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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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crestor y alcohol

Beta-blockade enhances the pleiotropic effects of statins on endothelial function. The mechanism should be confirmed by further studies.

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High-intensity statin therapy alters the progressive nature of diabetic coronary atherosclerosis, yielding regression of disease in diabetic and nondiabetic patients.

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In this open-labeled, placebo-controlled, randomized, two-period, crossover trial with a washout period of 15 days, 12 healthy male volunteers were administered daily oral doses of 5 mg warfarin for 14 days. Either rosuvastatin 40 mg/day (treatment A) or placebo (treatment B) was concomitantly administered on days 8-14. The pharmacodynamic parameters prothrombin time (PT) and international normalized ratio (INR) were evaluated on all 14 days pre-dose during both study periods. On the 8th, 10th, 12th, and 14th days of each study period, PT and INR were also measured at 4 h post-dose of rosuvastatin or placebo. Bleeding time and clotting time were assessed on the 1st, 8th, and 14th days pre-dose.

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Attenuated plaque is present in a significant number of nonculprit segments in patients enrolled in IVUS progression trials and remains stable during follow-up. There is a relationship with mixed calcified lesions. These findings challenge the prior assumption that attenuated plaque is a finding limited to culprit lesions associated with acute clinical presentation.

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Statin-fibrate combination therapy has been used to treat patients with acute coronary syndrome (ACS) complicated by elevated triglycerides (TG) and decreased high density lipoprotein cholesterol (HDL-C). The purpose of this study was to evaluate the influence of the combination therapy on lipids profile and apolipoprotein A5 (apoA5) level in patients with ACS.

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Consistent with recent evidence-based Canadian Cardiovascular Society guidelines for primary prevention, the JUPITER trial demonstrates that rosuvastatin 20 mg significantly reduces major cardiovascular events among men and women with elevated hsCRP and "intermediate risk" defined either as 5% to 10% or 10% to 20% 10-year risk.

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24 subjects were included in this single-dose, open-label, randomized, two-way crossover study following an overnight fast. A 2-week wash out period was applied. Blood samples were drawn up to 72 hours following drug administrations. Rosuvastatin plasma concentrations were determined by liquid chromatography-tandem mass spectrometry method with TurboIon-Spray mode. Pharmacokinetic parameters AUC(0-t), AUC(0-∞), and Cmax were determined and used for bioequivalence evaluation after log-transformation, whereas tmax ratios were evaluated nonparametrically.

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This is a prespecified analysis of a prospective, randomized, open-label, blinded end point (PROBE) study ( identifier: NCT01010516). Patients (n = 100) with mixed dyslipidaemia on a standard statin dose who had not achieved lipid targets were randomized to switch to the highest dose of rosuvastatin (40 mg/day) or to add-on-statin extended release nicotinic acid (ER-NA)/laropiprant (LRPT) or to add-on-statin micronized fenofibrate for a total of 3 months.

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Careful review of both results and methods used in the trial and comparison with expected data.

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Administration of P-OM3 with rosuvastatin did not affect the pharmacokinetics of rosuvastatin under steady-state conditions in healthy individuals.

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PTEN(loxp/cre) or PTEN(+/-) mice received ND or WD without or with ROS (10 mg/kg/day). Wild-type mice received ND or WD without or with ROS, CIL (10 mg/kg/day), or ROS+CIL for 30 days. Fasting insulin and glucose tolerance test were measured as well as PTEN and P-AKT levels in skeletal muscle.

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Homocysteine (50-1000 μmol/L) significantly increased the production and activation of MMP-2, the expression of TIMP-2, and the migration of VSMCs in a dose-dependent manner. Additional extracellular rosuvastatin can decrease the excessive expression and activation of MMP-2 and abnormal migration of VSMCs induced by homocysteine.

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At the LDL-C target of 2.6 mmol L(-1) and the non-HDL-C target of 3.4 mmol L(-1), the measured apoB values were significantly higher than consensus apoB target values. The difference was most marked for c-LDL-C in hypertriglyceridaemic subjects and for non-HDL-C in patients without hypertriglyceridaemia. A similar pattern was seen using centile-derived consensus values but the differences were accentuated because this approach generates lower equivalent consensus apoB values.

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Rosuvastatin treatment was associated with a 49% reduction in LDL-C-C, a 34% reduction in total cholesterol, an 8.0% increase in HDL-C and a 16% reduction in triglycerides (all P < 0.0001 compared with placebo). The difference in rate of mean maximum CIMT progression between the rosuvastatin and placebo groups (based on near and far wall measurements from both left and right common carotid and internal carotid segments and carotid bifurcation) was not statistically significant after 6 months (0.0023 mm year(-1) and 0.0106 mm year(-1), respectively P = 0.34). After 12 months, CIMT progression rates were significantly different between the groups: 0.0032 mm year(-1) and 0.0133 mm year(-1) in the rosuvastatin-treated and placebo-treated groups, respectively (P = 0.049). This divergence grew with further follow-up: -0.0009 mm year(-1) and 0.0131 mm year(-1) after 18 months (P < 0.001) and -0.0014 mm year(-1) and 0.0131 mm year(-1) after 24 months of treatment (P < 0.001). Results were stronger for the mean common CIMT progression (based on near and far wall measurements from both left and right common carotid segments).

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Takotsubo cardiomyopathy is a disorder characterized by left ventricular apical ballooning with preceding emotional and/or physical stressors. This condition is also an important differential diagnosis of acute coronary syndrome. We herein describe a case of Takotsubo cardiomyopathy, a significant clinical phenomenon, triggered by delayed-onset rhabdomyolysis following the administration of long-term statin treatment, without any preceding stressors or changes in the patient's medical condition, in association with complaints of non-specific muscle-related symptoms. Although an electrocardiogram showed remarkable ST-segment elevation, a careful reading of the electrocardiogram findings revealed the features of Takotsubo cardiomyopathy. Withdrawing the statin therapy improved the patient's cardiac function.

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Animal studies have consistently demonstrated the ability of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors to limit the damage induced by ischemia-reperfusion (IR) in the cardiac, cerebral and mesenteric circulation through a mechanism dependent on the upregulation of cyclooxygenase-2 (COX-2). Our group performed studies aimed at investigating the mechanism of HMG-CoA reductase inhibitor-mediated endothelial protection from IR injury, in particular the role of COX-2, in a human in vivo model of IR-induced endothelial dysfunction. We demonstrated that HMG-CoA reductase inhibition protects against IR-induced endothelial damage, an effect that was lost upon COX-2 inhibition. These observations may suggest a mechanistic explanation for the cardioprotection observed in clinical settings such as percutaneous coronary interventions and coronary artery bypass surgery and may also propose a mechanistic hypothesis for the reported cardiotoxic effects of cyclooxygenase-2 inhibitors observed in clinical studies. These studies are summarized and discussed in the present paper.

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Randomized controlled and uncontrolled before-and-after trials evaluating the dose response of different fixed doses of rosuvastatin on blood lipids over a duration of three to 12 weeks.

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Hypercholesterolemia is a major risk factor for cardiovascular disease and requires continuous management. The role of primary physicians in this regard is important, yet the factors associated with successful lipid lowering treatments in primary clinics have not been clearly identified. We aimed to evaluate the rate of successful hypercholesterolemia treatment in Korean primary care, and to identify the factors associated with achieving low density lipoprotein cholesterol (LDL-C) targets.

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Rosuvastatin treatment reduced insulin resistance without affecting body weight or WAT loss in HFD rats. Reduction of leptin and JNK, and enhancement of SIRT-1, p53, PGC-1α, PPAR-γ and GLUT-4 expression in WAT could contribute to insulin sensitization. Normalization of SIRT-1 expression in WAT could be considered a key novel mechanism that aids in explaining the beneficial effects of rosuvastatin on the amelioration of glucose metabolism and the arrangement of multiple signaling pathways participating in insulin resistance in overweight HFD rats.

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The results of this study show that ciprofibrate and rosuvastatin or a combination of both can be considered an effective, safe and well-tolerated lipid-lowering treatment for patients with AIDS on highly active antiretroviral therapy.

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crestor dosage amounts 2015-07-15

This was a prospective observational study including patients with dyslipidemia and IFG (IFG group, n = 49) matched with normoglycemic patients with dyslipidemia (control group, n = 64). Study participants, following dietary intervention, were prescribed rosuvastatin 10 or 20 mg/d to achieve LDL-C goals. Baseline as well as 24 weeks posttreatment changes buy crestor online in the serum lipid profile were evaluated. Moreover, analysis of the LDL subfraction profile was conducted using a polyacrylamide tube gel electrophoresis method.

crestor cost comparison 2015-03-21

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 buy crestor online the elimination of rosuvastatin.

crestor prescription cost 2017-08-31

Gemfibrozil increased rosuvastatin plasma concentrations buy crestor online approximately 2-fold, which is similar to the effect of gemfibrozil on pravastatin, simvastatin acid, and lovastatin acid plasma concentrations and substantially less than the effect observed for cerivastatin. Gemfibrozil inhibition of OATP2-mediated rosuvastatin hepatic uptake may contribute to the mechanism of the drug-drug interaction. Care is warranted when gemfibrozil is coadministered with rosuvastatin and other statins.

crestor and alcohol 2016-08-03

A 66-year-old man with diabetes and hypertension using statin buy crestor online was admitted to the hospital with progressive myalgia. He had been on rosuvastatin for five months. After beginning the use of phosphodiesterase-5 inhibitors, he presented with severe muscle pain and maintained penile erection. Several days after interruption of therapy, muscle pain and penile erection disappeared. This case demonstrates the interaction of sildenafil with rosuvastatin might result in myopathy.

crestor 1 mg 2017-10-06

This study shows that: 1 buy crestor online .rosuvastatin exerts a beneficial effect on the conduction of the fastest sensory fibres;2.these effects are independent of blood pressure and lipid changes.

crestor 80 mg 2016-11-30

Long-term ROS can induce diabetes by upregulating PTEN. CIL attenuates these changes. Partial knockdown buy crestor online of PTEN also ameliorates ROS-induced insulin resistance. Further studies are needed to assess the effects of increasing cAMP levels to prevent the induction of diabetes by statins.

crestor dosage 2015-02-18

Despite the demonstrated benefits of low-density lipoprotein cholesterol (LDL-C) reduction in reducing the risk of coronary heart disease, many patients receiving lipid-lowering therapy fail to achieve LDL-C goals. We compared the effects of rosuvastatin and atorvastatin in reducing LDL-C and achieving LDL-C goals buy crestor online in patients with primary hypercholesterolemia.

crestor generic rosuvastatin 2015-04-27

Although large-scale statin trials have demonstrated significant reductions in cardiovascular risk, there are many patients who have a cardiovascular event despite receiving statin therapy. There is increasing evidence that larger reductions in low-density lipoprotein cholesterol (LDL-C) are associated with greater improvements in cardiovascular morbidity and mortality, which highlights the need for more efficacious statins. This article will review the lipid-altering effects of two new statins, rosuvastatin and pitavastatin. Rosuvastatin represents an advance in buy crestor online the pharmacological and clinical properties of other available agents. The large LDL-C reductions observed with rosuvastatin, even at the start dose of 10 mg and in patients switched from other statins to rosuvastatin 10 mg, should help to improve goal attainment, while reducing the need for dose titration. The ability of rosuvastatin to improve other elements of the lipid profile, such as high-density lipoprotein cholesterol (HDL-C), triglycerides and non-HDL-C, may be of utility in patients with diabetes and the metabolic syndrome. Increases in HDL-C, along with the greater efficacy of rosuvastatin for reducing LDL-C and non-HDL-C, may obviate the need for combination therapy. Results of a number of outcome studies with rosuvastatin are expected over the next 5 years, which will contribute to the evidence base for statin therapy and cardiovascular disease prevention.

crestor generic availability 2016-03-29

IMEA-043-CESAR was a phase II open-label pilot trial that enrolled patients under suppressive ART and CD4 <500/mm. Patients received buy crestor online rosuvastatin (20 mg/d) 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.

crestor pills 2017-08-25

We conducted a hospital-based observational buy crestor online study. Totally 80 non-CHD patients and 120 CHD patients without statin treatment were previously enrolled in this study. All the CHD patients received statin treatment, and 63 of them were followed after 3 months of regular statin treatment. HDL sample of each patient was isolated by density gradient ultracentrifugation from fasting venous plasma, and HDL-apoCIII of each patient was measured by ELISA method.

crestor low dose 2016-11-18

Statins did not alter the replication of influenza A in vitro or enhance its clearance from the lung in vivo. Statins neither attenuated the severity buy crestor online of influenza A-induced lung injury nor had an effect on influenza A-related mortality. Our data suggest that the association between HMG CoA reductase inhibitors and improved outcomes in patients with sepsis and pneumonia are not attributable to their effects on influenza A infection.

crestor drug reviews 2016-02-08

Thirty healthy Chinese male volunteers were enrolled. The serum lipids, high-sensitivity C-reactive protein, and plasma fibrinogen were determined before and 72 hours after administration of 20 mg of rosuvastatin. The differentially expressed genes of peripheral leukocytes after administration of rosuvastatin were screened using human oligonucleotide microarray gene expression chips. Then four of the differentially expressed genes including ATM, CASP8, IL8RB and buy crestor online S100B were verified by real-time polymerase chain reaction (PCR).

crestor 40mg tab 2017-11-05

Double-blind, randomized clinical trial. buy crestor online

crestor 10 mg 2015-08-31

Double-blind, Prograf Drugs multicenter, 6-week, parallel-group study in hypercholesterolemic patients (n = 2959). Patients were randomized based on stratification by low-density lipoprotein cholesterol (LDL-C) levels to ezetimibe/simvastatin or rosuvastatin, respectively, at the usual starting (10/20 or 10 mg/day), the next highest (10/40 or 20 mg/day), and maximum doses (10/80 or 40 mg/day).

crestor reviews 2015-12-14

Cytotoxicity of the four drugs was tested in MCF-7, HeLa and HepG2 cells by the neutral red assay method and also the effect Biaxin Vs Generic of rosuvastatine and doxazosin against Ehrlich Ascities Carcinoma Cells (EACC) by trypan blue assay.

crestor 10mg medication 2017-10-01

Clinical studies suggest that statins reduce proteinuria and slow the decline in kidney function in chronic kidney disease. Given a rich literature identifying podocyte apoptosis as an early step in the pathophysiological progression to proteinuria and glomerulosclerosis, we hypothesized that rosuvastatin Propecia Generic Brand protects podocytes from undergoing apoptosis. Regarding a potential mechanism, our lab has shown that the cell cycle protein, p21, has a prosurvial role in podocytes and there is literature showing statins upregulate p21 in other renal cells. Therefore, we queried whether rosuvastatin is prosurvival in podocytes through a p21-dependent pathway.

crestor orphan drug 2016-04-10

A sensitive liquid chromatography/tandem mass spectrometric (LC-MS/MS) method was developed and validated for the determination of rosuvastatin in human plasma. The plasma samples were prepared using liquid-liquid extraction with ethyl ether. Chromatographic separation was accomplished on a Zorbax XDB-C18 (150 mm x 4.6 mm i.d., 5 microm) column. The mobile phase consisted of methanol-water (75:25, v/v, adjusted to pH 6 by aqueous ammonia). Detection of rosuvastatin and the internal standard (IS) hydrochlorothiazide was achieved by ESI MS/MS in the negative ion mode. The lower limit of quantification was 0.020 ng/ml by using 200 microl aliquots of plasma. The linear range of the method was from 0.020 to 60.0 ng/ml. The intra- and inter-day precisions were lower than 8.5 Generic Amoxil 30x500mg % in terms of relative standard deviation (RSD), and the accuracy was within -0.3 to 1.9% in terms of relative error (RE). Compared with the existing methods, the validated method offered increased sensitivity. The method was successfully applied for the evaluation of pharmacokinetics of rosuvastatin after single oral doses of 5, 10 and 20 mg rosuvastatin to 10 healthy volunteers.

crestor 60 mg 2017-08-07

Short-term rosuvastatin but not allopurinol administration Vermox Suspension decreases MMP-2 and -9 and increases TIMP-2 levels.

crestor 5mg reviews 2016-02-23

Ten apparently healthy subjects were given 40 mg of simvastatin and tested for urinary α1 Vermox Drug -microglobulin, albumin, creatinine and cystatin C, up to 24 h after administration. Additionally, urine samples of 76 statin-treated and 456 untreated patients presenting with micro-albuminuria (albuminuria range between 20 and 200 mg/L) were tested for α1-microglobulin and albumin. α1-Microglobulin/albumin ratios were compared. Total cholesterol was measured in 50 patients on statin therapy.

crestor go generic 2016-01-09

These data suggest that the ABCB1 c.1236C-c.2677G-c.3435C and Lamictal Overdose Death c.1236T-c.2677T-c.3435T haplotypes play no significant role in the interindividual variability in the pharmacokinetics of fluvastatin, pravastatin, lovastatin, and rosuvastatin.