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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:
Alipid, Alvastin, Ampliar, Anvistat, Anzitor, Atacor, Atasin, Atenfar, Ateroclar, Ateroz, Atocor, Ator, Atorin, Atoris, Atorlip, Atorpharm, Atorsan, Atorva, Atorvastatina, Atorvin, Atorvox, Atova, Atovarol, Atovin, Atroact, Avas, Avascare, Avastatin, Axo, Aztor, Biger, Biostatina, Caduet, Card-ok, Cardyl, Cardyn, Cholvast, Colastin l, Colostat, Danelip, Delipost, Dislipat, Divastin, Divator, Doss-medichrom, Finlipol, Fluxol, Holisten, Hypolip, Kolestor, Larus, Liparex, Lipex ariston, Lipibec, Lipicon, Lipidan, Lipidra, Lipigan, Lipinor, Lipitaksin, Lipitin, Lipium, Lipivastin, Lipizem, Lipizim, Lipobi, Lipocambi, Lipodial, Lipofin, Liponorm, Liporest, Lipostatin, Lipostop, Lipovast, Lipovastatin, Liprimar, Liptor, Livas, Locol, Lorvaten, Lowlipen, Nor lipox, Orva, Pharmastatin, Plan, Prevencor, Saphire, Sortis, Stacor, Stator, Storvas, Tahor, Tarden, Tarimyl, Taven, Tcl-r, Tiginor, Torid, Torivas, Torva, Torvacard, Torvalipin, Torvaplipin, Torvast, Torvazin, Totalip, Trova, Tulip, Vasolip, Vass, Vastatin, Vastina, Visvas-ez, Voredanin, Xelitor, Xelpid, Zarator, Zoamco, Zurinel, Zydus atorva

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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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Eleven male patients with primary hyperlipidemia received 20 mg atorvastatin daily for 4 weeks. Blood was collected at baseline, 12 h, 36 h, 1 and 4 weeks after the start of treatment.

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Clopidogrel decreased MCP-1 expression in the carotid artery at 4 weeks after irradiation. Expression of VCAM-1, ICAM-1, thrombomodulin, tissue factor and eNOS was unchanged in atorvastatin and clopidogrel-treated mice. Neither drug inhibited either age-related or radiation-induced atherosclerosis. Furthermore, loss of the inflammatory mediator CD40L did not influence the development of age-related and radiation-induced atherosclerosis.

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All four patients repeatedly distinguished blinded statin therapy from placebo. Strength testing confirmed weakness during statin therapy that reversed during placebo use. Muscle biopsies showed evidence of mitochondrial dysfunction, including abnormally increased lipid stores, fibers that did not stain for cytochrome oxidase activity, and ragged red fibers. These findings reversed in the three patients who had repeated biopsy when they were not receiving statins. Creatine kinase levels were normal in all four patients despite the presence of significant myopathy.

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In this triple-blind controlled randomized clinical trial, 190 candidates for elective PCI, who were already using statins and/or other lipid lowering agents such as fibrates, were randomly assigned to two equal groups to receive either atorvastatin (80 mg) or placebo within 24 hours before the procedure. Serum levels of creatinine kinase myocardial isoenzyme (CK-MB), cardiac troponin I (cTNI) and high-sensitive C-reactive protein (hs-CRP) were measured at baseline and then 6 and 12 hours following PCI. Post-procedural MI was defined as troponin elevation>5-fold in patients with normal baseline or >20% in those with elevated baseline measurements with or without chest pain or ST segment or T wave abnormalities.

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This multicenter, randomized, double-blind study compared the effects of atorvastatin 40 mg/day versus placebo over 12 weeks on endothelial function (the primary endpoint) measured by peripheral arterial tone (PAT). Secondary endpoints included office blood pressure (BP), early carotid atherosclerosis, arterial stiffness measured by pulse wave velocity (PWV), and metabolic parameters.

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In clinical trials which have which have included over 40,000 patients there was no difference in all cause mortality for patients randomised to a fibrate compared to placebo. Treatment with a fibrate was associated with a small reduction in the risk of non-fatal cardiovascular events.

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This review shows that there is clear evidence in favor of calcium channel blockers and iloprost (oral and IV) to treat secondary RP. For all other interventions, only limited, conflicting, or no evidence was found. More high-quality, well-designed RCTs are needed in this field, especially for new interventions based on recent knowledge about the pathophysiology of secondary RP.

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Total cholesterol was reduced by 40.6+/-11.2% (p<0.001), low density lipoproteins cholesterol by 55.4+/-14% (p<0.001), triglycerides by 29.6% (p<0.05) and high density lipoproteins cholesterol was increased by 24.7% (p<0.05) in atorvastatin group after 6 months of therapy. No significant lipid changes were observed in the control group. Sixteen target segments in the treatment group and 12 segments in the control group were selected for primary efficacy parameter. The vasoconstrictor reaction to acetylcholine was similar at baseline in both groups: -16.8%+/-11.6% of diameter in atorvastatin group and -14.2%+/-13.7% in control group (p=0.58) at dose 10(-6) mol/l, -43.5%+/-21.2% in atorvastatin group and -41.2%+/-22.4% in control group (p=0.79) at dose 3.3x10(-6) mol/l, -64.5%+/-12.4% in atorvastatin group and -57.4%+/-15.6% in control group (p=0.35) at dose 10(-5) mol/l. Treatment with high doses of atorvastatin markedly decreased acetylcholine - induced vasoconstriction: -6.5%+/-14.5% of diameter in atorvastatin group versus -18.3%+/-14.0% in control group (p=0.04) at dose 10(-6) mol/l, -19.7%+/-22.8% in atorvastatin group versus -40.0%+/-25.0% in control group (p=0.034) at dose 3.3x10(-6) mol/l, -29.9%+/-21.3% in atorvastatin group (6 segments) versus -48.7%+/-19.0% in control group (3 segments, p=0.24) at dose 10(-5) mol/l.

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The Sanjiao theory is useful in guiding the treatment of hyperlipidemia.

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In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events, despite a small increase in the incidence of hemorrhagic stroke. ( number, NCT00147602 [].).

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lipitor going generic 2017-06-30

Itraconazole increased the area under the concentration--time curve from time zero to 72 hours [AUC(0-72)] and the elimination half-life of atorvastatin acid about threefold (p < 0.001), whereas the peak serum concentration was not significantly changed. The AUC(0-72) of atorvastatin lactone was increased about fourfold (p < 0.001), and the peak serum concentration and half-life were increased more than twofold (p < 0.01). Itraconazole decreased the peak serum Lozol Generic Name concentration and AUC(0-72) of 2-hydroxyatorvastatin acid (p < 0.01) and 2-hydroxyatorvastatin lactone (p < 0.01). Itraconazole significantly (p < 0.01) increased the half-life of 2 hydroxyatorvastatin lactone. The AUC(0-72) values of active and total HMG-CoA reductase inhibitors were increased 1.6-fold (p < 0.001) and 1.7-fold (p < 0.001), respectively.

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Fourth-year students at the Altace Generic Ramipril University of Miami Miller School of Medicine exposed to Lipitor promotional items had more favorable implicit attitudes about that brand-name drug compared to the control group (IAT effect: 0.66 vs 0.47; P = .05), while the effect was reversed at the University of Pennsylvania School of Medicine (IAT effect: 0.22 vs 0.52; P = .002) where restrictive policies are in place limiting pharmaceutical marketing (interaction effect: P = .003). No significant effect was observed among third-year students. On a "skepticism" scale, University of Miami students held more favorable attitudes toward pharmaceutical marketing compared to University of Pennsylvania students (0.55 vs 0.42; P < .001) but the results were similar to those of a previously published national study (0.42 vs 0.43; P = .53).

lipitor generic recall 2015-05-19

Although their primary Flomax Generic Substitute therapeutic indications are different, aminobisphosphonates and statins target enzymes in the mevalonate pathway, which is critical for bone homeostasis. Previous studies have shown that some polymorphisms of the gene encoding farnesyl diphosphate synthase (FDPS), the main target of aminobisphosphonates, modulate the response to these drugs. In this study, we explored whether those single nucleotide polymorphisms (SNPs) also influence the changes in bone mineral density (BMD) following therapy with statins. Sixty-six patients with coronary heart disease were studied at baseline and after 1-year therapy with atorvastatin. BMD was measured by DXA. Three SNPs of the FDPS gene (rs2297480, rs11264359 and rs17367421) were analyzed by using Taqman assays. The results showed that there was no association between the SNPs and basal BMD. However, rs2297480 and rs11264359 alleles, which are in linkage disequilibrium, were associated with changes in hip BMD following atorvastatin therapy. Thus, patients with AA genotype at the rs2297480 locus had a 0.8 ± 0.8 % increase in BMD at the femoral neck, whereas in patients with AC/CC genotypes, BMD showed a 2.3 ± 0.8 % decrease (p = 0.02). Similar results were obtained regarding changes of BMD at the femoral trochanter and when alleles at the rs11264359 locus were analyzed. However, there was no association between BMD and rs17367421 alleles. In conclusion, these results suggest that polymorphisms of the FDPS gene may influence the bone response to various drugs targeting the mevalonate pathway, including not only aminobisphosphonates but also statins.

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Two randomized crossover studies were conducted. In study 1, 10 healthy volunteers took 600 mg rifampin or placebo once daily for 5 days. Keflex Generic On day 6, they ingested a single 40-mg dose of atorvastatin. In study 2, 10 healthy volunteers took 600 mg gemfibrozil or placebo twice daily for 5 days. On day 3, they ingested a single 20-mg dose of atorvastatin. Plasma concentrations of atorvastatin (in nanograms per milliliter) and its metabolites (in arbitrary units) were measured by liquid chromatography-tandem mass spectrometry up to 48 to 72 hours after dosing.

lipitor prices 2016-05-23

Statins, which inhibit 3-hydroxy-3-methylglutaryl CoA reductase, have been shown recently to promote proinflammatory responses. We show in this study that both atorvastatin and simvastatin induced proinflammatory responses in mitogen-activated PBMCs by increasing the number of T cells secreting IFN-gamma. This is abolished by the presence of mevalonate, suggesting that statins act specifically by blocking the mevalonate pathway for cholesterol synthesis to promote the proinflammatory response. Both statins at low concentrations induced a dose-dependent increase in the number of IFN-gamma-secreting T cells in mitogen-activated PBMCs, whereas at higher concentrations the effect was abolished. The proinflammatory effect of statins was not seen in purified T cells per se activated with mitogen. However, conditioned medium derived from statin-treated PBMCs enhanced the number of IFN-gamma-secreting cells in activated purified T cells. This effect was not blocked by mevalonate, but was abolished by neutralizing Abs to IL-18 and IL-12. Similarly, the up-regulation of IFN-gamma-secreting T cells in PBMCs costimulated with statins and mitogens was blocked by the neutralizing anti-IL-18 and anti-IL-12. We showed that simvastatin stimulates the secretion of IL Prandin Online -18 and IL-1beta in monocytes. Active caspase-1, which is required for the processing and secretion of IL-18 and IL-1beta, was activated in simvastatin-treated monocytes. This was blocked by mevalonate and the caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone. Taken together, the proinflammatory response mediated by statins in activated PBMCs is mediated mainly via the activation of caspase-1 and IL-18 secretion in the monocytes and to a lesser extent by IL-12.

lipitor online 2015-01-06

Prophylactic 80-mg atorvastatin administration for 4 d failed to reduce the number of intravascular bubbles observed following a 60-ft, 80-min dry chamber dive despite significant acute reductions in lipid levels. Several hypotheses may explain why statins failed to decrease bubble volume: (1) differential influence of statins Crestor Generic Costco on the venous vs. arterial vasculature; (2) failure to elicit an improvement in endothelial function and, therefore, the hypothesized endothelial conditioning in younger patients possessing normal baseline; and (3) the ordinal grading system encompassing a substantial variation in bubble volume (bubbles Scm(-2)).

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High-dose atorvastatin potentiated the decline in inflammation in patients with acute coronary syndromes. This supports the Vasotec Cost value of early statin therapy in these patients.

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This study shows for the first time that myocardial expression of Cxs is downregulated during CVB3-induced myocarditis and that immunomodulation by atorvastatin could restore the impaired Order Viagra gap junction channels and improve the outcome of viral myocarditis.

lipitor generic drug 2016-04-28

The ABCG2 c.421C>A single-nucleotide polymorphism (SNP) was determined in 660 healthy Finnish volunteers, of whom 32 participated in a pharmacokinetic crossover study involving the administration of 20 mg atorvastatin and rosuvastatin. The frequency of the c.421A variant allele was 9.5% (95% confidence interval 8.1-11.3%). Subjects with the c.421AA genotype (n = 4) had a 72% larger mean area under the plasma atorvastatin concentration-time curve from Risperdal Injection Cost time 0 to infinity (AUC(0-infinity)) than individuals with the c.421CC genotype had (n = 16; P = 0.049). In participants with the c.421AA genotype, the rosuvastatin AUC(0-infinity) was 100% greater than in those with c.421CA (n = 12) and 144% greater than in those with the c.421CC genotype. Also, those with the c.421AA genotype showed peak plasma rosuvastatin concentrations 108% higher than those in the c.421CA genotype group and 131% higher than those in the c.421CC genotype group (P < or = 0.01). In MDCKII-ABCG2 cells, atorvastatin transport was increased in the apical direction as compared with vector control cells (transport ratio 1.9 +/- 0.1 vs. 1.1 +/- 0.1). These results indicate that the ABCG2 polymorphism markedly affects the pharmacokinetics of atorvastatin and, even more so, of rosuvastatin-potentially affecting the efficacy and toxicity of statin therapy.

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To study the effects of atorvastatin on matrix metalloproteinase- Lioresal Online 9 (MMP-9) and high sensitive C-reactive protein (hs-CRP) - markers of the proteinolytic and inflammatory activity.

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Seventy-four overweight [body-mass index (BMI) > 25 kg/m(2) , fat-mass > 30%], statin-free patients, with carotid stenosis, but without indications for intervention were enrolled. Thirty-eight age-, sex- and BMI-matched healthy subjects served as healthy controls (HC). All patients received gradual titrated (10-80 mg) atorvastatin therapy to target LDL-C < 100 mg/dL. GSM score, blood pressure (BP), fat-mass, lipid profile, and serum high-sensitivity C-reactive protein (hsCRP), apelin and visfatin levels were obtained at baseline Aricept Medication Generic and after 24 months.