No abstract available.
Hyperkalemia ; Paralysis ; Polyneuropathies ; Spironolactone

Introduction: Resistant hypertension (RH) is defined as a blood pressure (BP) reading that remains above goal despite concurrent use of three optimally dosed antihypertensives of different classes, including a diuretic. Spironolactone, a mineralocorticoid receptor antagonist, has shown significant benefit in reduction of BP in recent trials and is used empirically as an add-on therapy for RH. The researchers’ objective is to evaluate the BP-lowering efficacy of spironolactone in patients with resistant hypertension. Methods: A meta-analysis was performed on randomized controlled trials (RCTs) comparing office or home BP reduction using spironolactone with placebo or an alternative drug regimen on top of standard-triple drug therapy among patients with RH. The study was conducted in reference to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Results: Five RCTs were included comprising a total of 662 patients. Three of these studies were found to have low risk of bias while two had unclear risk of bias. Compared to placebo, the addition of spironolactone significantly decreased office systolic BP (weighted mean difference [WMD]= -16.33, 95% confidence interval [CI]=-24.68 to -7.97, P=0.0001) and office diastolic BP (WMD=-6.12, 95% CI= -9.35 to -2.89, P=0.0002). Compared to an alternative drug regimen, additional spironolactone resulted in a significantly greater reduction in office systolic BP (WMD=-4.58mmHg, 95% CI=-7.19, -1.97, P= 0.0006) and home systolic BP (WMD= -4.33, 95% CI= 5.55, -3.12, P< 0.00001); while the addition of spironolactone had no significant difference compared to an alternative drug regimen in reducing office diastolic BP (WMD=-3.35, 95% CI=-12.08 to +5.38, P=0.45) and home diastolic BP (WMD= 0.00, 95 % CI=-0.73 to 0.73, P=1.0). Conclusion Spironolactone, when added to triple-drug anti-hypertensive therapy, showed significant reduction of systolic office and home BP. It should be considered as the add-on medication of choice for BP reduction in patients with RH.
Antihypertensive Agents ; Spironolactone ; Blood Pressure

BACKGROUND/AIMS: Transtubular potassium gradient(TTKG) is known as the most accurate indicator of aldosterone activity. TTKG may be used to monitor the effectiveness of aldosterone antagonist which is prescribed generally for the management of cirrhotic ascites. Spot urine [Na]/[K] ratio may also be used for the same purpose. METHODS: After measuring TTKG, spot urine [Na]/[K] ratio, and plasma aldosterone concentration in each of the 23 patients all who had cirrhotic ascites, 100 mg of spiron-olactone was prescribed to be taken daily for 5 days. When no diuretic response occurred and TTKG was more than 3.5 at the end of 5 days, the dose of spironolactone was increased by 100 mg/day at the interval of 5 days until TTKG decreased to below 3.5. Furosemide was added to the non-responders if their TTKG had dropped to below 3.5. RESULTS: Basal plasma concentration of aldosterone was higher than upper normal limit in 13(57%) patients, and correlated with TTKG significantly(r=0.60, p=0.002). TTKG was calculated to be 3.5+/-0.67 when assuming the aldosterone activity has been completely blocked. Spot urine [Na]/[K] ratio had significant negative correlation with TTKG before and after the administration of spironolactone. In most patients, diuretic response appeared with the fall of TTKG (especially below 3.5) and with the rise of spot urine [Na]/[K] ratio. In patients who did not respond to a low dose spironolactone, further treatment plan (to increase dose of spironolactone or to add furosemide) was guided by TTKG, and all were successful. CONCLUSIONS: TTKG and spot urine [Na]/[K] ratio are good indicators of aldosterone activity, and might be used as useful guidelines in the diuretic management of cirrhotic ascites.
Aldosterone ; Ascites* ; Furosemide ; Humans ; Plasma ; Potassium* ; Spironolactone

Introduction: Gitelman Syndrome (GS), a rare autosomal recessive inherited disorder, is frequently unrecognized in the clinical setting. GS typically manifests with severe hypokalemia with debilitating and potentially fatal consequences if untreated. As of writing, confirmatory genetic assays are currently unavailable in the country, and the diagnosis of GS is primarily based on several biochemical laboratory tests. This results in the difficulty with prompt diagnosis of GS in the locality. Case: We present a 52-year-old male who came in with chronic, intermittent paraparesis associated with persistent hypokalemia. A diagnosis of GS was made biochemically based on renal wasting of potassium and magnesium, hypocalciuria, and metabolic alkalosis. Electrolyte correction with lifelong supplementation, and administration of Spironolactone resulted in the resolution of bilateral leg weakness. Electrolyte levels were maintained within normal limits in the outpatient setting. Conclusion GS is an uncommon potentially debilitating disorder that may lead to problematic, potentially fatal consequences to electrolyte abnormalities if left untreated. The lack of awareness and consequent delay in the diagnosis, and the unavailability of confirmatory genetic testing remains a clinical challenge. Timely recognition and initiation of treatment leads to early control of electrolyte levels, and better prognosis.
Gitelman&rsquo ; s Syndrome ; Paraparesis ; Hypokalemia ; Hypomagnesemia ; Spironolactone ; Case Report

A 19 year old female patient presented with diffuse alopecia as her chief medical complaint. A clinical examination revealed hirsutism limited only to the on midline lower abdomen with elevated DHEA-S(dehydroepiandrosterone sulfate) and total testosterone levels. Polycystic ovarian disease (PCOD) was diagnosed during the treatment with dexamethasone and spironolactone, which was effective to improve her alopecia. We believe that, with increasing, concerns about hair conditions of teen-age girls there should be increasing chances for dermatologists to care for patients of PCOD first before other specialities in medicine.
Abdomen ; Alopecia* ; Dexamethasone ; Female* ; Hair ; Hirsutism ; Humans ; Ovarian Diseases* ; Spironolactone ; Testosterone ; Young Adult

BACKGOUND: Gitelman's syndrome is manifested by hypokalemia, metabolic alkalosis, normal blood pressure, hyperreninemic hyperaldosteronism, hypomagnesemia and hypocalciuria. This study was carried out to investigate the effects of magnesium supplementation for correcting hypokalemia in Gitelman syndrome. METHODS: A Gitelman patient without hyperaldosteronism in our hospital was studied, oral supplementation periods of regimens for 60 days were divided into eight stages (each stage is at least over 5 days) such as 1 stage:no regimen supplementation period 2 stage:spironolactone 100 mg, alone period 3 stage:spironolactone 100 mg, MgO 1 g mixed period, 4 stage:spironolactone 100 mg, alone period, 5 stage:spironolactone 100 mg, MgO 1 g mixed period, 6 stage:spironolactone 150 mg, MgO 1 g mixed period, 7 stage: spironolactone 150 mg, MgO 1.5 g mixed period, 8 stage:spironolactone 150 mg, MgO 1.5 g, KCl 3.6 g mixed period. RESULTS: The highest value of plasm [K] was 3.3 mEq/L, the lowest value of TTKG was 2.6 during 3 stage, plasm [K] had tendency to increased and TTKG decreased, however next during 4 stage, the tendency of correcting hypokalemia diminished. The highest value of plasm [K] was only 3.3 mEq/L during 7 stage, the highest value of plasm [K] was 4.6 mEq/L during 8 stage. And the highest value of plasm ionized [Mg++] was 0.44 mmol/L during MgO 1.5 g supplementation. CONCLUSION: Magnesium alone fails to completely correct potassium and magnesium depletion despite tendency of correcting. Therefore, the optimal therapeutic regimens for correcting hypokalemia in Gitelman syndrome without hyperaldosteronism would be the magnesium and additional K supplementation.
Alkalosis ; Blood Pressure ; Gitelman Syndrome* ; Humans ; Hyperaldosteronism ; Hypokalemia* ; Magnesium* ; Potassium ; Spironolactone ; Gitelman Syndrome

Primary aldosteronism is present in approximately 1% of unselectd hypertensive patients. Adrenal adenoma is a known as one of the surgically curable form of the hypertension. Hypertension is one of the contributing factors for the development of aortic dissection. Cincurrence of aortic dissection in patient with primary aldosteronism is extemely rare. Only one case wasconfirmed by autopsy and reported in the world literature. We report a case of DeBakey type 3 anortic aneursm in a 49-year old hypertensive female patient with primary aldosteronism due to left adrenal adenoma. She underwent left adrenalectomy uneventfully after stabilization of her blood pressure with maximal medical management including nitroprusside, aldactone, enalapril and inderal.
Adenoma ; Adrenalectomy ; Autopsy ; Blood Pressure ; Enalapril ; Female ; Humans ; Hyperaldosteronism ; Hypertension ; Middle Aged ; Nitroprusside ; Propranolol ; Spironolactone

A sensitive high performance liquid chromatography-electrospray ionization-mass spectrometry (HPLC-ESI-MS) method was established for the determination of eplerenone (EP) in human plasma. The plasma samples of EP were extracted with ethyl acetate and separated by HPLC on a reversed phase C18 column with a mobile phase of 10 mmol x L(-1) ammonium acetate water solution-methanol (30 : 70, v/v). EP was determined with electrospray ionization-mass spectrometry (ESI-MS) in the selected ion monitoring (SIM) mode. The calibration curves were linear over the range of 2-4 000 ng x mL(-1) for EP. The lower limit of quantification was 2 ng x mL(-1). The method has been successfully applied in the pharmacokinetic study of the EP tablets. The main pharmacokinetic parameters of EP after oral administration of 25 mg, 50 mg, 100 mg were as follows, t1/2: (4.9 +/- 2.1), (4.7 +/- 1.5), (5.9 +/- 1.2) h; AUC(0-infinity): (4 402 +/- 1 735), (8 150 +/- 2 509), (13 783 +/- 4 102) microg x h x L(-1); and MRT: (6.2 +/- 2.1), (6.6 +/- 1.3), and (7.2 +/- 1.6) h. Parameters of EP after oral administration of multiple doses of 50 mg were as follows, t1/2: (6.1 +/- 1.7) h; AUC(ss): (10 071 +/- 4220) microg x h x L(-1); MRT: (8.1 +/- 2.3) h; and DF: (3.2 +/- 1.0).
Chromatography, High Pressure Liquid ; methods ; Humans ; Spectrometry, Mass, Electrospray Ionization ; methods ; Spironolactone ; analogs & derivatives ; blood ; pharmacokinetics

BACKGROUND: Previous studies have shown that aldosterone antagonists have a proteinuria-lowering effect in patients with proteinuria and progressive proteinuric disease not adequately controlled by the use of angiotensin receptor blockers (ARBs). Aldosterone antagonists, in combination with ARBs, might improve proteinuria in patients with glomerulonephritis (GN). METHODS: In the present retrospective study, we evaluated the proteinuria-lowering effect and drug safety of low-dose spironolactone (12.5 mg/day) in 42 patients with GN being treated with an ARB. RESULTS: Proteinuria decreased from a mean total-protein-to-creatinine (TP/Cr) ratio of 592.3 ± 42.0 mg/g at baseline to 335.6 ± 43.3 mg/g after three months of treatment with spironolactone (P < 0.001). After the initial three months, the mean TP/Cr ratio increased progressively at six, nine, and 12 months; however, it was still less than the baseline value (P = 0.001, < 0.001, and < 0.001, respectively). Although serum Cr levels increased significantly at three and nine months compared with baseline (P = 0.036 and 0.026, respectively), there was no time effect of treatment (P = 0.071). Serum potassium levels tended to increase with time (P = 0.118), whereas systolic and diastolic blood pressures decreased with time (P = 0.122 and 0.044, respectively). CONCLUSION: Low-dose spironolactone in combination with an ARB reduced proteinuria in patients with GN, which could represent a novel treatment option in individuals whose proteinuria is not optimally controlled by the use of ARBs alone.
Angiotensin Receptor Antagonists ; Angiotensins* ; Glomerulonephritis* ; Humans ; Mineralocorticoid Receptor Antagonists ; Potassium ; Proteinuria ; Retrospective Studies ; Spironolactone*

PURPOSE: Primary aldosteronism due to an adrenal cortical adenoma is a surgically curable disease. However, hypertension is known to persist postoperatively in many patients. The aim of this study was to determine the factors influencing the long-term outcome of blood pressure after an adrenalectomy for a primary aldosteronism and to evaluate the changing pattern of renin and aldosterone. METHODS: Forty-two cases of primary aldosteronism, which were operated on and followed up at the Department of Surgery, Seoul National University Hospital from January 1986 to June 2001 were included in this study. The subjects were classified into a normotensive group and a hypertensive group and the two groups were compared according to the clinical, biochemical and pathological parameters. RESULTS: After surgery, the aldosterone concentration was decreased and the plasma renin activity was increased. During a mean follow-up period of 28 months, 31 patients (73.8%) had a normal blood pressure without an antihypertensive treatment. The significant risk factors for persistent hypertension were a family history of hypertension, a long duration of preoperative hypertension, a poor response of preoperative spironolactone. The hypertensive group had a higher level of postoperative plasma renin activity and an aldosterone concentration in the long-term follow-up period after surgery. CONCLUSION: A family history of hypertension, the duration of hypertension and the response to spironolactone were factors influencing persistent hypertension after surgery for a primary aldosteronism. A high level of plasma renin activity and aldosterone during the follow-up period is related to the persistent hypertension. Therefore, early detection and surgery for a primary aldosteronism would reduce the preoperative cardiovascular changes and improve the postoperative outcome.
Adrenalectomy ; Adrenocortical Adenoma ; Aldosterone ; Blood Pressure ; Follow-Up Studies ; Humans ; Hyperaldosteronism* ; Hypertension ; Plasma ; Renin ; Risk Factors ; Seoul ; Spironolactone