by an intravenous saline infusion test or captopril challenge test and subtype differentiation was performed by adrenal computed tomography scanning and adrenal vein sampling, using strict criteria to define successful cannulation and lateralization of aldosterone production. RESULTS: A total of 1,672 primary care patients with hypertension (569 newly diagnosed and 1,103 patients already diagnosed with arterial hypertension) were included in the study. A total of 99 patients (5.9%) were diagnosed with PA and conclusive subtype differentiation by adrenal vein sampling was made in 91 patients (27 patients with an APA and 64 patients with BAH). The overall prevalence of PA increased with the severity of hypertension, from 3.9% in stage 1 hypertension to 11.8% in stage 3 hypertension. Patients with PA more frequently displayed target organ damage and cardiovascular events compared with those without PA, independent of confounding variables. CONCLUSIONS: Our results demonstrated that PA is a frequent cause of secondary hypertension, even in the general population of patients with hypertension, and indicates that most of these patients should be screened for PA.

Prevalence and characteristics of the metabolic syndrome in primary aldosteronism.

CONTEXT: Patients with hypertension have a high prevalence of concurrent metabolic abnormalities, including obesity, dyslipidemia, and hyperglycemia. Clustering of these cardiovascular risk factors, defined as metabolic syndrome, causes a more pronounced target organ damage. Aldosterone excess has been found to be associated with glucose disorders and may contribute to cardiovascular damage. OBJECTIVE: The aim of our study was to assess the prevalence and the characteristics of the metabolic syndrome in a group of patients with hypertension due to primary aldosteronism compared with patients with essential hypertension. METHODS: The National Cholesterol Education Program Adult Treatment Panel III definition of the metabolic syndrome was used. Eighty-five patients with primary aldosteronism and 381 patients with essential hypertension were studied. Most patients were not receiving antihypertensive therapy during the investigation. RESULTS: Blood glucose and systolic blood pressure were higher (P < 0.05 and P < 0.01, respectively) and duration of hypertension was longer (P < 0.05) in primary aldosteronism than in essential hypertension. The prevalence of metabolic syndrome was higher in primary aldosteronism than in essential hypertension (41.1% vs. 29.6%; P < 0.05). Distribution of single components of the metabolic syndrome other than hypertension showed a higher prevalence of hyperglycemia in primary aldosteronism than in essential hypertension (27.0% vs. 15.2%; P < 0.05). CONCLUSIONS: Our findings confirm a negative effect of aldosterone excess on glucose metabolism and suggest that the recently reported higher rates of cardiovascular events in primary aldosteronism than in essential hypertension might be due to increased prevalence of the metabolic syndrome in the former condition.

QT interval in patients with primary aldosteronism and low-renin essential hypertension.

INTRODUCTION: QT interval prolongation increases the risk of sudden death in several medical conditions. Patients with primary aldosteronism and salt-sensitive hypertension experience more cardiovascular events than those with normal-renin essential hypertension. QT interval prolongation might represent one of the risk factors for cardiovascular events in these patients. The aim of the present study was to evaluate the QT interval in patients with primary aldosteronism and low-renin essential hypertension (LREH). METHODS: Twenty-seven patients with primary aldosteronism, 17 patients with LREH, 117 patients with essential hypertension and 25 healthy individuals were studied. Plasma aldosterone, plasma renin activity, and aldosterone to plasma renin activity ratio (ARR) were determined. Corrected QT intervals (QTcs) were measured from a 12-lead electrocardiogram. RESULTS: The QTc was longer in primary aldosteronism (434 +/- 23 ms) and LREH (430 +/- 18 ms) compared with essential hypertension (419 +/- 22 ms) and healthy controls (412 +/- 19 ms) (P = 0.0004). The prevalence of QTc longer than 440 ms was higher in primary aldosteronism (48%) and LREH (23%) compared with essential hypertension (11%) and healthy controls (4%) (P < 0.0001). QTc correlated with plasma aldosterone (P = 0.01), ARR (P = 0.02), and diastolic blood pressure (P = 0.01). ARR (P = 0.01) and systolic blood pressure (P = 0.01) were identified as independent predictors of QTc. CONCLUSIONS: We postulate that the elevated aldosterone secretion contributes to the prolongation of the QT interval in patients with primary aldosteronism and LREH through both a depletion of intracellular potassium concentration and higher blood pressure values. QTc measurement might represent one simple, non-invasive and reproducible index to characterize the cardiovascular risk in patients with primary aldosteronism and LREH.

Long-term cardio- and cerebrovascular events in patients with primary aldosteronism.

BACKGROUND: Aldosterone plays a detrimental role on the cardiovascular system and PA patients display a higher risk of events compared with EH. OBJECTIVES: The objectives of the study were to compare cardio- and cerebrovascular events in patients with primary aldosteronism (PA) and matched essential hypertension (EH). METHODS: We retrospectively compared the percentage of patients experiencing events at baseline and during a median follow-up of 12 years in 270 PA patients case-control matched 1:3 with EH patients and in PA subtypes [aldosterone-producing adenoma (n = 57); bilateral adrenal hyperplasia (n = 213)] vs matched EH. RESULTS: A significantly higher number of PA patients experienced cardiovascular events over the entire period of the study (22.6% vs 12.7%, P < .001). At the diagnosis of PA, a higher number of patients had experienced total events (14.1% vs 8.4% EH, P = .007); furthermore, during the follow-up period, PA patients had a higher rate of events (8.5% vs 4.3% EH, P = .008). In particular, stroke and arrhythmias were more frequent in PA patients. During the follow-up, a higher percentage of PA patients developed type 2 diabetes. Parameters that were independently associated with the occurrence of all events were age, duration of hypertension, systolic blood pressure, presence of diabetes mellitus, and PA diagnosis. After division into PA subtypes, patients with either aldosterone-producing adenoma or bilateral adrenal hyperplasia displayed a higher rate of events compared with the matched EH patients. CONCLUSIONS: This study demonstrates in a large population of patients the pathogenetic role of aldosterone excess in the cardiovascular system and thus the importance of early diagnosis and targeted PA treatment.

Genes implicated in insulin resistance are down-regulated in primary aldosteronism patients.

Primary aldosteronism (PA) patients display an increased incidence of insulin resistance. Herein we demonstrate the decreased gene expression of lipid metabolism genes PCK1, PLIN, ADIPOQ and PPARG in the visceral adipose tissue (VAT) of PA patients compared to age-, sex- and BMI-matched controls. In VAT, the expression of PCK1, PLIN, ADIPOQ and PPARG was inversely correlated with aldosterone levels; furthermore, PLIN and ADIPOQ gene expression was correlated with potassium levels. Therefore, raised aldosterone and low potassium may contribute to the reduced expression of these genes in PA patients. Finally, incubation of primary cultures of human adipocytes with aldosterone resulted in a decrease in the expression of PCK1, PLIN and ADIPOQ and this effect was blocked by eplerenone. Therefore, the characteristic aldosterone excess of PA patients may mediate the down-regulation of PCK1, PLIN and ADIPOQ in VAT that in turn may contribute to the insulin resistance observed in PA patients.

Concurrent primary aldosteronism and subclinical cortisol hypersecretion: a prospective study.

BACKGROUND: Primary aldosteronism is the most frequent cause of secondary hypertension and is responsible for an increased risk of cardiometabolic complications. A concomitant subtle cortisol hyperproduction could enhance cardiovascular risk. We prospectively estimated the occurrence of subclinical hypercortisolism in primary aldosteronism patients. METHODS: In a large population of hypertensive patients without clinical signs of hypercortisolism, 76 consecutive patients with primary aldosteronism were investigated. Differential diagnosis between unilateral and bilateral aldosterone hypersecretion was made by computed tomography/MRI and/or adrenal venous sampling (AVS). Subclinical hypercortisolism was defined as failure to suppress plasma cortisol to less than 50 nmol/l after 1 mg-overnight dexamethasone, used as screening test, and at least one of two other abnormal hormonal parameters, that is, adrenocorticotrophin (ACTH) less than 2 pmol/l and urinary cortisol more than 694 nmol/24 h. RESULTS: Three out of 76 patients had postdexamethasone plasma cortisol more than 50 nmol/l. Only one also showed low-normal ACTH and mildly elevated urinary cortisol. The patient had a right 4 cm adrenal mass. Laparoscopic adrenalectomy was followed by short-term steroid replacement to prevent adrenal insufficiency. In-situ hybridization showed CYP11B1 expression exclusively in tumoral tissue, whereas CYP11B2 was expressed only in a peritumoral region composed of zona glomerulosa-like cells, suggesting the co-existence of a cortisol-producing adenoma and an aldosterone-producing hyperplasia in the same adrenal. The restoration of hormone abnormalities to normal levels was confirmed at 12 months of follow-up. CONCLUSION: Concurrent aldosterone and subclinical cortisol hypersecretion seems to be a rare event in primary aldosteronism patients; however, its detection by appropriate testing is important to avoid AVS misinterpretation.

Ventricular repolarization before and after treatment in patients with secondary hypertension due to renal-artery stenosis and primary aldosteronism.

A prolonged QT interval is a risk factor for ischemic heart disease in hypertensive subjects. Patients with renal-artery stenosis and primary aldosteronism (PA) are at increased risk of cardiovascular events. The objective of the present study was to evaluate the QT interval in patients with renovascular hypertension (RV) and PA before and after treatment. A total of 24 patients with RV and 38 with PA were studied; 89 patients with essential hypertension (EH) served as control group. Corrected QT intervals (QTcH) were measured from a 12-lead ECG. Basal QTcH was longer in RV (429±30 ms) and PA (423±23 ms) compared with EH controls (407±18 ms; P<0.001). The prevalence of QTcH >440 ms was higher in RV (29%) and PA patients (29%) compared with EH controls (4%; P<0.001). QTcH interval was evaluated after treatment in 19 RV and 15 PA patients. QTcH was reduced after renal-artery angioplasty in RV patients (419±14 ms; P=0.02), and after spironolactone or adrenalectomy in PA (403±12 ms; P=0.01). In conclusion, QT interval was prolonged in patients with RV and PA compared with controls with EH. After angioplasty of renal-artery stenosis in RV, and treatment with spironolactone or adrenalectomy in PA, the cardiovascular risk of such patients may be reduced by concomitant blood pressure lowering and QT duration shortening.

Psychological assessment of primary aldosteronism: a controlled study.

OBJECTIVE: Our objective was to investigate psychological correlates in a population with primary aldosteronism (PA) using methods found to be sensitive and reliable in psychosomatic research. METHODS: Twenty-three PA patients (12 male, 11 female; mean age 50 ± 9 yr) were compared with 23 patients with essential hypertension (EH) (15 male, eight female; mean age 47 ± 8 yr) and 23 matched normotensive subjects. A modified version of the Structural Clinical Interview for DSM-IV, a shortened version of the structured interview for the Diagnostic Criteria for Psychosomatic Research, and two self-rating questionnaires, the Psychosocial Index and the Symptom Questionnaire, were administered. RESULTS: Twelve of 23 patients with PA (52.2%) suffered from an anxiety disorder compared with four of 23 with EH (17.4%) and one control (4.3%) (P < 0.001). Generalized anxiety disorder was more frequent in PA than in EH patients and controls (P < 0.05). As assessed by Diagnostic Criteria for Psychosomatic Research, irritable mood was more frequent in PA and EH compared with controls (P < 0.05) but did not differentiate PA from EH. According to Psychosocial Index results, patients with PA had higher levels of stress (P < 0.01) and psychological distress (P < 0.01) and lower level of well-being (P < 0.05) than controls. Compared with EH patients, PA patients had higher scores in stress subscale (P < 0.05). The Symptom Questionnaire showed higher levels of anxiety (P < 0.01), depression (P < 0.01) and somatization (P < 0.01) and lower physical well-being (P < 0.05) in PA than controls. CONCLUSION: A role of mineralocorticoid regulatory mechanisms in clinical situations concerned with anxiety and stress is suggested.

Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms).

Primary aldosteronism (PA) is the most frequent cause of secondary hypertension, and patients display an increased prevalence of cardiovascular events compared with essential hypertensives. To date, 3 familial forms of PA have been described and termed familial hyperaldosteronism types I, II, and III (FH-I to -III). The aim of this study was to investigate the prevalence and clinical characteristics of the 3 forms of FH in a large population of PA patients. Three-hundred consecutive PA patients diagnosed in our unit were tested by long-PCR of the CYP11B1/CYP11B2 hybrid gene that causes FH-I, and all of the available relatives of PA patients were screened to confirm or exclude PA and, thus, FH-II. Urinary 18-hydroxycortisol and 18-oxocortisol were measured in all of the familial PA patients. Two patients were diagnosed with FH-I (prevalence: 0.66%), as well as 21 of their relatives, and clinical phenotypes of the 2 affected families varied markedly. After exclusion of families who refused testing and those who were not informative, 199 families were investigated, of which 12 were diagnosed with FH-II (6%) and an additional 15 individuals had confirmed PA; clinical and biochemical phenotypes of FH-II families were not significantly different from sporadic PA patients. None of the families displayed a phenotype compatible with FH-III diagnosis. Our study demonstrates that familial forms of hyperaldosteronism are more frequent than previously expected and reinforces the recommendation of the Endocrine Society Guidelines to screen all first-degree hypertensive relatives of PA patients.

Evaluation of primary aldosteronism.

PURPOSE OF REVIEW: The purpose of this review is to briefly summarize current knowledge on diagnosis and treatment of primary aldosteronism, the most frequent cause of endocrine hypertension. RECENT FINDINGS: The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. The detection of primary aldosteronism is of particular importance, not only because it provides an opportunity for a targeted treatment but also because it has been extensively demonstrated that patients affected by primary aldosteronism are more prone to cardiovascular events and target organ damage than patients with essential hypertension. The diagnosis of primary aldosteronism is a three-step process; screening, confirmation and subtype diagnosis. SUMMARY: We review, the strategies to correctly identify primary aldosteronism, highlighting the central role of the new guidelines and the diagnostic aspects still under debate.