ライフサイエンスコーパス: spironolactone

1 mitted after 1 week (patiromer) and 3 weeks (spironolactone).

2 ear accumulation of MR more efficiently than spironolactone.

3 ine and reduced by the antihypertensive drug Spironolactone.

4 dine-derived selective MR antagonist, and by spironolactone.

5 for any reason were significantly reduced by spironolactone.

6 (n=6551) or were not (n=12 301) treated with spironolactone.

7 at week 12 in the proportion of patients on spironolactone.

8 mulation was blocked by mifepristone but not spironolactone.

9 d to evaluate amiloride as an alternative to spironolactone.

10 r a previous large fall in blood pressure on spironolactone.

11 angiotensin-converting enzyme inhibitors or spironolactone.

12 pokalemia (<3.4 mmol/l) that were rescued by spironolactone.

13 al of 840 patients had new prescriptions for spironolactone.

14 ravated with furosemide and is attenuated by spironolactone.

15 is blocked by the competitive MR antagonist spironolactone.

16 and (3) adrenalectomy plus dexamethasone and spironolactone.

17 e mineralocorticoid receptor (MR) antagonist spironolactone.

18 annels could be a relevant in vivo target of spironolactone.

19 aldosterone was inhibited with NSC23766 and spironolactone.

20 easing evidence of MR-independent effects of spironolactone.

21 y define a subgroup with warranting trial of spironolactone.

22 Salt appetite was inhibited by spironolactone.

23 ase 9 inhibition, and myocardial fibrosis by spironolactone.

24 heart failure were significantly reduced by spironolactone.

25 n of MR are inhibited by both finerenone and spironolactone.

26 Patients in the ramipril (0.7%) or spironolactone (0.7%) group were less likely to develop

27 ntrast, 24 h exposure with the MR antagonist spironolactone (1-10 microM), the GR antagonist RU-486 (

28 Spironolactone 100 mg and bendroflumethiazide 5 mg cause

29 bendroflumethiazide 5 mg was as effective as spironolactone 100 mg in lowering blood pressure, despit

30 High-dose spironolactone (100 mg) vs placebo or 25 mg spironolacto

31 on fraction of 45% or more to receive either spironolactone (15 to 45 mg daily) or placebo.

32 , and four weeks of ALDO/salt + furosemide + spironolactone (200 mg/kg/day in divided doses by twice-

33 re frequently in survivors with PLE included spironolactone (21 [68%]), octreotide (7 [21%]), sildena

34 ailure guidelines were randomized to receive spironolactone 25 mg daily or placebo in a double-blind

35 After an active run-in phase with spironolactone 25 mg once daily, 112 patients with stage

36 n fraction <35% randomized to treatment with spironolactone 25 mg or placebo in the Randomized Aldact

37 mg/day) were randomized to add-on therapy of spironolactone 25 mg, hydrochlorothiazide (HCTZ) 12.5 mg

38 Participants were randomized to spironolactone 25 mg, which could be titrated to 50 mg,

39 zed stepped-care antihypertensive treatment, spironolactone 25 mg/d, bisoprolol 10 mg/d, prazosin 5 m

40 Patients were randomized to 6 months of oral spironolactone 25 mg/day or matching placebo.

41 ents to placebo, losartan (100 mg daily), or spironolactone (25 mg daily) for 48 wk.

42 tassium canrenoate (200 mg) followed by oral spironolactone (25 mg once daily) for 6 months in additi

43 day on the first postoperative day only), or spironolactone (25 mg/day).

44 2 weeks of once daily treatment with each of spironolactone (25-50 mg), bisoprolol (5-10 mg), doxazos

45 occupied by metastasis: control = 68 +/- 13, spironolactone = 26 +/- 8, P < 0.05) or inhibition of al

46 fter 21 were excluded, 285 patients received spironolactone, 282 doxazosin, 285 bisoprolol, and 274 p

47 lthy participants received the MR antagonist spironolactone (300 mg) or a placebo and underwent a str

48 sure than either bendroflumethiazide 5 mg or spironolactone 50 mg (P<0.005).

49 re traditional therapy were given amiloride, spironolactone, a combination of the two drugs, or place

50 Here we demonstrate that spironolactone, a mineralocorticoid receptor antagonist

51 Spironolactone, a nonselective mineralocorticoid recepto

52 ism, pharmacological inhibition of NER using spironolactone abolished SIRT2-mediated TC-NER activity

53 treating severe heart failure patients with spironolactone, acceptance of this drug was overwhelming

54 Spironolactone accounted for 99.4% of MRA use.

55 Last, spironolactone acutely lowered blood pressure, which was

56 arked vascular calcification, treatment with spironolactone allowed for replacement of calcification

57 erting-enzyme inhibitors, beta-blockers, and spironolactone) alone or in combination with cardiac-res

58 Spironolactone also modestly increased serum potassium l

59 Spironolactone also reduced the expression of osteoinduc

60 ar conditions for high-risk medications (eg, spironolactone, amiodarone).

61 0.55 [95% CI, -0.92 to -0.18] with high-dose spironolactone and -0.49 [95% CI, -0.98 to -0.14] with u

62 pg/mL among the group treated with high-dose spironolactone and 3753 (1968-7633) pg/mL among the grou

63 up, 131 patients completed therapy-64 taking spironolactone and 67 placebo.

64 Two doses each of spironolactone and bendroflumethiazide were compared.

65 -11.2%, P = 0.007) in the group assigned to spironolactone and by 16.8% (95% CI, -37.3%, +10.5%, P =

66 Cs, an effect inhibited by the MR antagonist spironolactone and by MR knock down with small interferi

67 There was a significant interaction of spironolactone and change in E/e' on VO2 (p = 0.039).

68 ence in home systolic blood pressure between spironolactone and each of the other two drugs.

69 Although steroidal antagonists such as spironolactone and eplerenone are clinically useful for

70 ineralocorticoid receptor antagonists (MRAs) spironolactone and eplerenone have proved valuable addit

71 eralocorticoid receptor antagonists, such as spironolactone and eplerenone that are used to treat sid

72 the mineralocorticoid receptor antagonists, spironolactone and eplerenone.

73 ving no or low-dose (12.5 mg or 25 mg daily) spironolactone and had NT-proBNP levels of 1000 pg/mL or

74 ar decreases in systolic blood pressure with spironolactone and HCTZ but not with placebo.

75 -EC adhesion, an effect that is inhibited by spironolactone and ICAM1 blocking antibody, supporting t

76 d from 12.7 (SD, 3.6) to 12.1 (SD, 3.7) with spironolactone and increased from 12.8 (SD, 4.4) to 13.6

77 One het group received spironolactone and lisinopril starting at 8 weeks of lif

78 Moreover, WRF (17% vs. 7% for spironolactone and placebo groups, p < 0.001) was associ

79 veraged home systolic blood pressure between spironolactone and placebo, followed (if significant) by

80 ence in home systolic blood pressure between spironolactone and the average of the other two active d

81 Physician education of the risks of spironolactone and the need for follow-up is essential.

82 The diuretics spironolactone and trichlormethiazide, but not amiloride

83 To assess the effect of high-dose spironolactone and usual care on N-terminal pro-B-type n

84 c therapy in approximately 70% and both oral spironolactone and vasodilators in approximately 90%, eu

85 alance calculation identified dexamethasone, spironolactone, and 6-alpha-methylprednisolone as major

86 before the widespread use of beta-blockers, spironolactone, and defibrillators-interventions known t

87 e treatment includes estrogens, finasteride, spironolactone, and gonadotropin-releasing hormone (GnRH

88 as they were abolished by the MR antagonist, spironolactone, and mimicked by the MR-agonist, aldoster

89 progesterone and the antihypertensive agent spironolactone, and the binding selectivity of cortisol

90 in both treatment arms, participants in the spironolactone arm had lower mortality rates at all pota

91 tion and those with WRF, particularly in the spironolactone arm, but the substantial net benefit of s

92 This study suggests Spironolactone as a new candidate for chemotherapy.

93 METHODS AND First, we identified spironolactone as a potent inhibitor of Panx1 in an unbi

94 The MR binds progesterone and spironolactone as antagonists in human MR but as agonist

95 he adequacy of monitoring patients receiving spironolactone as well as spironolactone's relationship

96 meeting enrollment criteria, 24.1% received spironolactone, as compared with 17.4% of those not meet

97 that the lamprey CR expresses an ancestral, spironolactone-as-agonist structural motif and that spir

98 cular mechanisms of action of finerenone and spironolactone at several key steps of the MR signaling

99 s these losses, whereas its combination with spironolactone attenuates these responses to prevent bon

100 patients in the patiromer group remained on spironolactone (between-group difference 19.5%, 95% CI 1

101 Spironolactone blocked the aldosterone-induced decrease

102 Central infusions of spironolactone blocked the increased intake of 1.8% sali

103 We recently discovered that spironolactone blocks EBV virion production by inhibitin

104 We found that spironolactone blunted the development of GJR and also p

105 ne or amiloride; plasma renin rose 4-fold on spironolactone but only 2-fold on bendroflumethiazide (P

106 oth the AT1 receptor blocker losartan and by spironolactone, but not by aldosterone synthase inhibiti

107 In conclusion, the addition of spironolactone, but not losartan, to a regimen including

108 urrent VT/VF and who were not candidates for spironolactone by current heart failure guidelines were

109 d by the ICD and who were not candidates for spironolactone by current heart failure guidelines, spir

110 Although spironolactone can act at the mineralocorticoid receptor

111 mineralocorticoid receptor via antagonists (spironolactone, canrenoate, and eplerenone) rescues GC-i

112 Since spironolactone causes degradation of xeroderma pigmentos

113 +/- 759 microg/24 h, respectively), whereas spironolactone co-treatment attenuated (p < 0.05) these

114 alt and ALDO/salt + furosemide, but not with spironolactone co-treatment.

115 less hyperkalemia and more hypokalemia with spironolactone compared with non-AAs and seemed to deriv

116 , mineralocorticoid receptor antagonism with spironolactone decreased aldosterone-mediated reactive o

117 ft ventricular ejection fraction assigned to spironolactone did not achieve a significant reduction i

118 lactone by current heart failure guidelines, spironolactone did not delay the first recurrence of VT/

119 preserved ejection fraction, treatment with spironolactone did not significantly reduce the incidenc

120 , non-AAs were more likely to attain maximal spironolactone dose (13.9% versus 5.8%; P=0.04) and had

121 Persistent spironolactone enablement in this population of patients

122 the vascular wall with MR antagonists (i.e., spironolactone, eplerenone) may therefore account for th

123 Raptor-small interfering RNA or treated with spironolactone/eplerenone, aldosterone or pulmonary arte

124 rticipants at 12 months, those randomized to spironolactone experienced greater reductions from basel

125 pitation assays revealed that, as opposed to spironolactone, finerenone inhibits MR, steroid receptor

126 f hyperkalemia in healthy young women taking spironolactone for acne is equivalent to the baseline ra

127 yperkalemia among healthy young women taking spironolactone for acne is unclear.

128 f hyperkalemia in healthy young women taking spironolactone for acne was calculated.

129 ring is unnecessary for healthy women taking spironolactone for acne.

130 perkalemia in 974 healthy young women taking spironolactone for acne.

131 spective study of healthy young women taking spironolactone for acne.

132 Many patients treated with spironolactone for CHF do not receive needed follow-up o

133 m, as has flutamide (250 mg) twice daily and spironolactone for more severe cases.

134 come occurred in 320 of 1722 patients in the spironolactone group (18.6%) and 351 of 1723 patients in

135 talized longer than those in the ramipril or spironolactone group (6.8+/-8.2 days vs. 5.7+/-3.2 days

136 7.8% in the ramipril group, and 25.9% in the spironolactone group (p=.95).

137 CFR improved with treatment in the spironolactone group as compared with the HCTZ group and

138 onth, mean potassium levels increased in the spironolactone group but not in the placebo group (4.54+

139 The spironolactone group showed improvement in exercise capa

140 e had a significantly lower incidence in the spironolactone group than in the placebo group (206 pati

141 tients in the placebo group, patients in the spironolactone group were extubated sooner after surgery

142 Adjusted mean changes in KCCQ for the spironolactone group were significantly better than thos

143 68.7% in the placebo group and 84.7% in the spironolactone group.

144 us did not ingest the aldosterone antagonist spironolactone had lower distal nephron H+ secretion (29

145 Spironolactone has been demonstrated to reduce heart fai

146 Spironolactone has been shown to be an effective treatme

147 Blockade of aldosterone with spironolactone has been shown to be particularly effecti

148 yocardial compliance attributed to fibrosis, spironolactone has not been shown to alter outcomes-perh

149 : 1.3 to 2.6) but not in those randomized to spironolactone (hazard ratio: 1.1, 95% confidence interv

150 st (aldosterone; EC50 1.3 nM) or antagonist (spironolactone; IC50 1.6 nM), and 53 gene expression dif

151 We further revealed that Spironolactone impairs Rad51 foci formation, sensitizes

152 We evaluated whether spironolactone improved congestion at 4 months and wheth

153 Spironolactone improved congestion compared with placebo

154 Treatment with spironolactone improved coronary microvascular function,

155 ment with heart failure drugs lisinopril and spironolactone improves skeletal muscle pathology in Duc

156 usion criteria and were randomly assigned to spironolactone in addition to double-blind treatment wit

157 Of TGW, 9 (38%) took spironolactone in addition to estradiol.

158 Potassium increased with spironolactone in non-AAs (4.29+/-0.5-4.55+/-0.49 mmol/L

159 endroflumethiazide, would be as effective as spironolactone in overcoming the Na+ retention and lower

160 end toward improvement in LS associated with spironolactone in patients enrolled in the Americas but

161 pressures during 12 months of treatment with spironolactone in patients with chronic HF with preserve

162 er patiromer to allow more persistent use of spironolactone in patients with chronic kidney disease a

163 However, the use of spironolactone in patients with chronic kidney disease c

164 We evaluated the effects of spironolactone in patients with heart failure and a pres

165 changes and possible clinical benefits with spironolactone in patients with heart failure and preser

166 The benefits of spironolactone in patients with heart failure with eithe

167 ning renal function (WRF) on the efficacy of spironolactone in patients with severe heart failure (HF

168 alemia was less likely in patients receiving spironolactone in the Americas with no significant treat

169 entify improvement in exercise capacity with spironolactone in the subset of patients with HFpEF with

170 lated with Raptor-small interfering RNA plus spironolactone in vivo, which decreased arteriole muscul

171 receptor antagonists, such as eplerenone and spironolactone, in improving blood pressure control in p

172 d mineralocorticoid receptor (MR) antagonist spironolactone indirectly and directly target MR.

173 Spironolactone induced reverse remodeling (left ventricu

174 Next, spironolactone inhibited alpha-adrenergic vasoconstricti

175 The mineralocorticoid receptor antagonist spironolactone inhibited AngII-induced increases in NADP

176 In addition, spironolactone inhibits expression of other SM-dependent

177 l capsid antigen is highly SM dependent, and spironolactone inhibits viral capsid antigen synthesis a

178 congestive heart failure (CHF) patients with spironolactone initiation after publication of RALES.

179 Spironolactone interacted with NYHA (P<0.001).

180 Spironolactone is an effective antihypertensive drug, es

181 We tested the hypothesis that spironolactone is associated with reduced mortality also

182 Spironolactone is effective at reducing blood pressure i

183 0 patients with diastolic heart failure with spironolactone is in its final phases of planning.

184 The use of spironolactone is inversely associated with fractures in

185 The antihypertensive benefit of spironolactone is not limited to patients with demonstra

186 e primary objective was to determine whether spironolactone is superior to placebo in improving diast

187 verse cardiovascular effects in CKD and that spironolactone is worthy of further study as a treatment

188 Intravitreal injections of spironolactone-loaded microspheres and systemic delivery

189 ffinity for the MR than either eplerenone or spironolactone, Ly caused no hyperkalemia.

190 The net benefits of spironolactone may be lower outside the clinical trial s

191 Although some data suggest that spironolactone might improve outcomes in these patients,

192 g intracerebroventricular infusion (10 d) of spironolactone (MR antagonist) or RU486 (GR antagonist).

193 previous systolic blood pressure response to spironolactone of > or = 20 mm Hg.

194 orgia, and there was no detectable impact of spironolactone on any outcomes.

195 essed effects of 12 months of treatment with spironolactone on biomarkers reflecting myocardial stres

196 rcise E/e' mediates the beneficial effect of spironolactone on exercise capacity.

197 s were randomly assigned to receive 25 mg of spironolactone once daily (n=213) or matching placebo (n

198 ension in the 10% hypomorphs is corrected by spironolactone or amiloride at doses that do not change

199 ommon in patients with RHTN, and addition of spironolactone or amiloride to the standard 3-drug antih

200 umethiazide to be less effective than either spironolactone or amiloride; plasma renin rose 4-fold on

201 Spironolactone or eplerenone prevented or reversed pulmo

202 ition of the mineralocorticoid receptor with spironolactone or eplerenone, which attenuated hypoxia-i

203 ificantly higher with the addition of either spironolactone or losartan.

204 seline and after 12 months of treatment with spironolactone or placebo were available in 204 patients

205 terone Antagonist (TOPCAT) and randomized to spironolactone or placebo.

206 e levels were not significantly altered with spironolactone or RU486 in either genotype.

207 hibitors or ARBs were randomized to continue spironolactone or to receive a matching placebo.

208 These effects were abrogated by spironolactone or vascular gene transfer of G6pd.

209 with or without dexamethasone (Dex), RU-486, spironolactone, or vehicle.

210 cologic blockade of aldosterone effects with spironolactone (percentage of lung occupied by metastasi

211 eceived (1) vehicle, (2) aldosterone, or (3) spironolactone plus aldosterone.

212 ps muscles from dystrophic mice treated with spironolactone plus lisinopril (IC50 0.1 nM) compared wi

213 Secondary measures included spironolactone prescriber profiles and potassium monitor

214 We assessed spironolactone prescriptions at hospital discharge in pa

215 Spironolactone prescriptions increased markedly after th

216 In rats with aldosteronism, spironolactone preserves skeletal strength.

217 The MR antagonists BR-4628 and spironolactone prevent these alterations.

218 erone (DHT), testosterone, R1881, estradiol, spironolactone, progesterone, and cortisol resulting in

219 haracteristics and achieved study drug dose, spironolactone reduced the combined end point of death o

220 Spironolactone reduced the total number of signs of cong

221 at the mineralocorticoid receptor antagonist spironolactone reduced vascular and soft tissue calcific

222 The use of spironolactone reduces left ventricular mass and improve

223 l mineralocorticoid receptor (MR) antagonist spironolactone reduces signs of CNV in patients refracto

224 ial was designed to test the hypothesis that spironolactone reduces the incidence of VT/VF in patient

225 The increase in CFR with spironolactone remained significant after controlling fo

226 Spironolactone restored beta-catenin-N-cadherin complexi

227 Compared with placebo, the use of spironolactone resulted in significant improvements in l

228 Spironolactone reversed interstitial fibrosis, attenuate

229 + hydrochlorothiazide (RSG+HCTZ), (4) RSG + spironolactone (RSG+SPIRO), and (5) discontinuation of R

230 patients receiving spironolactone as well as spironolactone's relationship to hyperkalemia.

231 ect due, at least in part, to stimulation of spironolactone-sensitive, PIT1-dependent osteoinductive

232 In six of the 285 patients who received spironolactone, serum potassium exceeded 6.0 mmol/L on o

233 In 30 subjects, 3 months of treatment with spironolactone significantly increased FMD (2.5+/-1.7 ve

234 terone was demonstrated by the evidence that spironolactone significantly reduced blood pressure and

235 rol with no further treatment (CONT; n = 6); spironolactone (SP) alone (200 mg/kg per d, by gavage, n

236 locorticoid and androgen receptor antagonist spironolactone (SP) was recently identified as an inhibi

237 Spironolactone (SP), an FDA approved aldosterone antagon

238 he potential of repurposing the FDA-approved spironolactone (SP), as one such drug.

239 Here, we found that spironolactone (SPIR), an FDA-approved diuretic drug wit

240 A separate group received spironolactone (Spiro), an aldosterone receptor antagoni

241 8.4 g once daily), in addition to open-label spironolactone (starting at 25 mg once daily) and their

242 ngiotensin receptor blockers, beta-blockers, spironolactone) stratified by socioeconomic circumstance

243 The superiority of spironolactone supports a primary role of sodium retenti

244 We studied the adoption of spironolactone therapy after publication of the Randomiz

245 The impact of spironolactone therapy on measures of cardiac structure

246 tone arm, but the substantial net benefit of spironolactone therapy remained.

247 Twelve to 18 months of spironolactone therapy was not associated with alteratio

248 rements obtained among young women receiving spironolactone therapy, yielding a hyperkalemia rate of

249 ntricular dysfunction who were randomized to spironolactone, titrated to 25 or 50 mg daily or placebo

250 sought to determine whether the addition of spironolactone to angiotensin-converting enzyme (ACE) in

251 However, in humans, the relationship of spironolactone to fractures is not known.

252 65 healthy young women taking and not taking spironolactone to obtain a profile for the baseline rate

253 an Aldosterone Antagonist; n=3445) comparing spironolactone to placebo for heart failure (for which s

254 The SPIronolactone to Reduce ICD Therapy (SPIRIT) trial was

255 Adding treatment with high-dose spironolactone to usual care for patients with AHF for 9

256 effects of aldosterone were reversed by both spironolactone treatment and PIT1 silencing and were mit

257 We derived propensity scores for spironolactone treatment based on 41 covariates.

258 lactone-as-agonist structural motif and that spironolactone treatment in vivo increases osmoregulator

259 Depletion of XPB protein, by spironolactone treatment or by siRNA transfection, inhib

260 , blockade of mineralocorticoid receptors by spironolactone treatment reversibly restored the elevate

261 4%, beta-blocker uptake from 12% to 41%, and spironolactone uptake from 3% to 20%.

262 ave been raised about the appropriateness of spironolactone use in some patients with heart failure.

263 Spironolactone use increased >7-fold (3.0% to 21.3% P<0.

264 rpose of this study was to determine whether spironolactone use is associated with fractures in men w

265 Spironolactone use was also associated with a shorter du

266 After adjustment for covariates, spironolactone use was inversely associated with total f

267 tervals of having a fracture associated with spironolactone use were estimated using conditional logi

268 spironolactone (100 mg) vs placebo or 25 mg spironolactone (usual care) daily for 96 hours.

269 is an ongoing randomized controlled trial of spironolactone versus placebo for heart failure with pre

270 Peak VO2 did not significantly change with spironolactone vs placebo (from 16.3 [SD, 3.6] mL/min/kg

271 ntrol procedure) and MR-availability (400 mg spironolactone vs. placebo) in a randomized, placebo-con

272 for propensity scores, the hazard ratio for spironolactone was 1.05 (95% confidence interval, 1.00-1

273 for propensity scores, the hazard ratio for spironolactone was 1.11 (95% confidence interval, 1.02-1

274 Use of spironolactone was an independent predictor of improved

275 Compared with placebo, spironolactone was associated with a similar risk of VT/

276 preserved ejection fraction patients, use of spironolactone was associated with an improvement in HF-

277 Treatment with spironolactone was associated with increased serum creat

278 ance of potassium and creatinine, the use of spironolactone was associated with less hypokalemia and

279 When spironolactone was given with dexamethasone, it did not

280 The absolute benefit of spironolactone was greatest in patients with reduced eGF

281 The treatment benefit of spironolactone was maintained at least until potassium e

282 tive prognosis, yet the mortality benefit of spironolactone was maintained.

283 Spironolactone was not associated with alterations in ca

284 lation of HF with reduced ejection fraction, spironolactone was not associated with reduced mortality

285 ot be generalizable, and eplerenone was, but spironolactone was not, studied in mild HF.

286 Spironolactone was prescribed to 22.8% of patients with

287 Spironolactone was reported by one prospective randomize

288 reduction in home systolic blood pressure by spironolactone was superior to placebo (-8.70 mm Hg [95%

289 However, spironolactone was the more effective natriuretic agent,

290 Spironolactone was the most effective add-on drug for th

291 Spironolactone was the most effective blood pressure-low

292 Finally, spironolactone was used to inhibit calcification in kl/k

293 of potassium levels on the effectiveness of spironolactone were assessed in a landmark analysis and

294 of these populations and their responses to spironolactone were explored.

295 Moreover, we showed that, in contrast to spironolactone, which activates the S810L mutant MR resp

296 ent with the aldosterone receptor antagonist spironolactone, which has been shown to diminish sudden

297 e mineralocorticoid receptor (MR) antagonist spironolactone, which significantly reduced sodium appet

298 led more patients to continue treatment with spironolactone with less hyperkalaemia.

299 trate that molecules structurally related to spironolactone with similar antimineralocorticoid blocki

300 used by excessive sodium retention, and that spironolactone would therefore be superior to non-diuret