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Lipitor (Atorvastatin)

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Generic Lipitor is an extremely strong medical preparation which is taken in treatment of high cholesterol diseases. Generic Lipitor can also be helpful for patients with heart complications caused by type 2 diabetes or coronary heart disease. Generic Lipitor acts as an anti-high cholesterol remedy.

Other names for this medication:

Similar Products:
Atorlip-10, Atorlip-20, Atorlip-5


Also known as:  Atorvastatin.


Generic Lipitor is made by highly educated specialists to combat high cholesterol diseases (heart attack, stroke). Target of Generic Lipitor is to control and decrease level of cholesterol.

Generic Lipitor acts as an anti-high cholesterol remedy. Generic Lipitor operates by reducing decrease level of cholesterol.

Lipitor is also known as Atorvastatin, Atorbest, Agitor, Attor, Atorlip, Lipvas, Sortis, Torvast, Torvacard, Totalip, Tulip.

Generic Lipitor is HMG-CoA reductase inhibitor (statin).

Generic name of Generic Lipitor is Atorvastatin.

Brand name of Generic Lipitor is Lipitor.


Generic Lipitor can be taken in tablets. You should take it by mouth.

It is better to take Generic Lipitor once a day at the same time with meals or without it.

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


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


Store at room temperature between 20 to 25 degrees C (68 to 77 degrees F) away from moisture and heat. 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 Lipitor 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 Generic Lipitor if you are allergic to Generic Lipitor components.

Be careful with Generic Lipitor if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Lipitor can ham your baby.

Be careful with Generic Lipitor usage in case of having liver disease.

Be careful with Generic Lipitor in case of taking erythromycin (E.E.S., E-Mycin, Erythrocin); cimetidine (Tagamet); ketoconazole (Nizoral) and itraconazole (Sporanox); spironolactone (Aldactone); oral contraceptives (birth control pills); cyclosporine (Neoral, Sandimmune); digoxin (Lanoxin); cholesterol-lowering medications as fenofibrate (Tricor), gemfibrozil (Lopid), and niacin (nicotinic acid, Niacor, Niaspan).

Use Generic Lipitor with great care in case you want to undergo an operation (dental or any other).

If you experience drowsiness and dizziness while taking Generic Lipitor you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

Elderly people should be very careful with Generic Lipitor.

Keep low-cholesterol and low-fat diet.

Do not stop taking Generic Lipitor suddenly.

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Recent evidence suggests that higher doses of statins could improve clinical outcomes compared to conventional doses, but whether this benefit is due to "additional" pleiotropic effects is uncertain. We tested the hypothesis that atorvastatin 80 mg/day would have beneficial effects on indices of matrix remodelling (matrix metalloproteinase-1, MMP-1, and its tissue inhibitor, TIMP-1) in high-risk cardiovascular disease. We studied 27 "high-risk" patients (inclusion criteria: severe triple vessel but rejected for by-pass for extensive coronary disease, severe effort angina after coronary artery by-pass and premature coronary disease with > or =3 risk factors) with an abnormal lipid profile despite atorvastatin 40 mg/day, at baseline and at 3 months after increasing the statin dose to 80 mg/day. Baseline results in patients were compared to 22 healthy controls. At baseline, patients had lower levels of MMP-1 compared to controls. When atorvastatin was increased to 80 mg/day, significant reduction in LDL-cholesterol was observed, whereas MMP-1 and TIMP-1 levels were increased. These, despite of atorvastatin 40 mg daily, 'high-risk' patients still demonstrated abnormal extracellular remodelling indices. Doubling the dose of atorvastatin resulted in significant improvement in extracellular remodelling indices.

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Medline/Ovid and EMBASE search and manual search of bibliography of key papers, on the effects of statins on bone metabolism including in vitro and in vivo studies, as well as clinical trials on the effects of statins on bone mineral density and fracture risk.

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Chronic kidney disease (CKD) is associated with inflammation. The effects of atorvastatin on biomarkers of inflammation were assessed in CKD patients in the LORD trial.

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Statins do not always decrease coronary heart disease mortality, which was speculated based on increased serum plant sterols observed during statin treatment. To evaluate plant sterol atherogenicity, we fed low density lipoprotein-receptor deficient (LDLr(+/-)) mice for 35 weeks with Western diets (control) alone or enriched with atorvastatin or atorvastatin plus plant sterols or stanols. Atorvastatin decreased serum cholesterol by 22% and lesion area by 57%. Adding plant sterols or stanols to atorvastatin decreased serum cholesterol by 39% and 41%. Cholesterol-standardized serum plant sterol concentrations increased by 4- to 11-fold during sterol plus atorvastatin treatment versus stanol plus atorvastatin treatment. However, lesion size decreased similarly in the sterol plus atorvastatin (-99% vs. control) and the stanol plus atorvastatin (-98%) groups, with comparable serum cholesterol levels, suggesting that increased plant sterol concentrations are not atherogenic. Our second study confirms this conclusion. Compared with lesions after a 33 week atherogenic period, lesion size further increased in controls (+97%) during 12 more weeks on the diet, whereas 12 weeks with the addition of plant sterols or stanols decreased lesion size (66% and 64%). These findings indicate that in LDLr(+/-) mice 1) increased cholesterol-standardized serum plant sterol concentrations are not atherogenic, 2) adding plant sterols/stanols to atorvastatin further inhibits lesion formation, and 3) plant sterols/stanols inhibit the progression or even induce the regression of existing lesions.

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Adverse reactions in two patients who received HMG CoA reductase inhibitor therapy were reinvestigated because of their rarity. A case of permanent forearm myalgia was thought to be caused by atorvastatin. Closer evaluation and work-up revealed underlying lateral epicondylitis, and atorvastatin was not considered the cause of the disability. In another patient, rhabdomyolysis was suspected to be secondary to simvastatin. However, after an extensive review, the reaction was believed to be compartment syndrome of the anterior tibial area. An adverse drug reaction report requires careful and judicious assessment to assign the correct probability for the event.

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Compared with in the water group, the AUC(0,48 h) of atorvastatin acid significantly increased by 1.40 fold (95% CI 1.02, 1.92; P < 0.05) when atorvastatin was taken with GFJ. AUC(0,48 h) and C(max) of atorvastatin lactone significantly increased by 1.56 (95% CI 1.33, 1.83; P < 0.001) and 1.29 fold (95% CI 1.09, 1.51; P < 0.01), respectively, when atorvastatin was taken with GFJ. No significant changes were detected in any pravastatin pharmacokinetic parameter examined when pravastatin was taken with GFJ. However, AUC(0,24 h) of pravastatin lactone increased 1.31 fold (95% CI 1.01, 1.71; P < 0.05) with GFJ intake.

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This study found that the difference in adherence between treatment groups may have underestimated the true effect of the treatment differential. Usage of prospective randomized open label endpoint evaluation design should be carefully considered when well-known treatments are compared with rather new ones and especially in segments where patients could be more vulnerable, as in the elderly. Nonadherers in a clinical trial may be at especially high risk of fatal and nonfatal endpoints from various diseases and should be carefully monitored.

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Lesinurad interacted in vitro with OATP1B1, OCT1, and OAT1/3 transporters. Co-administration of lesinurad 200 mg did not significantly alter plasma exposure (maximum concentration [C max] and area under the concentration-time curve [AUC]) of total atorvastatin (atorvastatin + hydroxyl-metabolites) or atorvastatin, while co-administration of lesinurad 400 mg increased the C max of total atorvastatin and atorvastatin by 17-26 %, but had no effect on AUC. Co-administration of lesinurad 400 mg had no effect on the plasma exposure of metformin. Furosemide plasma AUC was reduced by 31 % in the presence of lesinurad 400 mg, but furosemide renal clearance and diuretic activity were unchanged.

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Seven trials involving 1529 patients were included. Pitavastatin reduced LDL-C level as effectively as atorvastatin (mean difference 0.97%, 95% CI -0.48% to 2.42%). The reductions in TC and TG levels were also comparable between the two drugs. The mean differences were 1.22% (95% CI -0.55% to 2.99%) and 2.3% (95% CI -1.06% to 5.65%), respectively. However, HDL-C levels increased significantly more with pitavastatin than with atorvastatin (mean difference 1.78%, 95% CI 0.20-3.36%, P=0.03).

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According to epidemiological studies, dyslipidaemia is the commonest risk factor of atherosclerosis in the Polish population. It is estimated that 18 million adult Poles are affected by dyslipidaemia.

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The most common side-effect of statins, mainly during dose titration, is liver toxicity, In these cases, sufficient control of low density lipoprotein cholesterol (LDL-C) in patients with heterozygous familial hypercholesterolaemia (HFH) becomes problematical. In patients with intolerance to resins as well, especially in the presence of coronary artery disease (CAD), it is practically impossible to reach the LDL-C treatment goal. This study included seven HFH patients with CAD, who presented with alanine amino transferase levels greater than three times the upper normal limit during dose titration of atorvastatin or simvastatin of from 20 mg/day to 40 mg/day. They could not tolerate concomitant cholestyramine administration, and presented with LDL-C levels significantly higher than the treatment goal (100 mg/dl; 2.6 mmol/l). In these patients, a combination of two statins with different pharmacokinetics (20 mg/day of atorvastatin plus 40mg/day of pravastatin) was administered for a mean period of one year. Efficacy was compared with that of monotherapy with each drug alone and with that of 40 mg of atorvastatin in 13 patients, who could also not tolerate resin co-administration, and that of 40 mg/day of atorvastatin plus 12 g of cholestyramine in 30 patients, with similar pretreatment LDL-C levels. No increase in serum transaminases and no symptom or sign of myopathy was recorded during the administration of the combination of the two statins for a mean period of 12 months. The atorvastatin plus pravastatin regimen was more effective than both monotherapies and equally effective with the 40 mg of atorvastatin and the 40 mg of atorvastatin plus 12 g of cholestyramine regimens in reducing LDL-C (59% vs. 57% and 61%, respectively) and triglyceride levels (31% vs. 32% and 28%, respectively), while it also had a better effect on high density lipoprotein cholesterol (13% vs. 7% and 8%). The data suggest that the atorvastatin-pravastatin combination has a highly beneficial effect on all lipid parameters, without causing hepatotoxicity, in HFH patients with CAD who are sensitive to higher doses of statins in monotherapy. These results require confirmation in larger studies.

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The underlying disorder in the vast majority of cases of cardiovascular disease is atherosclerosis, for which low-density lipoprotein cholesterol is recognized as a major risk factor. Data from epidemiologic studies have suggested that lower cholesterol levels are associated with a lower overall risk of morbidity and mortality due to coronary heart disease. Numerous clinical trials with lipid-lowering agents support these epidemiologic data. Of these, studies with the HMG-CoA (3-hydroxy 3-methylglutaryl coenzyme A) reductase inhibitors, or statins, have shown the greatest lipid-lowering effects. Data from recent trials such as the Atorvastatin Versus Revascularization Treatment contribute to a growing body of evidence that suggests that aggressive reduction of cholesterol can yield additional clinical benefits above and beyond that observed with less robust treatment regimens. Aggressive cholesterol-lowering strategies have the potential therefore to have a significant impact on levels of atherosclerotic disease throughout the westernized world. Such effects argue in favor of renaming the entire class of drugs as anti- atherosclerotic rather than lipid-lowering agents.

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A prospective, randomized, open-label, blinded-end-point trial involving 108 participants with hypercholesterolemia was conducted. Participants received 20 mg atorvastatin daily, 400 mg etidronate daily, or both drugs daily. The primary end point was the percent change in maximal vessel wall thickness of atherosclerotic plaques in the thoracic and abdominal aortas as measured by magnetic resonance imaging after 12 months of treatment. In both the combination therapy and atorvastatin groups, maximal vessel wall thickness of the thoracic aorta was reduced by 13.8% (95% confidence interval, -16.4 to -11.3) and 12.3% (95% confidence interval, -14.9 to -9.7), respectively. These reduction rates were comparable between groups (P=0.61). Meanwhile, in the etidronate group, maximal vessel wall thickness of the thoracic aorta remained unchanged (2.2%; 95% confidence interval, -0.3 to 4.8). Conversely, maximal vessel wall thickness of the abdominal aorta was reduced more effectively in the combination therapy group (-11.4%) than in the atorvastatin group (-0.9%; P<0.001) and the etidronate group (5.5%; P=0.006).

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Seventy-two consecutive patients including 48 women with primary hypercholesterolemia, were assigned prospectively to treatment with atorvastatin (10mg/day) for 3 months. We measured fasting lipid concentrations, thiobarbituric acid reactive substances (TBARS) as marker of lipid peroxide, fibrinolytic parameters, and endothelial function by flow-mediated vasodilation of the brachial artery (FMD), at baseline and after 3 months of therapy. We assessed the impact of gender on temporal differences in these parameters. In men, atorvastatin decreased total, low-density lipoprotein (LDL), and small, dense LDL-cholesterol concentrations, and increased FMD after 3 months. In women, atorvastatin decreased TBARS, triglyceride, and total, LDL, small, dense LDL, and remnant-like lipoprotein particle-cholesterol concentrations, and increased FMD after 3 months. Fibrinolytic parameters did not change significantly in either men or women. With respect to the percent change in those parameters after 3 months, TBARS (-17.6+/-12.4 vs. -0.4+/-18.8%, p<0.01) and small, dense LDL-cholesterol (-96.7+/-8.3 vs. -68.6+/-29.7%, p<0.01) decreased to a greater degree in women, although the relative changes in other parameters were similar between men and women.

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This Phase 3 study will randomize approximately 18,000 patients to receive biweekly injections of alirocumab (75-150 mg) or matching placebo beginning 1 to 12 months after an index hospitalization for acute myocardial infarction or unstable angina. Qualifying patients are treated with atorvastatin 40 or 80 mg daily, rosuvastatin 20 or 40 mg daily, or the maximum tolerated and approved dose of one of these agents and fulfill one of the following criteria: LDL-C ≥ 70 mg/dL, non-high-density lipoprotein cholesterol ≥ 100 mg/dL, or apolipoprotein B ≥ 80 mg/dL. The primary efficacy measure is time to first occurrence of coronary heart disease death, acute myocardial infarction, hospitalization for unstable angina, or ischemic stroke. The trial is expected to continue until 1613 primary end point events have occurred with minimum follow-up of at least 2 years, providing 90% power to detect a 15% hazard reduction. Adverse events of special interest include allergic events and injection site reactions. Interim analyses are planned when approximately 50% and 75% of the targeted number of primary end points have occurred.

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These data suggest that the effect on apoA-I levels observed with atorvastatin at higher drug doses in humans may be caused at least in part by enhanced HDL apoA-I catabolism, which is not entirely offset by a concomitant increase in apoA-I production. Whether this finding results from an effect of atorvastatin on HDL particle composition or on receptors involved in circulating HDL holoparticle clearance will require further study.

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A parallel group, randomized, PROBE, multicenter study was conducted to compare the efficacy of 10 mg/d atorvastatin with that of 10 mg/d simvastatin and 20 mg/d simvastatin in patients with primary hypercholesterolemia. After a 6-week diet-placebo lead-in period, 272 patients with LDL cholesterol > or = 160 mg/dL and triglycerides < or = 300 mg/dL were randomized to 6 weeks of treatment with atorvastatin 10 mg (109 patients), simvastatin 20 mg (109 patients), or simvastatin 10 mg (54 patients). In the main analysis, which tested the equivalence of atorvastatin 10 mg and simvastatin 20 mg, the mean percent change in LDL cholesterol for atorvastatin 10 mg (-37.0%) was greater than and not equivalent to simvastatin 20 mg (-33.8%). In the secondary analysis, which compared the efficacy of atorvastatin 10 mg with that of simvastatin 10 mg, the mean decrease in LDL cholesterol was significantly greater (P < .001) for atorvastatin 10 mg than for simvastatin 10 mg (-37.0% vs. -28.9%). The two drugs were well tolerated, with an incidence of clinical and biochemical side effects similar among the 3 treatment groups.

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The administration of conventional doses of atorvastatin plus trimetazidine three days before PCI is able to protect the perioperative patients from myocardial injury.

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Steady-state rivaroxaban did not affect the pharmacokinetic profile of steady-state digoxin (n = 17). Digoxin did not significantly influence the pharmacokinetic profile of single-dose rivaroxaban and had minimal effects on rivaroxaban-induced inhibition of Factor Xa activity and prolongation of clotting time. Similarly, steady-state atorvastatin did not affect the pharmacokinetic profile or the pharmacodynamics of rivaroxaban and vice versa (n = 19). All drugs (alone or in combination) were well tolerated.

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In this observational case report, we share our experience of achieving >40% LDL cholesterol reduction in four Chinese homozygous familial hypercholesterolaemia children below 8 years of age with a triple combination of atorvastatin, probucol, and ezetimibe for >6 years. Within a follow-up duration of 6-13 years, this triple therapy achieved significant reduction of LDL cholesterol as well as an impressive regression of xanthomas in all paediatric cases. All the children remained free from treatment-related adverse responses and cardiovascular events throughout follow-up.

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The primary endpoint was the difference in the percent change of ApoB/ApoA1 at 12 weeks, and secondary endpoints were changes in lipid profiles, glycosylated hemoglobin (HbA1c), homeostatic model assessment (HOMA) index, and C-reactive protein.

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To investigate the genotoxic potential of atorvastatin on human lymphocytes in vitro standard comet assay was used in the evaluation of basal DNA damage and to investigate possible oxidative DNA damage produced by reactive oxygen species (ROS) Fpg-modified version of comet assay was also conducted. In addition to these techniques the new criteria for scoring micronucleus test were applied for more complete detection of baseline damage in binuclear lymphocytes exposed to atorvastatin 80 mg/day in different time periods by virtue of measuring the frequency of micronuclei, nucleoplasmic bridges and nuclear buds. All parameters obtained with the standard comet assay and Fpg-modified comet assay were significantly higher in the treated than in control lymphocytes. The Fpg-modified comet assay showed a significantly greater tail length, tail intensity, and tail moment in all treated lymphocytes than did the standard comet assay, which suggests that oxidative stress is likely to be responsible for DNA damage. DNA damage detected by the standard comet assay indicates that some other mechanism is also involved. In addition to the comet assay, a total number of micronuclei, nucleoplasmic bridges and nuclear buds were significantly higher in the exposed than in controlled lymphocytes. Regression analyses showed a positive correlation between the results obtained by the comet (Fpg-modified and standard) and micronucleus assay. Overall, the study demonstrated that atorvastatin in its highest dose is capable of producing damage on the level of DNA molecule and cell.

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Patients with symptomatic coronary artery disease who are treated with aggressive lipid lowering have improvement of symptom status and ischemia that appears to reflect improved vascular function but not atheroma burden.

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Atrial fibrillation (AF) is one of the most common postoperative arrhythmias in patients who undergo coronary artery bypass grafting (CABG). The aim of this study was to evaluate the effect of preoperative atorvastatin on postoperative atrial fibrillation following coronary artery bypass grafting with cardiopulmonary bypass (CCABG). One hundred consecutive patients undergoing elective CCABG, without history of AF or previous statin treatment, were enrolled and randomly assigned to a statin group (atorvastatin 20 mg/d, n = 49) or a control group (placebo, n = 51) starting 7 days preoperatively. The primary endpoint was the occurrence of postoperative AF. C-reactive protein (CRP) levels were assessed in all selected patients before surgery and every 24 hours postoperatively until discharge from hospital. Atorvastatin significantly reduced the incidence of postoperative AF and postoperative peak CRP level versus placebo (18% versus 41%, P = 0.017; 129.3 ± 24.3 mg/L versus 149.3 ± 32.5 mg/L, P < 0.0001). Kaplan-Meier curves confirmed a significantly better postoperative atrial fibrillation-free survival in the statin group (χ(2) = 7.466, P = 0.006). Logistic regression analysis showed preoperative atorvastatin treatment was an independent factor associated with a significant reduction in postoperative AF (OR = 0.235, P = 0.007), whereas high postoperative CRP levels were associated with increased risk (OR = 2.421, P = 0.015). Preoperative atorvastatin administration may inhibit inflammatory reactions to prevent atrial fibrillation following coronary artery bypass grafting with cardiopulmonary bypass.

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Interferon-γ (IFN-γ) has been widely used to treat various malignant tumors including human non-small-cell-lung carcinomas (NSCLCs). However, the tumor-inhibitory effect of IFN-γ displays not satisfactory in NSCLC treatment due to the lack of immunogenicity of NSCLCs. This study demonstrated that inhibition of RhoA activity led to significant inhibition of NSCLC cell growth accompanied by decreased expression of c-myc and cyclin D1 and increased levels of major histocompatibility complex (MHC) class I and peptide transporter protein 1 (TAP1) which are involved in tumor immunity. Combination treatment of atorvastatin and IFN-γ resulted in a synergistic inhibition of NSCLC cell growth both in vitro and in vivo. Though IFN-γ alone exerted minimal inhibitory effect on RhoA activity, additional administration of atorvastatin could result in a significant inhibition of RhoA activity, thus substantially suppressing NSCLC cell growth. Specifically, atorvastatin could induce specific deposition of endogenous IFN-γ in tumors while not in other normal tissues in LLC-harbored mice. In conclusion, atorvastatin can enhance IFN-γ sensitivity in NSCLCs both in vitro and in vivo, probably through induction of a synergistic inhibitory effect on RhoA activity. This study also suggests a potential alternative of combination of atorvastatin and IFN-γ in clinical therapy against NSCLCs.

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Atorvastatin can inhibit leptin release and mRNA expression, and reduces serum leptin level in hypercholesterolemic rabbits.

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Pro- and anti-inflammatory cytokines play a major role in the development of acute myocardial infarction (AMI). This paper tests the hypothesis that atorvastatin may attenuate the severity of myocardial ischemic injury by restoring the balance between pro-inflammatory and anti-inflammatory mediators.

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All patients aged 66 or older without diabetes who started treatment with statins from 1 August 1997 to 31 March 2010. The analysis was restricted to new users who had not been prescribed a statin in at least the preceding year. Patients with established diabetes before the start of treatment were excluded.

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lipitor generic dosage 2017-08-06

Increased exposure to statins in Asian subjects versus Caucasians may buy lipitor represent a more general class phenomenon than previously recognized.

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Both buy lipitor ATV and SL reduce myocardial infarct size (IS) by enhancing expression and activity of NOS isoforms. We investigated whether atorvastatin (ATV) and sildenafil (SL) have synergistic effects on myocardial infarct size (IS) reduction and enhancing nitric oxide synthase (NOS) expression.

lipitor brand name 2016-02-24

The present study was designed to evaluate effectiveness of 1.2% atorvastatin (ATV buy lipitor ) gel, as an adjunct to scaling and root planing (SRP) in the treatment of intrabony defects in chronic periodontitis (CP) in patients with type 2 diabetes mellitus (t2DM).

lipitor 60 mg 2016-05-25

Following 8 weeks of treatment, we observed that atorvastatin-mediated reduction in cholesterol levels attenuated atherogenesis in LDLr.B6 mice but failed to significantly reduce atherosclerotic lesion size in LDLr.Sle mice, in spite of a significant reduction in serum cholesterol levels. Treatment with MMF and MMF-A attenuated atherogenesis in LDLr.B6 and LDLr.Sle mice. In addition, MMF-containing regimens inhibited recruitment of CD4+ T cells buy lipitor to atherosclerotic lesions in LDLr.Sle mice. In these mice, MMF also reduced the proportion of activated splenic T cells, as well as interleukin 10 secretion by T cells. With regard to lupus activity, MMF had no overt effect on anti-double-stranded DNA (dsDNA) antibody titres or kidney function and pathology.

lipitor normal dosage 2017-11-01

The loss of patent protection for proprietary statins offers affordability advantages to payers, but some clinicians still question the efficacy of generic formulations in real- buy lipitor world clinical applications.

lipitor generic dose 2017-10-15

Time being sedentary increased and physical activity levels decreased in the total sample over 6 months of drug treatment, independent of group assignment. Our results suggest that statins do not influence physical activity levels any differently buy lipitor from placebo, and the lack of inclusion of a placebo condition may provide insight into inconsistencies in the literature.

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Western University, London, Ontario, Canada buy lipitor .

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This randomized sequence, open-label, two-period crossover study with a one-week washout period between doses was performed in 24 fasting healthy Chinese males. They were randomly assigned to receive 20 mg of either the test (national made) or reference (imported) formulation orally. The blood samples were collected over a 72-hour period. Plasma concentrations of parent atorvastatin (AT), ortho-hydroxy-atorvastatin (o-OAT) and para-hydroxy-atorvastatin (p-OAT) were simultaneously determined using the validated liquid chromatography-tandem mass spectrometry buy lipitor method, the bioequivalence was also evaluated throughout the study.

lipitor 40 mg 2016-02-27

At baseline, 25(OH)D was negatively associated with BMI (r = -0.37; P = 0.004), total cholesterol (r = -0.31 buy lipitor ; P = 0.01) and LDL-C (r = -0.32; P = 0.02). After 24 weeks, 25(OH)D increased significantly in both groups (P < 0.001), although higher levels were obtained with calcifediol as compared with cholecalciferol (P < 0.001). Only in the calcifediol group, a significant reduction of LDL-C (P = 0.01) and an increase of HDL-C (P = 0.02) were obtained, even after adjustment for age, and baseline BMI, 25(OH)D and lipid levels (P < 0.05). The percentage changes in 25(OH)D levels were associated with the variations of LDL-C (r = -0.44; P = 0.01) and HDL-C levels (r = 0.30; P = 0.10).

lipitor pill cutter 2016-10-10

Forty-seven elderly Brazilian subjects (> or = 65 years old) with LDL cholesterol (LDL-c) > or = 130 mg/dL were randomly assigned, in a double-blinded manner, to receive either placebo (n = 23) or 20 mg/day of atorvastatin (n = 24) for 4 weeks. Exclusion criteria included diabetes, serious hypertension, obesity, steroid use, hormone replacement, and statin use within the previous six months. All patients underwent clinical examinations, laboratory tests (glucose, lipids, liver enzymes, creatine phosphokinase and high sensitivity buy lipitor C-reactive protein) and assessment of vasomotor function by high-resolution ultrasound examination of the brachial artery (flow-mediated dilation and sublingual nitrate), both before and after treatment.

lipitor 80 mg 2015-06-20

A hospital-base observation study enrolled 40 stroke patients with middle cerebral artery (MCA) or/and basilar artery (BA) stenosis. All participants had hyperlipidemia and were given atorvastatin 40 buy lipitor mg per day for at least six months. IAS was assessed by magnetic resonance angiogram (MRA) at the time of enrollment and then at least six months later. The primary outcome was the progression of IAS. All patients were also given antiplatelet agents for stroke prevention.

lipitor reviews 2013 2016-05-27

Aggressive lipid-lowering therapy is associated buy lipitor with a significant reduction in arterial wall strain. The reduction in biomechanical strain may be associated with reductions in plaque inflammatory burden.

lipitor 20 mg 2017-09-30

These first-in-man findings demonstrate that high-dose atorvastatin rapidly buy lipitor inhibits the pro-atherogenic Rho/ROCK pathway, independent of cholesterol reduction. This inhibition may contribute to the clinical benefits of statins. Rho/ROCK may provide a useful therapeutic target in patients with atherosclerosis.

lipitor versus generic 2016-07-02

Dyslipidemia rat model was produced with high-fat and high-cholesterol diet administration. Thereafter, atorvastatin, rosiglitazone or atorvastatin combined with rosiglitazone were prescribed for 2 weeks. At baseline, 6 weeks of dyslipidemia model production, and 2 weeks of medical intervention, fasting blood buy lipitor was drawn for parameters of interest evaluation. At the end, myocardium was used for 15-deoxy-delta-12,14-PGJ2 (15-d-PGJ2) assessment.

lipitor tabs 2016-08-30

The metabolic syndrome (MS) is a constellation of coronary risk factors. Atherogenic dyslipidemia is an important factor in cardiovascular risk in these patients, and treatment of atherogenic dyslipidemia has been identified as an important goal of therapy in patients with MS. This post hoc analysis of data from a 6-week, randomized, open-label, parallel-group, comparative trial (Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin [STELLAR]) assessed the effects of rosuvastatin 10, 20, and 40 mg, atorvastatin 10, 20, 40, and 80 mg, simvastatin 10, 20, 40, and 80 mg, and pravastatin 10, 20, and 40 mg on plasma lipids in hypercholesterolemic patients (low-density lipoprotein cholesterol >/=160 and <250 mg/dl; triglycerides <400 mg/dl) who had >/=3 of the 5 National Cholesterol Education Program Adult Treatment Panel III criteria for MS (body mass index >30 kg/m(2) substituted for waist circumference). Of 2,268 patients, 811 met criteria for MS. Percent reductions in low-density lipoprotein cholesterol ranged from 20% in the pravastatin 10-mg group to 55% in the rosuvastatin 40-mg group. In patients with MS, triglyceride reductions were 22% to 34% with rosuvastatin, 23% to 33% with atorvastatin, 15% to 23% with simvastatin, and 12% to 15% with pravastatin. High-density lipoprotein cholesterol increased by 8% to 11% with rosuvastatin, 5% to 9% with atorvastatin, 8% to 10% with simvastatin, and 3% to 7% with pravastatin. Rosuvastatin, atorvastatin, simvastatin, and pravastatin treatment had favorable effects in hypercholesterolemic patients on the atherogenic dyslipidemia associated with MS. Prandin 4 Mg Rosuvastatin had the most favorable effect on the atherogenic lipid profile of MS overall.

lipitor 8 mg 2017-07-08

Patients with CHD and CKD are at increased risk of cardiovascular events. Compared with usual care, focused atorvastatin treatment decreased cardiovascular risk for established patients in real-world settings, with no significant difference Trileptal Drug Class in treatment effects observed between patients with and without CKD.

lipitor dosage forms 2015-11-15

HMDM-PON2 expression is reduced in Evista Dosage Forms patients with hypercholesterolemia as a result of their increased cellular cholesterol content. Atorvastatin therapy reduced both macrophage oxidative stress and cholesterol content, and upregulated PON2 expression, thus contributing to attenuation of foam cells formation.

lipitor 5mg dosage 2017-07-10

It was concluded that atorvastatin therapy in dyslipidemic patients decreases the level Adalat 90 Mg of oxidative stress and increases PON activity, especially in patients with HDL levels above 35mg/dl.

lipitor user reviews 2017-08-01

This trial Luvox Weight Reviews compared the efficacy and tolerability of pitavastatin and atorvastatin in hypercholesterolemic Korean adults.

lipitor generic equivalent 2017-01-24

Atorvastatin and simvastatin (members of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor family) are widely prescribed as cholesterol-lowering agents. As they have been shown to exhibit potent immunomodulatory effects, they may become a future treatment option for autoimmune disease in general and multiple sclerosis (MS) in particular. Several recent reports have demonstrated that statins prevent and reverse chronic and relapsing experimental autoimmune encephalomyelitis, an animal model of MS. An open-label clinical trial assessing simvastatin in MS revealed a significant decrease in the number and volume of new MRI lesions and a favorable safety profile Avodart Medication Price . The results of a large multicenter, placebo-controlled clinical trial assessing atorvastatin in patients with clinically isolated syndrome (a disease that predisposes to development MS) are expected soon. However, prospective placebo-controlled trials of atorvastatin or simvastatin in definite MS are difficult to perform due to ethical and financial objections. In this review, we discuss the backgrounds, mechanisms of action and future perspectives of atorvastatin and simvastatin as putative future treatment options in MS.

lipitor 20mg tablets 2016-10-09

We demonstrate that treatment of human esophageal adenocarcinoma Zanaflex Pill Identification cells with simvastatin attenuates growth, by decreasing cell viability, decreasing cell proliferation, and increasing apoptosis, and attenuates metastatic potential, by decreasing expression of key metastatic markers. These findings identify simvastatin as a potential therapeutic and chemopreventive modality to thwart the progression of esophageal adenocarcinoma.

lipitor mg 2016-07-26

A 71-year-old African American woman presented with a past medical history significant for diabetes mellitus, coronary artery disease, hypertension and hyperlipidemia. She was being treated with atorvastatin and verapamil in addition to a few other medications. She complained of nausea, vomiting, myalgia, generalized weakness and dark urine. Initial evaluation revealed clinical icterus and mild mental confusion. Admission laboratory results showed features of multiple organ dysfunction. Over the course of four to five days the patient deteriorated to multiple organ failure resulting in death. Extensive work up for the etiology for multiple organ failure was noncontributory. We presume the cause for multiple organ failure could be the result of drug-drug interaction, atorvastatin and verapamil, as verapamil is known to increase Tab Urispas D the serum concentration of atorvastatin significantly.

lipitor 25 mg 2016-10-02

This analysis assumed that statin efficacy is the same in real life as in trials, and used titration and Zofran Pill switching patterns not based on patients' goal attainment. However, sensitivity and scenario analyses showed that the model was less sensitive to these parameters than to cost-related parameters.

lipitor usual dosage 2015-11-07

Fifty-one type 2 diabetes patients receiving Prednisone Replacement Drug oral antidiabetes drugs, not taking statins, with baseline low-density lipoprotein cholesterol between 2.6 mmol/L and 4.1 mmol/L were included. Forty-three patients (21 in placebo group and 22 in atorvastatin group) completed the study and were taken up for final analysis. Fasting blood samples were obtained at baseline and at 12 weeks to determine levels of blood glucose, lipid profile, insulin, C-peptide and glycosylated hemoglobin (A1C).

lipitor reviews 2017-02-14

Tofacitinib-associated elevated total and LDL-cholesterol and triglycerides were rapidly and significantly reduced by atorvastatin. Further investigation is required to explore the Duricef Suspension Dosing significance of reductions in RA disease activity in patients receiving tofacitinib and atorvastatin. (Pfizer protocol A3921109).

lipitor generic brand 2016-10-16

Although lipid-lowering therapy with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) decreases the progression of coronary artery and aortic valve calcification, the mechanism of action of these drugs to inhibit the calcification process remains unclear. In this study, we investigated the effect of statins such as cerivastatin and atorvastatin on vascular calcification by utilizing an in vitro model of inflammatory vascular calcification. Cerivastatin and atorvastatin dose-dependently inhibited in vitro calcification of human vascular smooth muscle cells (HVSMCs) induced by the following inflammatory mediators (IM): interferon-gamma, 1alpha,25-dihydroxyvitamin D3, tumor necrosis factor-alpha, and oncostatin M. These statins also depressed expression of alkaline phosphatase (ALP) in HVSMCs induced by these factors. Mevalonate and geranylgeranylpyrophosphate reversed the inhibitory effect of cerivastatin on ALP expression in HVSMCs, while farnesylpyrophosphate showed no effect on the ALP activities inhibited by this drug, suggesting that inhibition of Rho and its downstream target, Rho kinase may mediate the inhibitory effect of cerivastatin. Cerivastatin prevented RhoA activation in HVSMCs induced by the IM. A specific inhibitor of Rho kinase (Y-27632) inhibited in vitro calcification and induction of ALP in HVSMCs. These findings provide a possible mechanism of statins to prevent the progression of calcification in inflammatory vascular diseases such as atherosclerosis and cardiac valvular calcification.

lipitor 20mg dosage 2017-06-26

We evaluated the disease modifying effect of simvastatin and atorvastatin in Dextran Sulfate Sodium (DSS) model of colitis.

lipitor 90 mg 2016-04-07

We tested the hypothesis that atorvastatin active metabolite (ATM), on the basis of its distinct structural features and potent antioxidant activity, preferentially inhibits lipid oxidation in human small dense low-density lipoprotein (sdLDL) and other small lipid vesicles. LDL, sdLDL, and various subfractions were isolated from human plasma by sequential ultracentrifugation, treated with ATM, atorvastatin, pravastatin, rosuvastatin, or simvastatin and were subjected to copper-induced oxidation. Lipid oxidation was measured spectrophotometrically as a function of thiobarbituric acid reactive substances formation. Similar analyses were performed in reconstituted lipid vesicles enriched in polyunsaturated fatty acids and prepared at various sizes. ATM was found to inhibit sdLDL oxidation in a dose-dependent manner. The antioxidant effects of ATM in sdLDL were 1.5 and 4.7 times greater (P < 0.001) than those observed in large buoyant LDL and very low-density lipoprotein subfractions, respectively. ATM had similar dose- and size-dependent effects in reconstituted lipid vesicles. None of these effects were reproduced by atorvastatin (parent) or any of the other statins examined in this study. These data suggest that ATM interacts with sdLDL in a specific manner that also confers preferential resistance to oxidative stress. Such interactions may reduce sdLDL atherogenicity and improve clinical outcomes in patients with cardiovascular disease.

lipitor good reviews 2015-08-18

Low dose atorvastatin treatment improves endothelial function and reduces the expression of proinflammatory cytokines and adhesion molecules in patients with ischemic heart failure, an effect partly depressed by vitamin E.

lipitor medication 2016-10-05

HMG-CoA reductase inhibition has a biphasic dose-dependent effect on angiogenesis that is lipid independent and associated with alterations in endothelial apoptosis and vascular endothelial growth factor signaling. Statins have proangiogenic effects at low therapeutic concentrations but angiostatic effects at high concentrations that are reversed by geranylgeranyl pyrophosphate. At clinically relevant doses, statins may modulate angiogenesis in humans via effects on geranylated proteins.