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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.

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Actalipid, Docsimvasta, Doctiverine, Dosavastatin, Lipex, Lipinorm, Lodales, Normotherin, Simbastatin, Simcard, Simgal, Simvastatina, Simvastatinum, Simvofix, Simvor, Sinvacor, Sivastin, Statinal, Vasilip, Zeid, Zocord, Zorced, Zorstat, Zosta, Zostin, Zostine, Zovast, Zovastin, Zovatin, Zurocid

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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.

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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.

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Data on simvastain utilization, prices, and expenditures between 1997 and 2007 in the United Kingdom and four other countries were obtained from an outside vendor.

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Cerebral cavernous malformation (CCM) is a common vascular dysplasia that affects both systemic and central nervous system blood vessels. Loss of function mutations in the CCM2 gene cause CCM. Here we show that targeted disruption of Ccm2 in mice results in failed lumen formation and early embryonic death through an endothelial cell autonomous mechanism. We show that CCM2 regulates endothelial cytoskeletal architecture, cell-to-cell interactions and lumen formation. Heterozygosity at Ccm2, a genotype equivalent to that in human CCM, results in impaired endothelial barrier function. On the basis of our biochemical studies indicating that loss of CCM2 results in activation of RHOA GTPase, we rescued the cellular phenotype and barrier function in heterozygous mice with simvastatin, a drug known to inhibit Rho GTPases. These data offer the prospect for pharmacological treatment of a human vascular dysplasia with a widely available and safe drug.

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There is little evidence to show that strict dietary modification alone confers any significant impact on cardiac events in primary and secondary prevention of coronary heart disease. Given the efficacy of the statins, the need for strict dietary modification in patients on statin therapy has been questioned. This study was performed to assess 1) the added benefit on serum lipid levels of a strict low-fat dietary regimen in patients with hypercholesterolaemia already treated with simvastatin; 2) the efficacy of simvastatin on the lipid profile of our sample Asian population; and 3) the tolerability and side-effect profile of simvastatin. This study was a prospective evaluation of 60 patients with hypercholesterolaemia treated with simvastatin who were subjected to either a normal diet or a dietitian guided low-fat diet. Assessment of the effects on serum lipid levels, side-effects, biochemical and haematological markers were performed. After 24 weeks of treatment, a strict dietitian guided low-fat diet conferred no additional benefit over and above what was achieved by simvastatin alone. Furthermore, a higher dose of simvastatin was needed in the dietitian guided diet group to achieve the target LDL-cholesterol level. Simvastatin resulted in a significant positive alteration of lipid profiles in all patients. The drug was well tolerated, with no significant change in either haematological or biochemical indices. Simvastatin is a highly effective cholesterol-lowering drug with a beneficial effect on the entire lipid spectrum in a cross-section of Asian patients, and is well tolerated. A dietitian guided dietary approach confers no additional advantage once statin therapy has been initiated.

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This study shows that simvastatin therapy leads to a reversal of the cyclosporine A-induced bone loss, which may be mediated by downregulation of interleukin-1beta and prostaglandin E(2) production.

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Statin therapy is associated with changes in low-density, very low-density, and high- density lipoprotein metabolism. The effect of statin therapy on a minor high-density lipoprotein particle containing glycosylphosphatidylinositol-specific phospholipase D has not been examined. Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) has been implicated in triglyceride metabolism. A double-blind, crossover design comparing the effect of simvastatin (80 mg) and atorvastatin (80 mg) on serum lipid and glycosylphosphatidylinositol-specific phospholipase D levels was conducted in 13 patients with low high-density lipoproteins. Both statins reduced cholesterol, triglycerides, and apolipoprotein B and significantly lowered serum glycosylphosphatidylinositol-specific phospholipase D levels (16%). This statin effect seems to occur in the plasma compartment as neither statin altered GPI-PLD mRNA levels in HepG2 cells. Serum glycosylphosphatidylinositol-specific phospholipase D levels are regulated by statins and may represent an additional biochemical mechanism for affecting serum triglyceride levels.

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Low doses of statins rapidly induce the translocation of Akt to discrete sites in endothelial cell plasma membrane that colocalize with F-actin-positive, focal adhesion kinase (FAK)-negative lamellipodia and filopodia. This translocation event requires the lipid-binding, pleckstrin homology domain of Akt. Treatment with phosphoinositide 3-kinase (PI 3-kinase) inhibitors or the HMG-CoA reductase reaction product L-mevalonate blocks the translocation of Akt in response to statin stimulation. Furthermore, the ability of statins to promote Akt activation and translocation to the membrane is inhibited by cholesterol delivery to cells, but cholesterol loading had no effect on VEGF-induced Akt activation.

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This observational study used merged administrative data from VHA and a predominant regional PHIP to select veterans < 65 years of age, residing in two Midwestern US states, and simultaneously enrolled in both VHA and the PHIP during fiscal years (FY) 2001-2010. Primary outcome measures included counts of prescriptions dispensed from VHA and non-VHA pharmacies, and frequencies of medications dispensed by non-VHA pharmacies based on PHIP claims.

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In this study, simvastatin, atorvastatin, ezetimibe, and ezetimibe + simvastatin combination were administered to arthritic rats, first to determine their effects on the inflammatory response, employing a low-dose adjuvant-induced arthritis model in rats. Arthritis was induced by the subcutaneous injection of a suspension of Mycobacterium tuberculosis (100 μg) in mineral oil [complete Freund's adjuvant used (CFA)] into the plantar surface of the hind paws. Simvastatin(40 mg/kg), atorvastatin(10 mg/kg), ezetimibe(10 mg/kg), ezetimibe(10 mg/kg) + simvastatin(20 mg/kg or 40 mg/kg) were given intragastrically and the treatment began on the day of CFA injection and continued daily up to the 28th day after arthritis induction. The ezetimibe + simvastatin combination was more effective in reducing the inflammatory response in arthritic rats than in atorvastatin, simvastatin, or ezetimibe monotherapy. The observed effect seems to be cholesterol-independent as there were no changes in plasma cholesterol levels. In spite of the benefits on joint lesions, treatment with ezetimibe + simvastatin combination caused a marked increment in liver, kidneys, spleen size, and plasma transaminases activities. Therefore, animals treated with the ezetimibe(10 mg/kg) + simvastatin(40 mg/kg) combination were also submitted to liver perfusion experiments. In this regard, ezetimibe + simvastatin did not improve the liver metabolic alterations seen in control arthritic rats, on the contrary, a worsening was observed in liver production of glucose from alanine, as well as in oxygen uptake. All of these metabolic changes appear to be induced by treatment with ezetimibe + simvastatin combination, as the same metabolic effects were observed in normal and treated arthritic animals.

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IMPROVE-IT study demonstrated that the addition 10 mg of ezetimibe to 40 mg of simvastatin in patients after acute coronary syndrome reduces significantly not only their LDL-cholesterol, but also the number of cardiovascular events. Recently published subanalysis of this study was focused on whether these combinations of drugs is more preferable for patients with diabetes mellitus or for patients without diabetes. The addition of ezetimibe to a simvastatin resulted in a greater decline of LDL-cholesterol level in diabetic group than in patients without diabetes. In patients with diabetes mellitus their cardiovascular morbidity and mortality were decreased significantly; reduction of these clinical end-points in the group of patients without diabetes were not statistically significant.

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Large-scale randomized controlled trials (RCTs) have well demonstrated the beneficial effects of cholesterol-lowering treatment with statins in patients at high risk of vascular disease. However, large statin RCTs were usually restricted to the typical 5-6 years. Moreover, non-cardiovascular events, especially the risk of cancer, probably failed to emerge within a restricted period of 6 years. The aim of this study was to evaluate the long-term efficacy and safety of statin treatment by performing a meta-analysis of statin RCTs with extended follow-up beyond 6 years. Six RCTs with post-trial follow-up were eligible for inclusion, involving 47,296 patients with total follow-up ranging from 6.7 to 14.7 years. During the post-trial period, all the surviving participants were advised to take a statin and the cholesterol level were almost identical between the original statin group and the original placebo group. Over the entire 6.7-14.7 years of follow-up, a significant reduction in the rates of all-cause mortality (relative risk 0.90, 95% confidence interval 0.85-0.96; P=0.0009), cardiovascular mortality (0.87, 0.81-0.93; P<0.0001) and major coronary events (0.79, 0.72-0.86; P<0.00001) was observed in favour of the original statin group. During 2-year post-trial period, further reduction in all-cause mortality (0.83, 0.74-0.93; P=0.001), cardiovascular mortality (0.81, 0.69-0.95; P=0.01) and major coronary events (0.77, 0.63-0.95; P=0.01) was observed among initially statin-treated patients. Over the entire follow-up period, statin treatment did not increase the incidence of cancers (0.99, 0.95-1.04; P=0.79), deaths from cancers (1.00, 0.93-1.07; P=0.98) and non-cardiovascular mortality (0.95, 0.90-1.00; P=0.07). In conclusion, statin treatment beyond 6 years is effective and safe in patients at high risk of vascular events. Moreover, earlier treatment with statin may not only preserve the initial benefit but also have further survival benefit for additional 2 years. Further studies are called for to explore the underlying mechanisms.

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Puerarin inhibits the formation and development of AS plaque and suppresses the migration and reproduction of vascular smooth muscle cells by decreasing PCNA and PDGF-A expressions in the rabbit. This is encouraging in terms of cardiovascular disease prevention/treatment.

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Low-density lipoprotein receptors (LDLRs) mediate the uptake of lipoprotein particles into cells, as studied mainly in peripheral tissues. Here, we show that nerve growth factor (NGF) increases LDLR levels in PC6.3 cells and in cultured septal neurons from embryonic rat brain. Study of the mechanisms showed that NGF enhanced transcription of the LDLR gene, acting mainly via Tropomyosin receptor kinase A receptors. Simvastatin, a cholesterol-lowering drug, also increased the LDLR expression in PC6.3 cells. In addition, pro-NGF and pro-brain-derived neurotrophic factor, acting via the p75 neurotrophin receptor (p75NTR) also increased LDLRs. We further observed that Myosin Regulatory Light Chain-Interacting Protein/Inducible Degrader of the LDLR (Mylip/Idol) was down-regulated by pro-NGF, whereas the other LDLR regulator, proprotein convertase subtilisin kexin 9 (PCSK9) was not significantly changed. On the functional side, NGF and pro-NGF increased lipoprotein uptake by neuronal cells as shown using diacetyl-labeled LDL. The addition of serum-derived lipoprotein particles in conjunction with NGF or simvastatin enhanced neurite outgrowth. Collectively, these results show that NGF and simvastatin are able to stimulate lipoprotein uptake by neurons with a positive effect on neurite outgrowth. Increases in LDLRs and lipoprotein particles in neurons could play a functional role during brain development, in neuroregeneration and after brain injuries. Nerve growth factor (NGF) and pro-NGF induce the expression of low-density lipoprotein receptors (LDLRs) in neuronal cells leading to increased LDLR levels. Pro-NGF also down-regulated myosin regulatory light chain-interacting protein/inducible degrader of the LDLR (Mylip/Idol) that is involved in the degradation of LDLRs. NGF acts mainly via Tropomyosin receptor kinase A (TrkA) receptors, whereas pro-NGF stimulates p75 neurotrophin receptor (p75NTR). Elevated LDLRs upon NGF and pro-NGF treatments enhanced lipoprotein uptake by neurons. Addition of LDL particles further led to the stimulation of neurite outgrowth in PC6.3 cells after NGF or simvastatin treatments, suggesting a stimulatory role of lipoproteins on neuronal differentiation. In contrast, pro-NGF had no effect on neurite outgrowth either in the absence or presence of LDL particles. The precise mechanisms by which increased lipoproteins uptake can affect neurite outgrowth warrant further studies.

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Oral administration of rapamycin effectively attenuated inflammation, inhibited progression and enhanced stability of Arjuna Online atherosclerotic plaques in rabbits, without altering serum lipid levels. Our findings suggest a novel approach to the treatment of atherosclerosis.

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We describe the case of a 69-year-old man with a history of muscular symptoms dating back to his childhood; McArdle's disease (glycogen-storage disease V) was diagnosed following an episode of myositis in which a statin and physical exertion appear to have been precipitating factors. This case demonstrates that the ischaemic lactate-ammonia test still has a place in screening patients with symptoms suggestive of McArdle's disease and emphasizes the importance of carrying out glycogen phosphorylase histochemistry on the skeletal muscle biopsy to confirm the diagnosis. In patients who develop a raised plasma creatine kinase level or muscular symptoms during lipid-lowering therapy, the clinician should be alert to the possibility Noroxin Generic of an underlying myopathy.

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Association of statins with autoimmune disorders is rarely reported. We report a case of an apparently healthy 76-year-old woman who was on long-term statin therapy presenting with severe rhabdomyolysis, autoimmune hepatitis, and positive lupus antibodies. Patient presented with Zetia 20 Mg Prices complaints of worsening fatigue, leg cramps, and progressive weakening of lower extremities over 3 weeks. The patient was on simvastatin daily for several years. Clinical examination on admission included muscle tenderness, lower extremity edema, and ascites. Her laboratory values on admission showed elevated creatine kinase and transaminases. Immunologic workup revealed positive ANA, anti-dsDNA and anti-SSA antibodies. F-actin antibody was also positive at high titer. Magnetic resonance imaging of the lower extremities showed findings consistent with myositis. Patient underwent biopsy of the thigh muscles, which showed inflammatory myositis. Liver biopsy was characteristic of autoimmune hepatitis. Patient responded well to immunosuppressive therapy with azathioprine and prednisone. Although statins are generally considered safe, recent data from long-term follow-up on patients who are on statins for long duration suggest that prolonged exposure to statins may trigger autoimmune reactions. The exact mechanism of statin-induced autoimmune reaction is unclear. Statins, as proapoptotic agents, release nuclear antigen into the circulation and may induce the production of pathogenic autoantibodies. The role of statins in inducing an endoplasmic reticular stress response with associated upregulation of major histocompatibility complex-1 expression and antigen presentation by muscle fibers has also been reported. Systemic immunosuppressive therapy has proven to be effective in many reported cases.

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Of 197 hypercholesterolaemic patients on stable low-fat low-cholesterol diet Ziac Generic Side Effects , 49 were put on atorvastatin 10 mg per day, 48 on fluvastatin 40 mg per day, 50 on pravastatin 20 mg per day and 50 on simvastatin 10 mg per day.

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CAs were induced in Sprague-Dawley rats with or without oral administration of simvastatin. The size and media thickness of CAs was evaluated 3 months after aneurysm induction. Expression of macrophage chemoattractant protein-1, vascular cell adhesion molecule-1, endothelial nitric oxide synthase, interleukin-1beta, inducible nitric oxide synthase, matrix Benicar Medication Generic metalloproteinase-2, and matrix metalloproteinase-9 in aneurysmal walls was examined by reverse transcriptase-polymerase chain reaction and immunohistochemistry. To examine whether simvastatin has a suppressive effect on preexisting CAs, simvastatin administration started at 1 month after aneurysm induction.

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Besides hyperglycemia and hypertension, a recently recognized risk factor for diabetic retinopathy (DR) appears to be hyperlipidemia. While studies using earlier generation Cordarone Generic lipid lowering agents in DR were disappointing, a randomized trial using HMG-CoA Reductase Inhibitors has strong rationale, though hitherto not attempted. The aim of the present study was to compare the HMG-CoA Reductase Inhibitor, simvastatin, with placebo in patients having DR in a double-blind randomized placebo-controlled trial. Fifty patients with diabetes mellitus (Type 1 and 2) with good glycemic control and hypercholesterolemia and having DR (non-clinically significant macular edema and visual acuity 6/24 or better) in either or both eyes were randomized to simvastatin 20-mg per day or placebo, and were followed up for 180 days. On simvastatin therapy, total cholesterol and low-density lipoprotein cholesterol (LDL-C) decreased (P < 0.001, respectively), and the level of high-density lipoprotein cholesterol (HDL-C) increased (P < 0.001). VA improved in four patients using simvastatin, (not statistically different from placebo group) and worsening of VA occurred in seven patients in the placebo group and none in the simvastatin group (P = 0.009). Fundus fluorescein angiography and color fundus photograph showed improvement in one patient in the simvastatin group, while seven patients showed worsening in the placebo group (P = 0.009). The observations of the current study suggest that the HMG-CoA Reductase Inhibitor simvastatin significantly retards the progression of retinopathy in diabetic patients with hypercholesterolemia. The potential of this class of drugs for the primary prevention of DR and other microvascular complications needs to be explored further.

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To evaluate the effect of statins on aneurysm growth in a group of consecutive patients under surveillance for infrarenal aortic aneurysms (AAA Crestor Generic Coupon ).

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Experimental cements were prepared with TCP containing simvastatin and atorvastatin. Cell proliferation, cell adherence on a dentin disc, alkaline phosphatase (ALP) activity, expression of osteogenic/odontoblastic markers, and mineralization of the human dental Ranbaxy Lipitor Generic Name pulp cells on experimental cement and MTA were assessed.

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There is considerable evidence that more aggressive lowering of low-density lipoprotein (LDL) cholesterol is associated with increased benefits in reducing atherosclerotic disease burden, supporting the notion of 'the lower, the better.' However, achievement of currently recommended goals has proven difficult with lipid-lowering agents at the commonly used doses. Current options for achieving greater LDL cholesterol reductions include use of high doses of the most effective of the available statins and use of high or moderate statin doses in combination with agents that work in a complementary manner (e.g. bile acid sequestrants or niacin). Near-term options may include statins with increased LDL cholesterol-lowering effectiveness and better-tolerated secondary agents that can be combined with statin therapy. Rosuvastatin (Crestor, AstraZeneca) is a new statin that may prove to be of considerable utility in achieving greater LDL cholesterol reductions than are currently possible with existing statins. Recent phase III clinical trials have shown that this agent produces significantly greater LDL cholesterol reductions Buy Cheap Online Augmentin than atorvastatin, simvastatin, or pravastatin in patients with primary hypercholesterolemia and significantly greater reductions than the maximal dose of atorvastatin in patients with familial hypercholesterolemia.

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A simple, precise, and rapid stability-indicating reversed-phase column liquid chromatographic (RP-LC) method has been developed and subsequently validated for simultaneous estimation of simvastatin (SIM) and ezetimibe (EZE) from their combination drug product. The proposed RP-LC method utilizes a LiChrospher 100 C18, 5 microm, 250 x 4.0 mm id column at ambient temperature; optimum mobile phase consisting of acetonitrile-water-methanol (60 + 25 + 15, v/v/v) with apparent pH adjusted to 4.0 +/- 0.1; mobile phase flow rate of 1.5 mL/min; and ultraviolet detection at 238 nm. SIM, EZE, and their combination drug product were exposed to thermal, photolytic, hydrolytic, and oxidative stress conditions, and the stressed samples were analyzed by the proposed method. There were no other coeluting, interfering peaks from excipients, impurities, or degradation products due to variable stress conditions, and the method is specific for the estimation of SIM and EZE in the presence of degradation products. The described method was linear over the range of 1-80 and 3-80 microg/mL for SIM and EZE, respectively. The mean recoveries were 99.17 and 100.43% for SIM and EZE, respectively. The intermediate precision data were obtained under different experimental Diovan Generic Price conditions, and the calculated value of the coefficient of variation was found to be less than the critical value. The proposed method can be useful in the quality control of bulk manufacturing and pharmaceutical dosage forms.

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Diagnostic cluster methodology groups patients having similar medical conditions according to their International Classification of Diseases, 9th Revision codes. Episodes of care related to the diagnostic cluster can then be tracked from the claims data to determine the total charges associated with patient management. A retrospective claims analysis using an episode registry database was conducted to determine the 1-year (July 1, 1995, to June 30, 1996) covered charge for statin therapy, the overall cost of treating related cardiovascular (CV) disease, and the cost impact of coadministration of drugs that potentially compete for hepatic metabolism. The three statin treatment groups (lovastatin, pravastatin, and simvastatin) were similar with respect to age, gender, mean number of prescription refills, rate of refill compliance, and prevalence of the coadministration of potentially interacting agents. Before adjustment for severity of illness, there were no significant differences between groups in prescription drugs/services (statin Rx/Svc) or total CV charges. After adjustment for severity of illness, the pravastatin group had the lowest statin Rx/Svc and total CV charges. Within the group with the greatest severity of illness, statin Rx/Svc charges were significantly lower with pravastatin than with lovastatin and simvastatin. The statin Rx/Svc charges were not significantly different between lovastatin and simvastatin. Coadministration of a potentially interacting agent significantly increased both the statin Rx/Svc and total CV charges within the simvastatin-treated group but did not significantly influence costs in the lovastatin- or pravastatin-treated groups. The estimates of direct costs derived from this analysis are consistent with findings in the published literature and demonstrate that pravastatin has cost advantages compared with lovastatin and simvastatin. Diagnostic cluster methodology also generated valuable information regarding drug surveillance and the health care cost impact of potential drug-drug interactions with selected statins.

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Statins, used as cholesterol-lowering drugs, were reported to reduce the progression of Alzheimer's disease (AD). However, the molecular mechanisms underlying these findings remain to be clarified and it is not well understood whether this beneficial effect is due to simply lowering cholesterol levels. This study was aimed to investigate the neuroprotective effect of simvastatin and lovastatin, lipophilic statins that can transverse the blood brain barrier, against the toxicity triggered by the AD-associated amyloid-beta (Abeta) peptides and to analyze if such protection is cholesterol-independent. Using primary cultures of cortical neurons treated with Abeta1-40 peptide, we have demonstrated that pre-incubation with statins prevents the rise in cytosolic Ca2+ concentration and the accumulation of reactive oxygen species induced by Abeta through mechanisms independent of cholesterol reduction. The neuroprotective actions of statins were rather attributable to their ability to reduce isoprenyl intermediates levels in the cholesterol biosynthetic pathway since their effect was reversed by geranyl pyrophosphate while cholesterol addition was ineffective. Consequently, statins were shown to rescue cortical neurons from Abeta-40-induced caspase-3-dependent apoptosis. Moreover, our results revealed that simvastatin, at neuroprotective concentrations against Abeta-induced toxicity, is not able to activate Akt or ERK2, two signaling kinases with neuroprotective roles against apoptosis.

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Concomitant administration of midazolam with almorexant at steady-state levels, achieved within 4-5 days, resulted in an increase of 1.2-fold [90 % confidence interval (CI) 1.0-1.4], 1.4-fold (90 % CI 1.2-1.6), and 1.3-fold (90 % CI 1.2-1.4) in the maximum plasma concentration (C(max)), area under the concentration-time curve from time 0 to infinity (AUC(0-∞)), and terminal half-life (t(1/2)), respectively, of midazolam; the time to peak plasma concentration (t(max)) was unchanged. Whereas C(max) and t(max) were not influenced by almorexant, the AUC(0-∞) of hydroxy-midazolam increased by 1.2-fold (90 % CI 1.1-1.4) and the t(1/2) by 1.3-fold (90 % CI 1.0-1.5). Concomitant administration of simvastatin with almorexant at steady-state resulted in an increase of 2.7-fold (90 % CI 2.0-3.7) and 3.4-fold (90 % CI 2.6-4.4) in C(max) and AUC(0-∞), respectively, for simvastatin; the t(1/2) and t(max) were unchanged. The C(max) and AUC(0-∞) of hydroxyacid simvastatin both increased by 2.8-fold, with 90 % CIs of 2.3-3.5 and 2.2-3.5, respectively; the t(max) increased by 2 h and the t(1/2) was unchanged. The urinary 6-β-hydroxycortisol/cortisol ratio was unaffected by almorexant.

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The STASH trial did not detect any benefit in the use of simvastatin for long-term or short-term outcome in patients with aneurysmal subarachnoid haemorrhage. Despite demonstrating no safety concerns, we conclude that patients with subarachnoid haemorrhage should not be treated routinely with simvastatin during the acute stages.