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Zetia (Ezetimibe)

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Generic Zetia is a high-quality medication which is taken in treatment of heart disease and stroke. It also prevents clogged arteries and decreases triglyceride and cholesterol rate. Generic Zetia acts by reducing the general amount of cholesterol, LDL cholesterol and protein which is used to create cholesterol.

Other names for this medication:

Similar Products:
Lipitor, Zocor, Crestor, Zetia, Mevacor, Tricor


Also known as:  Ezetimibe.


Generic Zetia is a perfect remedy in struggle against heart disease and stroke. It also prevents clogged arteries and decreases triglyceride and cholesterol rate.

Generic Zetia acts by reducing the general amount of cholesterol, LDL cholesterol and protein which is used to create cholesterol. It is cholesterol-lowering drug.

Zetia is also known as Ezetimibe, Ezetrol.

Generic name of Generic Zetia is Ezetimibe.

Brand name of Generic Zetia is Zetia.


The usual dose of Generic Zetia is 10 mg a day taken with water.

You should take Generic Zetia 2 hours before or 4 hours after using colesevelam (such as Welchol), colestipol (such as Colestid) or cholestyramine (such as Prevalite, Locholest, Questran).

Take Generic Zetia tablets orally with or without food.

Do not crush or chew it.

Take Generic Zetia at the same time once a day.

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


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


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zetia 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 Zetia if you are allergic to Generic Zetia components.

Do not take Generic Zetia if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Zetia can ham your baby.

Generic Zetia cannot be taken by children under 10 years.

Generic Zetia cannot be used together with fibrates (such as Lopid, Tricor).

Try to be careful using Generic Zetia if you take cyclosporine (such as Sandimmune, Neoral, Gengraf); another cholesterol "lowering drugs fenofibrate (such as Tricor), (gemfibrozil (such as Lopid), clofibrate (such as Atromid-S), lovastatin (such as Altocor, Mevacor), pravastatin (such as Pravachol), fluvastatin (such as Lescol) or simvastatin (such as Zocor), atorvastatin (such as Lipitor).

It can be dangerous to use Generic Zetia if you suffer from or have a history of liver disease.

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

Avoid alcohol.

Keep low-cholesterol and low-fat diet.

Do not stop taking Generic Zetia suddenly.

zetia generic launch

This was a retrospective study including consecutive subjects ≥ 65 years old (n = 465) with a follow-up ≥ 3 years. Low-density lipoprotein cholesterol (LDL-C), blood pressure (BP) and glycated hemoglobin (HbA1c) goal achievement were recorded according to European Society of Cardiology/European Atherosclerosis Society (ESC/EAS), European Society of Hypertension (ESH)/ESC and European Association for the Study of Diabetes (EASD) guidelines.

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Our results suggest that fatty acids and desaturase activity associate with the development and progression of NAFLD, and that ezetimibe may be a novel treatment for this disorder.

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A randomized, double-blind, placebo-controlled, crossover trial was performed in 215 African- and European-American men.

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Mean LDL-C was reduced by 28%/27% (study 1/ study 2) compared with baseline values (on statin monotherapy). Mean total cholesterol was decreased by 22% in each study, mean triglycerides by 16/17%, and mean high density cholesterol (HDL-C) was increased by 9/10%. Adverse events were reported in 0.3% and 0.2% of patients, respectively.

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Ezetimibe inhibits cholesterol absorption by blocking Niemann-Pick C1-like 1 proteins (NPC1L1) expressed in the small intestine. Because NPC1L1 is also expressed in human liver, ezetimibe conceivably alters biliary lipid compositions. Here, we performed a clinical trial investigating the effect of ezetimibe on biliary lipids using transnasal endoscopy for bile collection.

zetia reviews

Statins remain the cornerstone of hypolipidaemic drug treatment. The recent American College of Cardiology (ACC)/American Heart Association (AHA) lipid guidelines suggest using percent reductions of low density lipoprotein cholesterol (LDL-C), according to cardiovascular disease (CVD) risk, rather than specific LDL-C targets. These guidelines raised concerns and other Societies (US, International, European) have not endorsed them. The implementation of previous guidelines in clinical practice is suboptimal due to attitudes of physicians and restrictions in health care systems. Monoclonal antibodies that inhibit proprotein convertase subtilisin/ kexin type 9 (PCSK9), which degrades the LDL receptor, like alirocumab and evolocumab, are in phase 3 trials. These drugs are suitable for statin intolerant or resistant patients, heterozygous familial hypercholesterolaemia (HeFH) and some forms of homozygous FH (HoFH). Mipomersen (antisense oligonucleotide against apolipoprotein B) and lomitapide (microsomal triglyceride transfer protein blocker) have already been approved for HoFH. Eventually, silencing micro-RNA oligonucleotides may also become available. The repair or silencing of genes implicated in hyperlipidaemia and/or atherosclerosis is also on the horizon. If the new therapeutic options mentioned above prove to be effective and safe then by combining them with statins and/or ezetimibe we should be able to effectively control acquired or hereditary dyslipidaemias and substantially further reduce CVD morbidity and mortality.

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Options for treatment of severe heterozygous and homozygous familial hypercholesterolemia prior to the statin era were limited by significant side effects and morbidity. The advent of both the statins and technology for the selective removal of LDL via apheresis have revolutionized management but challenges remain.

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Standard and aggressive lipid targets can be safely maintained in diabetic patients. Standardized algorithms, point-of-care lipid testing, and nonphysician providers facilitate care delivery.

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To review the clinical and cost-effectiveness of ezetimibe as a combination therapy or monotherapy for the treatment of primary hypercholesterolaemia in the UK.

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This was a prospective, open-label, crossover study, with subjects randomly assigned to group 1 (raltegravir 400 mg twice daily, raltegravir plus ezetimibe 10 mg once daily, wash-out period, ezetimibe) or group 2 (ezetimibe, raltegravir plus ezetimibe, wash-out period, raltegravir); all phases lasted for 10 days. Steady-state full PK sampling was performed at days 10, 20 and 40. Raltegravir and ezetimibe PK parameters were determined by non-compartmental methods and comparisons in the presence of the potentially interactive drug measured by geometric mean ratio (GMR) and 95% confidence intervals (CIs).

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Recent trends suggest a decreased use of ezetimibe/simvastatin combination and coadministered ezetimibe plus statin therapies.

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In Japanese patients with type 2 diabetes or impaired glucose tolerance and coronary artery disease, adding ezetimibe (10 mg/day) to atorvastatin (10 mg/day) significantly improved the lipid profile compared with atorvastatin monotherapy at 20 mg/day.

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Among 703,484 patients 68% had at least one lab test performed in the 6 months before treatment. Performing an LDL test was negatively associated with several patient characteristics, including recent hospitalization (OR = 0.32, 95% CI: 0.29-0.34), MI (OR = 0.77, 95% CI: 0.69-0.85), or carotid revascularization (OR = 0.37, 95% CI: 0.25-0.53). Patient demographics, diagnoses, and procedures predicted well who would have a lab test performed (AUC = 0.89 to 0.93). Among those with test results available claims data explained only 14% of variation.

zetia user reviews

In patients admitted for acute coronary syndrome (ACS), the guidelines of the European Society of Cardiology give a Class I, Level A recommendation for the prescription of high-intensity statins to be initiated as early as possible, regardless of the low-density lipoprotein cholesterol (LDL-C) level. Although statins are widely prescribed after ACS, the intensity of therapy and the proportion of patients achieving target LDL-C values are often not in line with recommendations due to a lack of compliance with guidelines by the physicians, a lack of compliance with treatment or poor tolerance by patients, and poor dose adaptation. In this context, a group of French physicians came together to define strategies to facilitate and improve the management of lipid-lowering therapy after ACS. This paper outlines the scientific rationale for the use of statins at the acute phase of ACS, the utility of ezetimibe, the measurement of LDL-C during the course of ACS, the opportunities for detecting familial hypercholesterolaemia and the results of the consensus for the management of lipid-lowering therapy, illustrated in two decision-making algorithms.

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Hypercholesterolaemia is a pivotal risk factor for cardiovascular and cerebrovascular disease and is treated with many effective lipid-lowering agents. Statins are often used alone or in combination with ezetimibe. Combination therapy is more effective because of its complementary approach, which has major benefits for patients with unmanageable lipid levels. Extensive application of combination therapy has resulted in an increased incidence of side-effects, which has raised our concern.

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Aiming to improve the dissolution rate of ezetimibe (EZE) and lovastatin (LOV) in a fixed dose combination (FDC), co-amorphous systems and ternary solid dispersions were prepared by quench cooling and spray drying, respectively.

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Baseline apoB and the apoB/apoA-I ratio were significantly predictive of CV events only for the placebo group (HR: 1.17 [p = 0.018] and HR: 1.19 [p = 0.016]). Baseline and on-study Lp(a) were predictive of CV events in both simvastatin plus placebo (baseline HR: 1.24 [p = 0.002] and on-study HR: 1.21 [p = 0.017]) and the simvastatin plus ERN group (baseline HR: 1.25 [p = 0.001] and on-study HR: 1.18 [p = 0.028]). The ERN modestly increased 1-year apoA-1 (7%), decreased apoB (13%), decreased the ApoB/ApoA-1 ratio (19%), and decreased Lp(a) 21%, but did not reduce CV events.

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Three months of ezetimibe treatment significantly decreased the total cholesterol (TC) (-10.1%), low-density lipoprotein (LDL-C) (-12.0%) (p < 0.001) and triglyceride (Tg) (-8%) levels (p < 0.05). After 6 and 12 months of treatment reduction in TC, LDL-C and Tg levels were even more pronounced. The genotype distribution of the patients were 2/2: 4.8%, 2/3: 7.9%, 3/3: 68.3%, 3/4: 19.0%. There were no patients with 2/4 and 4/4 genotypes. In patients with 2/3, 3/3 or 3/4 genotype, the ezetimibe treatment tended to be more effective on TC and LDL-C levels than in the 2/2 group, and the efficacy of ezetimibe on Tg levels were slightly better in 2/2 carriers compared to other patients.

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Ezetimibe is a lipid-lowering drug indicated for the treatment of hypercholesterolemia as co-administration with HMG-CoA reductase inhibitors (statins) or as monotherapy. The primary objectives of this study were to evaluate the pharmacodynamic effects and safety of the co-administration of ezetimibe and the new statin rosuvastatin. A secondary objective was to examine the potential for a pharmacokinetic interaction between ezetimibe and rosuvastatin.

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Compared with simvastatin/ezetimibe (10/10 mg), rosuvastatin (10 mg) appears to more effectively improve arterial wall stiffness that may be mediated by modulation of the ROCK activity.

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To examine the association of this announcement with national patterns of ezetimibe prescribing, including medication initiation and discontinuation, as well as predictors of use.

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We stratified patients with hyperlipidemia according to the risk categories outlined by the Adult Treatment Panel III of the National Cholesterol Education Program. On the basis of this classification, patients were started on background lipid-lowering therapy with diet alone or diet plus atorvastatin at a dose of 10 mg daily, atorvastatin at a dose of 80 mg daily, or atorvastatin at a dose of 80 mg daily plus ezetimibe at a dose of 10 mg daily, for a run-in period of 4 to 12 weeks. Patients with an LDL cholesterol level of 75 mg per deciliter (1.9 mmol per liter) or higher were then randomly assigned in a 2:1 ratio to receive either evolocumab (420 mg) or placebo every 4 weeks. The primary end point was the percent change from baseline in LDL cholesterol, as measured by means of ultracentrifugation, at week 52.

zetia 10mg tablets

Relationships between hsCRP and lipid factors in older patients were weak at baseline and somewhat stronger after treatment. HDL-C was inversely and consistently correlated with baseline and 12-week on-treatment hsCRP and with therapy-induced changes in HDL-C and hsCRP.

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Proprotein convertase subtilisin kexin type 9 (PCSK9) is a circulating protein that impairs LDL clearance by promoting the LDL receptor (LDLR) degradation. PCSK9 has emerged as a new pharmacological target for hypercholesterolemia, and different PCSK9 inhibitors are now evaluated in clinical trials. Here, we propose an overview of the clinical perspectives of PCSK9. First, we describe the clinical features of patients with PCSK9 mutations, and how these variations impact the cardiovascular risk. Then, we extensively discuss the potential role of circulating PCSK9 as a new biomarker of lipid metabolism. Indeed, many studies conducted in healthy and type 2 diabetic patients have tested the association of circulating PCSK9 with LDL-cholesterol as well as with multiple metabolic parameters. The overall picture of the clinical relevance of circulating PCSK9 is complicated by the effect of nutritional status and hypolipidemic drugs such as statins, fibrates, ezetimibe on plasma PCSK9 concentrations. Finally, we present a brief overview of the available therapeutic strategies to inhibit PCSK9.

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Time and care is needed to address SAMS because they impair drug adherence. For most patients it is possible to continue the statin therapy. However, combination therapy is wanted if the maximally tolerated statin dose is not sufficient to reach LDL targets.

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zetia drug interactions 2017-08-24

Sitosterolemia is a recessively buy zetia inherited disorder that results from mutations in either ABCG5 or G8 proteins, with hyperabsorption of dietary sterols and decreased hepatic excretion of plant sterols and cholesterol. As a consequence of markedly elevated plasma and tissue sitosterol and campesterol levels, premature atherosclerosis develops.

zetia max dose 2015-04-15

Ezetimibe treatment significantly reduced serum levels of low-density lipoprotein cholesterol (LDL-C) and malondialdehyde-modified low-density lipoprotein (MDA-LDL). In addition, the values of body mass index, body weight, waist circumference, plasma HbA1c and urinary albumin were significantly decreased in group E compared to those in group C. On the other hand, high-density lipoprotein cholesterol (HDL-C) and adiponectin levels were significantly increased in group E compared to those in group C. The values of brachial-ankle pulse wave velocity (ba-PWV), mean arterial blood pressure (m-ABP), and % of flow-mediated dilation (FMD) were significantly improved in group E. Furthermore, ultrasonic studies demonstrated amelioration of the vascular stiffness of common carotid arteries in group E buy zetia but not in group C. These vascular protective effects of ezetimibe were statistically correlated with the decreased values of MDA-LDL and MDA-LDL-to-LDL-C ratio but not with those of LDL-C.

zetia replacement drug 2017-10-27

This study assessed the efficacy and tolerability of colesevelam added to maximally buy zetia tolerated, stable-dose combination treatment with a statin + ezetimibe.

zetia generic 2016-09-15

The study revealed a 32.5% reduction in mean Lp-PLA(2) values (baseline 181.1±41.5 vs 122.1±28.1 ng/mL after treatment; P<.001). The change observed in LDL-C was 41%, (baseline 126.2±43 vs 73.9±37.7mg/dL after treatment), which also was significant (P < .001). However, a Pearson correlation test analysis revealed buy zetia only a weak positive association between changes in Lp-PLA(2) and LDL-C (r(2)=0.052, P < .001).

zetia overdose 2015-10-15

This was a post-hoc analysis of data from a randomized, double-blind, placebo-controlled trial designed to evaluate the low-density lipoprotein cholesterol (LDL-C)-lowering efficacy and safety of adding ezetimibe 10 mg/day versus placebo to ongoing, open-label statin treatment for 8 weeks in hypercholesterolemic patients. Qualifying LDL-C levels and target LDL-C goals were based on National Cholesterol Education Program risk categories. The DM subgroup buy zetia were patients who entered the study with a prior diagnosis of DM. Patients were classified as having MetS if they met 3 or more of the following criteria at baseline: triglycerides (TG) > or = 150 mg/dL (1.69 mmol/L); high-density lipoprotein cholesterol (HDL-C) < 40 mg/dL (1.04 mmol/L) for men or < 50 mg/dL (1.29 mmol/L) for women; fasting serum glucose (FSG) > or = 110 mg/dL (> or = 6.1 mmol/L); a diagnosis of hypertension or taking hypertension medication or blood pressure > or = 130/> or = 85 mmHg; waist circumference > 88 cm (women) or > 102 cm (men). DM patients were excluded from the MetS subgroup analysis.

zetia 5 mg 2017-12-16

No differences were buy zetia noted in levothyroxine absorption after gastric acid suppression with 1 week of famotidine or esomeprazole. A simultaneously administered dose of ezetimibe did not significantly change levothyroxine absorption.

zetia maximum dosage 2017-11-10

All study participants had established CV disease and atherogenic dyslipidemia. Participants received simvastatin (or simvastatin plus ezetimibe) at a dose sufficient to maintain LDL-C at 40 - 80 mg/dL (1.03-2.07 mmol/L) and were randomized to receive extended-release niacin or matching placebo. The primary end point is time to the first occurrence of coronary heart disease death, nonfatal myocardial infarction, ischemic stroke, hospitalization for buy zetia acute coronary syndrome or symptom-driven coronary or cerebral revascularization with average follow-up of 4.1 years.

zetia 10 mg 2015-12-10

Endogenously synthesized H2S protects vascular tissues from atherogenic damage by reducing vessel intimal proliferation and inhibiting adhesion molecule expression. Decreased endogenous H2S production predisposes the animals to vascular remodeling and early development of atherosclerosis. The CSE/H2S pathway is an important buy zetia therapeutic target for protection against atherosclerosis.

zetia reviews 2016-05-02

Exogenous cholesterol uptake involves a complex process in the intestines for the absorption of cholesterol and bile acids. This process is buy zetia regulated by intestinal nuclear transcription factors such as LXR that affect sterol transporters NPC1L1, ABCG5/G8, and ABCG1, and enzymes such as ACAT-2. Plant sterol/stanols, ezetimibe, and bile acid sequestrants have a variety of effects on these various transporters, and new insights into their mechanism(s) of action have provided a plethora of exciting targets for metabolic diseases, dyslipidemia, and atherosclerosis.

zetia usual dosage 2016-11-18

Persistent treatment with lipid-lowering therapies is important for buy zetia achieving optimal clinical outcomes. To date, no study has evaluated the real-world use of colesevelam and the factors associated with persistent colesevelam treatment.

zetia 10mg tablets 2016-05-23

This post-hoc analysis of a multicenter, randomized, double-blind, 6-week parallel study assessed the proportion of T2DM patients who attained specified LDL-C levels and non-HDL-C, ApoB, and hs-CRP with usual, recommended starting doses of E/S (10/20 mg) vs A (10 or 20 mg) and next highest doses of E/S (10/40 mg) vs A (40 mg) by logistic regression. Baseline triglyceride and hs-CRP effects buy zetia were also evaluated.

zetia dosing 2015-04-20

The obtained results indicate that the presence of isolated hypercholesterolemia is associated with abnormal hormonal function of the adipose tissue. They also show that ezetimibe induces relatively small changes in adipose tissue hormonal function and systemic inflammation in patients with elevated cholesterol levels. buy zetia

zetia tabs 2017-08-29

In the setting of stable coronary artery disease (CAD), it is not known if the pleiotropic effects of cholesterol reduction differ between combined ezetimibe/simvastatin and high-dose simvastatin alone. buy zetia

zetia generic price 2016-09-08

Despite statin use, residual cardiovascular risk remains. Therapeutic options include more potent statins or addition of ezetimibe. There is no clinical outcome data on the use of buy zetia ezetimibe in such patients.

zetia prices usa 2016-05-05

Statins should be Propecia Generic Pricing prescribed to older patients with CKD, and to younger patients with CKD who are at high CVD risk.

zetia dosage information 2017-06-04

This prespecified analysis compared outcomes in patients stratified by achieved LDL-C level at 1 month in the Improved Reduction of Outcomes: Vytorin Efficacy International Trial and adjusted for baseline characteristics during 6 years' median follow-up. Patients were enrolled from Diovan 220 Mg October 26, 2005, to July 8, 2010, and the data analysis was conducted from December 2014 to February 2017.

zetia online 2017-07-21

Patients with rare homozygous familial hypercholesterolaemia are at Ilosone Generic Name risk of dying at a very young age. When liver transplantation is not feasible, treatment is based on regular LDL apheresis sessions, a burdensome and inconvenient procedure, and on high-dose statins in combination with ezetimibe. Lomitapide acts by inhibiting the synthesis of LDL constituents. It has been granted EU marketing authorisation as adjunctive therapy for homozygous familial hypercholesterolaemia. Clinical evaluation of lomitapide is based on a non-comparative trial in 29 adults. When added to standard therapy, lomitapide led to about a 40% reduction in absolute LDL cholesterol levels. Longer follow-up is needed to determine whether this is sufficient to prevent cardiovascular complications. Seven of the 13 patients under-going LDL apheresis were able to increase the interval between sessions or stop them altogether. Nearly all patients treated with lomitapide experienced gastrointestinal adverse effects, including diarrhoea, nausea, vomiting and dyspepsia. Lomitapide was associated with hepatic abnormalities in about one-third of patients in the short-term. It remains to be seen whether the hepatic steatosis observed in some patients progresses to fibrosis or cirrhosis with long-term use. Lomitapide is extensively metabolised by cytochrome P450 isoenzyme CYP3A4 and also inhibits P-glycoprotein, hence a risk of multiple pharmacokinetic interactions. In particular, lomitapide increases the plasma concentrations of statins, and their toxicity. Lomitapide was teratogenic in experimental animals. In practice, lomitapide should be strictly reserved for patients with homozygous familial hypercholesterolaemia. Clinical evaluation must continue in these rare patients at high risk of early death.

zetia tablets 2017-01-16

Aortic valve stenosis and atherosclerotic disease have several risk factors in common, in particular, hypercholesterolemia. Histologically, the diseased valves appear to Benicar Generic have areas of inflammation much like atherosclerotic plaques. The effect of lipid-lowering therapy on the progression of aortic stenosis (AS) is unclear, and there are no randomized treatment trials evaluating cardiovascular morbidity and mortality in such patients. The Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) Study is a randomized, double-blind, placebo-controlled, multicenter study of a minimum 4 years' duration investigating the effect of lipid lowering with ezetimibe/simvastatin 10/40 mg/day in patients with asymptomatic AS with peak transvalvular jet velocity 2.5 to 4.0 m/s. Primary efficacy variables include aortic valve surgery and ischemic vascular events, including cardiovascular mortality, and second, the effect on echocardiographically evaluated progression of AS. The SEAS Study randomly assigned 1,873 patients (age 68+/-10 years, 39% women, mean transaortic maximum velocity 3.1+/-0.5 m/s) from 173 sites. Other baseline characteristics were mean blood pressure of 145+/-20/82+/-10 mm Hg (51% hypertensive); 55% were current or previous smokers; and most were overweight (mean body mass index 26.9 kg/m2). At baseline, mean total cholesterol was 5.7+/-1.0 mmol/L (222 mg/dl), low-density lipoprotein cholesterol was 3.6+/-0.9 mmol/L (139 mg/dl), high-density lipoprotein cholesterol was 1.5+/-0.4 mmol/L (58 mg/dl), and triglycerides were 1.4+/-0.7 mmol/L (126 mg/dl). The SEAS Study is the largest randomized trial to date in patients with AS and will allow determination of the prognostic value of aggressive lipid lowering in such patients.

zetia generic availability 2016-07-15

A total of 5936 adult patients from a primary care practice with Aricept 5mg Tablet a low-density lipoprotein measurement were categorized by coronary heart disease risk into 1 of 4 lipid-modifying therapy groups: unrestricted (fluvastatin, lovastatin, pravastatin, or simvastatin monotherapy); restricted (atorvastatin, rosuvastatin, or simvastatin/ezetimibe fixed-dose combination); other (lipid-modifying combination statin therapy or a nonstatin lipid-modifying therapy); and no lipid-modifying therapy. The primary outcome was low-density lipoprotein cholesterol goal attainment by lipid-modifying therapy group. Logistic regression identified associated demographic and clinical factors.

zetia pills 2016-12-30

An indirect response Imax model, based on the 2863 LDL-C concentrations of 378 patients, successfully and quantitatively described the time course for the LDL-C lowering effects of three statins. The combination of ezetimibe, a cholesterol absorption inhibitor, decreased the LDL synthesis rate (Kin ) by 10.9%. A simulation indicated that the combined treatment of ezetimibe with rosuvastatin (2.5 mg day(-1) ) led to superior clinical responses than those with high doses of rosuvastatin (5.0 mg day(-1) ) monotherapy, even in patients with higher baseline LDL-C concentrations Cardura Drug Class prior to the treatment.

zetia user reviews 2016-08-14

The study evaluated the efficacy and Lopressor Generic Drug safety of long-term coadministration of ezetimibe and simvastatin in adolescents with heterozygous familial hypercholesterolemia (HeFH).

zetia 4 mg 2017-10-07

ApoE ko and apoE/eNOS double ko (dko) mice received a high fat diet with or without 0.05% Ezetimibe. Ezetimibe significantly reduced plasma cholesterol concentrations and atherogenic lipoproteins in both genotypes to a similar extent. Moreover, the drug reduced vascular inflammation, as it significantly reduced vascular cell adhesion molecule-1 (VCAM-1) expression and vascular CD14 expression, a marker for mononuclear cell infiltration, in both genotypes. Neither NOS protein expression nor vascular reactivity of aortic rings was changed in apoE Lopid 100 Mg ko mice following Ezetimibe treatment. Significant lesion reduction was seen in Ezetimibe-treated male and female apoE ko and apoE/eNOS dko animals (p

zetia generic glenmark 2016-03-21

This post-hoc analysis calculated LDL-C and non-HDL-C levels corresponding to an Apo B of 0.9 g/L following treatment with 1) statin monotherapy (baseline) and 2) ezetimibe/simvastatin 10/20mg or rosuvastatin 10mg (study end). The percentages of patients reaching LDL-C, non-HDL-C, and Apo B targets were calculated at study end.

zetia 10mg generic 2017-05-28

Hypercholesterolemia and fatty liver were induced by high cholesterol (containing 2% cholesterol and 0.5% cholic acid) diet in male Wistar rats for 6 and 12 weeks. Kampo formulas Boiogito, Bofutsushosan, Keishibukuryogan and ezetimibe were added to the high-cholesterol diet, respectively. After 6 and 12 weeks, body and liver weights, blood chemistry, cholesterol concentrations, fat-related and inflammatory-related factors were examined.

medication zetia 2015-05-06

In SHARP, the proportional reductions per 1mmol/L of low-density lipoprotein (LDL) cholesterol reduction with simvastatin plus ezetimibe in all major atherosclerotic events of 20% (95% CI, 6%-32%) and in the costs of vascular hospital episodes of 17% (95% CI, 4%-28%) were similar across participant categories by cardiovascular risk and CKD stage. The 5-year reduction in major atherosclerotic events per 1,000 participants ranged from 10 in low-risk to 58 in high-risk patients and from 28 in CKD stage 3 to 36 in patients on dialysis therapy. The net cost per major atherosclerotic event avoided with simvastatin plus ezetimibe compared to no LDL-lowering regimen ranged from £157,060 in patients at low risk to £15,230 in those at high risk (£30,500-£39,600 per QALY); and from £47,280 in CKD stage 3 to £28,180 in patients on dialysis therapy (£13,000-£43,300 per QALY). In scenario analyses, generic high-intensity statin regimens were estimated to yield similar benefits at substantially lower cost.

zetia generic name 2017-01-10

Over the past 2 years two unsuccessful clinical trials of lipid-modifying agents, the ILLUMINATE Study for raising high-density lipoprotein and the ENHANCE Study for lowering low-density lipoprotein, have been reported. These results have surprised the field and led to a reassessment of the scientific and clinical basis for the overall mechanisms.

zetia and alcohol 2015-02-09

Cholesterol gallstones are associated with slow intestinal transit in humans as well as in animal models, but the molecular mechanism is unknown. We investigated in C57L/J mice whether the components of a lithogenic diet (LD; 1.0% cholesterol, 0.5% cholic acid and 17% triglycerides), as well as distal intestinal infection with Helicobacter hepaticus, influence small intestinal transit time. By quantifying the distribution of 3H-sitostanol along the length of the small intestine following intraduodenal instillation,we observed that, in both sexes, the geometric centre (dimensionless) was retarded significantly (P <0.05) by LD but not slowed further by helicobacter infection (males, 9.4±0.5 (uninfected), 9.6±0.5 (infected) on LD compared with 12.5±0.4 and 11.4±0.5 on chow). The effect of the LD was reproduced only by the binary combination of cholesterol and cholic acid. We inferred that the LD-induced cholesterol enrichment of the sarcolemmae of intestinal smooth muscle cells produced hypomotility from signal-transduction decoupling of cholecystokinin (CCK), a physiological agonist for small intestinal propulsion in mice. Treatment with ezetimibe in an amount sufficient to block intestinal cholesterol absorption caused small intestinal transit time to return to normal. In most cholesterol gallstone-prone humans, lithogenic bile carries large quantities of hepatic cholesterol into the upper small intestine continuously, thereby reproducing this dietary effect in mice. Intestinal hypomotility promotes cholelithogenesis by augmenting formation of deoxycholate, a pro-lithogenic secondary bile salt, and increasing the fraction of intestinal cholesterol absorbed.

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Fenofibrate/ezetimibe was as effective as fenofibrate and more effective than ezetimibe in reducing remnant-like particle cholesterol (-36.2% and -30.7% vs -17.3%, respectively), and in increasing LDL size (+2.1% and +1.9% vs + 0.7%, respectively), apolipoprotein AI (+7.9% and +5.1% vs +0.2%, respectively) and apolipoprotein AII (+24.2% and +21.2% vs +2.7%, respectively). Fenofibrate/ezetimibe and fenofibrate were equally effective in reducing TG (both -38.3%) and in increasing HDL-C (+11.5% and + 7.9%, respectively; p = 0.282). Ezetimibe had minor effects on TG (-10.4%) and HDL-C (+2.2%). Among patients with low HDL-C at baseline (<1.29 mmol/L [<50 mg/dL] in women, <1.03 mmol/L [<40 mg/dL] in men), normalization of HDL-C was observed in 52.9% with fenofibrate/ezetimibe and in 58.8% with fenofibrate, compared with 20.0% with ezetimibe. Changes in hsCRP were -25.9% with fenofibrate/ezetimibe, -27.8% with fenofibrate, and -10.2% with ezetimibe (not statistically significant). None of the treatments altered glucose metabolism parameters.