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Crestor (Rosuvastatin)

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Crestor is a high-quality medication which is taken for the treatment of high level of cholesterol. This remedy is acting by slowing the production of cholesterol in the body. It is HMG-CoA reductase inhibitor (statin).

Other names for this medication:

Similar Products:
Altocor, Altoprev, Lescol, Mevacor, Pravachol, Crestor, Lipitor, Livalo, Zocor, Baycol, Lescol XL


Also known as:  Rosuvastatin.


Crestor is indicated to treat high level of cholesterol.

This remedy is acting by slowing the production of cholesterol in the body.

Crestor is also known as Rosuvastatin calcium, Rosuvas, Rozavel.

Crestor is HMG-CoA reductase inhibitor (statins).


Take Crestor tablets orally with or without food.

Do not crush or chew it.

Take Crestor once a day at the same time every day with water.

If you want to achieve most effective results do not stop taking Crestor suddenly.


If you overdose Crestor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Crestor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Crestor if you are allergic to Crestor components.

Do not take Crestor if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Crestor if you suffer from or have a history of liver, thyroid or kidney disease.

Be careful with Crestor if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Crestor if you have allergies to medicines, foods, or other substances.

Do not eat fattening food that is high in cholesterol.

Use Crestor with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Do not stop taking Crestor suddenly.

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Prospective follow-up evaluation of the ARDS Clinical Trials Network Statins for Acutely Injured Lungs from Sepsis trial of rosuvastatin versus placebo in 568 mechanically ventilated patients with sepsis-associated ARDS, with blinded 6-month outcome assessment performed in the 272 eligible survivors for age-adjusted and sex-adjusted 36-Item Short Form Health Survey (SF-36) physical function and mental health domains, and in 84 eligible survivors for the 6 min walk test, along with secondary outcomes evaluations of survival, and additional patient-reported and performance-based measures at 6-month and 12-month follow-up.

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Simultaneous and spontaneous bilateral quadriceps tendon rupture is an uncommon injury that is usually seen in association with multiple medical conditions and some medications. We report a case of simultaneous and spontaneous bilateral quadriceps tendon rupture that may be related to the long-term use of a statin.

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These data show that the use of rosuvastatin plus a standard HF therapy results in a significant additional improvement in HF and cardiac remodelling in a rat model of HFpEF. These beneficial effects were independent of BP and plasma lipid changes, and seem to be due, at least in part, to decreased myocardial inflammation.

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To compare the cost-effectiveness of rosuvastatin 10 mg and atorvastatin 10 mg in lowering LDL-C and achieving guideline goals after 12 weeks of treatment. The LDL-C goals were those recommended by the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III and the Third Joint European Task Force.

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This study shows that gene expression analysis together with bioinformatics pathway analysis has the potential to help predict and identify drug combination-specific complementary and side effects.

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Although the difference in PCSK9 between 2 groups was transient, that in both campesterol and lathosterol persisted until 52 weeks. These results demonstrated simultaneous inhibition of cholesterol absorption and synthesis provides stable and greater decrease in LDL-C levels.

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This prospective, open-label pilot study was conducted in consecutively referred male and female patients aged 38 to 80 years with primary high LDL-C (mean, 177 mg/dL) at The Cholesterol Center, Jewish Hospital, Cincinnati, Ohio. Patients were instructed in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) therapeutic lifestyle changes diet. Rosuvastatin 5 mg/d was administered to patients categorized by NCEP ATP III risk stratification as moderately high risk, and rosuvastatin 10 mg/d was administered to patients categorized as high or very high risk. End points included acceptability (assessed using patient-initiated discontinuation of rosuvastatin), effectiveness (absolute and percentage reductions in LDL-C and triglycerides), and safety profile (aspartate and alanine aminotransferases [AST and ALT, respectively] >3 times the laboratory upper limit of normal [xULN] or elevations in creatine kinase [CK]>10xULN).

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In patients with mild to moderate aortic stenosis due to a BAV, the presence of Type I valve orientation was associated with significantly greater aortic root parameters compared to Type II valve orientation.

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The incremental prognostic value of high-sensitive troponin T (hs-cTnT) in heart failure (HF) beyond that of high-sensitivity C-reactive protein and amino-terminal probrain natriuretic peptide is debated. We examined the prognostic value of hs-cTnT in a subgroup of patients from the Controlled Rosuvastatin Multinational Trial in HF (CORONA) study.

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The purpose of this study is to compare the cost-effectiveness of the most commonly prescribed statins in Canada with respect to 1) lowering low-density lipoprotein cholesterol level (LDL-C) and 2) achieving National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) LDL-C goal.

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Our data documented leukocyte recruitment prior to lipid accumulation and subsequent inhibition by rosuvastatin. The underlying mechanism seemed to involve oxidative stress and an anti-inflammatory effect on the endothelium of atheroprone vessels.

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In a prospective pharmacokinetic drug interaction study, six HIV-seronegative, healthy adult volunteers received single 10-mg doses of RSV at baseline and after 6 days of ATV/RTV and FPV/RTV, with 6-day washout periods. Plasma concentrations of RSV and its metabolites, N-desmethyl-RSV and RSV-lactone, were measured by using a internally validated tandem mass spectrometric (LC-MS/MS) method over 24 hours.

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The healthy endothelium plays a key roll in vascular regulation. This function can be examined non-invasively by use of B-mode ultrasound on the brachial artery. The aim of this study was to measure the effect of low-dose and high-dose lipid-lowering treatment with rosuvastatin on the endothelial function evaluated with endothelium-dependent and endothelium-independent flow-mediated dilatation (FMD).

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With cardiovascular disease being the leading cause of morbidity and mortality in the United States, cholesterol-lowering medications have become a prominent focus of medical management and cardiovascular risk reduction, including the use of statins making them the most widely prescribed class of medications in the United States and are the cornerstone of management of hyperlipidemia. This case report describes a 29-year-old female with probable familial hypercholesterolemia (FH) who had allergic reactions to statin therapy on two separate occasions. She required statin therapy based on her elevated carotid intima media thickness test, historic LDL-C ≥ 190 mg/dL, elevated Lp(a), and family history significant for premature coronary heart disease. In this report, we document a case of successful oral desensitization to rosuvastatin and propose a replicable statin desensitization protocol.

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Vascular lesion development initiated by endothelial cell damage is moderated by bone marrow-derived progenitor cells. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibition promotes bone marrow-dependent reendothelialization and diminishes vascular lesion development. These findings may help to establish novel pathophysiological concepts and therapeutic strategies in the treatment of various cardiovascular diseases.

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The trial was flawed. It was discontinued (according to prespecified rules) after fewer than 2 years of follow-up, with no differences between the 2 groups on the most objective criteria. Clinical data showed a major discrepancy between significant reduction of nonfatal stroke and myocardial infarction but no effect on mortality from stroke and myocardial infarction. Cardiovascular mortality was surprisingly low compared with total mortality-between 5% and 18%-whereas the expected rate would have been close to 40%. Finally, there was a very low case-fatality rate of myocardial infarction, far from the expected number of close to 50%. The possibility that bias entered the trial is particularly concerning because of the strong commercial interest in the study.

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One hundred sixty candidate single-nucleotide polymorphisms for effects on circulating lipid levels or statin-induced LDL-cholesterol lowering were tested for association with response of LDL subfractions and non-HDL-C to rosuvastatin or placebo for 1 year among 7046 participants from the Justification for Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial. Of the 51 single-nucleotide polymorphisms associated with statin response for ≥ 1 of the LDL subfractions or non-HDL-C, 20 single-nucleotide polymorphisms could be clustered according to effects predominantly on LDL particle size, predominantly on LDL particle number, and on apolipoprotein B but not on LDL cholesterol or non-HDL-C.

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Serial intravascular ultrasound (IVUS) was used to compare the effects of moderate doses of rosuvastatin and atorvastatin on plaque regression in patients with intermediate coronary stenosis.

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One hundred and four patients with ACS were recruited and randomly assigned into two groups: one was statin group (n = 52), given atorvastatin (20 mg QN) or other statins with equivalent dosages; the other was combination group (n = 52), given the same dose of statin plus bezafibrate (200 mg BID). Follow-up visits were scheduled at the end of 6 and 12 weeks post treatment. Serum apoA5 levels were determined using a commercial available ELISA kit.

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INVESTIGATIONAL PRODUCT: Rosuvastatin (Crestor; Astra Zeneca).

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The combination of ezetimibe and rosuvastatin apparently diminishes lipid levels and plaque burden and improves plaque stability, which may be associated with the potent inhibitory effects of ezetimibe and rosuvastatin on inflammatory cytokines.

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The constellation of risk factors known as the metabolic syndrome increases the risk of coronary artery disease at any low-density lipoprotein (LDL) cholesterol level. We performed an exploratory analysis of data from 5 trials to study the effects of rosuvastatin 10 mg on lipid levels and ratios in hypercholesterolemic patients (LDL cholesterol > or =160 mg/dL and <250 mg/dL) who met a modified National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) definition of the metabolic syndrome. Of 580 patients completing 12 weeks of treatment with rosuvastatin 10 mg, 194 (33%) met the definition of the metabolic syndrome by exhibiting > or =3 of the following: body mass index >30; triglycerides > or =150 mg/dL; high-density lipoprotein (HDL) cholesterol <40 mg/dL in men and <50 mg/dL in women; blood pressure > or =130/> or =85 mm Hg or receiving current medication for hypertension; and fasting blood glucose > or =110 mg/dL. Patients with the metabolic syndrome had higher triglyceride, non-HDL cholesterol, apolipoprotein B, and lipid ratios, and lower HDL cholesterol and apolipoprotein A-I levels, at baseline compared with patients without the metabolic syndrome. In patients with the metabolic syndrome, rosuvastatin 10 mg improved LDL cholesterol (-47%), non-HDL cholesterol (-43%), non-HDL cholesterol/HDL cholesterol ratio (-47%), apolipoprotein B (-37%), apolipoprotein B/apolipoprotein A-I ratio (-40%), triglycerides (-23%), apolipoprotein A-I (+7%), and HDL cholesterol (+10%)-in a manner similar to that in hypercholesterolemic patients who did not meet these criteria. Among patients who met the metabolic syndrome criteria and who had triglycerides > or =200 mg/dL, 64% met their ATP III non-HDL goals.

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This study aimed to evaluate the 1-year efficacy and safety of rosuvastatin in combination with fenofibric acid in a subgroup of patients treated for 12 weeks with rosuvastatin 10 mg + fenofibric acid 135 mg and subsequently treated for up to 52 weeks with rosuvastatin 20 mg + fenofibric acid 135 mg.

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The relaxant effect of the methyl ester of rosuvastatin was evaluated on aortic rings from male Wistar rats (250-300 g, 6 rats for each experimental group) with and without endothelium precontracted with 1.0 µM phenylephrine. The methyl ester presented a slightly greater potency than rosuvastatin in relaxing aortic rings, with log IC50 values of -6.88 and -6.07 M, respectively. Unlike rosuvastatin, the effect of its methyl ester was endothelium-independent. Pretreatment with 10 µM indomethacin did not inhibit, and pretreatment with 1 mM mevalonate only modestly inhibited the relaxant effect of the methyl ester. Nω-nitro-L-arginine methyl ester (L-NAME, 10 µM), the selective nitric oxide-2 (NO-2) inhibitor 1400 W (10 µM), tetraethylammonium (TEA, 10 mM), and cycloheximide (10 µM) partially inhibited the relaxant effect of the methyl ester on endothelium-denuded aortic rings. However, the combination of TEA plus either L-NAME or cycloheximide completely inhibited the relaxant effect. Inducible NO synthase (NOS-2) was only present in endothelium-denuded aortic rings, as demonstrated by immunoblot with methyl ester-treated rings. In conclusion, whereas rosuvastatin was associated with a relaxant effect dependent on endothelium and hydroxymethylglutaryl coenzyme A reductase in rat aorta, the methyl ester of rosuvastatin exhibited an endothelium-independent and only slightly hydroxymethylglutaryl coenzyme A reductase-dependent relaxant effect. Both NO produced by NOS-2 and K+ channels are involved in the relaxant effect of the methyl ester of rosuvastatin.

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This paper contains detailed results of a sub-population of the prospective randomized RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study.

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The results showed that LVEDP, CVF, and P-p38 MAPK expression were drastically elevated in the four MI groups in comparison to the sham-operated group (p<0.001). Rosuvastatin elevated the left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF). Both rosuvastatin and torasemide improved the haemodynamic parameters. No significant difference was detected in LVEDP between the R group and the T1 group (p=0.37). In contrast, LVEDP was significantly higher in the R group than in the T2 group (p <0.05). CVF (%) was markedly decreased in the R group compared to the C, T1, and T2 groups (decreased by 47.4%, 28%, and 20.1%, respectively). Immunohistochemical analysis showed that the indices of P-p38 MAPK positive cells were significantly decreased in the R group in comparison with the C, T1, and T2 groups (decreased by 44.6%, 36.6%, and 21.4%, respectively). Western blot analysis demonstrated that P-p38 MAPK expression was markedly reduced in the R group compared with the C and T1 groups (reduced by 67% and 40.5%, respectively). The level of P-p38 MAPK in the R group was slightly higher than in the T2 group. However, the difference was not statistically significant (p>0.05).

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crestor generic coupon 2016-02-10

Patients with T2DM and hypercholesterolemia with detectable sd LDL-C after receiving 10mg/day atorvastatin for ≥ 24 weeks were randomly assigned to receive rosuvastatin (5mg/day; switched treatment) or atorvastatin (10mg/day; continued treatment) for 12 weeks. The primary endpoints were changes in sd LDL-C levels and sd LDL-C/total LDL-C ratio evaluated using the buy crestor LipoPhor AS(®) system.

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We studied 2268 adults aged 35-75 without cardiovascular disease in a population-based study in Switzerland in 2003-2006. We assessed the eligibility for statins according to the Adult Treatment Panel III (ATPIII) guidelines, and by adding "strict" (hs-CRP≥2.0 mg/L and LDL-cholesterol <3.4 mmol/L), and "extended" (hs-CRP≥2.0 mg/L alone) JUPITER-like criteria. We estimated the proportion of CHD deaths potentially prevented over 10 years in the Swiss buy crestor population.

crestor 80 mg 2017-05-20

In case of equivalent degree of the decrease in LDL-C levels, 24-week combination therapy with atorvastatin and ezetimibe, unlike rosuvastatin treatment, induced increases in basal glycemia, insulinemia, HbA1c, and HOMA-IR buy crestor index irrespective of the presence of carbohydrate metabolism disturbances before treatment. Our data suggest that adiponectin and leptin are involved in the mechanisms of adverse metabolic effects of the combination of atorvastatin and ezetimibe.

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These results identify key membrane transporters buy crestor as modulators of skeletal muscle statin exposure and toxicity.

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This study suggests that the CYP2C9 polymorphism may be involved in the lipid-lowering efficacy of rosuvastatin in patients with hyperlipidemia buy crestor .

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Our findings indicate that statin therapy intensified buy crestor by ezetimibe may reduce the incidence of cardiovascular events within the first 12 months after vascular surgery. Nonetheless, whether the use of ezetimibe as an add-on therapy to reduce cardiovascular risk in these patients needs to be tested in larger future studies.

crestor reviews australia 2016-06-03

HIV-IP who are aged between 30 and 60 years, with a CD4 count. greater than 200 cells/mm(3). Patients must be stable on combination antiretroviral buy crestor therapy (cART) for at least 12 months and have a 10-year CVD risk of less than 20% (using the Framingham risk score).

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Cardiovascular disease (CVD) can occur in individuals with low low-density buy crestor lipoprotein (LDL) cholesterol (LDL-C). We investigated whether detailed measures of LDL subfractions and other lipoproteins can be used to assess CVD risk in a population with both low LDL-C and high C-reactive protein who were randomized to high-intensity statin or placebo.

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These results indicated that the two formulations of rosuvastatin were bioequivalent; therefore, buy crestor they may be prescribed interchangeably.

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Statins are efficacious in reducing the risk of major cardiovascular events for both primary and secondary prevention, yet long-term adherence is poor. Their effectiveness could be compromised in actual practice when patients are not adherent to the treatments. Higher copayments have been shown to be associated buy crestor with lower adherence to statins.

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Rosuvastatin may have a beneficial effect on bone metabolism in patients with type 2 diabetes and hypercholesterolemia by stimulating osteoblast function and bone formation, which seems to be independent of buy crestor its cholesterol-lowering effect.

crestor dosage levels 2015-10-11

With particular emphasis on interactions between cholesterol homeostasis and drug metabolism buy crestor we investigate the transcriptome of human primary hepatocytes treated by two commonly prescribed cholesterol lowering drugs atorvastatin and rosuvastatin and by rifampicin that serves as an outgroup as well as a model substance for induction of nuclear pregnane X receptor.

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This study utilized data from a randomized clinical trial of rosuvastatin in HIV-infected adults on ART. Incidental findings were reported from chest computed tomography (CT) scans obtained buy crestor for coronary artery calcium score at entry, week 48 and 96. Markers of immune activation and inflammation were measured concurrently. Poisson regression and generalized estimating equations were used.

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Rosuvastatin has demonstrated clinical superiority over atorvastatin, pravastatin, and simvastatin Mysoline Dosage in reducing LDL-C levels and in enabling patients to reach goals established by the JAS.

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IMEA-043-CESAR was a phase II open-label pilot trial that enrolled patients under suppressive ART and CD4 <500/mm. Patients received rosuvastatin (20 mg/d Crestor Medicine Reviews ) for 12 weeks. The primary outcome was the variation at week 12 (W12) in the proportion of CD38HLA-DRCD8 T lymphocytes. Secondary outcomes included evolution of other markers of T-cell activation and of inflammatory biomarkers between baseline, W12, and W24.

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Rosuvastatin showed a superior lipid-lowering effect compared to fluvastatin in stable RTR receiving everolimus. The combination of everolimus/rosuvastatin seems to be as safe as the everolimus/ Suprax Suspension Coupon fluvastatin combination.

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This study reports on the antifungal activities Asacol Maximum Dosage of statins combined with an antifungal compound secreted by Penicillium chrysogenum, PAF. Several species belonging in the class Zygomycetes are considered to be agents of human or animal mycoses; other species have significance as postharvest plant pathogens. In the present work, four species (Rhizopus stolonifer, Mortierella wolfii, Syncephalastrum racemosum and Mycotypha africana) that exhibited different sensitivities to lovastatin and PAF in previous experiments were investigated. The efficiencies with which four statins (lovastatin, simvastatin, rosuvastatin and atorvastatin) inhibited sporangiospore germination in the absence or in the presence of a constant concentration of PAF were studied. PAF and lovastatin acted synergistically on the sporangiospore germination of Mycotypha africana, and similar effects of the combinations PAF-rosuvastatin and PAF-atorvastatin were observed on S. racemosum.

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Ratios for rosuvastatin area under the plasma concentration-time curve from time 0 to the time of the last quantifiable concentration were 2.31, 1.91, and 1.63 and ratios for maximum plasma concentration were 2.36, 2.00, and 1 Viagra Online Sales .68 in Chinese, Malay, and Asian-Indian subjects, respectively, compared with white subjects. Similar increases in exposure to N-desmethyl rosuvastatin and rosuvastatin-lactone were observed. SLCO1B1 genotypes did not account for the observed pharmacokinetic differences between Asians and white subjects.

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The study sought to explore sex-related differences Diflucan Brand Name in coronary atheroma regression following high-intensity statin therapy.

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The co-primary end points Vantin Cost were percentage changes from baseline in HDL-C and LDL-C after 12 weeks of treatment.

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Rosuvastatin and fenofibrate are Claritin Maximum Dosage lipid-regulating agents with different modes of action. Patients with dyslipidemia who have not achieved treatment targets with monotherapy may benefit from the combination of these agents.

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The study involved 30 healthy subjects as well as 30 patients with angiographically confirmed coronary artery disease who despite at least 6 months hypolipidemic treatment did not achieve LDL-C <70mg/dl. The following parameters studied included homocysteine level, lipid peroxidation in plasma and lipidogram parameters. Our study showed increase of homocysteine level, lipid peroxidation in plasma, LDL-C concentration and total cholesterol level. After six months therapy, the following changes were observed in comparison to the values before therapy: decrease of Imodium Online homocysteine level in plasma - R15 20%, A40 26% and A+E 28%; decrease of lipid peroxidation in plasma - R15 31%, A40 27% and A+E 32%; decrease of LDL-C cholesterol level - R15 18%; A40 17% and A+E 33% and decrease of total cholesterol level - R15 9%, A40 15% and A+E 17%.

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SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin) employed serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. The treatment groups did not differ significantly in change from baseline of percent atheroma volume (PAV) or total atheroma volume (TAV) on intravascular ultrasound, nor in Imitrex Cost safety or clinical outcomes.

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A linear two-compartment model with first-order absorption and elimination processes adequately described the combined dataset. Weight and gender were significant covariates for CL/F, with moderate between-patient variability remaining (coefficient of variation (CV) 40 %): CL/F in female children was approximately 30 % lower than in male children, and there was a twofold mean difference in CL/F across the observed weight range. Age was not a significant covariate after accounting for weight and gender differences. However, weight and gender only reduced between-patient variability from 45 (without covariates) to 40 % and are considered Aricept Max Dosage unlikely to be clinically relevant.

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Patients under lipid Micardis Overdose Death lowering therapy and managed by general practitioners were included. LDL-cholesterol therapeutic objective was defined according to the number of cardiovascular risk factors associated with dyslipidemia (AFSSAPS-2005 guidelines).

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High dose rosuvastatin loading before PCI significantly improved 12-month clinical outcomes in patients with ACS who underwent an early invasive strategy.

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Rosuvastatin is a cost-effective therapy in the treatment of hypercholesterolemia versus simvastatin, atorvastatin and pitavastatin, especially in specific profiles of patients with high and very high cardiovascular risk factors, according to the SCORE system, in Spain.

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The present study was carried out to evaluate the protective effect of different statins on isoproterenol (ISO) induced myocardial necrosis. Atorvastatin, rosuvastatin, fluvastatin, simvastatin and pravastatin (10 mg/kg/day) were administered for 12 weeks. After pretreatment of 12 weeks myocardial necrosis was induced by subsequent injection of ISO (85 mg/kg/day, s.c.) to wistar rats. Serum biochemical parameters like glucose, lipid profile, cardiac markers and transaminases were evaluated. Animals were killed and heart was excised for histopathology and antioxidant study. Statins pretreated rats showed significant protection against ISO induced elevation in serum biochemical parameters and serum level of cardiac marker enzymes and transaminase level as compared to ISO control group. Mild to moderate protection was observed in different statins treated heart in histopathology and TTC stained sections. Result from our study also revealed that statins could efficiently protect against ISO intoxicated myocardial necrosis by impairing membrane bound enzyme integrity and endogenous antioxidant enzyme levels. Amongst all statins used, rosuvastatin and pravastatin were found to have maximum cardio-protective activity against ISO induced myocardial necrosis as compared to other statins.