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Baseline total cholesterol levels, LDL cholesterol levels, HDL cholesterol levels, and triglyceride levels were similar in the two groups. At six months, the total cholesterol, LDL cholesterol, and triglyceride levels were greatly reduced in both groups, with greater reductions in the simvastatin group than in the pravastatin group. Only modest increases were noted in HDL cholesterol levels in the two groups. No significant adverse effects were noted, and no complications with drug withdrawals occurred. Patient compliance exceeded 97%.
(+)-Dapoxetine hydrochloride, (R)-Etodolac; Abatacept, ABT-510, Adalimumab, Agatolimod sodium, Alemtuzumab, Alvocidib hydrochloride, Aminolevulinic acid methyl ester, Aripiprazole, AS01B, AS02B, AS02V, Azacitidine; Becatecarin, Bevacizumab, Bevirimat, Bortezomib, Bremelanotide; CAIV-T, Canfosfamide hydrochloride, CHR-2797, Ciclesonide, Clevidipine; Darbepoetin alfa, Decitabine, Degarelix acetate, Dendritic cell-based vaccine, Denosumab, Desloratadine, DMXB-Anabaseine, Duloxetine hydrochloride, Dutasteride; Ecogramostim, Eicosapentaenoic acid/docosahexaenoic acid, Eletriptan, Enzastaurin hydrochloride, Erlotinib hydrochloride, Escitalopram oxalate, Etoricoxib, Everolimus, Ezetimibe, Ezetimibe/simvastatin; Ferumoxytol, Fesoterodine fumarate, Fulvestrant; Gefitinib, GM-CSF DNA, GSK-690693; H5N1 avian flu vaccine, Hepatitis B hyperimmunoglobulin, Human Fibroblast Growth Factor 1, Hypericin-PVP; Icatibant acetate, Iclaprim, Immunoglobulin intravenous (human), Ipilimumab, ISS-1018; L19-IL-2, Lapuleucel-T, Laropiprant, Liposomal doxorubicin, LP-261, Lumiracoxib, LY-518674; MDV-3100, MGCD-0103, Mirabegron, MyoCell; NASHA/Dx, Niacin/laropiprant; O6-Benzylguanine, Ocrelizumab, Olmesartan medoxomil, Omalizumab; P-276-00, Paclitaxel nanoparticles, Paclitaxel nanoparticles, Padoporfin, Paliperidone, PAN-811, Pegaptanib octasodium, Pegfilgrastim, Pemetrexed disodium, PF-00299804, Pimecrolimus, Prasugrel, Pregabalin; Reolysin, Rimonabant, Rivaroxaban, Rosuvastatin calcium; Satraplatin, SCH-697243,Selenite sodium, Silodosin, Sorafenib, Sunitinib malate; Talarozole, Taxus, Temsirolimus, Tocilizumab, Tolevamer potassium sodium, Tremelimumab, TTP-889; Uracil; V-260, Valsartan/amlodipine besylate, Vardenafil hydrochloride hydrate, Varenicline tartrate, Varespladib, Vitespen, Voclosporin, VX-001; Xience V; Zotarolimus-eluting stent.
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Simvastatin is among the most commonly used prescription medications for cholesterol reduction and the most common statin-related adverse drug reaction is skeletal muscle toxicity. Multiple factors have been shown to influence simvastatin-induced myopathy. In addition to age, gender, ethnicity, genetic predisposition, and dose, drug-drug interactions play a major role. This is particularly true for drugs that are extensively metabolized by cytochrome P450 (CYP)3A4. We describe a particularly severe case of rhabdomyolysis after the introduction of ciprofloxacin, a weak CYP3A4 inhibitor, in a patient who previously tolerated the simvastatin-amlodipine combination.
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It is concluded that SIM co-administration attenuated ISO-induced cardiac lesions including LVH by inhibiting iNOS expression in cardiomyocytes.
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Hypocholesterolemic apolipoprotein A1 (apoA1) knockout mice were administered high dose simvastatin twice daily for 3 days.
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In two separate experiments, diabetic db/db mice received fasudil (10 mg x kg(-) x day(-) i.p.) or simvastatin (40 mg x kg(-) x day(-) p.o.) for 16 weeks. Untreated db/db and db/m mice served as controls.
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Endothelial progenitor cells (EPCs) are involved in endothelium repair of acute lung injury (ALI). Numerous studies have demonstrated that statins can promote EPC function in vitro and in vivo; therefore, the purpose of this study was to determine whether simvastatin enhances the function of EPCs participating in the repair of ALI.
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Both hypertension and aortic valve stenosis induce left ventricular hypertrophy. However, less is known about the influence of concomitant hypertension on left ventricular structure in patients with aortic valve stenosis.
Previously recognized pharmacogenomic associations with drug efficacy have been further validated (e.g. with clopidogrel and warfarin) and shown to influence clinically important outcomes. The clinical significance of variants modulating toxicity (e.g. SLCO1B1 with simvastatin) has also been confirmed. The genetic contribution to variable efficacy and toxicity of other important classes of cardiovascular drugs, such as beta-blockers, is becoming increasingly recognized. Prospective trials testing whether the use of genomic information improves clinical care are underway. Guidance based on the most well-established pharmacogenomic findings has appeared in prescribing labeling and is in the early stages of being implemented into routine clinical care.
These observations show that statins decrease LOX-1 expression, a novel oxidized-LDL endothelial receptor, and uptake of oxidized-LDL in HCAECs. The effect of statins on LOX-1 expression is associated with an increase in PKB activity in HCAECs.
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This was a phase 3, multicenter, randomized, double-blind, active-controlled study. A total of 657 patients with mixed dyslipidemia (low-density lipoprotein cholesterol [LDL-C] > or =130 mg/dL, triglycerides [TGs] > or =150 mg/dL, and high-density lipoprotein cholesterol [HDL-C]<40 mg/dL [men] or <50 mg/dL [women]) were randomized to 12 weeks of treatment with ABT-335 + simvastatin (20 or 40 mg) combination therapy, ABT-335 monotherapy (135 mg), or simvastatin monotherapy (20, 40, or 80 mg).
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These results demonstrate that an independent family medicine physician practice can successfully perform statin therapeutic substitution during routine patient care. Equivalent clinical outcomes with regards to changes in lipid fractions and NCEP LDL-C goal attainment were observed in conjunction with the potential for reduced costs for patients.
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The overall incidence of hospitalization due to severe hepatic injury was low among statin initiators with chronic liver disease. Only high-dose atorvastatin was associated with increased risk.
University research center.
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A large healthcare maintenance organisation.
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Convenient access to prescription drugs produced outside the US has been facilitated by the Internet. Of greatest concern to clinicians and policymakers is product quality and patient safety. The Food and Drug Administration has issued warnings to potential buyers that the safety of drugs purchased through the Internet cannot be guaranteed and may present consumers with a health risk from substandard products.
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Statin treatment is proposed to be a new potential therapy for multiple sclerosis (MS), an inflammatory demyelinating disease of the central nervous system. The effects of statin treatment on brain cells, however, are hardly understood. We therefore evaluated the effects of simvastatin treatment on the migratory capacity of brain microglial cells, key elements in the pathogenesis of MS. It is shown that exposure of human and murine microglial cells to simvastatin reduced cell surface expression of the chemokine receptors CCR5 and CXCR3. In addition, simvastatin treatment specifically abolished chemokine-induced microglial cell motility, altered actin cytoskeleton distribution, and led to changes in intracellular vesicles. These data clearly show that simvastatin inhibits several immunological properties of microglia, which may provide a rationale for statin treatment in MS.
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In patients at high risk for cardiovascular events, comprehensive management under daily practice conditions leads to improvement of lipid, glucose, and blood pressure parameters. There is a need to improve secondary prevention among high-risk patients.
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Ocimum sanctum (OS) has a lipid-lowering action in both normal and diabetic animals. Because OS leaves are rich in oil, the present study was conducted to explain the anti-hyperlipidemic and organ-protective effect of OS fixed oil in rats fed with a high fat (HF) diet. OS fixed oil was extracted by hexane and the fatty acids composition identified by GC-MS. Four groups of male Wistar rats included a normal control group, a high fat fed-diet (HF) group, a HF group treated with OS fixed oil, and a HF group treated with a reference drug simvastatin. The results show that OS fixed oil contains five kinds of fatty acids, of which alpha-linolenic acid was the major fatty acid. OS fixed oil depressed high serum levels of total cholesterol, triglyceride, LDL-C, and AI, whereas no significant effect on HDL-C was observed. OS fixed oil also suppressed high levels of liver cholesterol and triglyceride with no significant effect on both lipids in feces. In addition, OS fixed oil normalized the high serum levels of LDH and CK-MB but no significant effect on high serum levels of ALT, AST, and ALP was obtained. We conclude that treatment with OS fixed oil during the last three weeks of HF diet feeding decreased the high serum lipid profile and expressed antiartherogenic and cardioprotective actions against hyperlipidemia. The anti-hyperlipidemic action of OS fixed oil was mainly resulted from the suppression of liver lipid synthesis. Linolenic acid and linoleic acid contained in OS fixed oil were possibly responsible for both lipid-lowering and cardiac protective action against hyperlipidemia.
With the 80-mg dose, the mean serum cholesterol level decreased from 12.30 +/- 4.96 to 5.29 +/- 1.24 mmol/L (mean reduction, 54%) and the mean serum triglyceride level decreased from 8.77 +/- 7.16 to 3.61 +/- 1.33 mmol/L (-48%); this was due to a decrease in very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) lipids. There was a decrease in the ratio of VLDL cholesterol to serum triglycerides and in the apolipoproteins B and E, suggesting a reduction in the amount of circulating atherogenic remnant particles. Except for a slight increase in serum alanine aminotransferase levels in three patients, no side effects were observed.
This is an update of a Cochrane review first published in 2001 and then updated in 2009. Vascular risk factors including high cholesterol levels increase the risk of dementia due to Alzheimer's disease and of vascular dementia. Some observational studies have suggested an association between statin use and lowered incidence of dementia.
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These results indicated that HA-CD44 interactions down-regulate RANKL expression and osteoclastogenesis via activation of the Rho kinase pathway.