ライフサイエンスコーパス: rosuvastatin

1 hree substrates (TCA, estrone-3-sulfate, and rosuvastatin).

2 d atorvastatin, and with a limited effect by rosuvastatin.

3 role of Oatp1a1 in the renal reabsorption of rosuvastatin.

4 ations with higher doses of atorvastatin and rosuvastatin.

5 raction between coenzyme Q and the effect of rosuvastatin.

6 ues <103 pmol/l (868 pg/ml) may benefit from rosuvastatin.

7 in the presence of higher concentrations of rosuvastatin.

8 yrimidine precursor to the blockbuster drug, rosuvastatin.

9 tected between the 2 groups after 2 years of rosuvastatin.

10 placebo, followed by 12 weeks of open-label rosuvastatin.

11 cyte subsets were increased in PWH receiving rosuvastatin.

12 Acute kidney injury was more common with rosuvastatin.

13 rimary end point (hazard ratio of placebo to rosuvastatin, 0.87; 95% confidence interval, 0.77 to 0.9

14 mg lowered UPCR significantly more than did rosuvastatin 10 mg (-15.6%, 95% CI -28.3 to -0.5; p=0.04

15 Subjects received rosuvastatin 10 mg daily or placebo for 24 weeks.

16 ctivation or inflammation were randomized to rosuvastatin 10 mg daily or placebo for 96 weeks.

17 Rosuvastatin 10 mg daily reduces plasma cystatin C and s

18 occurred in 69 (60%) of 116 patients in the rosuvastatin 10 mg group versus 79 (64%) of 123 patients

19 enrolled 353 patients: 118 were assigned to rosuvastatin 10 mg, 124 to rosuvastatin 40 mg, and 111 t

20 astatin 80 mg, 1.02 (0.88-1.18; p=0.83) with rosuvastatin 10 mg, and 0.96 (0.83-1.11; p=0.53) with ro

21 assigned participants to atorvastatin 80 mg, rosuvastatin 10 mg, or rosuvastatin 40 mg for 52 weeks.

22 derate-dose statins (atorvastatin 20-<40 mg, rosuvastatin 10-<20 mg, simvastatin 40-<80 mg), and 12.9

23 re randomised equally to either receive oral rosuvastatin (10 mg once daily) or no intervention (cont

24 k who did not have cardiovascular disease to rosuvastatin (10 mg per day) or placebo and to candesart

25 The combination of rosuvastatin (10 mg per day), candesartan (16 mg per day

26 tudy, designed to investigate the effects of rosuvastatin (10 mg/daily) on markers of cardiovascular

27 vastatin, 40 mg/d; atorvastatin, 20 mg/d; or rosuvastatin, 10 mg/d) with or without evacetrapib, 100

28 ontrast, among the 8900 (50%) patients given rosuvastatin 20 mg (who had a median on-treatment LDL-ch

29 ated safe and effective LDL-C reduction with rosuvastatin 20 mg alone or added to ezetimibe and/or ap

30 ng Rosuvastatin) primary prevention trial of rosuvastatin 20 mg compared with placebo among men and w

31 LDL-C <130 mg/dl were randomly allocated to rosuvastatin 20 mg daily or placebo, and followed up for

32 cestry who were randomly allocated to either rosuvastatin 20 mg daily or placebo.

33 Individuals allocated to receive rosuvastatin 20 mg daily with baseline and on-treatment

34 isease or diabetes were randomly assigned to rosuvastatin 20 mg or placebo and followed up for up to

35 by a computer-generated sequence to receive rosuvastatin 20 mg per day or placebo, with participants

36 For 17,802 patients in the JUPITER trial, rosuvastatin 20 mg per day reduced the incidence of the

37 d, double-blind, 12-week, crossover study of rosuvastatin 20 mg versus placebo, followed by 12 weeks

38 high dose statins (atorvastatin 40-80 mg or rosuvastatin 20 mg), and low/medium dose statins (all ot

39 s at baseline and after random allocation to rosuvastatin 20 mg/d or placebo were associated with fir

40 tatin) before and after random allocation to rosuvastatin 20 mg/d or placebo, with outcomes reported

41 atin (JUPITER) trial before randomization to rosuvastatin 20 mg/d or placebo.

42 (CVD) before and after random allocation to rosuvastatin 20 mg/d or placebo.

43 tatins included atorvastatin 40 or 80 mg and rosuvastatin 20 or 40 mg.

44 y statins included atorvastatin 40 to 80 mg, rosuvastatin 20 to 40 mg, and simvastatin 80 mg.

45 ed high-dose statins (atorvastatin 40-80 mg, rosuvastatin 20-40 mg, simvastatin 80 mg), 28.6% moderat

46 Patients were then switched to rosuvastatin (20 mg/d), and a follow-up 12/24-hour PK in

47 Twelve months of rosuvastatin (20 mg/day) did not change cholesterol effl

48 els of 2.0 mg per liter or higher to receive rosuvastatin, 20 mg per day, or placebo.

49 in prescription (atorvastatin, 40-80 mg, and rosuvastatin, 20-40 mg) within 30 days of discharge.

50 oma multiplicity by 76% compared to low-dose Rosuvastatin (29%) and DFMO (46%), suggesting additive e

51 (-15.6%, 95% CI -28.3 to -0.5; p=0.043) and rosuvastatin 40 mg (-18.2%, -30.2 to -4.2; p=0.013).

52 </=0.8) nontarget lesion (NTL) to intensive (rosuvastatin 40 mg daily) or standard-of-care lipid-lowe

53 o atorvastatin 80 mg, rosuvastatin 10 mg, or rosuvastatin 40 mg for 52 weeks.

54 ts with and without DM (non-DM) who received rosuvastatin 40 mg for 8-12 weeks and underwent intracor

55 group versus 79 (64%) of 123 patients in the rosuvastatin 40 mg group versus 63 (57%) of 110 patients

56 ary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months.

57 were assigned to rosuvastatin 10 mg, 124 to rosuvastatin 40 mg, and 111 to atorvastatin 80 mg; of th

58 tin 10 mg, and 0.96 (0.83-1.11; p=0.53) with rosuvastatin 40 mg.

59 and stratified by hospital to receive either rosuvastatin (40 mg loading dose and then 20 mg daily un

60 e strategy were randomly assigned to receive rosuvastatin (40 mg on admission, followed by 20 mg/day;

61 g]) or high-intensity (atorvastatin [80 mg], rosuvastatin [40 mg]) statin.

62 nt with either atorvastatin, 80 mg daily, or rosuvastatin, 40 mg daily, to compare the effect of thes

63 (maximal: atorvastatin calcium, 80 mg/d, or rosuvastatin, 40 mg/d; submaximal: all other dosages).

64 torvastatin [10 mg], simvastatin [40 mg], or rosuvastatin [5 mg]) or high-intensity (atorvastatin [80

65 Prevention: An Intervention Trial Evaluating Rosuvastatin), a randomized primary prevention trial tha

66 For rosuvastatin, a cholesterol-lowering drug and OATP1A/1B

67 igher level of HDL cholesterol achieved with rosuvastatin, a similar degree of regression of PAV was

68 Treatment of Nf1(+/-) mice with rosuvastatin, a stain with anti-inflammatory properties,

69 Among 3386 rosuvastatin-allocated individuals, both CRP and LDL-C l

70 Among rosuvastatin-allocated individuals, on-treatment HDL-P h

71 Among rosuvastatin-allocated individuals, on-treatment HDL-P r

72 gh-sensitivity C-reactive protein >/=2 mg/l, rosuvastatin-allocated participants attaining LDL-C <50

73 litus were not significantly different among rosuvastatin-allocated participants with and without LDL

74 This is the first report on Rosuvastatin alone or combination strategy using clinica

75 rosuvastatin or 20 mg atorvastatin or 10 mg rosuvastatin alone.

76 f 2 mg/L or more benefit from treatment with rosuvastatin, although absolute rates of cardiovascular

77 /-SD) ventilator-free days (15.1+/-10.8 with rosuvastatin and 15.1+/-11.0 with placebo, P=0.96).

78 in 60-day in-hospital mortality (28.5% with rosuvastatin and 24.9% with placebo, P=0.21) or in mean

79 or diabetes were met by 1 participant in the rosuvastatin and 3 in the placebo arm by week 96.

80 fferent cholesterol lowering abilities, with rosuvastatin and atorvastatin being the most effective,

81 Maximal doses of rosuvastatin and atorvastatin resulted in significant re

82 treatment, animals were fed diets containing Rosuvastatin and difluromethylornithine (DFMO) individua

83 (per 100 person-years) in JUPITER women for rosuvastatin and placebo (0.57 and 1.04, respectively) w

84 .99 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ra

85 Although the median change in Lp(a) with rosuvastatin and placebo was zero, rosuvastatin nonethel

86 In contrast, rosuvastatin and simvastatin significantly reduced total

87 ticipants assigned to combined therapy (with rosuvastatin and the two antihypertensive agents) with t

88 DFMO, Rosuvastatin and/or combinations significantly decreased

89 three different statin drugs (atorvastatin, rosuvastatin, and fluvastatin).

90 reported by five participants randomised to rosuvastatin, and one serious adverse event in each grou

91 ding, atorvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin.

92 ariant toward substrates estrone sulfate and rosuvastatin are similar to the well characterized full-

93 lacebo arm (HR, 1.35; 95% CI, 1.03-1.76) and rosuvastatin arm (HR, 1.60; 95% CI, 1.27-2.03).

94 ebo arm was 1.99 (95% CI, 1.64-2.42); in the rosuvastatin arm, 2.06 (95% CI, 1.74-2.43).

95 not a clinical diagnosis of diabetes in the rosuvastatin arm.

96 aimed to assess the lipid-lowering effect of rosuvastatin as compared with fluvastatin in RTR receivi

97 marginally improved among those allocated to rosuvastatin as compared with placebo.

98 ase and were at intermediate risk to receive rosuvastatin at a dose of 10 mg per day or placebo.

99 Treatment with rosuvastatin at a dose of 10 mg per day resulted in a si

100 torvastatin 80 mg daily and atorvastatin and rosuvastatin at doses equivalent to simvastatin 20 mg da

101 ive cardiac surgery to receive perioperative rosuvastatin (at a dose of 20 mg daily) or placebo.

102 Even the most efficacious statin, rosuvastatin, at its highest dose has not achieved such

103 Mean rosuvastatin AUC0-24 was 157+/-61.7 ng*h/mL, approximate

104 Prevention: An Intervention Trial Evaluating Rosuvastatin) before and after random allocation to rosu

105 n patients receiving 10 mg TA-8995 and 10 mg rosuvastatin by 157.5%.

106 nsporters increases the systemic exposure of rosuvastatin by reducing its hepatic extraction ratio.

107 ed secondary aim was to assess the effect of rosuvastatin calcium on T2DM.

108 Rosuvastatin calcium, 20 mg/d, or placebo.

109 The PROteKT study tested the hypothesis that rosuvastatin can inhibit aminoglycoside-induced nephroto

110 urpose of this study is to determine whether rosuvastatin can reduce the proinflammatory response ind

111 els and the absence of efficient alternative rosuvastatin clearance mechanisms.

112 nd ABCG2 c.421C>A (P<0.01) were important to rosuvastatin concentration (adjusted R(2)=0.56 for the f

113 Finally a rosuvastatin (Crestor(R)) intermediate is produced using

114 All subjects received 40 mg of rosuvastatin daily for 8 to 12 weeks, when the nonculpri

115 assigned in a 1:1 ratio to receive 20 mg of rosuvastatin daily or placebo.

116 METHODS AND We compared 10 mg rosuvastatin daily with placebo in patients with ischemi

117 Rosuvastatin did not lead to any changes in levels of T-

118 rmacokinetic (PK) interaction potential of a rosuvastatin/everolimus combination in RTR.

119 preventive measures on-admission, high-dose rosuvastatin exerts a protective effect against contrast

120 Rosuvastatin exhibits anti-inflammatory effects and redu

121 combination with other risk factors received rosuvastatin for 2 years, starting at 5 mg once daily, w

122 Treatment with rosuvastatin for 3 months yielded diminished macrophage

123 interaction between hs-CRP and the effect of rosuvastatin for most end points whereby rosuvastatin tr

124 ents: 63.2% with atorvastatin and 68.5% with rosuvastatin for PAV (P=0.07) and 64.7% and 71.3%, respe

125 n JUPITER (N = 8,749), a randomized trial of rosuvastatin for primary prevention of CVD, component GR

126 already receiving fluvastatin, switching to rosuvastatin further decreased LDL cholesterol and total

127 High-dose rosuvastatin given on admission to statin-naive patients

128 rates of pulmonary embolism were 0.09 in the rosuvastatin group and 0.12 in the placebo group (hazard

129 e occurred in 235 participants (3.7%) in the rosuvastatin group and in 304 participants (4.8%) in the

130 (occurring in 277 participants [4.4%] in the rosuvastatin group and in 363 participants [5.7%] in the

131 ion did not differ significantly between the rosuvastatin group and the placebo group (21.1% and 20.5

132 After 104 weeks of therapy, the rosuvastatin group had lower levels of LDL cholesterol t

133 ein cholesterol level was 26.5% lower in the rosuvastatin group than in the placebo group.

134 At 6 months, 19 (36%) of 53 patients in the rosuvastatin group versus 29 (38%) of 77 in the placebo

135 f days with delirium was 34% (SD 30%) in the rosuvastatin group versus 31% (29%) in the placebo group

136 In the rosuvastatin group, there was no excess of diabetes or c

137 placebo group but little association in the rosuvastatin group.

138 n-years in the placebo group (n = 8,150) and rosuvastatin groups without LDL-C <50 mg/dl (n = 4,000)

139 L <130 mg/dl and hs-CRP levels >/= 2.0 mg/l, rosuvastatin had an incremental cost-effectiveness of $2

140 he effect of statins by type of statin, with rosuvastatin having the lowest risk on venous thromboemb

141 atory endothelial responses are regulated by rosuvastatin in a mechanism that appears to involve KLF2

142 in cholesterol (LDL-C) levels <50 mg/dl with rosuvastatin in apparently healthy adults in the JUPITER

143 Study to Evaluate the Efficacy and Safety of Rosuvastatin in Children and Adolescents With Homozygous

144 g trial to assess the efficacy and safety of rosuvastatin in children with FH aged 6 to 17 years, we

145 Effect of rosuvastatin in expression of the atheroprotective facto

146 rosclerosis and Treating Unhealthy Bone With Rosuvastatin in HIV (SATURN-HIV) trial is a randomized,

147 rosclerosis and Treating Unhealthy Bone With Rosuvastatin in HIV (SATURN-HIV) trial randomized 147 pa

148 mporary heart failure trials, the Controlled Rosuvastatin in Multinational Trial Heart Failure (CORON

149 onal studies, this trial shows no benefit of rosuvastatin in reducing delirium in intensive care or c

150 Rosuvastatin in situ gel (1.2%), when delivered locally

151 Prevention: an Intervention Trial Evaluating Rosuvastatin) individuals and clinical outcomes of indiv

152 n, genome-wide significant associations with rosuvastatin-induced change in Lp-PLA(2) activity were o

153 ed with LDL-C reduction were associated with rosuvastatin-induced CRP change after multiple testing c

154 The genetic determinants of rosuvastatin-induced CRP reduction differ from, and are

155 ct correlated with a significant increase of rosuvastatin-induced KLF2.

156 Neither variant was associated with rosuvastatin-induced LDL-C reduction or with CRP reducti

157 f, the major pharmacogenetic determinants of rosuvastatin-induced LDL-C reduction.

158 treatment by demonstrating that benefit from rosuvastatin is as strongly related to genetic risk from

159 Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) and performed replication in a me

160 Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) and synthesized the results with

161 Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) participants, we tested whether l

162 Prevention: an intervention Trial Evaluating Rosuvastatin (JUPITER) reignited attention on the link b

163 Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial (NCT00239681).

164 Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial before randomization to ros

165 Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial of rosuvastatin users ident

166 Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial.

167 Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), HDL size and HDL-P were measured

168 Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), to a target population of trial-

169 ative uptake transporters at higher systemic rosuvastatin levels and the absence of efficient alterna

170 cal variables to avoid high atorvastatin and rosuvastatin levels is described; further study will det

171 Rosuvastatin lowered low-density lipoprotein cholesterol

172 interquartile range] age, 66 [60-71] years), rosuvastatin lowered the levels of LDL particles (-39.6%

173 Despite high-dose rosuvastatin lowering plasma lipid concentrations to a g

174 12.9% low-dose statins (atorvastatin <20 mg, rosuvastatin <10 mg, simvastatin <40 mg).

175 els, and therefore, a more potent agent like rosuvastatin maybe needed.

176 Prevention: An Intervention Trial Evaluating Rosuvastatin], minor allele frequency=0.018) was used to

177 heart failure enrolled in CORONA (Controlled Rosuvastatin Multinational Study in Heart Failure) and r

178 in a population with HF from the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORON

179 onths in patients enrolled in the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORON

180 and prognosis measured in CORONA (Controlled Rosuvastatin Multinational Trial in Heart Failure), coul

181 Mortality and Morbidity], CORONA [Controlled Rosuvastatin Multinational Trial in Heart Failure], and

182 n a subgroup of patients from the Controlled Rosuvastatin Multinational Trial in HF (CORONA) study.

183 HARM-Added HF-REF trials, and the Controlled Rosuvastatin Multinational Trial in HF-REF (CORONA).

184 Primary outcome data was available for 88% (rosuvastatin n = 20, control n = 24).

185 Fifty (rosuvastatin n = 23, control n = 27) participants were r

186 n=777) or > or = 2.0 mg/L (placebo, n=1694; rosuvastatin, n=1711).

187 protein (hs-CRP) <2.0 mg/L (placebo, n=779; rosuvastatin, n=777) or > or = 2.0 mg/L (placebo, n=1694

188 p(a) with rosuvastatin and placebo was zero, rosuvastatin nonetheless resulted in a small but statist

189 Rosuvastatin not alter plasma levels of IL-6, soluble (s

190 assessed the effect of 2-year treatment with rosuvastatin on carotid IMT in children with HeFH.

191 20 mg atorvastatin; 10 mg TA-8995 plus 10 mg rosuvastatin or 20 mg atorvastatin or 10 mg rosuvastatin

192 nalysis of splenic NK cells exposed to DFMO, Rosuvastatin or combination resulted in an increase of N

193 esponse of LDL subfractions and non-HDL-C to rosuvastatin or placebo for 1 year among 7046 participan

194 randomly assigned to receive either enteral rosuvastatin or placebo in a double-blind manner.

195 an ancestry randomly allocated to 20 mg/d of rosuvastatin or placebo in the JUPITER trial.

196 rotein >/=2 mg/L) were randomized to receive rosuvastatin or placebo.

197 emic systolic HF) randomly assigned to 10 mg rosuvastatin or placebo.

198 lesterol </=130 mg/dL to blinded 10 mg daily rosuvastatin or placebo.

199 rome, current treatment with atorvastatin or rosuvastatin or simvastatin, hepatitis C virus infection

200 n and by 1.22% (95% CI, -1.52 to -0.90) with rosuvastatin (P=0.17).

201 ed IL-6 and IL-8 production was inhibited by rosuvastatin, particularly at higher doses.

202 atorvastatin, and by 63.3% in patients given rosuvastatin plus 10 mg TA-8995 (p<0.0001).

203 Low-dose Rosuvastatin plus DFMO suppressed colon adenocarcinoma m

204 The patient responded modestly to maximum rosuvastatin plus ezetimibe therapy, even in combination

205 ITER-based strategy becomes cost-saving at a rosuvastatin price of < $0.86 per day.

206 Prevention-an Intervention Trial Evaluating Rosuvastatin) primary prevention trial of rosuvastatin 2

207 o and 396 mg/dl (range: 130 to 700 mg/dl) on rosuvastatin, producing a mean 85.4 mg/dl (22.3%) differ

208 ither confirm nor refute the hypothesis that rosuvastatin protects against aminoglycoside nephrotoxic

209 Atorvastatin and rosuvastatin provided net benefit at lower 10-year risks

210 Rosuvastatin reduced coenzyme Q but there was no interac

211 Rosuvastatin reduced coenzyme Q, but even in patients wi

212 ITER demonstrated that in primary prevention rosuvastatin reduced CVD events in women with a relative

213 ne low-density lipoprotein was the same, and rosuvastatin reduced low-density lipoprotein by 47% in b

214 Rosuvastatin reduces by more than half the incidence of

215 Rosuvastatin reduces first cardiovascular events and all

216 high-sensitivity C-reactive protein levels, rosuvastatin reduces the incidence of major cardiovascul

217 The JUPITER trial found that rosuvastatin reduces vascular events in apparently healt

218 Rosuvastatin renal clearance, although still minor, was

219 Rosuvastatin (RSV) and atorvastatin (ATV) are known to i

220 Rosuvastatin (RSV) and atorvastatin (ATV) have shown bon

221 ffectiveness of subgingivally delivered 1.2% rosuvastatin (RSV) gel incorporated into a methylcellulo

222 Rosuvastatin (RSV) is a new synthetic, second-generation

223 In this study, we investigated the effect of rosuvastatin (RSV) on atherogenesis in Apolipoprotein E-

224 Conversely, administration of rosuvastatin (RSV) to hamsters increased hepatic Acsl1 e

225 Hypolipidemic statin drugs, particularly rosuvastatin (RSV), are known to be associated with alve

226 The combination of everolimus/rosuvastatin seems to be as safe as the everolimus/fluva

227 Rosuvastatin showed a superior lipid-lowering effect com

228 Similarly, rosuvastatin showed benefits on biomarkers but not on ph

229 Rosuvastatin significantly reduced incident cardiovascul

230 In this trial of apparently healthy persons, rosuvastatin significantly reduced the occurrence of sym

231 In intervention studies, therapy with rosuvastatin significantly reduced venous thromboembolis

232 Prevention: An Intervention Trial Evaluating Rosuvastatin]), statin therapy led to a greater relative

233 Prevention: An Intervention Trial Evaluating Rosuvastatin) study reduced cardiovascular events among

234 r surgery were lower in patients assigned to rosuvastatin than in those assigned to placebo (P<0.001)

235 heroma volume (TAV), was more favorable with rosuvastatin than with atorvastatin: -6.39 mm(3) (95% CI

236 activity at baseline and after 12 months of rosuvastatin therapy (20 mg/d) among 6851 participants o

237 Seventy-two participants were randomized to rosuvastatin therapy and 75 to placebo.

238 Rosuvastatin therapy did not improve clinical outcomes i

239 Rosuvastatin therapy did not result in beneficial effect

240 Rosuvastatin therapy in the JUPITER (Justification for t

241 The impact of 48 weeks of rosuvastatin therapy on inflammation and immune activati

242 Twenty-four weeks of rosuvastatin therapy significantly decreased the level o

243 Compared with placebo, rosuvastatin therapy was associated with significantly g

244 We hypothesized that rosuvastatin therapy would improve clinical outcomes in

245 Rosuvastatin therapy, as compared with placebo, was asso

246 ociated with incident T2DM, including during rosuvastatin therapy.

247 null, and ranged from 0.21 (0.02, 2.82) for rosuvastatin to 2.16 (0.06, 75.0) for gemfibrozil.

248 Use of rosuvastatin to prevent cardiovascular disease may reduc

249 per 100 patient-years of follow-up) and 498 rosuvastatin-treated (12.2 per 100 patient-years of foll

250 per 100 patient-years of follow-up) and 532 rosuvastatin-treated (12.6 per 100 patient-years) patien

251 -treated (8.3 per 100 patient-years) and 192 rosuvastatin-treated (9.7 per 100 patient-years) patient

252 per 100 patient-years of follow-up) and 188 rosuvastatin-treated (9.8 per 100 patient-years of follo

253 Signal changes in rosuvastatin-treated rabbits correlated with reduced mac

254 +)) monocytes (-38.8% vs -11.9%, P = .04) in rosuvastatin-treated vs placebo-treated subjects.

255 Rosuvastatin treatment effectively lowered markers of mo

256 Rosuvastatin treatment for 2 years resulted in significa

257 Rosuvastatin treatment for JUPITER-eligible patients app

258 We compared: 1) hs-CRP testing followed by rosuvastatin treatment for patients with hs-CRP levels >

259 The increased incidence of diabetes with rosuvastatin treatment in Justification for the Use of S

260 Rosuvastatin treatment prevented leukostasis when both r

261 mized primary prevention trial that compared rosuvastatin treatment to placebo in individuals with no

262 of rosuvastatin for most end points whereby rosuvastatin treatment was associated with better outcom

263 in patients with a low baseline coenzyme Q, rosuvastatin treatment was not associated with a signifi

264 imus AUC0-12 was not affected by concomitant rosuvastatin treatment, 80.3+/-21.3 mug*h/L before and 7

265 Prevention: an Intervention Trial Evaluating Rosuvastatin trial, the 'C' category representing 'chole

266 adding children and adults from a prior HoFH rosuvastatin trial.

267 Prevention: an Intervention Trial Evaluating Rosuvastatin) trial data demonstrate that statins reduce

268 Prevention: an Intervention Trial Evaluating Rosuvastatin) trial results into clinical practice.

269 Prevention: An Intervention Trial Evaluating Rosuvastatin) trial were adults without diabetes or CVD,

270 rogression Observation: Measuring Effects of Rosuvastatin) trial.

271 Prevention: an Intervention Trial Evaluating Rosuvastatin) trial.

272 l Evaluating Rosuvastatin (JUPITER) trial of rosuvastatin users identified a sub-genome-wide associat

273 take transporters on the pharmacokinetics of rosuvastatin using wild-type and Oatp1a/1b-null mice.

274 eroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial in

275 ssing mortality and ventilator-free days for rosuvastatin versus placebo for patients with sepsis-ass

276 ous adverse event among older persons in the rosuvastatin versus placebo group was 1.05 (CI, 0.93 to

277 thors sought to assess the LDL-C efficacy of rosuvastatin versus placebo in HoFH children, and the re

278 protein cholesterol <130 mg/dL randomized to rosuvastatin versus placebo.

279 developed diabetes during follow-up (270 on rosuvastatin vs 216 on placebo; HR 1.25, 95% CI 1.05-1.4

280 abetes by 5.4 weeks (84.3 [SD 47.8] weeks on rosuvastatin vs 89.7 [50.4] weeks on placebo).

281 Among those with moderate CKD, rosuvastatin was associated with a 45% reduction in risk

282 Rosuvastatin was equally effective in preventing a first

283 Rosuvastatin was not associated with an increased incide

284 tration (15 mg/kg), intestinal absorption of rosuvastatin was not impaired in Oatp1a/1b-null mice, bu

285 up 12/24-hour PK investigation of everolimus/rosuvastatin was performed after 1 month.

286 Whilst no protective effect of rosuvastatin was seen, there was a lower than expected l

287 he magnitude of relative risk reduction with rosuvastatin was similar among participants with high or

288 The biliary excretion of rosuvastatin was very fast, with 60% of the dose elimina

289 After 24 weeks of rosuvastatin, we found significant decreases in plasma l

290 Median LDL-C reductions on rosuvastatin were 40, 48, 51, 55, 60, and 64 mg/dL, resp

291 If the effectiveness of rosuvastatin were 50% of that observed in JUPITER, the i

292 Pravastatin and rosuvastatin were associated with reduced Alzheimer dise

293 post-hoc analysis, participants allocated to rosuvastatin were categorized as to whether or not they

294 te reductions in event rates associated with rosuvastatin were greater in older persons.

295 ciation (P<5x10(-8)) with LDL-C reduction on rosuvastatin were identified at ABCG2, LPA, and APOE, an

296 n total, 299 patients taking atorvastatin or rosuvastatin were prospectively recruited at an outpatie

297 well as side effect profiles associated with rosuvastatin were similar among those with and without C

298 The benefits of rosuvastatin were substantial and consistent regardless

299 ared with placebo, participants allocated to rosuvastatin who achieved LDL cholesterol less than 1.8

300 taking the highest doses of atorvastatin or rosuvastatin, with an overall AE profile similar to plac