Effect of rosuvastatin on low-density lipoprotein cholesterol in patients with hypercholesterolemia

Olsson, Anders; Pears, John; McKellar, John; Mizan, Jacques; Raza, Ali

doi:10.1016/s0002-9149(01)01727-1

Cited by 183 publications

(112 citation statements)

References 16 publications

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“…Statins also have beneficial effects on other lipid parameters, including increase in high-density lipoprotein cholesterol levels and decrease in triglyceride levels, and are predominantly metabolized by cytochrome P450 [14]. Mixture of Capryol 90: Maisine 35-1 and LAS as oil phase respectively has the capability to minimize variability in absorption as well as to avoid first pass metabolism of ROC as it could produce more uniform drug concentration in the systemic circulation and avoids first pass metabolism, which leads to improvement in bioavailability [15].…”

Section: Lipid Profilementioning

confidence: 99%

Development and Evaluation of Solid Self Nano- Emulsifying Formulation of Rosuvastatin Calcium for Improved Bioavailability

Kulkarni¹,

Ranpise²,

Mohan³

2015

Trop. J. Pharm Res

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Section: Lipid Profilementioning

confidence: 99%

Development and Evaluation of Solid Self Nano- Emulsifying Formulation of Rosuvastatin Calcium for Improved Bioavailability

Kulkarni¹,

Ranpise²,

Mohan³

2015

Trop. J. Pharm Res

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“…In clinical trials, rosuvastatin (1-80 mg) produced highly significant dose-dependent reductions in low-density lipoprotein cholesterol (up to 65%) and was welltolerated [1].…”

Section: Introductionmentioning

confidence: 99%

Lack of effect of ketoconazole on the pharmacokinetics of rosuvastatin in healthy subjects

Cooper

Martín

Dane

et al. 2003

Brit J Clinical Pharma

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Aims To examine in vivo the effect of ketoconazole on the pharmacokinetics of rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. Methods This was a randomized, double-blind, two-way crossover, placebocontrolled trial. Healthy male volunteers ( n = 14) received ketoconazole 200 mg or placebo twice daily for 7 days, and rosuvastatin 80 mg was coadministered on day 4 of dosing. Plasma concentrations of rosuvastatin, and active and total HMG-CoA reductase inhibitors were measured up to 96 h postdose. Results Following coadministration with ketoconazole, rosuvastatin geometric least square mean AUC(0, t ) and C max were unchanged compared with placebo (treatment ratios (90% confidence intervals): 1.016 (0.839, 1.230), 0.954 (0.722, 1.260), respectively). Rosuvastatin accounted for essentially all of the circulating active HMGCoA reductase inhibitors and most ( > 85%) of the total inhibitors. Ketoconazole did not affect the proportion of circulating active or total inhibitors accounted for by circulating rosuvastatin. Conclusions Ketoconazole did not produce any change in rosuvastatin pharmacokinetics in healthy subjects. The data suggest that neither cytochrome P450 3A4 nor P-gp-mediated transport contributes to the elimination of rosuvastatin.

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“…Miller et al concluded in their analysis that rosuvastatin proved to be more cost effective than atorvastatin, pravastatin or simvastatin 4) . Although these clinical benefits were demonstrated in Western patients treated with 10 to 40 mg of rosuvastatin, the dose-response data showed that reductions in LDL-C with 5 to 10 mg of rosuvastatin in Western populations were comparable to the LDL-C reductions achieved with 2.5 to 5 mg of rosuvastatin in the Japanese population 5,6) . This study was conducted to assess the efficacy of rosuvastatin 2.5 mg in moderate to high risk patients in achieving lipid targets defined for Japanese patients under the JAS Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases (2007), the guidelines most commonly referred to in clinical practice.…”

Section: Introductionmentioning

confidence: 90%

Effect of Rosuvastatin 2.5 mg on Achieving Lipid Goals Defined by the 2007 Japan Atherosclerosis Society Guidelines

Ohbayashi

2008

J Rural Med

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Objective: The aim of the study was to assess the effect of rosuvastatin 2.5 mg, an inhibitor of HMG-CoA reductase, on achieving lipid goals defined by the 2007 Japan Atherosclerosis Society guidelines. Subjects and Methods: Thirty-seven patients with moderate to high risk hypercholesterolemia (Mean age: 64.8 ± 8.4) were treated with 2.5 mg/day of rosuvastatin and their lipid and hepatic function parameters were measured at the baseline and at Weeks 4 and 8. Results: At 4 and 8 weeks after start of treatment, 74.1% and 92.6% of moderate risk patients, as well as 70% and 80% of high risk patients, achieved their LDL-C goals, respectively. In both moderate and high risk patients, the mean LDL-C/HDL-C ratio, which is considered as a prospective index for plaque regression, was significantly reduced (p<0.001 for both the moderate and high risk groups), and the mean LDL-C/HDL-C ratio decreased to less than 2 in moderate risk patients. No abnormal changes were observed in hepatic function tests during the study. Conclusion: More than 80% of moderate to high risk patients with hypercholesterolemia achieved their lipid goals and the mean LDL-C/HDL-C ratio was significantly reduced after the 8-week short treatment of rosuvastatin 2.5 mg, suggesting the clinical possibility of continuous use of rosuvastatin for plaque regression.

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Effect of rosuvastatin on low-density lipoprotein cholesterol in patients with hypercholesterolemia

Cited by 183 publications

References 16 publications

Development and Evaluation of Solid Self Nano- Emulsifying Formulation of Rosuvastatin Calcium for Improved Bioavailability

Development and Evaluation of Solid Self Nano- Emulsifying Formulation of Rosuvastatin Calcium for Improved Bioavailability

Lack of effect of ketoconazole on the pharmacokinetics of rosuvastatin in healthy subjects

Effect of Rosuvastatin 2.5 mg on Achieving Lipid Goals Defined by the 2007 Japan Atherosclerosis Society Guidelines

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