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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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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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Twelve and 24-hour post-PCI Creatine Kinase Muscle and Brain (CK-MB) elevation >3× occurred more frequently in the CG than in the RG and in the AG (at 24-h: 25.0 vs 7.1; p=0.003 and 25.0 vs 6.1; p=0.001). At 30-day, 6-and 12-month follow-up the incidence of cumulative MACCE was higher in CG than in the RG or AG (at 12-month: 41.0% vs 11.4% vs 12.0%; p=0.001). There was no difference between the RG and AG in terms of myocardial post-procedural necrosis and MACCE occurrence at follow-up.

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The study enrolled 12 healthy Chinese volunteers (6 men: mean [SD] age, 22.3 [1.5] years; mean [SD] weight, 61.8 [2.4] kg [range, 59-64 kg]; 6 women: mean [SD] age, 21.6 [1.4] years; mean [SD] weight, 56.4 [6.4] kg [range, 50-64 kg]). Geometric mean (SD) C(max) values of 10.22 (8.05), 25.86 (18.77), and 44.99 (17.99) ng/mL were achieved at a median T(max) of 2.5 hours after administration of single doses of 5, 10, and 20 mg of rosuvastatin, respectively; the corresponding geometric mean (SD) values of AUC(0-t) were 73.67 (48.78), 210.21 (178.70), and 303.81 (193.29) ng/mL . h(-1), and the mean (SD) apparent elimination t(1/2) values were 13.01 (8.68), 13.33 (5.21), and 15.40 (5.43) hours after administration. The Student-Newman-Keuls test results found that C(max) and AUC(0-t) were both linearly related to dose. In men, the mean (SD) C(max) values were 7.57 (6.49), 20.43 (14.10), and 36.80 (15.64) ng/mL, and the mean (SD) AUC(0-t) values were 51.74 (33.92), 136.35 (97.18), and 232.25 (101.66) ng/mL x h(-1), with the 5-, 10-, and 20-mg doses of rosuvastatin, respectively. In women, the corresponding C(max) values were 13.40 (9.27), 32.44 (23.10), and 54.82 (16.78) ng/mL, and AUC(0-t) values were 99.99 (54.07), 298.85 (223.66), and 430.21 (194.61) ng/mL x h-1. Results of the t tests of (lg)C(max) and (lg)AUC(0-t) found no significant differences between the male and female groups. However, C(max) and AUC(0-t) values of 0.82 ng/mL and 6.87 ng/mL x h-1, respectively, after oral administration of 10 mg of rosuvastatin in the fed state were significantly different from the corresponding values under fasting conditions (both, P < 0.05). Two adverse events (pharyngitis and nausea) were reported in 3 subjects (2 women, 1 man) at the 20-mg fasting state. Two cases of elevated laboratory values (bilirubin, from 16.1 micromol/L at baseline to 31.4 micromol/L; phosphocreatine, from 141 U/L at baseline to 307 U/L) were found at the poststudy follow-up immediately after study completion in 2 volunteers (1 man, 1 woman) at the 10-mg fed state; both values had returned to normal 5 days later.

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Two-year change in GSM did not significantly differ between rosuvastatin and placebo in the total population, with a mean difference in the rate of change in GSM of 1.13 (95% confidence interval, -1.00 to 3.25). The effect of rosuvastatin differed across quintiles of baseline GSM values (P for interaction = .01). In the lowest quintile (n = 175) (i.e., in those with the most echolucent intima-media), the difference in the rate of change in GSM between rosuvastatin and placebo was 4.18 (95% confidence interval, -0.23 to 8.58). Increases in GSM were significantly related to decreasing low-density lipoprotein cholesterol levels in the lowest quintile (β = 0.76; 95% confidence interval, 0.26 to 1.25).

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Platelet-vessel wall interaction and thrombosis take place under dynamic conditions involving the interaction of the exposed damaged vascular wall with the circulating blood cells and proteins. Blood was perfused over type I collagen at different wall shear rates, and platelet deposition was measured by confocal microscopy. Perfused effluent blood was collected, platelets were sequentially extracted based on differential protein solubility, and proteins were separated by 2D gel electrophoresis. Blockade of 3-hydroxy-3-methylglutaryl-coenzyme A reductase significantly reduced platelet deposition and modulated the expression pattern of 18 proteins in the platelet subproteome. Among them, an increase in platelet surface 78-kDa glucose-regulated protein (GRP78), a stress-inducible multifunctional endoplasmic reticulum protein, was clearly apparent. Immunoprecipitation of platelet GRP78 revealed its interaction with tissue factor. Moreover, blockade of surface GRP78 resulted in a substantial increase in platelet deposition and tissue factor procoagulant activity and in a decrease in clotting time.

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Carotid artery stenting (CAS) is a worldwide diffuse intervention, but may be associated with distal plaque component embolization, and sometimes major and minor stroke. Statin use has been demonstrated to reduce atherosclerotic plaque burden, but its effect in reducing distal embolization during carotid stenting has not yet been well validated.

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Pubmed, EMBASE, Cochrane Central Register of Controlled Trials and ISI Web of Science databases were systematically searched for randomized controlled trials (RCTs) up to June 2015. We assessed the incidence of MACE and PMI in all enrolled patients for subgroups stratified by clinical presentation and previous statin therapy during the follow-up period.

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ODYSSEY Outcomes will determine whether the addition of the PCSK9 antibody alirocumab to intensive statin therapy reduces cardiovascular morbidity and mortality after ACS.

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Ezetimibe has been reported to provide significant incremental reduction in low-density-lipoprotein cholesterol (LDL-C) when added to a statin; however, its effect on coronary atherosclerosis has not yet been evaluated in detail. The aim of this study was to investigate the add-on effect of ezetimibe to a statin on coronary atherosclerosis evaluated by intravascular ultrasound (IVUS).In this prospective randomized open-label study, a total of 51 patients with stable coronary artery disease (CAD) requiring percutaneous coronary intervention (PCI) were enrolled, and assigned to a combination group (n = 26, rosuvastatin 5 mg/day + ezetimibe 10 mg/day) or a monotherapy group (n = 25, rosuvastatin 5 mg/day). Volumetric IVUS analyses were performed at baseline and 6 months after the treatment for a non-PCI site. LDL-C level was significantly reduced in the combination group (-55.8%) versus that in the monotherapy group (-36.8%; P = 0.004). The percent change in plaque volume (PV), the primary endpoint, appeared to decrease more effectively in the combination group compared with the monotherapy group (-13.2% versus -3.1%, respectively, P = 0.050). Moreover, there was a significant group × time interaction in the effects of the two treatments on PV (P = 0.021), indicating the regressive effect of the combination therapy on PV was greater than that of monotherapy for subtly different values of baseline PV in the two treatment groups. Moreover, percent change in PV showed positive correlations with percent change of LDL-C (r = 0.384, P = 0.015).Intensive lipid-lowering therapy with ezetimibe added to usual-dose statin may provide significant incremental reduction in coronary plaques compared with usual-dose statin monotherapy.

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Treatment with yellow wine increased NO production, eNOS activity, and eNOS protein expression, which decreases iNOS and ICAM-1 protein expression. We conclude that yellow wine may have similar beneficial effects as rosuvastatin on the cardiovascular system. These effects may be attributed to their anti-atherosclerotic actions.

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Expression of the organic anion transporting polypeptide 1B1 (OATP1B1) is regulated by transcription factor hepatic nuclear factor (HNF) 1alpha. The aim of this study was to investigate the effect of ursodeoxycholic acid (UDCA), an inhibitor of transcription factor HNF1alpha, on rosuvastatin and bilirubin kinetics in human healthy volunteers. Both substances are substrates of OATP1B1. Twelve subjects with OATP1B1(*)1b/(*)1b genotype predicting high transport activity were recruited for this randomized, crossover study. Each subject received a single p.o. dose of 20 mg of rosuvastatin after 14 days of p.o. intake of either 500 mg of UDCA or placebo. Plasma concentrations of rosuvastatin were determined on days 15 to 18 of each study period. Subjects were randomly assigned to UDCA or placebo group. Intake of UDCA led to a significant increase in rosuvastatin area under the curve (AUC)(0-72) from 128.5 ng/ml.h to 182.1 ng/ml.h(P = 0.008) compared with the control group. The oral clearance decreased from 155.2 l/h with placebo to 109.8 l/h with UDCA. In addition, the mean values of total bilirubin, conjugated bilirubin, and unconjugated bilirubin significantly increased to 139 +/- 39% (P = 0.003), 127 +/- 29% (P = 0.005), and 151 +/- 52% (P = 0.004), respectively, after UDCA treatment. These results in healthy volunteers confirm the findings from in vitro studies that UDCA inhibits OATP1B1 activity by inhibition of the transcription factor HNF1alpha. They highlight a novel mechanism of OATP1B1-based interaction that is mediated by transcription factor HNF1alpha.

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The mean systolic blood pressure (SBP) initially reached 164.26 mm Hg. During the whole follow-up, the reduction in mean SBP generally accounted for 22.6% (p = 0.000). At the study inclusion, the mean diastolic blood pressure (DBP) reached 99.38 mm Hg. The total decline in mean DBP was 19.3% (p = 0.000). The mean level of total cholesterol (TC) decreased significantly by 32.1% (p = 0.000); that of triglycerides (TG) also fell significantly by 31.8% (p = 0.04); that of high-density lipoproteins increased insignificantly by 11.1% (p = 0.599); that of low-density lipoproteins (LDL) dropped significantly by 47.5% (p = 0.000).

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Rosuvastatin ameliorates insulin sensitivity induced by HFD in rats. This effect is mediated by several mechanisms including reduction of leptin and enhancement of SIRT-1, PPAR-γ and GLUT-4 expression in white adipose tissue. SIRT1 could be considered a major mediator of the beneficial effects of rosuvastatin on insulin sensitivity in overweight rats induced by diet.

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The National Cholesterol Education Program Adult Treatment Panel III guidelines and the results of the Heart Protection Study have provided a stronger rationale to more aggressively treat high-risk patients to a low-density (LDL) cholesterol goal of less than 100 mL/dL. Two new therapies, ezetimibe and rosuvastatin, have recently been added to the lipid-lowering armamentarium to improve guideline adherence. Ezetimibe, a novel cholesterol absorption inhibitor, lowers LDL by 18% to 20% and can be used safely in combination with statins. Adding ezetimibe to a statin is comparable with the LDL-lowering efficacy of tripling the dose of the statin. Rosuvastatin is a highly efficacious statin providing 8% greater LDL reduction than equivalent doses of atorvastatin, and the starting dose of 10 mg/d provides nearly a 50% reduction in LDL cholesterol. There are several investigational drugs in development for the prevention and treatment of atherosclerosis. Of these investigational drugs, the most promising are the cholesterol ester transfer protein inhibitors, which have the potential to significantly raise high-density lipoprotein cholesterol and acetyl-coenzyme A: cholesterol acyltransferase inhibitors, which may directly inhibit the progression of atherosclerosis.

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Data were used from a trial on the effects of Rosuvastatin on rate of change in carotid intima-media thickness (CIMT). The reference treatment effect was derived from a complete data set. Scenarios and proportions of missing values in CIMT measurements were applied and LME analyses were used before and after MI. The added value of MI, in terms of bias and precision, was assessed using the mean-squared error (MSE) of the treatment effects and coverage of the 95% confidence interval.

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Thirty-six patients were randomly assigned to 10 mg/day of rosuvastatin (n = 18) or 20 mg/day of atorvastatin (n = 18) for 12 weeks. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-HDL-C, triglycerides (TG), fasting plasma glucose, insulin, homeostasis model assessment-insulin resistance (HOMA-IR), quantitative IS check index (QUICKI), adiponectin, leptin and high-sensitivity C-reactive protein (hsCRP) were measured at baseline and after 4 and 12 weeks.

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Fibrates activate peroxisome proliferator activated receptor α and exert beneficial effects on triglycerides, high-density lipoprotein cholesterol, and low density lipoprotein subspecies. Fenofibric acid (FA) has been studied in a large number of patients with mixed dyslipidemia, combined with a low- or moderate-dose statin. The combination of FA with simvastatin, atorvastatin and rosuvastatin resulted in greater improvement of the overall lipid profile compared with the corresponding statin dose. The long-term efficacy of FA combined with low- or moderate- dose statin has been demonstrated in a wide range of patients, including patients with type 2 diabetes mellitus, metabolic syndrome, or elderly subjects. The FA and statin combination seems to be a reasonable option to further reduce cardiovascular risk in high-risk populations, although trials examining cardiovascular disease events are missing.

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Rosuvastatin (RSV) is a synthetic statin with favourable pharmacologic properties, but its local effect in bone has yet to be investigated. The aim of this study was to evaluate the potential of absorbable collagen sponge (ACS) as a carrier for RSV to enhance bone formation in critical-size cortical bone defects adjacent to titanium implants. ACS, treated with different concentrations of RSV (R1 = 8.7 + or - 1.8 microg; R2 = 52.0 + or - 4.4 microg; R3 = 259.1 + or - 8.8 microg) or phosphate-buffered saline alone, were placed into the bone marrow through a defect made in the proximal tibial cortical bone of New Zealand White rabbits. One empty defect (SHAM) served as an internal control in each animal. After a healing time of 4 weeks, a concentration-dependent increase of alkaline phosphatase activity in ACS treated with RSV was detected in the bone fluid after removing the implants. In addition, a significant concentration-dependent increase in BMP-2 mRNA levels was found in the cortical bone tissue adjacent to the RSV-treated ACS. The cortical architecture of bone defects analysed by micro-computed tomography showed a trend towards higher bone volume in the ACS+R1 group compared with SHAM, which was accompanied by an increase in the bone mineral density. Evaluation of histological sections showed new bone formation in ACS treated with RSV but not in untreated ACS. These results indicate that RSV, when administered locally in bone, may have a potential effect in stimulating bone formation.

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With the growing clinical usage of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), the number of reports concerning serious drug-drug interaction has been increasing. Because recent studies have shown that conversion between acid and lactone forms occurs in the body, drug-drug interaction should be considered on both acid and lactone forms. Thus, we investigated the inhibitory effects of acid and lactone forms of eight statins, including one recently withdrawn, cerivastatin, and two recently developed, pitavastatin and rosuvastatin, on cytochrome P450 (CYP) 2C8, CYP2C9, and CYP3A4/5 metabolic activities and multidrug resistance protein 1 (MDR1) transporting activity.

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The results presented open the possibility that in humans, rosuvastatin may affect the metabolism of many drugs by influencing expression and activity of CYP2C6 (counterpart of human CYP2C9). Further studies are needed to elucidate the effects of this statin on CYP2C9 in humans.

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AMI and UA patients had higher NLRP3, cathepsin-B, interleukin-18 (IL-18), pro-IL-18, IL-1β, and pro-IL-1β expressions as compared with the control group (P<0.05). This corresponded with higher levels of serum total cholesterol, serum low-density lipoprotein cholesterol, and oxidized low-density lipoprotein in UA and AMI patients (P<0.05). Rosuvastatin at a concentration of 20 mg led to a significant decrease (P<0.05) in the expressions of NLRP3, cathepsin-B, and their downstream cytokines as compared with 5 mg rosuvastatin (P>0.05) from baseline to 4 weeks. This study also showed a positive correlation between NLRP3, cathepsin-B, and downstream inflammatory mediators.

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Rosuvastatin lowered free fatty acids (FFA), triglycerides, and increased insulin sensitivity, without affecting cholesterol. Rosuvastatin lowered the plaque volume, inhibited macrophage, lipid and oxLDL accumulation, and decreased the oxLDL-to-LDL ratio of plaques in the aortic arch. It increased superoxide dismutase 1 (SOD1), CD36, LXR-alpha, ABCA-1 and PPAR-gamma RNA expression in aortic extracts. SOD1 was the strongest inverse correlate of oxLDL. In THP-1 macrophages and foam cells, expression of SOD1 was lower than in THP-1 monocytes. Rosuvastatin restored expression of SOD1 in THP-1 macrophages and foam cells.

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Coronary Heart Disease (CHD) is the most important complication and the leading cause of death in patients with type 2 diabetes mellitus (T2DM). Hypercholesterolemia is an important modifiable risk factor for CHD. Statins are the first line drugs for the treatment of hypercholesterolemia in DM. Comparative studies between different statins are available but different doses of the same statin have not been compared in our population. The objective of this study is to compare mean reduction in serum LDL-C level after using 5mg and 10mg of rosuvastatin among T2DM patients with hypercholesterolemia. This study will help finding lowest effective dose of rosuvastatin to achieve internationally set low density lipoprotein cholesterol (LDL-C) goals.

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Large-scale randomized clinical trials have established the efficacy of cholesterol-lowering, blood pressure-lowering, and anti-platelet therapy to prevent cardiovascular diseases. A challenge for clinicians is to apply group-level buy crestor evidence from these trials to individual patients. Trials typically report a single treatment effect estimate which is the average effect of all participants, comprising patients who respond poorly, intermediately, and well. Clinicians would preferably make patient-tailored treatment decisions. Therefore, one would require an estimate of an individual patient's response to therapy. Although not yet widely recognized, trials contain this type of information. In this paper, we show how available information from landmark trials can be translated to an individual 'treatment score' through the use of multivariable therapeutic prediction models. These models provide an individual estimate of the absolute risk reduction in cardiovascular events given the specific combination of multiple clinical characteristics of a patient under care. Based on this individualized treatment estimate and metrics such as the individual number-needed-to-treat, clinicians together with their patients can decide whether drug treatment or what treatment intensity is worthwhile. Selective treatment of those who can anticipate the greatest benefit and the least harm on an individualized basis could reduce the number of unnecessary treatments and healthcare costs beyond that currently achievable by subgroup analyses based on single patient characteristics.

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This population-based study extends buy crestor previous evidence by exploring the potential association between statins use and risk of liver injury. Overall, we found that statin was not associated with risk of liver injury. Nevertheless, special concern should be paid to those who used statin ≥1 defined daily dose and rosuvastatin.

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Administration of meloxicam after lung contusion decreased the amount of neutrophil infiltration; however, marked hemorrhage and edema were still noticed. Administration of rosuvastatin decreased significantly cytokine levels that were increased after the blunt chest trauma. Rosuvastatin increased the expression of inducible nitric oxide (iNOS), COX-2, heme oxygenase-1 (HO-1), and prostaglandin E2 (PGE-2) in the bronchoalveolar lavage fluid of the rat contused lungs. Coadministration of meloxicam prevented these changes. buy crestor

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The buy crestor aim of this study was to evaluate the effect of statin treatment in primary prevention of cardiovascular events in different race/ethnic groups.

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RSV pretreatment was associated with more Treg accumulation, less inflammatory response, and myocardial injury, suggesting that such cardioprotection against IRI was partially mediated by Treg- buy crestor negative modulation of inflammation response, probably through the HMG-CoA reductase pathway.

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The primary end point was percentage change in calculated LDL-C from buy crestor baseline to 24 weeks (intent to treat).

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The objectives of this study were to determine the relationships among Type II diabetes (T2DM)-dependent elevations in platelet-derived reactive oxygen species (ROS), platelet-surface protein disulfide isomerase (psPDI) NO-releasing activity, and platelet aggregation and to evaluate the efficacy of rosuvastatin in normalizing these parameters in primary cells derived from a hamster model of prediabetic insulin resistance induced by fructose feeding. Platelets from rosuvastatin-treated non-fructose-fed (NFF) and fructose-fed (FF) hamsters were analyzed for aggregability and psPDI-denitrosation activity. Platelets from NFF animals treated with xanthine/xanthine oxidase (X/XO) were assessed for the same parameters and primary aortic endothelial cells (AEC) cultivated with a range of [rosuvastatin] +/- mevalonate were analyzed for ROS production. Platelets from FF hamsters displayed statistically significant enhanced ROS production, diminished psPDI-mediated NO-releasing activity, and hyperaggregability. Suggestively, platelets from NFF animals treated with X/XO displayed characteristics similar to platelets from FF animals. Rosuvastatin elicited a normalizing effect on all parameters measured in platelets from FF animals. Further, ROS production in primary AEC from FF animals could be blunted to that of NFF animals by concentrations of rosuvastatin in the range of those achieved in the bloodstream. Diminished psPDI-dependent NO-releasing activity and increased initial aggregation rates of FF platelets may result from elevated vascular ROS production under conditions of insulin resistance. Normalization of ROS production and platelet aggregation by rosuvastatin indicates buy crestor its potential use as a vasculoprotective agent.

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Eight-week-old male Sprague-Dawley rats were fed buy crestor control chow or HFHC diet. Half of the HFHC diet-fed rats were orally administered 2 mg/kg/day rosuvastatin for 12 weeks. Hepatic injury, steatosis, fibrosis and markers of lipid peroxidation/oxidant stress were evaluated.

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Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior mesenteric artery and the celiac trunk for 30 min, followed by reperfusion for 60 min. Rosuvastatin dissolved in physiological saline was administered intraperitoneally 60 min before ischemia. The severity of buy crestor the intestinal mucosal injury and inflammation were evaluated by several biochemical markers, as well as by histological findings. The protein levels of eNOS were determined by Western blot.

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We compared 10 mg rosuvastatin daily with placebo in patients with ischemic systolic heart failure according to baseline high sensitivity-C reactive protein (hs-CRP) <2.0 mg/L (placebo, n=779; rosuvastatin, n=777) or > or = 2.0 mg/L (placebo, n=1694; rosuvastatin, n=1711). The primary outcome was cardiovascular death, myocardial infarction, or stroke. Baseline low-density lipoprotein was buy crestor the same, and rosuvastatin reduced low-density lipoprotein by 47% in both hs-CRP groups. Median hs-CRP was 1.10 mg/L in the lower and 5.60 mg/L in the higher hs-CRP group, with higher hs-CRP associated with worse outcomes. The change in hs-CRP with rosuvastatin from baseline to 3 months was -6% in the low hs-CRP group (27% with placebo) and -33.3% in the high hs-CRP group (-11.1% with placebo). In the high hs-CRP group, 548 placebo-treated (14.0 per 100 patient-years of follow-up) and 498 rosuvastatin-treated (12.2 per 100 patient-years of follow-up) patients had a primary end point (hazard ratio of placebo to rosuvastatin, 0.87; 95% confidence interval, 0.77 to 0.98; P=0.024). In the low hs-CRP group, 175 placebo-treated (8.9 per 100 patient-years of follow-up) and 188 rosuvastatin-treated (9.8 per 100 patient-years of follow-up) patients experienced this outcome (hazard ratio, 1.09; 95% confidence interval, 0.89 to 1.34; P>0.2; P for interaction=0.062). The numbers of deaths were as follows: 581 placebo-treated (14.1 per 100 patient-years of follow-up) and 532 rosuvastatin-treated (12.6 per 100 patient-years) patients in the high hs-CRP group (hazard ratio, 0.89; 95% confidence interval, 0.79 to 1.00; P=0.050) and 170 placebo-treated (8.3 per 100 patient-years) and 192 rosuvastatin-treated (9.7 per 100 patient-years) patients in the low hs-CRP group (hazard ratio, 1.17; 95% confidence interval, 0.95 to 1.43; P=0.14; P for interaction=0.026).

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To evaluate the efficacy and safety of fenofibric buy crestor acid + statin combination therapy in this population.

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This study sought to examine the effect of statin buy crestor therapy hospitalizations for heart failure (HFH) in patients in the CORONA (Controlled Rosuvastatin Multinational Trial in Heart Failure) trial.

crestor mg dosage 2015-05-21

A specific, accurate, precise and reproducible high-performance liquid chromatography (HPLC) method was developed for the estimation of rosuvastatin (RST), a novel, synthetic and potent HMG-CoA inhibitor in rat plasma. The assay procedure involved simple liquid-liquid extraction of RST and internal standard (IS, ketoprofen) from a small plasma volume directly into acetonitrile. The organic layer was separated and evaporated under a gentle stream of nitrogen at 40 degrees C. The residue was reconstituted in the mobile phase and injected onto a Kromasil KR 100-5C18 column (4.6 x 250 mm, 5 microm). Mobile phase consisting of 0.05 m formic acid and acetonitrile (55:45, v/v) was used at a flow rate of 1.0 mL/min for the effective separation of RST and IS. The detection of the analyte peak was achieved by monitoring the eluate using a UV detector set at 240 nm. The ratio of peak area of analyte to IS was used for quantification of plasma samples. Nominal retention times of RST and IS were 8.6 and 12.5 min, respectively. The standard curve for RST was linear (r2 > 0.999) in the concentration range 0.02-10 microg/mL. Absolute recoveries of RST and IS were 85-110 and >100%, respectively, from rat plasma. The lower limit of quantification (LLOQ) of RST was 0.02 microg/mL. The inter- and intra-day precisions in the measurement of quality control (QC) samples, 0.02, 0.06, 1.6 and 8.0 microg/mL, were in the range 7.24-12.43% relative standard deviation (RSD) and 2.28-10.23% RSD, respectively. Accuracy in the measurement of QC samples was in the range 93.05-112.17% of the spiked nominal values. Both analyte and IS were stable in the battery of stability studies, viz. benchtop, autosampler and freeze-thaw cycles. RST was found to be stable for a period buy crestor of 30 days on storage at -80 degrees C. The application of the assay to determine the pharmacokinetic disposition after a single oral dose to rats is described.

crestor tablet image 2015-09-17

There were no statistically significant differences in the pre- and after treatment levels of the LDL-C between groups. TAC values were increased in both groups and statistically significant in the former group (p=0.007). There was no difference between the change percentages ((after treatment TAC-pretreatment TAC)/pretreatment level buy crestor ) of TAC between two treatment groups. The effects of two drugs on the other oxidative parameters were not significantly different.

crestor 10mg tab 2015-03-26

Itraconazole produced modest increases in rosuvastatin plasma concentrations, which are unlikely to be of clinical relevance. The results support previous in vitro metabolism findings Diovan 25 Mg that CYP3A4 plays a minor role in the limited metabolism of rosuvastatin.

crestor generic price 2015-02-05

The present work aimed to develop and characterize sustained release cuboidal lipid polymeric nanoparticles (LPN) of rosuvastatin calcium (ROS) by solvent emulsification-evaporation process. A three factor, two level (2(3)) full-factorial design was applied to study the effect of independent variables, i.e. amount of lipid, surfactant and polymer on dependent variables, i.e. percent entrapment efficiency and particle size. Optimized formulations were further studied for zeta potential, TEM, in vitro drug release and ex vivo intestinal permeability. Cuboidal nanoparticles exhibited average particle size 61.37 ± 3.95 nm, entrapment efficiency 86.77 ± 1.27% and zeta potential -6.72 ± 3.25 mV. Nanoparticles were lyophilized to improve physical stability and obtain free-flowing powder. Effect of type and concentration of cryoprotectant required to lyophilize nanoparticles was optimized using freeze-thaw cycles. Mannitol as cryoprotectant in concentration of 5-8% w/v was found to be Topamax Y Alcohol optimal providing zeta potential -20.4 ± 4.63 mV. Lyophilized nanoparticles were characterized using FTIR, DSC, XRD and SEM. Absence of C=C and C-F aromatic stretch at 1548 and 1197 cm(-1), respectively, in LPN indicated coating of drug by lipid and polymer. In vitro diffusion of ROS using dialysis bag showed pH-independent sustained release of ROS from LPN in comparison to drug suspension. Intestinal permeability by non-everted gut sac model showed prolonged release of ROS from LPN owing to adhesion of polymer to mucus layer. In vivo absorption of ROS from LPN resulted in 3.95-fold increase in AUC0-last and 7.87-fold increase in mean residence time compared to drug suspension. Furthermore modified tyloxapol-induced rat model demonstrated the potential of ROS-loaded LPN in reducing elevated lipid profile.

crestor 5mg dose 2015-04-04

After 3 months, the mean reduction in low-density lipoprotein (LDL) cholesterol levels was 43% in patients receiving rosuvastatin, from a mean baseline level of 100 mg per deciliter (2.6 mmol per liter). During a median follow-up period of 3.8 years, 396 patients in the rosuvastatin group and 408 patients in the placebo group reached the primary end point (9.2 and 9.5 events per Coumadin 3 Mg 100 patient-years, respectively; hazard ratio for the combined end point in the rosuvastatin group vs. the placebo group, 0.96; 95% confidence interval [CI], 0.84 to 1.11; P=0.59). Rosuvastatin had no effect on individual components of the primary end point. There was also no significant effect on all-cause mortality (13.5 vs. 14.0 events per 100 patient-years; hazard ratio, 0.96; 95% CI, 0.86 to 1.07; P=0.51).

crestor drug interactions 2015-06-23

ARH should be considered in cases of severe hypercholesterolaemia with a pattern of recessive inheritance. Combination therapy with high-dose statin and ezetimibe seems to be the treatment of choice Cozaar Name Brand in ARH and may reduce or eliminate the need for LDL apheresis treatment.

crestor 10 pill 2016-04-24

To evaluate efficacy of Rosuvastatin in achieving target HDL, LDL, triglycerides and total cholesterol levels in type 2 diabetes mellitus (T2DM) patients with newly diagnosed dyslipidaemia, but without known coronary artery disease Prevacid 45 Mg .

crestor 80 mg 2016-11-19

OR of interacting erythromycin versus comparator doxycycline did not differ between patients on interacting and comparator statins either in patients dispensed high or low statin doses (adjusted OR 0.87; 95% CI 0.60- Periactin Buy Uk 1.25 and 0.92; 95% CI 0.69-1.23). Interacting statins were less common among patients dispensed verapamil/diltiazem as compared to patients on amlodipine/felodipine (OR high dose 0.62; CI 0.56-0.68 and low dose 0.63; CI 0.58-0.68). Patients on any statin were to a lesser extent dispensed gemfibrozil compared to patients not dispensed a statin (OR high dose 0.65; CI 0.55-0.76 and low dose 0.70; CI 0.63-0.78). Mean DDD (SD) for any statin was substantially higher in patients co-dispensed gemfibrozil 178 (149) compared to patients on statin monotherapy 127 (93), (p<0.001).

crestor dosage 2015-06-07

Statin therapy prior Uroxatral Drug Interactions to percutaneous coronary intervention (PCI) is associated with reduced mortality and periprocedural myocardial injury after PCI. We studied whether single high dose statin loading is beneficial on the outcome of patients with acute coronary syndrome (ACS) underwent PCI.

crestor generic launch 2015-05-04

A simple, sensitive and rapid high-performance liquid chromatography/negative ion electrospray tandem mass Sinemet Online spectrometry method was developed and validated for the assay of fluvastatin in human plasma. Following solid-phase extraction, the analytes were separated using an isocratic mobile phase on a reversed-phase column and analyzed by mass spectrometry in the multiple reaction monitoring mode using the respective [M-H]- ions, m/z 410/348 for fluvastatin and m/z 480/418 for the internal standard. The assay exhibited a linear dynamic range of 2-500 ng/mL for fluvastatin in human plasma. The lower limit of quantification was 2 ng/mL with a relative standard deviation of less than 5%. Acceptable precision and accuracy were obtained for concentrations over the standard curve range. A run time of 1.5 min for each sample made it possible to analyze more than 400 human plasma samples per day. The validated method has been successfully used to analyze human plasma samples for application in pharmacokinetic, bioavailability or bioequivalence studies.

crestor 40mg tab 2017-12-20

Compared Cipro Drug Category with non-users, users of any drug within the statin class were 0.78 times less likely to develop C difficile infection in the hospital (95% CI 0.75 to 0.81) adjusting for potential confounders. Differences in estimates for specific statins were minimal. Niacin, fibrates and selective cholesterol absorption inhibitors showed no association with the risk of C difficile infection.