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Lipitor

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.

Description

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.

Dosage

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.

Overdose

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

Storage

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.

Contraindications

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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While HMG-CoA reductase inhibitors such as fluvastatin, lovastatin, pravastatin and simvastatin demonstrate lack of in vitro and in vivo mutagenicity and clastogenicity in bacterial and mammalian cells, long term rodent carcinogenicity studies resulted in an increased incidence in neoplasms at high doses. These effects may be attributable to an exaggeration of the desired biochemical effect of the drug and/or a tumor promoting effect. The genotoxicity of atorvastatin, a newly developed HMG-CoA reductase inhibitor, was evaluated in a variety of test systems. In bacterial mutagenicity tests, the E. coli tester strain WP2(uvrA) and S. typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538 were exposed to concentrations of atorvastatin as high as 5000 micrograms/plate both in the absence (S9-) and presence (S9+) of metabolic activation. Atorvastatin was not mutagenic in either E. coli or S. typhimurium. Chinese hamster lung V79 cell cultures were exposed to atorvastatin at concentrations of 50-300 micrograms/ml (S9-) and 100-300 micrograms/ml (S9+) and structural chromosome aberrations were assessed. Mutation at the hgprt locus was assessed at concentrations of 100-300 micrograms/ml (S9-) and 150-275 micrograms/ml (S9+). Atorvastatin was neither mutagenic nor clastogenic in the absence or presence of S9. The lack of in vitro genotoxicity was corroborated in vivo in a mouse micronucleus study in which single oral doses of atorvastatin were administered to male and female CD-1 mice at 1, 2500, or 5000 mg/kg. No biologically significant increases in the frequency of micronucleated polychromatic erythrocytes in bone marrow at 24, 48, or 72 h postdosing were observed. Thus, atorvastatin, as with the other tested HMG-CoA reductase inhibitors, is not genotoxic.

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We conclude that low-dose statins reduce progression of atherosclerosis as observed by carotid intima media thickness in Indian patients with known coronary heart disease and normal lipid values independent of lipid lowering. The study favors use of this therapy in patients with normal/below average cholesterol levels.

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Atorvastatin is a widely-used therapeutic statin given for hypercholesterolaemia and for prevention of cardiovascular events. We report herein the occurrence of a drug reaction with eosinophilia and systemic symptoms (DRESS) secondary to intake of this drug.

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Documentation on secondary prevention with statins in RA patients with coronary heart disease (CHD) is limited, despite the increased risk of CHD in RA. Our objective was to describe the effect of statin treatment on lipid levels and cardiovascular disease (CVD) events in patients with RA who participated in the incremental decrease in endpoints through aggressive lipid lowering (IDEAL) study.

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The capacity of FasL molecules expressed on melanoma cells to induce lymphocyte apoptosis contributes to either antitumor immune response or escape depending on their expression level. Little is known, however, about the mechanisms regulating FasL protein expression. Using the murine B16F10 melanoma model weakly positive for FasL, we demonstrated that in vitro treatment with statins, inhibitors of 3-hydroxy-3-methylgutaryl CoA reductase, enhances membrane FasL expression. C3 exotoxin and the geranylgeranyl transferase I inhibitor GGTI-298, but not the farnesyl transferase inhibitor FTI-277, mimic this effect. The capacity of GGTI-298 and C3 exotoxin to inhibit RhoA activity prompted us to investigate the implication of RhoA in FasL expression. Inhibition of RhoA expression by small interfering RNA (siRNA) increased membrane FasL expression, whereas overexpression of constitutively active RhoA following transfection of RhoAV14 plasmid decreased it. Moreover, the inhibition of a RhoA downstream effector p160ROCK also induced this FasL overexpression. We conclude that the RhoA/ROCK pathway negatively regulates membrane FasL expression in these melanoma cells. Furthermore, we have shown that B16F10 cells, through the RhoA/ROCK pathway, promote in vitro apoptosis of Fas-sensitive A20 lymphoma cells. Our results suggest that RhoA/ROCK inhibition could be an interesting target to control FasL expression and lymphocyte apoptosis induced by melanoma cells.

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Clinicians should be vigilant in monitoring the regimens of patients prescribed a statin with drugs that may increase the risk of myopathy. In particular, since nearly half of the patients prescribed amiodarone may also be prescribed a statin, then addition of amiodarone or changes in statin dose should trigger a drug regimen review and patient level monitoring. Clinicians should avoid simvastatin doses greater than 20 mg per day in patients taking amiodarone.

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The aim of the paper is to assess the compliance and efficacy of atorvastatin treatment according to usual care on carotid atheromatous plaque and lipids during follow-up for one year in patients with acute ischemic stroke. Sixty-six patients were included. Morphological plaque characteristics were described and a complete blood analysis was performed at admission and at one year. Nineteen patients stopped treatment. Lipid reduction was significant in triglycerides, cholesterol and LDL cholesterol, with an increase in HDL cholesterol. Morphological characteristics of carotid plaque were not modified. In conclusion, an irregular compliance has been seen in patients with acute ischemic stroke treated with atorvastatin according to usual care. Nearly one-third of our patients stopped the treatment before the course of a year. The effect on lipids and its pleiotropic effect on atheromatous carotid artery disease might support the long-term use of atorvastatin, regardless of the dose, in patients with acute ischemic stroke.

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After measuring the baseline levels of CRP and lipid fractions, the patients were divided into two groups. In Group A (n = 46), atorvastatin (20 mg/day) was administered in addition to classic antianginal treatment (beta-blocker, nitrate and aspirin). In Group B (n = 32), the usual antianginal treatment was continued. Following 4 weeks of treatment the same measurements were repeated.

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This study was designed to investigate the effect of atorvastatin on the serum levels of tumor necrosis factor alpha (TNF-α) and interleukin-1beta (IL-1β) following acute pulmonary embolism (PE). Forty New Zealand white rabbits were divided into control and atorvastatin groups. Acute PE was created by injection of autologous blood clots into the femoral vein. Enzyme-linked immunosorbent assay was used to measure TNF-α and IL-1β. At baseline, there was no significant difference in serum TNF-α (10.6 ± 1.3 versus 11.2 ± 1.9 pg/mL; P > .05) or IL-1β (8.2 ± 1.0 versus 8.6 ± 0.9 pg/mL; P > .05) between the control group and the atorvastatin group. In both groups, there was a significant increase in the serum TNF-α and IL-1β following acute PE. However, the levels of serum TNF-α and IL-1β in the atorvastatin group was significantly lower than in the control group following PE (P < .01). The authors conclude that acute PE is associated with a significant increase in serum proinflammatory factors TNF-α and IL-1β. Pretreatment with atorvastatin diminished the increase in TNF-α and IL-1β.

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Atorvastatin exerts an anti-inflammatory effect by inhibiting NLRP3 inflammasome through suppressing TLR4/MyD88/NF-κB pathway in PMA-induced THP-1 monocytes.

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Response amplitude was significantly decreased at all frequencies immediately after exposure to noise in all studied groups. The amplitude increased after 72 hours to a level higher than temporary threshold shift (TTS); this change was only significant in the group received 5 mg/kg atorvastatin.

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By means of the MCR-estimated diffraction patterns and concentration profiles, the trihydrate phase of the drug salt was found to dehydrate sequentially into two partially dehydrated hydrate structures upon heating from 25 to 110°C, with no associated breakage of the original crystal lattice. During heating from 110 to 140°C, the remaining water was lost from the solid drug salt, which instantly collapsed into a liquid crystalline phase. An isotropic melt was formed above 155°C. Thermogravimetric analysis, hot-stage polarized light microscopy, and hot-stage Raman spectroscopy combined with principal component analysis (PCA) was shown to provide consistent results.

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The cholesterol biosynthetic pathway produces numerous signaling molecules. Oxysterols through liver X receptor (LXR) activation regulate cholesterol efflux, whereas the non-sterol mevalonate metabolite, geranylgeranyl pyrophosphate (GGPP), was recently demonstrated to inhibit ABCA1 expression directly, through antagonism of LXR and indirectly through enhanced RhoA geranylgeranylation. We used HMG-CoA reductase inhibitors (statins) to test the hypothesis that reduced synthesis of mevalonate metabolites would enhance cholesterol efflux and attenuate foam cell formation. Preincubation of THP-1 macrophages with atorvastatin, dose dependently (1-10 microm) stimulated cholesterol efflux to apolipoprotein AI (apoAI, 10-60%, p < 0.05) and high density lipoprotein (HDL(3)) (2-50%, p < 0.05), despite a significant decrease in cholesterol synthesis (2-90%). Atorvastatin also increased ABCA1 and ABCG1 mRNA abundance (30 and 35%, p < 0.05). Addition of mevalonate, GGPP or farnesyl pyrophosphate completely blocked the statin-induced increase in ABCA1 expression and apoAI-mediated cholesterol efflux. A role for RhoA was established, because two inhibitors of Rho protein activity, a geranylgeranyl transferase inhibitor and C3 exoenzyme, increased cholesterol efflux to apoAI (20-35%, p < 0.05), and macrophage expression of dominant-negative RhoA enhanced cholesterol efflux to apoAI (20%, p < 0.05). In addition, atorvastatin increased the RhoA levels in the cytosol fraction and decreased the membrane localization of RhoA. Atorvastatin treatment activated peroxisome proliferator activated receptor gamma and increased LXR-mediated gene expression suggesting that atorvastatin induces cholesterol efflux through a molecular cascade involving inhibition of RhoA signaling, leading to increased peroxisome proliferator activated receptor gamma activity, enhanced LXR activation, increased ABCA1 expression, and cholesterol efflux. Finally, statin treatment inhibited cholesteryl ester accumulation in macrophages challenged with atherogenic hypertriglyceridemic very low density lipoproteins indicating that statins can regulate foam cell formation.

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HbA1c and fasting glucose levels were significantly different between baseline and 3 months among responders receiving atorvastatin; however, these differences were not statistically significant in nonresponders. Atherogenic ratios of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (LDL-C/HDL-C; p = 0.002), total cholesterol to HDL-C (TC/HDL-C; p<0.001) and AIP (the atherogenic index of plasma; p = 0.004) decreased significantly in responders receiving atorvastatin than in nonresponders. Moreover, responders receiving atorvastatin showed a significant increase in HDL-C levels but nonresponders receiving atorvastatin did not (p = 0.007). The multivariate model identified a significant association between metformin response (as the independent variable) and TG, TC, HDL-C and LDL-C (dependent variables; Wilk's λ = 0.927, p = 0.036).

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Patients with peripheral artery disease (PAD) are at heightened risk of both systemic cardiovascular adverse events, as well as limb-related morbidity. The optimal management of patients with PAD requires a comprehensive treatment strategy incorporating both lifestyle changes, including smoking cessation and exercise, as well as optimal medical therapy. Pharmacological therapies for patients with PAD are targeted both at modifying broad risk factors for major adverse cardiovascular events, as well as reducing limb-related morbidity. Observational data suggest that indicated pharmacological treatments are greatly underutilized in PAD, underscoring the need for improvements in patient identification and care delivery. Ongoing trials of novel therapies in patients with PAD will further inform pharmacological strategies to reduce both systemic cardiovascular risk and limb-related morbidity.

lipitor reviews 2013

It has been proposed that paraoxonase1 (PON1), a high density lipoprotein (HDL)-associated esterase/lactonase, has anti-atherosclerotic properties. The activity of PON1 is influenced by PON1 polymorphisms. However, the influence of PON1 polymorphisms on PON1 activity and oxidative stress in response to lipid-lowering drugs remains poorly understood. The objective of the present study was to investigate the effects of atorvastatin on PON1 activity and oxidative status. The influence of PON1 polymorphisms on PON1 activity and oxidative status in response to atorvastatin treatment was also evaluated. In total, 22 hypercholesterolemic patients were treated with atorvastatin at a dose of 10 mg/day for 3 months. Lipid profile, lipid oxidation markers (malondialdehyde (MDA), conjugated diene (CD), total peroxides (TP)), total antioxidant substance (TAS), oxidative stress index (OSI), and paraoxonase1 activity were determined before and after treatment. L55M, Q192R, and T(-107)C PON1 polymorphisms were also determined. Atorvastatin treatment significantly reduced the levels of total cholesterol (24.5%), low density lipoprotein (LDL) cholesterol (25.4%), triglycerides (24.4%), CD (4.4%), MDA (15.2%), TP (13.0%) and OSI (24.0%), and significantly increased the levels of TAS (27.3%), and PON1 activity (14.0%). Interestingly, the increase in PON1 activity and the reduction in oxidative stress in response to atorvastatin were influenced only by the PON1 T-107C polymorphism. Atorvastatin treatment improved the lipid profile, lipid oxidation, and oxidative/antioxidative status markers including the activity of PON1 towards paraoxon. These beneficial effects may be attributed to the antioxidant properties of statins and the increase in PON1 activity. The increase in PON1 activity was enhanced by the PON1 T-107C polymorphism.

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We identified 1239 incident simvastatin and atorvastatin users in the Rotterdam Study, a population-based cohort study. Associations between the polymorphisms in the CYP3A4 and ABCB1 gene and the time to a decrease in dose or a switch to another cholesterol lowering drug were studied using Cox proportional hazards.

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The present study aimed to assess the effects of a COX-2 inhibitor, celecoxib, a HMG-CoA reductase inhibitor, atorvastatin, and the association of both on monocrotaline (MC)-induced pulmonary hypertension in rats. Celecoxib (Cib, 25 mg kg(-1) day(-1)), atorvastatin (AS, 10 mg kg(-1) day(-1)) or vehicle, were given orally, separately or in combination, for 26 days to Wistar male rats injected or not with MC (60 mg/kg intraperitoneally). At 4 weeks, MC-injected rats developed a severe pulmonary hypertension, with an increase in lung to body weight ratio (L/BW), right ventricular pressure (RVP in mmHg, 31 +/- 3 and 14 +/- 1 for MC and control groups, respectively, P < 0.05) and right ventricle/left ventricle + septum weight ratio (RV/LV+S) associated with a decrease in acetylcholine- and sodium-nitroprusside-induced pulmonary artery vasodilation in vitro. Hypertensive pulmonary arteries exhibited an increase in wall thickness (wall thickness to external diameter ratio, 0.42 +/- 0.01 vs 0.24 +/- 0.01 for MC and control groups, respectively, P < 0.001). Whole lung eNOS expression was decreased, and an increase in apoptosis, evaluated by cleaved caspase-3 expression, was evidenced by Western blotting. Cib (RVP in mmHg, 19 +/- 3 and 31 +/- 3 for MC+Cib and MC groups, respectively, P < 0.05), but neither AS nor AS+Cib significantly limited the development of pulmonary hypertension (P < 0.05), although the three treatments exhibited protective effects against MC-induced lung and right ventricle hypertrophy evaluated by L/BW and RV/(LV+S) ratios, respectively (P < 0.05). AS, Cib and AS+Cib treatments reduced MC-induced thickening of small intrapulmonary artery wall (0.42 +/- 0.01, 0.24 +/- 0.01, 0.26 +/- 0.01 and 0.28 +/- 0.01 for MC, MC+AS, MC+Cib and MC+AS+Cib groups, respectively, P < 0.001). In control rats, Cib reduced acetylcholine-induced pulmonary artery vasorelaxation. Treatment of MC rats by either Cib or AS did not modify acetylcholine-induced pulmonary artery relaxation, whereas combination of both drugs significantly worsened it (P < 0.05). AS, but neither Cib nor the combination of both, prevented apoptosis (AS, P < 0.05) and partially restored eNOS expression (AS, P < 0.05) in whole lung of MC rats. In conclusion, celecoxib exhibited beneficial effects against the development of monocrotaline-induced pulmonary artery hypertension and right ventricular hypertrophy. These beneficial effects of celecoxib might be, at least partly, explained by its effects on pulmonary artery thickening and pulmonary hypertrophy, even if it did not show any effect on pulmonary artery vasorelaxation and whole lung eNOS expression or apoptosis. The combination of celecoxib and atorvastatin was unable to prevent MC-induced pulmonary hypertension, decreased endothelium-dependent vasorelaxation and showed a trend toward an increased in RVP that deserves further studies.

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Using a large historical database of interventions and outcomes in dialysis patients, we conducted an observational model of the 4D Study in dialysis patients who had type 2 diabetes and were prescribed a statin (5144 patients) and matched to a non-statin user (5144 control subjects) before multivariate modeling. Inclusion, exclusion, and outcome parameters of the study, as prespecified by the 4D Study, were strictly modeled in this analysis.

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Mutations of the tumor suppressor genes tuberous sclerosis complex (TSC)1 and TSC2 cause pulmonary lymphangioleiomyomatosis (LAM) and tuberous sclerosis (TS). Current rapamycin-based therapies for TS and LAM have a predominantly cytostatic effect, and disease progression resumes with therapy cessation. Evidence of RhoA GTPase activation in LAM-derived and human TSC2-null cells suggests that 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor statins can be used as potential adjuvant agents. The goal of this study was to determine which statin (simvastatin or atorvastatin) is more effective in suppressing TSC2-null cell growth and signaling. Simvastatin, but not atorvastatin, showed a concentration-dependent (0.5-10 μM) inhibitory effect on mouse TSC2-null and human LAM-derived cell growth. Treatment with 10 μM simvastatin induced dramatic disruption of TSC2-null cell monolayer and cell rounding; in contrast, few changes were observed in cells treated with the same concentration of atorvastatin. Combined treatment of rapamycin with simvastatin but not with atorvastatin showed a synergistic growth-inhibitory effect on TSC2-null cells. Simvastatin, but not atorvastatin, inhibited the activity of prosurvival serine-threonine kinase Akt and induced marked up-regulation of cleaved caspase-3, a marker of cell apoptosis. Simvastatin, but not atorvastatin, also induced concentration-dependent inhibition of p42/p44 Erk and mTORC1. Thus, our data show growth-inhibitory and proapoptotic effects of simvastatin on TSC2-null cells compared with atorvastatin. These findings have translational significance for combinatorial therapeutic strategies of simvastatin to inhibit TSC2-null cell survival in TS and LAM.

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Inflammation is important in atherogenesis. Interleukin (IL)-1 is the prototypic inflammatory cytokine. We hypothesized a dysbalance between inflammatory and anti-inflammatory mediators in the IL-1 family in coronary artery disease (CAD) and a possible modulation of these mediators by HMG-CoA inhibitors (statins).

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Patient age had a statistically significant impact on statin prescribing for patients in profile 1 (disorders of lipoprotein metabolism) and profile 3 (complex profiles) with a greater number of patented statins being prescribed for the youngest patients. For instance, patients older than 76 years with a complex profile were prescribed fewer patented statins than patients aged 68-76 years old with the same medical profile (coefficient: -0.225; p = 0.0008). By contrast, regardless of the patient's age, the medical profile did not affect the probability of prescribing a patented statin except in young patients with heart diseases who were prescribed a greater number of patented statins (coefficient: 0.3992; p = 0.0007). Prescribing was also statistically influenced by physician features, e.g., older male physicians were more likely to prescribe patented statins (coefficient: 0.245; p = 0.0417) and GPs practicing in groups were more likely to prescribe multiple sourced statins (coefficient: -0.178; p = 0.0338), which is an important finding of the study. GPs with a lower workload prescribed a greater number of patented statins.

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Inter-individual variability exists in the statin (HMG-CoA reductase inhibitor) lipid-lowering response, which is partially attributed to genetic factors. The polymorphic enzyme P450 oxidoreductase (POR) transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH) to cytochrome P450 (CYP) 3A enzymes, which metabolize atorvastatin and simvastatin. The POR*28 allele is associated with increased activity of CYP3A enzymes. We analyzed the association of the POR*28 allele with response to atorvastatin and simvastatin.

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lipitor drug card 2017-11-26

Th1 polarization exists in buy lipitor patients with CHF, and atorvastatin can modulate the Th1/Th2 response through inhibiting Th1 cytokine production.

lipitor tablets 2016-04-26

Under the current statin treatment guidelines a small number of statin eligible subjects with low CAC might not benefit from statin therapy within 5 years. However, the statin buy lipitor not eligible subjects with high CAC have high event rate attributing to loss of opportunity for effective primary prevention.

lipitor 60 mg 2017-07-20

Our findings provide buy lipitor new insight into the molecular mechanism by which statins induce apoptosis in ovarian cancer cells and may lead to novel therapies for advanced ovarian cancer.

lipitor 300 mg 2016-02-02

We studied prospectively 33 stable, iron-repleted haemodialysis patients with low-density lipoprotein cholesterol (LDL) > or =2.58 mmol/L, who received 20 mg atorvastatin aiming to achieve the target of LDL <2.58 mmol/L, over a period of 9 months. Twenty-five patients completed the study, 15 men, with mean age 66. buy lipitor 1 +/- 8.2 years. The duration of haemodialysis was 56.6 +/- 63.1 months and 5/25 patients were diabetics. Total serum cholesterol, triglycerides, high-density lipoprotein cholesterol, LDL, haemoglobin, albumin, intact parathyroid hormone, serum iron, ferritin, total iron binding capacity, CRP and weekly dose of erythropoietin/body weight/haemoglobin were analysed.

lipitor brand name 2015-03-20

Familial hypercholesterolaemia (FH) affects 1 in 500 people in the UK population and is associated with premature morbidity and mortality buy lipitor from coronary heart disease. In 2008, National Institute for Health and Care Excellence (NICE) recommended genetic testing of potential FH index cases and cascade testing of their relatives. Commissioners have been slow to respond although there is strong evidence of cost and clinical effectiveness. Our study quantifies the recent reduced cost of providing a FH service using generic atorvastatin and compares NICE costing estimates with three suggested alternative models of care (a specialist-led service, a dual model service where general practitioners (GPs) can access specialist advice, and a GP-led service).

lipitor generic price 2016-05-25

This report investigated the relationship between anthropometric measurements of body fat buy lipitor distribution and lipid response to statins in hypercholesterolemic hypertensive patients.

lipitor cutting tablets 2016-04-15

To investigate whether Atorvastatin (Ator) treatment improves the cardiac micro buy lipitor -environment that facilitates survival and differentiation of bone-marrow-derived mesenchymal stem cells (MSCs) implanted in the post-infarct myocardium.

lipitor dosage amounts 2016-04-04

Atherosclerosis is considered to be a chronic inflammatory disorder. Several large-scale clinical studies demonstrate that markers of inflammation, such as high-sensitivity C-reactive protein (hsCRP), fibrinogen, and soluble CD40 ligand, are potent buy lipitor and independent predictors of vascular risk.

lipitor side reviews 2015-04-19

Atorvastatin, estrogen and G-CSF could mobilize EPCs. The mobilization efficacy is as follows: G-CSF > atorvastatin 5 mg.k(-1).d(-1) > estrogen > atorvastatin 2.5 mg.k(-1).d(-1) > atorvastatin 10 mg.k(-1).d(-1). NO buy lipitor might partly contribute to the mobilizing effect of estrogen and atorvastatin.

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Perioperative atorvastatin treatment is not found to be associated with reduced postoperative atrial fibrillation and cardiac mortality in patients undergoing isolated buy lipitor coronary artery bypass grafting above the age of seventy years.

lipitor 10mg tablet 2015-07-24

Plasticity of vascular smooth muscle cells (VSMCs) plays a central role in the onset and progression of proliferative vascular diseases. In adult tissue, VSMCs exist in a physiological contractile-quiescent phenotype, which is defined by lack of the ability of proliferation and migration, while high expression of contractile marker proteins. After injury to the vessel, VSMC shifts from a contractile phenotype to a pathological synthetic phenotype, associated with increased proliferation, migration and matrix secretion. It has been demonstrated that PDGF-BB is a critical mediator of VSMCs phenotypic switch. Atorvastatin calcium, a selective inhibitor of 3-hydroxy-3-methyl-glutaryl l coenzyme A (HMG-CoA) reductase, exhibits various protective effects against VSMCs. In this study, we investigated the effects of atorvastatin calcium on phenotype modulation of PDGF-BB-induced VSMCs and the related intracellular signal transduction pathways. Treatment of VSMCs with atorvastatin calcium showed dose-dependent inhibition of PDGF-BB-induced proliferation. Atorvastatin calcium co-treatment inhibited the phenotype modulation and cytoskeleton rearrangements and improved the expression of contractile phenotype marker proteins such as α-SM actin, SM22α and calponin in comparison with PDGF-BB alone stimulated VSMCs. Although Akt phosphorylation was strongly elicited by PDGF-BB, Akt activation was attenuated when PDGF-BB was co-administrated with atorvastatin calcium. In conclusion, atorvastatin calcium inhibits phenotype modulation of PDGF-BB-induced VSMCs and activation of the Akt signaling pathway, indicating that buy lipitor Akt might play a vital role in the modulation of phenotype.

lipitor dosage information 2017-12-30

Statins are some of the most widely prescribed medications, and though generally well tolerated, can lead to a self-limited myopathy in a minority of patients. Recently, these medications have been associated with a necrotizing autoimmune myopathy (NAM). Statin-associated NAM is characterized by irritable myopathy on electromyography (EMG) and muscle necrosis with minimal inflammation on muscle biopsy. The case presented is a 63-year-old woman who has continued elevation of creatine kinase (CK) after discontinuation of statin therapy. She has irritable myopathy on EMG and NAM is confirmed by muscle biopsy. She subsequently tests positive for an experimental anti-3-hydroxy-3-methylglutaryl-coenzyme A (anti-HMGCoA) antibody buy lipitor that is found to be present in patients with statin-associated NAM. Though statin-associated NAM is a relatively rare entity, it is an important consideration for the general internist in patients who continue to have CK elevation and weakness after discontinuation of statin therapy. Continued research is necessary to better define statin-specific and dose-dependent risk, as well as optimal treatment for this condition.

lipitor reviews webmd 2016-11-17

This study assessed the relationships between baseline characteristics and changes in lipid variables, high-sensitivity C-reactive protein (hs-CRP) and attainment of prespecified low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL buy lipitor -C) levels in MetS patients treated with ezetimibe/simvastatin and atorvastatin.

cmi lipitor tablets 2015-09-08

Treatment with atorvastatin was associated with increased levels of myocardial tissue protein and lipid oxidative stress biomarkers and a reduced functional endogenous angiogenic response, but improved coronary microvascular reactivity. Increased oxidative stress in tissues may buy lipitor play a role in the reduced angiogenic response seen with atorvastatin treatment in other studies.

lipitor drug class 2015-02-28

The concentrations of crospovidone (CP), maltodextrin and microcrystalline Lexapro Starting Dose cellulose (MCC) have been optimized in the development of self-microemulsified tablets (SMET) to improve the oral bioavailability of an anti-hyperlipidemic drug, atorvastatin, and the in-vivo pharmacokinetic parameters of the optimized SMET were compared with those of a commercial tablet in rabbits.

atorvastatin lipitor reviews 2015-11-04

K-Ras is one of the most frequently mutated signal transducing human oncogenes. Ras signaling activity requires correct cellular localization of the GTPase. The spatial organization of K-Ras is controlled by the prenyl binding protein PDEδ, which enhances Ras diffusion in the cytosol. Inhibition of the Ras-PDEδ interaction by small molecules Augmentin Oral Suspension impairs Ras localization and signaling. Here we describe in detail the identification and structure guided development of Ras-PDEδ inhibitors targeting the farnesyl binding pocket of PDEδ with nanomolar affinity. We report kinetic data that characterize the binding of the most potent small molecule ligands to PDEδ and prove their binding to endogenous PDEδ in cell lysates. The PDEδ inhibitors provide promising starting points for the establishment of new drug discovery programs aimed at cancers harboring oncogenic K-Ras.

lipitor went generic 2015-04-23

Primary objective To quantify the effects of various doses of rosuvastatin on serum total Diovan User Reviews cholesterol, low-density lipoprotein (LDL)-cholesterol, high-density lipoprotein (HDL)-cholesterol, non-HDL-cholesterol and triglycerides in participants with and without evidence of cardiovascular disease. Secondary objectives To quantify the variability of the effect of various doses of rosuvastatin.To quantify withdrawals due to adverse effects (WDAEs) in the randomized placebo-controlled trials.

lipitor reviews 2014 2016-09-07

Achilles tendon xanthomas (ATX) have been associated with increased cardiovascular risk in Periactin 4mg Tablets patients with familial hypercholesterolemia (FH). The aim of this study was to evaluate clinical and ultrasonographic changes of ATX in patients with FH under statin treatment.

lipitor generic brand 2017-07-18

The median patient age was 66 years (interquartile range [IQR] 58 to 74 years), 60% were men and 80% were in the high 10-year risk category. The median low-density lipoprotein cholesterol level was 2.0 mmol/L (IQR 1.6 mmol/L to 2.5 mmol/L) and the median total cholesterol/high-density lipoprotein cholesterol ratio was 3.4 mmol/L (IQR 2.8 mmol/L to 4.1 mmol/L). However, based on the 2006 Canadian Cardiovascular Society recommendations, 37% of all patients did not have a low-density lipoprotein cholesterol level at goal or intervention target level, including 45% of high-risk category patients. The majority of patients received atorvastatin (50%) Imodium Recommended Dosage or rosuvastatin (37%) but primarily at low-to-medium doses, and a minority (14%) received additional lipid-modifying therapies.

lipitor 100 mg 2015-01-30

The effect of atorvastatin (3 mg kg(-1) day(-1)), simvastatin (3 mg kg(-1) day(-1)) and bezafibrate (100 mg kg(-1) day(-1)) administered for 4 weeks to male New Zealand white rabbits on enzyme activities related to lipid metabolism has been studied. Only the statins reduced plasma cholesterol values, while none of the drugs modified plasma triglyceride or high density lipoprotein (HDL)-cholesterol concentrations, nor the activity of enzymes such as hepatic diacylglycerol acyltransferase, lipoprotein lipase or hepatic lipase, directly involved in triglyceride metabolism. Both statins elicited similar increases in the hepatic microsomal 3-hydroxy-3-methyl-glutaryl Coenzyme A (CoA) reductase activity (147 and 109% induction for simvastatin and atorvastatin, respectively), and none of the drugs assayed modified hepatic acyl-coenzyme A:cholesterol acyltransferase activity significantly. Only bezafibrate induced a significant 57% reduction in the activity of hepatic microsomal cholesterol 7alpha- Stromectol 18 Mg hydroxylase. Regarding the rate limiting enzyme of phosphatidylcholine biosynthesis, CTP:phosphocholine cytidylyl transferase, atorvastatin and bezafibrate behaved similarly, decreasing the enzyme activity in the liver by 45% and 54%, respectively; simvastatin induced no modification of this activity. The reduction of CTP:phosphocholine cytidylyl transferase activity is not caused by a direct inhibition of the enzyme by bezafibrate and atorvastatin. Further, the inhibitory effect of atorvastatin appears to be unrelated to the inhibition of 3-hydroxy-3-methyl-glutaryl CoA reductase elicited in vivo.

cut lipitor pill 2017-12-08

HsCRP was associated with AF recurrence one and six months after successful CV of persistent AF. However, the association at one month was significant only after adjusting for atorvastatin treatment.

lipitor good reviews 2015-02-13

Greater reductions in LDL-C were achieved with rosuvastatin compared with equal doses of atorvastatin, enabling more patients with Type 2 diabetes to achieve European LDL-C goals.

lipitor 50mg tab 2016-12-21

Radiofrequency (RF) signals were obtained using an IVUS system with a 40-MHz catheter. The IB values of the RF signal were calculated and color-coded. The 3D reconstruction of the color-coded map was performed by computer software. A total of 18 IB IVUS images were captured at an interval of 1 mm in each plaque. A total of 52 patients with hyperlipidemia were randomized to treatment with pravastatin (20 mg/day, n = 17), atorvastatin (20 mg/day, n = 18), or diet (n = 17) for six months. The tissue characteristics of arterial plaque in each patient (one arterial segment per patient) were analyzed with 3D IB IVUS before and after treatment.

lipitor generic drug 2017-07-17

Altogether, these results show that administration of an high-fat diet in a model of type 2 diabetes increases cardiovascular risk and combined use of atorvastatin and insulin provides a superior control of cardiovascular risk markers in diabetic and hyperlipidemic subjects.

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Statins have been shown to inhibit oxidative stress, however it is still unclear if they influence antioxidant status. We performed a retrospective analysis of oxidative stress, as assessed by serum levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and vitamin E, a known antioxidant, in patients with metabolic syndrome (n=112) treated (n=30) or not (n=82) with statins. Statin-treated patients showed higher levels of vitamin E (p=0.02) and lower 8-OHdG (p<0.01) than statin-free patients. An inverse correlation between oxidative stress and vitamin E was observed (r=-0.670, p<0.001). These preliminary data suggest that statins enhance the antioxidant status likely by inhibiting oxidative stress.

lipitor normal dosage 2017-12-12

Breast cancer cells express enzymes that convert cholesterol, the synthetic precursor of steroid hormones, into estrogens and androgens, which then drive breast cancer cell proliferation. In the present study, we sought to determine whether oxidosqualene cyclase (OSC), an enzyme in the cholesterol biosynthetic pathway, may be targeted to suppress progression of breast cancer cells. In previous studies, we showed that the OSC inhibitor RO 48-8071 (RO) may be a ligand which could potentially be used to control the progression of estrogen receptor-α (ERα)-positive breast cancer cells. Herein, we showed, by real-time PCR analysis of mRNA from human breast cancer biopsies, no significant differences in OSC expression at various stages of disease, or between tumor and normal mammary cells. Since the growth of hormone-responsive tumors is ERα-dependent, we conducted experiments to determine whether RO affects ERα. Using mammalian cells engineered to express human ERα or ERβ protein, together with an ER-responsive luciferase promoter, we found that RO dose-dependently inhibited 17β-estradiol (E2)-induced ERα responsive luciferase activity (IC50 value, ~10 µM), under conditions that were non-toxic to the cells. RO was less effective against ERβ-induced luciferase activity. Androgen receptor (AR) mediated transcriptional activity was also reduced by RO. Notably, while ERα activity was reduced by atorvastatin, the HMG-CoA reductase inhibitor did not influence AR activity, showing that RO possesses broader antitumor properties. Treatment of human BT-474 breast cancer cells with RO reduced levels of estrogen-induced PR protein, confirming that RO blocks ERα activity in tumor cells. Our findings demonstrate that an important means by which RO suppresses hormone-dependent growth of breast cancer cells is through its ability to arrest the biological activity of ERα. This warrants further investigation of RO as a potential therapeutic agent for use against hormone-dependent breast cancers.

lipitor dosage forms 2015-09-26

This review examines current evidence to address the question whether rheumatoid arthritis (RA) is a coronary heart disease equivalent, similar to type 2 diabetes mellitus (DM2).

lipitor 40 mg 2015-09-07

The results suggest that α-TCP can be used for local delivery of statin as a pulp capping material to accelerate reparative dentin formation.

lipitor generic 2016-12-01

No statin-clopidogrel interaction nor any clinically relevant events were documented in the studied cohort. No interaction between CYP3A4 statins and a single loading dose of 600 mg clopidogrel was documented in this cohort.

lipitor drug 2016-12-13

In the present study we examined the disposition of atorvastatin, lovastatin, and simvastatin in acid and lactone forms and pravastatin in acid form in multidrug-resistant gene (mdr1a/b) knockout (KO), and wild-type (WT) mice. Each statin was administered s.c. to mdr1a/b KO and WT mice at 3.0 mg/kg (n > or = 3 mice/time point). Blood, brain, and liver samples were harvested at 0, 0.5, 1.5, and 3 h postdose. Plasma and tissue concentrations of the acid and lactone (only the acid form was determined for pravastatin) were determined using a liquid chromatography-mass spectrometry method. Both lactone and acid were observed in plasma when lactones were administered, but only acids were detected when the acid forms were administered. The plasma and liver concentrations of acid or lactone were similar between the KO and WT mice. Two- to 23-fold higher concentrations were observed in liver than in plasma, suggesting potential uptake transporters involved. A significantly higher (p < 0.05) brain penetration in the KO compared with the WT mice was observed for lovastatin acid (but the brain/plasma ratio was low for both KO and WT mice) and lactone and simvastatin lactone but not for atorvastatin or pravastatin. The present results suggest that mouse P-glycoprotein does not affect the lactone-acid interconversion or liver-plasma distribution. Furthermore, P-glycoprotein plays a limited role in restricting the brain penetration of the acid forms of atorvastatin, pravastatin, simvastatin, lovastatin, and atorvastatin lactone but may limit the brain availability of the lactone forms of simvastatin and lovastatin.