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1.
Effectiveness of Thermal Ablation for Aldosterone-Producing Adrenal Adenoma: A Systematic Review and Meta-Analysis of Clinical and Biochemical Parameters.
Liang, KW, Jahangiri, Y, Tsao, TF, Tyan, YS, Huang, HH
Journal of vascular and interventional radiology : JVIR. 2019;(9):1335-1342.e1
Abstract
PURPOSE To assess the effectiveness of thermal ablation for aldosterone-producing adrenal adenoma. MATERIALS AND METHODS A systematic search of the PubMed and CINAHL databases was performed to identify studies of thermal ablation for adrenal adenomas. Random effects meta-analysis models were used to compare pre- and post-treatment values of the following outcomes: systolic blood pressure (SBP), diastolic blood pressure (DBP), use of antihypertensive medications, and biochemical parameters (plasma aldosterone levels, aldosterone-to-renin ratio, and potassium levels). The rate of hypertension (HTN) resolution and improvement were also evaluated. RESULTS A total of 89 patients from 7 studies were included in the analysis. The mean postablation follow-up duration was 45.8 months. Pooled data analysis revealed a statistically significant decrease in SBP (-29.06 mm Hg; 95% confidence interval [CI], -33.93 to -24.19), DBP (-16.03 mm Hg; 95% CI, -18.33 to -13.73), and the number of antihypertensive medications used (-1.43; 95% CI, -1.97 to -0.89) after ablation. Biochemical parameters had returned to normal ranges after ablation in all studies. The cumulative rate of resolution or improvement in HTN status was 75.3%. On metaregression analysis, there was no statistically significant association between postablation blood pressure changes or serum aldosterone levels and study follow-up duration. CONCLUSIONS Thermal ablation for aldosterone-producing adrenal adenoma can be effective in controlling blood pressure, reducing the need for antihypertensive medications, and normalizing hormone secretion. Further higher-quality evidence is needed to confirm these results.
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2.
Expression and gene variation studies deny association of human HSD3B1 gene with aldosterone production or blood pressure.
Verwoert, GC, Hofland, J, Amin, N, Mattace-Raso, FU, Sijbrands, EJ, Hofman, A, van den Meiracker, AH, Uitterlinden, AG, van Duijn, CM, de Jong, FH, et al
American journal of hypertension. 2015;(1):113-20
Abstract
BACKGROUND Recent evidence suggests that the type I 3β-hydroxysteroid dehydrogenase, a steroidogenic enzyme encoded by the HSD3B1 gene, could be involved in aldosterone production and that genetic variation in HSD3B1 is associated with blood pressure. These findings challenge the long-standing hypothesis that all adrenocortical steroidogenesis is executed by the type II iso-enzyme, encoded by HSD3B2. METHODS To verify these findings, the adrenal presence of HSD3B1 and its effect on aldosterone synthesis and blood pressure were studied in expression and genetic association analyses, respectively. Expression of HSD3B1 and HSD3B2 was investigated in various adrenocortical tissues (n = 15) and in primary adrenal cell cultures (n = 5) after stimulation with adrenocorticotropin and angiotensin II. Six tagging single nucleotide polymorphisms within the HSD3B1 gene were studied for association with blood pressure and hypertension in a meta-analysis of 4 Dutch cohorts (n = 11,192). RESULTS HSD3B1 expression was minimal or absent in adrenocortical tissues, including 6 aldosterone-producing adenomas. In contrast with the ubiquitously expressed HSD3B2 mRNA, HSD3B1 levels were not stimulated by adrenocorticotropin or angiotensin II. No variants in the HSD3B1 gene were associated with blood pressure or the occurrence of hypertension. CONCLUSIONS We found no evidence to support confirmation that HSD3B1 is involved in aldosterone synthesis in the human adrenal cortex or that genetic variation in HSD3B1 affects blood pressure or hypertension, favoring the hypothesis that all adrenocortical steroidogenesis is primarily dependent on the type II 3β-hydroxysteroid dehydrogenase.
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3.
A Meta-Analysis of Somatic KCNJ5 K(+) Channel Mutations In 1636 Patients With an Aldosterone-Producing Adenoma.
Lenzini, L, Rossitto, G, Maiolino, G, Letizia, C, Funder, JW, Rossi, GP
The Journal of clinical endocrinology and metabolism. 2015;(8):E1089-95
Abstract
CONTEXT Due to selection biases and inadequate statistical power, individual studies may fail to identify the clinical features of patients with an aldosterone-producing adenoma (APA) harboring KCNJ5 mutations. When this failure occurs, meta-analysis can provide significant outcome data. OBJECTIVE The objective was to determine the clinical features of these APA patients. DESIGN We systematically searched the PubMed, Scopus, Web of Science, and Cochrane databases library in January 2015 applying the Population, Intervention, Comparison, and Outcome (PICO) strategy. The standardized differences in mean and corresponding 95% confidence interval of continuous variables were computed by random-effects modeling. SETTING We performed a meta-analysis of all available studies on somatic KCNJ5 mutations in APA. PATIENTS We could identify 13 studies that recruited 1636 patients (age 49 ± 4 years; 55% females). MAIN OUTCOMES AND MEASURES Differences between APA with and without KCNJ5 mutations in gender, plasma renin activity, plasma aldosterone, tumor size, serum potassium, and blood pressure were investigated. RESULTS The overall prevalence of KCNJ5 mutations was 43% (range = 12-80%). Their rate was lower (P < .003) in the studies done in Europe, the United States, and Australia (35%) than in Japan and China (63%); it correlated (r = 0.60, P = .029) with the mean daily urinary sodium excretion. Compared with the wild-type, the mutated APA patients were younger (45 ± 3 vs 52 ± 5 yrs), had higher plasma aldosterone (42 ± 8 vs 33 ± 8 ng/dl), larger tumors (16.1 ± 6.4 versus 14.9 ± 7.4 mm), and were more often females (67% vs 44%) (all P < .05). CONCLUSIONS Meta-analysis showed that more pronounced hyperaldosteronism, young age, female gender, and larger tumors are the phenotypic features of APA patients with KCNJ5 mutations. No significant differences in blood pressure and serum K(+) was found, which suggests that these clinical features do not help in identifying mutated APA patients.
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4.
Effects of T-type calcium channel blockers on renal function and aldosterone in patients with hypertension: a systematic review and meta-analysis.
Li, X, Yang, MS
PloS one. 2014;(10):e109834
Abstract
BACKGROUND High blood pressure can cause kidney damage, which can increase blood pressure, leading to a vicious cycle. It is not clear whether the protective effects of T-type calcium channel blockers (T-type CCBs) on renal function are better than those of L-type CCBs or renin-angiotensin system (RAS) antagonists in patients with hypertension. METHODS AND FINDINGS PUBMED, MEDLINE, EMBASE, OVID, Web of Science, Cochrane, CNKI, MEDCH, VIP, and WANFANG databases were searched for clinical trials published in English or Chinese from January 1, 1990, to December 31, 2013. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated and reported. A total of 1494 reports were collected, of which 24 studies with 1,696 participants (including 809 reports comparing T-type CCBs versus L-type CCBs and 887 reports comparing T-type CCB versus RAS antagonists) met the inclusion criteria. Compared with L-type CCBs, T-type CCBs resulted in a significant decline in aldosterone (mean difference = -15.19, 95% CI -19.65 - -10.72, p<1×10(-5)), proteinuria (mean difference = -0.73, 95% CI -0.88 - -0.57, p<1×10(-5)), protein to creatinine ratio (mean difference = -0.22, 95% CI -0.41 - -0.03, p = 0.02), and urinary albumin to creatinine ratio (mean difference = -55.38, 95% CI -86.67 - -24.09, p = 0.0005); no significant difference was noted for systolic blood pressure (SBP) (p = 0.76) and diastolic blood pressure (DBP) (p = 0.16). The effects of T-type CCBs did not significantly differ from those of RAS antagonists for SBP (p = 0.98), DBP (p = 0.86), glomerular filtration rate (p = 0.93), albuminuria (p = 0.97), creatinine clearance rate (p = 0.24), and serum creatinine (p = 0.27) in patients with hypertension. CONCLUSION In a pooled analysis of data from 24 studies measuring the effects of T-type CCBs on renal function and aldosterone, the protective effects of T-type CCBs on renal function were enhanced compared with L-type CCBs but did not differ from RAS antagonists. Their protective effects on renal function were independent of blood pressure.
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5.
Effects of low-sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review).
Graudal, NA, Hubeck-Graudal, T, Jürgens, G
American journal of hypertension. 2012;(1):1-15
Abstract
BACKGROUND The question of whether reduced sodium intake is effective as a health prophylaxis initiative is unsolved. The purpose was to estimate the effects of low-sodium vs. high-sodium intake on blood pressure (BP), renin, aldosterone, catecholamines, and lipids. METHODS Studies randomizing persons to low-sodium and high-sodium diets evaluating at least one of the above outcome parameters were included. Data were analyzed with Review Manager 5.1. RESULTS A total of 167 studies were included. The effect of sodium reduction in: (i) Normotensives: Caucasians: systolic BP (SBP) -1.27 mm Hg (95% confidence interval (CI): -1.88, -0.66; P = 0.0001), diastolic BP (DBP) -0.05 mm Hg (95% CI: -0.51, 0.42; P = 0.85). Blacks: SBP -4.02 mm Hg (95% CI: -7.37, -0.68; P = 0.002), DBP -2.01 mm Hg (95% CI: -4.37, 0.35; P = 0.09). Asians: SBP -1.27 mm Hg (95% CI: -3.07, 0.54; P = 0.17), DBP -1.68 mm Hg (95% CI: -3.29, -0.06; P = 0.04). (ii) Hypertensives: Caucasians: SBP -5.48 mm Hg (95% CI: -6.53, -4.43; P < 0.00001), DBP -2.75 mm Hg (95% CI: -3.34, -2.17; P < 0.00001). Blacks: SBP -6.44 mm Hg (95% CI: -8.85, -4.03; P = 0.00001), DBP -2.40 mm Hg (95% CI: -4.68, -0.12; P = 0.04). Asians: SBP -10.21 mm Hg (95% CI: -16.98, -3.44; P = 0.003), DBP -2.60 mm Hg (95% CI: -4.03, -1.16; P = 0.0004). Sodium reduction resulted in significant increases in renin (P < 0.00001), aldosterone (P < 0.00001), noradrenaline (P < 0.00001), adrenaline (P < 0.0002), cholesterol (P < 0.001), and triglyceride (P < 0.0008). CONCLUSIONS Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hypertensives), and a significant increase in plasma renin, plasma aldosterone, plasma adrenaline, and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride.
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6.
Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride.
Jürgens, G, Graudal, NA
The Cochrane database of systematic reviews. 2004;(1):CD004022
Abstract
BACKGROUND One of the controversies in preventive medicine is, whether a general reduction in sodium intake can decrease the blood pressure of a population and thereby reduce cardiovascular mortality and morbidity. In recent years the debate has been extended by studies indicating that reducing sodium intake has effects on the hormone and lipid profile. OBJECTIVES To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol and triglycerides. SEARCH STRATEGY "MEDLINE" and reference lists of relevant articles were searched from 1966 through December 2001. SELECTION CRITERIA Studies randomising persons to low sodium and high sodium diets were included if they evaluated at least one of the above outcome parameters. DATA COLLECTION AND ANALYSIS Two authors independently extracted the data, which were analysed by means of Review Manager 4.1. MAIN RESULTS In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. The median duration of the intervention was 8 days in the normal blood pressure trials (range 4-1100) and 28 days in the elevated blood pressure trials (range 4-365). Multiple regression analyses showed no independent effect of duration on the effect size. In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. The magnitude of blood pressure reduction was also greater in a single trial in Japanese patients. There was also a significant increase in plasma or serum renin, 304% (p < 0.0001), aldosterone, 322%, (p < 0.0001), noradrenaline, 30% (p < 0.0001), cholesterol, 5.4% (p < 0.0001) and LDL cholesterol, 4.6% (p < 0.004), and a borderline increase in adrenaline, 12% (p = 0.04) and triglyceride, 5.9% (p = 0.03) with low sodium intake as compared with high sodium intake. REVIEWER'S CONCLUSIONS The magnitude of the effect in Caucasians with normal blood pressure does not warrant a general recommendation to reduce sodium intake. Reduced sodium intake in Caucasians with elevated blood pressure has a useful effect to reduce blood pressure in the short-term. The results suggest that the effect of low versus high sodium intake on blood pressure was greater in Black and Asian patients than in Caucasians. However, the number of studies in black (8) and Asian patients (1) was insufficient for different recommendations. Additional long-term trials of the effect of reduced dietary sodium intake on blood pressure, metabolic variables, morbidity and mortality are required to establish whether this is a useful prophylactic or treatment strategy.
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7.
Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride.
Jürgens, G, Graudal, NA
The Cochrane database of systematic reviews. 2003;(1):CD004022
Abstract
BACKGROUND One of the controversies in preventive medicine is, whether a general reduction in sodium intake can decrease the blood pressure of a population and thereby reduce cardiovascular mortality and morbidity. In recent years the debate has been extended by studies indicating that reducing sodium intake has effects on the hormone and lipid profile. OBJECTIVES To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol and triglycerides. SEARCH STRATEGY "MEDLINE" and reference lists of relevant articles were searched from 1966 through December 2001. SELECTION CRITERIA Studies randomising persons to low sodium and high sodium diets were included if they evaluated at least one of the above outcome parameters. DATA COLLECTION AND ANALYSIS Two authors independently extracted the data, which were analysed by means of Review Manager 4.1. MAIN RESULTS In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. The median duration of the intervention was 8 days in the normal blood pressure trials (range 4-1100) and 28 days in the elevated blood pressure trials (range 4-365). Multiple regression analyses showed no independent effect of duration on the effect size. In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. The magnitude of blood pressure reduction was also greater in a single trial in Japanese patients. There was also a significant increase in plasma or serum renin, 304% (p < 0.0001), aldosterone, 322%, (p < 0.0001), noradrenaline, 30% (p < 0.0001), cholesterol, 5.4% (p < 0.0001) and LDL cholesterol, 4.6% (p < 0.004), and a borderline increase in adrenaline, 12% (p = 0.04) and triglyceride, 5.9% (p = 0.03) with low sodium intake as compared with high sodium intake. REVIEWER'S CONCLUSIONS The magnitude of the effect in Caucasians with normal blood pressure does not warrant a general recommendation to reduce sodium intake. Reduced sodium intake in Caucasians with elevated blood pressure has a useful effect to reduce blood pressure in the short-term. The results suggest that the effect of low versus high sodium intake on blood pressure was greater in Black and Asian patients than in Caucasians. However, the number of studies in black (8) and Asian patients (1) was insufficient for different recommendations. Additional long-term trials of the effect of reduced dietary sodium intake on blood pressure, metabolic variables, morbidity and mortality are required to establish whether this is a useful prophylactic or treatment strategy.