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Zocor (Simvastatin)

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Zocor is an HMG-CoA reductase inhibitor. Zocor is used to reduce the risk of heart attack, stroke, and death due to coronary heart disease. It also reduces the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina, it lows high cholesterol and triglycerides and increases high-density lipoprotein (HDL, "good") cholesterol levels. Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Other names for this medication:

Similar Products:
Crestor, Zetia, Tricor, Pravachol, Mevacor, Lipitor


Also known as:  Simvastatin.


Zocor is an HMG-CoA reductase inhibitor.

Zocor is used to: reduce the risk of heart attack, stroke, and death due to coronary heart disease; reduce the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina; low high cholesterol and triglycerides; increase high-density lipoprotein (HDL, "good") cholesterol levels.

Zocor is also known as Imvastatin, Simlup, Simcardis, Ranzolont, Simvador.

Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Generic name of Zocor is Simvastatin.

Brand name of Zocor is Zocor.


Take Zocor orally.

Take Zocor with or without food.

Do not use grapefruit or grapefruit juice while taking Zocor. Eating grapefruit or drinking grapefruit juice may increase the amount of Zocor in blood, what may increase the serious side effects.

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


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


Store at room temperature below 30 degrees C (86 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 Zocor 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 Zocor if you are allergic to Zocor components.

Be careful with Zocor if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Be careful with Zocor if you suffer from low blood pressure, kidney problems, diabetes, serious infection, metabolism problems, hormonal problems.

Do not use potassium supplements or salt substitutes.

Avoid eating grapefruit or drinking grapefruit juice while taking Zocor.

While taking Zocor, you can make laboratory tests (blood cholesterol levels, liver function tests, creatine phosphokinase blood levels) to monitor the condition of your health.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Zocor suddenly.

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We report a case of a 70-year-old obese white man with sudden onset of severe rhabdomyolysis with consecutive renal failure. His medication included low-dose simvastatin, which he had taken for 6 years up until the event. The statin was withdrawn immediately. After 3 days of veno-venous hemofiltration his renal function was completely restored.

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Insulin-like growth factor 1 (IGF-1) and IGF-1 receptor (IGF-1R) signaling plays an important role in tumor progression in patients with certain gastrointestinal tract cancers. In addition to lowering cholesterol in serum, statins have pleiotropic effects, including anti-oxidative, anti-inflammatory or anti-neoplastic effects. Therefore, the present study investigated whether statins could induce the apoptosis of colon cancer cells and regulate the expression of IGF-1R and its associated signaling pathways in the present study. It was demonstrated that simvastatin and pravastatin suppressed cell proliferation and induced cell death in human HT-29 cells, but simvastatin was more potent than pravastatin. Simvastatin induced apoptosis in a concentration-dependent manner. In addition, simvastatin suppressed the expression of IGF-1R and inhibited the activity of phosphorylated-extracellular signal-regulated kinase (ERK)1/2 and phosphorylated-Akt activated by IGF-1. Simvastatin and IGF-1 each stimulated the activity of phosphorylated ERK1/2. However, simvastatin inhibited cell proliferation and IGF-1 stimulated cell proliferation. Mevalonic acid and PD98059 reversed the ERK activation and apoptosis induced by treatment with simvastatin. It was concluded that simvastatin induces the apoptosis of human colon cancer cells and inhibits IGF-1-induced ERK and Akt expression via the downregulation of IGF-1R expression and proapoptotic ERK activation. Simvastatin may be beneficial for the treatment of colon cancer. The present study suggested that statin may possess therapeutic potential for the treatment of colon cancer.

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Coadministration of ezetimibe/simvastatin was significantly (P<.001) more effective than simvastatin alone in reducing LDL-C levels for the pooled ezetimibe/simvastatin vs pooled simvastatin analysis and at each specific dose comparison. The decrease in LDL-C levels with coadministration of ezetimibe and the lowest dose of simvastatin, 10 mg, was similar to the decrease with the maximum dose of simvastatin, 80 mg. A significantly (P<.001) greater proportion of patients in the ezetimibe/simvastatin group achieved target LDL-C levels compared with those in the monotherapy group. Treatment with ezetimibe/simvastatin also led to greater reductions in total cholesterol, triglyceride, non-high-density lipoprotein cholesterol, and apolipoprotein B levels compared with simvastatin alone; both treatments increased high-density lipoprotein cholesterol levels similarly. The safety and tolerability profiles for the ezetimibe/simvastatin and monotherapy groups were similar.

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Simvastatin treatment significantly increased EPC in the hypercholesterolemic group, but failed to improve the EPC levels in the SSc patients, mainly in patients with late disease. Baseline levels of CEC were significantly higher in SSc patients compared with controls and at the end of the treatment they were significantly decreased. Regarding other markers of endothelial activation, we found that all the cytokine levels decreased in a statistically significant manner in the treated patients.

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This post-hoc analysis of a multicenter, randomized, double-blind, 6-week parallel study assessed the proportion of T2DM patients who attained specified LDL-C levels and non-HDL-C, ApoB, and hs-CRP with usual, recommended starting doses of E/S (10/20 mg) vs A (10 or 20 mg) and next highest doses of E/S (10/40 mg) vs A (40 mg) by logistic regression. Baseline triglyceride and hs-CRP effects were also evaluated.

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Ezetimibe does not increase circulating PCSK9 concentrations while simvastatin does. When added to simvastatin, ezetimibe does not cause an incremental increase in PCSK9 concentrations. Changes in PCSK9 concentrations are tightly regulated and mainly influenced by baseline PCSK9 levels and changes in LDL cholesterol.

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There were no significant associations between the pharmacokinetic parameters of simvastatin lactone and gender. For simvastatin hydroxy acid, peak plasma concentrations (Cmax) and dose-normalized by the subject weight Cmax (NCmax) were higher in females than in males. Furthermore, NCmax and dose-normalized by the subject weight AUC (NAUC0-24h, NAUC0-∞) ratios of simvastatin hydroxy acid to simvastatin lactone in females were higher than in males.

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Although intensive-dose statin therapy was associated with a reduced risk for important CV events, it was also associated with an increased risk for statin-induced adverse events. Therefore, moderate-dose statin therapy may be the most appropriate choice for achieving CV risk reduction in the majority of individuals, whereas intensive-dose statin therapy may be reserved for those at highest risk.

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Four of 5 patients with 2 defective CYP2D6 alleles discontinued the therapy at a low daily dose because of adverse events, with a significant mean decrease in the cholesterol levels of 0.23 mmol/L per milligram of simvastatin in the daily dose. In the group of 28 patients with 1 mutated CYP2D6 gene, 13 did not tolerate the therapy, whereas a mean decrease in the cholesterol levels of 0.20 mmol/L per milligram of simvastatin was found. One patient with a multiplication of the CYP2D6 gene showed a cholesterol reduction of only 0.01 mmol/L per milligram of simvastatin, at a maximal daily dose of 40 mg. Only 9 patients of the group of 54 persons who were homozygous for the wild-type allele discontinued the therapy because of intolerance. In that group, a mean decrease of cholesterol of 0.10 mmol/L per milligram of simvastatin was observed.

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Evacetrapib, as monotherapy or with statins, significantly reduces the concentrations of atherogenic apoB-containing lipoproteins, including Lp(a), LDL-P, and sLDL.

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Data were collected from 96 patients with a median age of 56 years; patients exhibited tendinitis (n = 63) and tendon rupture (n = 33). Tendinopathy more often occurred within the first year after statin initiation (59%). Tendon manifestations were related to atorvastatin (n = 35), simvastatin (n = 30), pravastatin (n = 21), fluvastatin (n = 5), and rosuvastatin (n = 5). Statin was reinitiated in 7 patients, resulting in recurrence of tendinopathy in all cases.

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Simvastatin, a cholesterol-lowering drug, also stimulates oral bone growth when applied topically, without systemic side-effects. However, the mechanisms involved in vivo are not known. We hypothesized that bone morphogenetic protein-2, nitric oxide synthase, and cyclooxygenase-2 are involved, based on prior in vitro evidence.

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The beneficial effects of statins in reducing cardiovascular events have been attributed predominantly to their lipid-lowering effects, recent studies suggest that these effects might be due to their anti-inflammatory properties. We here investigate the in vivo and in vitro effects of simvastatin on cytokine production in pre-dialysis chronic renal failure patients.

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Forty Sprague-Dawley rats were randomly divided into: five groups, 8 rats in each group: control untreated group, atherosclerosis group, atherosclerosis with Shenshao Decoction (low dose) group, atherosclerosis with Shenshao Decoction (high dose) group, atherosclerosis with simvastatin group. To stimulate atherosclerosis, the rats were fed vitamin D3 and a high-cholesterol diet. Four weeks later, treatments were maintained for eight weeks. Morphology changes were investigated by hematoxylin and eosin staining. Serum levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) were obtained by enzymatic assays with use of an automated biochemical analyzer. The expression of malondialdehyde (MDA), glutathione peroxidase (GSH-PX) were detected by enzyme-enzymelinked immunosorbent assay. The expression levels of interleukin (IL)-1β, IL-17A, and IL-23 were detected by linked immunoblotting.

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In the IMPROVE-IT trial, post-ACS patients with mean low density lipoprotein cholesterol (LDL-C) of 93.8 mg/dL at presentation were randomized to simvastatin/ezetimibe or simvastatin/placebo. The primary endpoint was cardiovascular death, major coronary event or stroke, and the median follow-up was 6 years. Efficacy and safety endpoints were examined by prior CABG status. Among 18 134 patients, 1684 (9.3%) had a prior CABG (median age 69 years, 82% male). During the trial, the median time-weighted LDL-C level was 55.0 mg/dL with simvastatin/ezetimibe vs. 69.9 mg/dL with simvastatin/placebo in patients with prior CABG (P < 0.001), and it was 53.6 mg/dL vs. 69.5 mg/dL, respectively, in patients without prior CABG (P < 0.001). The rate of the primary endpoint was higher in patients with vs. without prior CABG [56% vs. 32%, adj. hazard ratio 1.45, 95% confidence interval (CI) 1.33-1.58]. Patients with prior CABG receiving simvastatin/ezetimibe had an 8.8% (95% CI 3.1-14.6%) lower absolute risk over simvastatin/placebo in the primary endpoint, whereas patients without prior CABG had a 1.3% (95% CI 0-2.6%) lower absolute risk (P-interaction = 0.02). There were no between-group significant differences in safety endpoints.

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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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Currently, 6 hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are marketed in the United States (US). Given the wide variation in the prices and efficacy of statins, formal cost-effectiveness analysis may improve drug selection decisions. To assess the cost-effectiveness of statin therapy in primary and secondary prevention of coronary heart disease, we developed a model of the costs and consequences of lipid-regulating therapy and estimated the incremental cost-effectiveness of 5 statins (atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin) at usual starting doses versus no therapy. Drug effects on serum lipids were assessed using data approved by the US Food and Drug Administration for product labeling. Annual risks of coronary event occurrence were estimated using Framingham Heart Study coronary risk equations developed for use in this model. Current estimates of direct medical costs of coronary heart disease were used to assign costs to health states and acute coronary events. Main outcome measurements were net cost (statin therapy minus savings in coronary heart disease treatment), gain in life expectancy, and cost per life-year saved. The maximum gain in life expectancy was achieved with atorvastatin, which also had a lower net cost than lovastatin, pravastatin, and simvastatin. Compared with fluvastatin, atorvastatin's greater effectiveness is attained at a lower cost per life-year saved. The cost-effectiveness of HMG-CoA reductase inhibition in primary and secondary prevention of coronary heart disease has been improved with the introduction of atorvastatin.

zocor 20 mg NCT01999309; EudraCT-number 2013-000834-36.

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These results provide rationale for evaluating intraosseous injection of simvastatin in poloxamer 407 to enhance implant fixation in patients with osteoporosis.

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Recent studies have suggested that simvastatin may exert endothelial-protective and anti-ischemic effects via nitric oxide (NO) mechanisms. The aim of this study was to evaluate, in isolated working rat hearts, the effect of acute simvastatin administration on endothelial and inducible NO-synthase (eNOS and iNOS) mRNA and on myocytic apoptosis after ischemia-reperfusion. We used isolated working rat hearts submitted to 15 min global, no-flow, normothermic ischemia and 180 min reperfusion. To detect myocytic apoptosis we used DNA agarose gel electrophoresis and Tunel technique; eNOS and iNOS expression were evaluated by multiplex reverse transcriptase-polymerase chain reaction; glyceraldehyde-3-phosphate dehydrogenase (G3PDH) was used as standard. The eNOS and iNOS mRNAs were expressed as G3PDH/eNOS and G3PDH/iNOS densitometric ratio (BioRad Gel Doc 1000). Hearts were divided into four groups: A) hearts excised and used as histological controls; B) untreated hearts submitted to ischemia and reperfusion; C) actinomicin D-treated (1.5 mg/kg) hearts, perfused with 25 microM simvastatin, subjected to ischemia and reperfusion; D) hearts treated with simvastatin 25 microM and submitted to ischemia and reperfusion. In Group B we evidenced a significant myocytic apoptotic damage, reduced in groups C and D. In Group B an increase in G3PDH/eNOS ratio vs Group A was detected; in Group D a reduction in G3PDH/eNOS ratio vs Group B occurred; no significant changes were observed between groups C and D. As for G3PDH/iNOS ratio, it was significantly increased in Group D with respect to groups A and B. Our data suggest that simvastatin in acute may modulate NO-synthase mRNA expression (induction of eNOS mRNA by means of post-transcriptional mechanisms and inhibition of iNOS postischemic overexpression) and reduce myocytic apoptosis.

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The hypothesis was tested by experiments in which rats with streptozotocin (STZ)-induced diabetes and retinal endothelial cells maintained in high-glucose medium were treated with simvastatin. Blood-retinal barrier (BRB) function was assayed by determining extravasation of albumin. Oxidative stress was assayed by measuring lipid peroxidation, protein nitration of tyrosine, dihydroethidine oxidation, and chemiluminescence. Immunoprobe techniques were used to determine the levels of NADPH oxidase subunit expression and STAT3 activation.

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Plasma phospholipid transfer protein (PLTP) is an important modulator of high-density lipoprotein (HDL) metabolism, regulating its particle size, composition, and mass. In patients with low HDL and cardiovascular disease (CVD), plasma PLTP activity is positively correlated with the concentration of HDL particles containing apo A-I but not apo A-II (Lp(A-1)). We recently completed a study to determine the effect of simvastatin and niacin (S-N) therapy on disease progression/regression in these patients, and found that this therapy selectively increased Lp(A-I). To determine if PLTP was also increased with this drug therapy, we measured the PLTP activity in the plasma of 30 of these patients obtained at baseline and after 12 months of therapy, and compared the changes to a similar group of 31 patients who received placebo for the drugs. No significant increase in PLTP activity was observed in either group of patients. However, changes in apo A-I and A-II between these two time points were correlated with the corresponding change in PLTP activity. The correlation coefficients were r=0.57 (P=0.001) and r=0.43 (P=0.02) for apo A-I, and r=0.54 (P=0.002) and r=0.41 (P=0.02) for apo A-II in the placebo and S-N group, respectively. At baseline, PLTP activity correlated positively with the percent of plasma apo A-I associated with Lp(A-I) (r=0.38, P=0.04) and the amounts of apo A-I in these particles (r=0.43, P=0.02). These relationships persisted in patients who took placebo for 12 months (r=0.46, P=0.009 and r=0.37, P=0.04, respectively), but was attenuated in those treated with S-N. These data indicate that S-N-induced increase in Lp(A-I) was PLTP-independent. It also confirms our previous observation that an interrelationship exists between PLTP and apo-specific HDL particle subclasses in CVD patients with low HDL, and that this relationship is altered by drug intervention.

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Since we recently demonstrated that high-density lipoprotein induced human coronary artery endothelial cell (HCEC) tube formation through Ras/Raf/ERK (extracellular-signal-regulated kinase) activation [Arterioscler. Thromb. Vasc. Biol. 23 (2003) 802], it is possible that lipid-lowering agents such as statins, which reduce the prenylation of Ras, could decrease such tube formation. Therefore, we investigated whether this event occurs through inhibition of the Ras/Raf/ERK pathway. We developed an in vitro model of EC tube formation on a matrix gel. Simvastatin inhibited serum-induced endothelial tube formation after 18 h. The inhibition of ERK activity suppressed serum-induced tube formation. Farnesylpyrophosphate (Fpp), which translocates Ras from the cytoplasm to the cell membrane, rescued this inhibition. In addition, farnesyltransferase I inhibitor, which inhibits Ras farnesylation, and dominant-negative Ras (N17) also inhibited serum-induced tube formation. Although Fpp activated Ras assessed by a Ras pull-down assay and phospho(p)-ERK1/2, Fpp-induced p-ERK1/2 activation was not inhibited by simvastatin. In conclusion, simvastatin-induced Ras/Raf/ERK inactivation is a potent signal in the anti-angiogenic phenotype of HCECs. Fpp counteracted simvastatin-induced Ras/Raf/ERK inactivation.

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We conducted a retrospective cohort study on data from an integrated healthcare system. We included patients with pancreatic cancer stage I-IIb who underwent resection for curative intent between January 2005 and January 2011. Baseline statin use was characterized as any prior use as well as active use of either simvastatin or lovastatin. Intensity of exposure was calculated as average daily dose prior to surgery. Overall and disease-free survival was assessed from surgery until the end of study (April 2014). We used the Kaplan-Meier method and Cox proportional hazards regression to evaluate the impact of baseline statin use on survival, adjusting for age, sex, Charlson comorbidity score, resection margin, disease stage, and receipt of adjuvant chemotherapy.

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zocor 20 mg 2016-12-17

A Markov state transition model, using individual subject data from the Australian Diabetes, Obesity and Lifestyle study, was constructed to simulate the effects of the treatment versus no treatment on CVD events, and costs over 10 years. In 1,991 individuals classified as MetS and free of existing diabetes mellitus or CVD, treatment with the polypill (or its components) was effective at reducing cardiovascular events [statin: 171, aspirin (actetylsalicylic acid): 201, antihypertensive: 186 per 1,000 individuals]. The more drug therapies employed the greater the reduction, with the polypill reducing up to 351 cardiovascular events per 10,000 individuals. Cost-effectiveness analyses were sensitive to drug treatment costs and effectiveness of treatment. At a cost of AUD$42 per person per annum, aspirin was considered cost saving. All other treatment strategies, including the polypill, were not cost effective buy zocor .

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The effects of short-term intensive lipid-lowering treatment on coronary plaque composition have not yet been sufficiently evaluated. We investigated the influence of short-term buy zocor intensive lipid-lowering treatment on quantitative and qualitative changes in plaque components of non-culprit lesions in patients with acute coronary syndrome.

zocor simvastatin reviews 2017-06-26

Fifty six Wistar rats were randomly assigned to non-diabetic group (n=28 buy zocor ), and streptozotocin-induced diabetic group (n=28). Abdominal sepsis was induced in 14 diabetic and in 14 non diabetic rats and the other 28 rats were allocated on sham group. Sepsis rats and sham rats (each with 7 animals) were treated with oral simvastatin (20 mg kg-1 day-1) or normal saline solution 0.9%. Peripheral blood TNFalpha, IL-1beta, IL-6, C-reactive protein, procalcitonin, leukocytes and neutrophils were tested in all the animals. Statistical analysis was done by ANOVA and Tukey test, with p<0.05.

zocor generic cost 2016-09-03

Previous studies have shown that patients with early onset of Alzheimer buy zocor disease and vascular dementia have higher levels of circulating brain-derived 24S-hydroxycholesterol (cerebrosterol). Two recent epidemiological studies indicated that treatment with inhibitors of cholesterol synthesis (statins) reduces the incidence of Alzheimer disease.

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Emerging evidence suggests that clinically important antiinflammatory effects of HMG-CoA reductase inhibition may extend buy zocor beyond cardiovascular disease to other inflammatory disorders, such as rheumatoid arthritis (RA). Protective bone-specific anabolic and antiresorptive effects of HMG-CoA reductase inhibitors have also been evaluated in normal and osteoporotic bone. The specific effect of statins on inflammation-induced bone loss has not previously been a focus of evaluation. We investigated whether simvastatin, a potent HMG-CoA reductase inhibitor, alters bone turnover in an animal model of RA, thus preventing periarticular bone loss.

zocor safe dosage 2015-06-01

The first clinical studies on hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors reported a low incidence of liver toxicity. The personal observation of a case of simvastatin-induced acute cholestatic hepatitis prompted us to evaluate the true incidence of hepatic side effects of these drugs in a large Italian population. One hundred patients taking simvastatin and ninety patients treated with pravastatin were followed-up six months with periodical evaluation of serum lipid levels and liver function test. In 5% of simvastatin-treated patients and 4.5% of pravastatin-treated patients significant liver toxicity was observed, which required drug discontinuation. The mechanism of liver damage was direct, idiosyncratic, but immunological features of drug toxicity could be hypothesized in buy zocor one patient.

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This study buy zocor aimed to investigate potential drug-drug interactions (pDDIs) with warfarin to minimize them, assess the acceptability of pharmaceutical interventions by the medical team and the impact on the international normalized ratio (INR) results.

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These results suggest that atorvastatin is the most buy zocor potent of the assayed statins with respect to suppression of IL-1β-induced MUC5AC mRNA expression, and may be considered as an anti-hypersecretory agent.

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Genome-wide association (GWA) buy zocor studies for pharmacogenomics-related traits are increasingly being performed to identify loci that affect either drug response or susceptibility to adverse drug reactions. Until now, only the largest effects have been detected, partly because of the challenges of obtaining large numbers of cases for pharmacogenomic studies. Since 2007, a range of pharmacogenomics GWA studies have been published that have identified several interesting and novel associations between drug responses or reactions and clinically relevant loci, showing the value of this approach.

zocor normal dosage 2016-01-31

Cardiotrophin-1 (CT-1) is a cytokine involved in the growth and survival of cardiac cells via activation of the Janus activated kinase/signal transducer activator of transcription (JAK/STAT). Statins, 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have effects that extend beyond cholesterol reduction and inhibit vascular smooth muscle cell (VSMC) proliferation and cardiac hypertrophy. However, whether stains also can inhibitin vitromyocardial hypertrophy or not still remains elusive. The purpose of this study was to explore the effects of simvastatin on the hypertrophy of cultured rat cardiomyocytes induced by CT-1 and buy zocor to investigate whether this effect was mediated via JAK-STAT signaling pathway.

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In this small study, short-term statin therapy appeared to significantly improve chronic vascular inflammation and endothelial dysfunction with no adverse effects in children complicated by CAA late after KD. However, long-term and randomized studies buy zocor are still needed to make further conclusions.

zocor and alcohol 2016-09-19

Patients with dyslipidemia were evaluated with regard to the 5 drugs regimen: simvastatin (average dose, 11.8 mg/day), gemfibrozil (dose 963 mg/day), bezafibrate (433 mg/day), fenofibrate (211 mg/day) and acipimox (667 mg/day). The responses to the drug were divided into different time periods and the magnitude of responses were presented either as average changes in per cent from baseline or as proportion of patients (also in %) whose levels changed by a predetermined percentage. These predetermined percentage took into account the variation observed among patients who had more than 3 measurements during baseline. These levels for significant changes were 16 per cent for total cholesterol (TC), 25-30 per cent for high- and low-density lipoprotein (HDL and LDL), and 44 per cent for triglyceride (TG). Our subjects responded to the drugs within the range reported by other investigators except for acipimox which produced no alteration. Sixty to 100 per cent of patients reduced their TC by 16 per cent with an average change in TC of around -16 per cent to -24 per cent. Simvastatin and fenofibrate appeared most effective in altering TC. The HDL increased 10 per cent to 29 per cent depending on the drug but in terms of proportion that responded by an increment greater than 25 per cent, this was seen in only 23 per cent to 45 per cent of the patients. Long term follow-up which was possible only on 42 patients showed 11 who lessened their response and 6 whose response became more marked.(ABSTRACT TRUNCATED AT buy zocor 250 WORDS)

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Simvastatin (SS) is an effective cholesterol-lowering medicine, and is hydrolyzed to simvastatin acid (SSA) after oral administration. Due to SS and SSA inter-conversion and its pH and temperature dependence, SS and SSA quantitation is analytically challenging. Here we report a high-throughput salting-out assisted liquid/liquid extraction (SALLE) method with acetonitrile and mass spectrometry compatible salts for simultaneous LC-MS/MS analysis of SS and SSA. The sample preparation of a 96-well plate using SALLE was completed within 20 min, and the SALLE extract was diluted and injected into an LC-MS/MS system with a cycle time of 2.0 min/sample. The seamless interface Zofran 8mg Dosage of SALLE and LC-MS eliminated drying down step and thus potential sample exposure to room or higher temperature. The stability of SS and SSA in various concentration ratios in plasma was evaluated at room and low (4 degrees C) temperature and the low temperature (4 degrees C) was found necessary to maintain sample integrity. The short sample preparation time along with controlled temperature (2-4 degrees C) and acidity (pH 4.5) throughout sample preparation minimized the conversion of SS-->SSA to < or = 0.10% and the conversion of SSA-->SS to 0.00% The method was validated with a lower limit of quantitation (LLOQ) of 0.094 ng mL(-1) for both SS and SSA and a sample volume of 100 microL. The method was used for a bioequivalence study with 4048 samples. Incurred sample reproducibility (ISR) analysis of 362 samples from the study exceeded ISR requirement with 99% re-analysis results within 100+/-20% of the original analysis results.

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The drug-drug interaction model between simvastatin and itraconazole was simultaneously modeled using a one Famvir Loading Dose compartment parent-metabolite model for simvastatin, and a two-compartment model for itraconazole.

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There are sufficient data to support evening administration of simvastatin Norvasc 10mg Medication to achieve optimal lowering of LDL-C levels. Rigorous and robust trials are necessary to determine the best administration time to achieve optimal LDL-C lowering for lovastatin, pravastatin, rosuvastatin, atorvastatin, and fluvastatin.

zocor with alcohol 2016-10-07

Objective. The aim of this study was to investigate the role of hyperlipidemia in the microstructure of parotid gland and its possible amelioration through statin treatment on Wistar rats. Methods. Forty Wistar rats (111.06 ± 3.36 g) were divided into 4 groups (A1, A2 controls, B1, B2 experimental). Groups A1 Tofranil And Alcohol and A2 consumed normal cereal rodents diet during the experimental hyperlipidemic mixture. The A2 and B2 were treated with simvastatin (Zocor) 40 mg/kg/daily p.o. for 3 months. Results. Total cholesterol, triglycerides, high density lipoproteins, and low density lipoproteins were increased in groups B1 and B2 while the parotid weight was decreased. The histological findings demonstrated changes in the parotid gland morphology of the B1 and B2, such as the presence of chronic inflammation, fibrosis, lipocytes, and foci of lymphocytic infiltration. Conclusions. The influence of statin tended to predominate over the chronic inflammation while the lipocytes were decreased and remodelling of the parotid's structure occurred.

zocor 40mg medication 2015-04-25

Of 2394 patients who received SIMVA or EZE/SIMVA and for whom MetS status at baseline could be determined, 31% were identified as having MetS. In the entire cohort, treatment with EZE/SIMVA led to a significant incremental reduction in low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B, triglyceride (TG), and C-reactive protein compared to SIMVA and these effects were similar across the MetS and non-MetS subgroups. EZE/SIMVA was well Periactin Patient Reviews tolerated in both the MetS and non-MetS subgroups.

zocor cold medicine 2017-10-16

These findings suggest that simvastatin reduces inflammation in atherosclerotic Minipress Overdose plaques and in blood mononuclear cells more than expected for the lipid reduction achieved.

zocor online 2016-06-18

BALB/c mice were sensitized to ovalbumin over 4 weeks and exposed to 1% ovalbumin aerosol over 2 weeks. Simvastatin (40 mg/kg) or simvastatin plus mevalonate 30 Mg Singulair (20 mg/kg) was injected intraperitoneally before each ovalbumin exposure.

zocor 500 mg 2017-02-19

To verify Trileptal With Alcohol the effect of hypercholesterolemia on fatty infiltration and the quality of tendon-to-bone healing and its reversibility by lowering the cholesterol level in a chronic tear model using the rabbit supraspinatus.

zocor 40 mg 2016-10-10

The treatment of proliferating murine tubular cells (MCT) with simvastatin induced apoptosis in a time- and dose-dependent manner (0.1 to 1 micromol/L). Apoptosis was correlated with Bcl-xL mRNA and protein down-regulation. Tegretol User Reviews By contrast, the treatment with simvastatin did not modify the expression of the proapoptotic protein Bax. Simvastatin treatment was associated with cytochrome C release from the mitochondria to the cytosol. We also observed the presence of active caspase 9 and 3 during apoptosis induced by simvastatin. These effects were reversed by mevalonate, farnesylpyrophosphate (FPP), and geranylgeranylpyrophosphate (GGPP), suggesting the involvement of protein prenylation. Simvastatin appears to alter the balance between cell-life and death-promoting genes, as reflected by the decreased Bcl-xL/Bax ratio. Supporting this hypothesis, overexpression of Bcl-xL reduced the amount of apoptosis induced by simvastatin by 80% when compared with control vector-expressing cells. The overexpression of Bcl-xL also prevented the activation of caspase 9 and 3.

zocor maximum dosage 2017-03-19

We measured the serum concentration of hsCRP at 30 days (n=3813) and 4 months in patients with non-ST-elevation or ST-elevation acute coronary syndrome randomly assigned to an early intensive versus delayed conservative simvastatin strategy in the Aggrastat-to-Zocor Trial. Patients with hsCRP >3 mg/L at 30 days had significantly higher 2-year mortality rates than those with hsCRP 1 to 3 mg/L or hsCRP <1 mg/L (6.1% versus 3.7% versus 1.6%, P<0.0001). Results were similar with hsCRP measured at 4 months. After adjusting for age, gender, diabetes, smoking, cardiovascular history, index event, lipid levels, and randomly assigned treatment, patients with hsCRP >3 mg/L were at more than 3-fold higher risk of death (HR, 3.7; 95% CI, 1.9 to 7.2) compared with those with hsCRP <1 mg/L. "Average" levels of hsCRP (1 to 3 mg/L) were also associated with increased risk compared with those with Diamox Er Dosage hsCRP <1 mg/L (HR, 2.3; 95% CI, 1.2 to 4.6). Patients allocated to early intensive statin therapy were more likely to achieve hsCRP levels <1 mg/L at 30 days (P=0.028) and 4 months (P<0.0001).

zocor mg 2017-04-08

The study has delimited the region responsive to transcription factors to a sequence surrounding the C(-107)T polymorphism of the paraoxonase-1 gene, and demonstrated an interaction at this sequence between Sp1 and SREBP-2. SREBP-2 and statin strongly up-regulated the C, but not the T allele. The results suggest a pharmacogenetic interaction between the promoter and simvastatin, which can influence serum paraoxonase in Nolvadex Tablets patients.

zocor generic name 2016-06-29

Clinacanthus nutans is used traditionally in many parts of Asia to improve well-being, but there are limited studies on Desyrel Tabs 50mg its efficacy. We explored the potential use of C. nutans for prevention of high fat and high cholesterol diet-(HFHC-) induced insulin resistance in rats.

zocor blockbuster drug 2017-05-10

In the 2002 - 2006 period the total consumption of statins increased by 261%, while the number of patients treated with statins increased by 252%. Simvastatin had the greatest share in the total Zantac 6 Tablets consumption, while atorvastatin consumption recorded the greatest individual increase.

zocor dosage information 2016-06-08

Simvastatin may decrease pulmonary arterial pressure in a subset of patients with pulmonary hypertension.

zocor 10mg tablets 2016-06-03

To compare change in low-density lipoprotein cholesterol (LDL-C) levels and National Cholesterol Education Program (NCEP) Adult Treatment Panel III LDL-C goal attainment in diabetic patients treated with rosuvastatin versus other statins in a large, managed care health plan.

buy online zocor 2017-03-30

A total of 89,703 patients with average follow up of 5.0 ± 3.5 years were included in this study. In the 56,044 patients receiving statins, 5698 (10%) had new-onset AF vs. 5010 (15%) in the 33,659 patients serving as controls. The adjusted Cox regression analysis showed significant reduction in new-onset AF (HR 0.83, 95% CI 0.80-0.87, p < 0.001) in statin users. Adjustment for propensity score yielded nearly identical results (HR 0.82, 95% CI 0.78-0.85, p < 0.001). Furthermore, patients compliant to statin treatment had significant reduction in new-onset AF (HR 0.84, 95% CI 0.80-0.87, p < 0.001). Finally, simvastatin and atorvastatin were significantly more effective than pravastatin (both p < 0.01) in reducing new-onset AF.

zocor dosage timing 2017-09-30

Atorvastatin reduced the liver-derived acute-phase reactants, CRP and SAA, whilst the effect of simvastatin was small or absent. Small and inconsistent effects were seen for both statins on plasma levels of IL-6 and ICAM-1.

zocor dosage forms 2015-05-12

We identified 85 incident simvastatin users, for whom a cholesterol measurement both before and after the start of simvastatin therapy was available. Associations between the ABCB1 gene variants and reductions in cholesterol levels were analyzed. In our analysis we stratified for gender, because the level of P-gp expression in the liver is higher in men than in women.