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Crestor

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:
Cresadex, Creston, Dorosur, Liparon, Provisacor, Richstatin, Rosumed, Rosuva, Rosuvas, Rosuvast, Rosuvastatina, Rosuvastatinum, Rosuvastin, Rovartal, Rovast, Rozavel, Simestat, Sinlip, Turbovas, Visacor, Zyrova

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

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Also known as:  Rosuvastatin.

Description

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).

Dosage

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.

Overdose

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

Storage

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.

Contraindications

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.

crestor benefits reviews

Incident fracture was a prespecified secondary end point of JUPITER. Fractures were confirmed by radiographs, computed tomography, bone scan, or other methods. Cox proportional hazards models were used to calculate hazard ratios (HRs) and associated 95% confidence intervals for the risk of fracture according to randomized treatment assignment, as well as increasing tertiles of hs-CRP, controlling for potential confounders.

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OBJECT Coil embolization is a safe, efficient, and minimally invasive technique for the treatment of intracranial aneurysms. However, coil embolization is associated with a higher risk of recurrence than clip ligation. In this study, the authors explore a new approach through the promotion of endothelial progenitor cells (EPCs) to optimize endothelialization of the aneurysm neck and reduce the risk of recurrence. METHODS A coiled aneurysm model was created in 48 adult male Sprague-Dawley rats via microsurgery. Half of these animals were treated with rosuvastatin (20 mg/kg) in saline via gavage for 10, 20, or 30 days. The other half were administered saline without rosuvastatin. An additional 15 rats underwent "mock surgery" (identical anesthesia and saline gavage but no surgery). The endothelial repair process in the coiled aneurysms was evaluated via flow cytometry, im-munostaining, and electronic microscopy. The mock surgery group was used for comparison in flow cytometry studies. The effects of rosuvastatin on viability and functioning of Sprague-Dawley rat bone marrow-derived EPCs were also explored via MTT, migration, and tube formation assays. RESULTS The aneurysm neck repair score was significantly higher in the rosuvastatin-treated rats than in the untreated rats (p < 0.05). The circulating EPC count was increased and maintained at a higher level in rosuvastatin-treated rats compared with the aneurysm rats that did not receive rosuvastatin (p < 0.05). Immunostaining showed that the aneurysm neck endothelium was more integrated and the number of kinase insert domain receptor-positive cells was increased in the rosuvastatin-treated rats. Further study demonstrated that rosuvastatin promoted EPC proliferation, migration, and tube formation. CONCLUSIONS Rosuvastatin promoted endothelialization of the coiled aneurysm neck via induction of EPCs, suggesting that promoting endothelialization provides an additional therapeutic opportunity during vascular endothelium repair.

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The effects of different hypolipidemic treatment strategies on emerging atherosclerosis risk factors remain unknown.

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Rosuvastatin reduces first cardiovascular events and all-cause mortality among men and women with LDL-C <130 mg/dl, elevated hsCRP, and concomitant evidence of moderate CKD. (JUPITER-Crestor 20 mg Versus Placebo in Prevention of Cardiovascular [CV] Events; NCT00239681).

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Although statin therapy is known to increase concentrations of PCSK9, whether this effect is related to the magnitude of LDL reduction is uncertain. This study was undertaken to understand the extent of this effect and examine the relationship between PCSK9 and LDL cholesterol (LDL-C) reduction.

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Congestive heart failure (HF) is characterised by increased proinflammatory stimulation and impaired endothelial function. Statin treatment exerts a beneficial effect on endothelial function and inflammatory process in patients with atherosclerosis. However, its effect in patients with HF is not well studied. Therefore, in the present study we compared the effect of short-term treatment with rosuvastatin or ezetimibe on endothelial function in patients with HF.

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Compared with healthy controls, HIV patients already have abnormal lipoprotein concentrations before the initiation of highly active antiretroviral therapy (HAART), which worsen with the therapy. HAART-associated dyslipidaemia features fundamental proatherogenic changes such as increased plasma triglycerides (TGs), increased total cholesterol and low-density lipoprotein cholesterol as well as decreased high-density lipoprotein cholesterol (HDL-C). The current guidelines for managing HIV-associated dyslipidaemia recommend diet and exercise counselling, alteration of HAART regimen or addition of lipid-lowering medications such as statins, fibrates and omega-3 (OM-3) fatty acids. Given that cardiovascular risk significantly increases with elevated lipid levels, selecting a drug to manage dyslipidaemia is particularly important. A case is described of an HIV patient who had severe hypertriglyceridaemia and bad metabolic parameters treated with rosuvastatin and OM-3 fatty acids. So we obtained a more marked reduction of TG levels than has never been described before in the literature, associated with a significant increase in HDL-C levels.

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The results show that doctors may overestimate patient adherence to lipid-lowering treatment. Based on data from the National Health Insurance Fund Administration of Hungary, satisfaction of doctors with high lipid level appears to be high. There is a need to optimize not only patient adherence, but adherence of doctors to lipid guidelines too.

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crestor go generic 2017-01-24

20-week-old Zucker obese and 16-week-old ZDF rats were treated with Rosuvastatin (25 mg/kg/day) or Enalapril (20 mg/kg/day) for 12 weeks. We examined metabolic parameters, indices of oxidative stress Keflex Canine Dosage and vascular dysfunction in ventricular and mesenteric small arteries (75-175 microm intraluminal diameter) from lean, Zucker obese and ZDF rats (untreated and treated).

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A total of 325 patients were identified. These patients were aged 63 ± 10 years, 50% male and prescription was mostly for primary prevention of cardiovascular disease (CVD) (59%). Co-morbidities included: established CVD present in 41%, type 2 diabetes mellitus (15%), hypertension (74%) and smoking (9%). Adverse effects had been documented to simvastatin (75%) or atorvastatin (63%). A total of 289 patients (89%) tolerated rosuvastatin well and were still adherent after a median follow-up of 14.9 (3-79) months. The remainder (n = 36; 11%) discontinued the medication after median 5 months' treatment due to adverse effects. Efficacy was assessed in 224 patients who had adequate data. Baseline lipids were total cholesterol (TC) 7.41 ± 1.50 mmol/L, triglycerides (TG) 2.26 (range 0.36-18.4) mmol/L; high density lipoprotein cholesterol (HDL-C) 1.43 ± 0.47 mmol/L and low density lipoprotein cholesterol (LDL-C) 4.76 ± 1. Zofran 80 Mg 38 mmol/L. Daily rosuvastatin (n = 134) reduced mean TC by 31%, TG 15% and LDL-C 43% (p < 0.001). Rosuvastatin 5 mg 2-3 times weekly (n = 79) reduced TC 26%, TG 16% and LDL-C 32% (p < 0.001). Weekly rosuvastatin (n = 11) reduced TC 17%, LDL-C by 23% (p < 0.001) but had no effect on TGs. Targets were attained in 17% of CHD-risk equivalent patients and 41% of primary prevention patients by National Cholesterol Education Program criteria and 27% and 68% using UK targets. No myositis or rhabdomyolysis was observed and alanine aminotransferase (ALT) and creatine kinase (CK) were similar to baseline.

crestor monthly cost 2017-03-07

Rosuvastatin protects against ADR- and PA-induced apoptosis in podocytes. Further, exposure to rosuvastatin increases p21 levels in podocytes in vitro. ADR induces apoptosis in p21 -/- mouse podocytes, but rosuvastatin's protective effect is not seen in the absence of p21. Reconstituting p21 in p21 -/- podocytes restores Altace Max Dose rosuvastatin's prosurvival effect.

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There are Symmetrel Drug Summary insufficient data available on the efficacy and safety of lipid-lowering therapy for patients with dyslipidaemia complicated by multiple metabolic abnormalities.

crestor 30 mg 2017-11-16

This 12-week, randomized, open-label, 2-arm, parallel-group trial was conducted at 210 centers in Finland, Iceland, and Ireland. Patients aged > or =18 years with a high risk for CHD and primary hypercholesterolemia (LDL-C >3.5 mmol/L [>135 mg/dL]) were randomized (2:1) to receive rosuvastatin 10 mg or atorvastatin 10 mg PO OD for 12 weeks. Before randomization, statin-naive patients underwent 6 weeks of dietary counseling, whereas patients receiving treatment with a starting dose of another lipid-lowering therapy but with an LDL-C level >3.1 mmol/L (>120 mg/dL) were switched to study drug immediately after they were determined eligible for the study Patients were assessed for fasting lipid levels at weeks 0 and 12, and the proportions of patients attaining 1998 and 2003 JTF lipid Bactroban Cost goals (1998: LDL-C, <3.0 mmol/L [<116 mg/dL]; TC, <5.0 mmol/L [<193 mg/dL]; 2003: LDL-C, <2.5 mmol/L [<97 mg/dL]; TC, <4.5 mmol/L [<174 mg/dL]) were calculated. Tolerability was monitored for the 12-week study and for an additional 36-week optional extension period.

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In patients with mild to moderate Propecia Normal Dosage asymptomatic AS, rosuvastatin did not attenuate the progression of diastolic dysfunction.

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Most patients with STEMI are prescribed statin therapy at discharge. Despite this, the target LDL-C is attained in Altace Generic Medication a minority of the patients due to suboptimal statin dosing. The formulation of statin did not affect LDL-C goal attainment. High-dose statin therapy is underused in real-world clinical practice. These findings emphasize the opportunities to improve outcomes of STEMI patients with evidence-based therapies.

crestor 10 mg 2015-03-01

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 Ceftin Dosing Dialysis 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.