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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:
Ezedoc, Ezetimiba, Ezetrol, Zient

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Lipitor, Zocor, Crestor, Zetia, Mevacor, Tricor

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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.

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Statin intolerance limits many patients from achieving optimal low-density lipoprotein cholesterol (LDL-C) concentrations. Current options for such patients include using a lower but tolerated dose of a statin and adding or switching to ezetimibe or other non-statin therapies.

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The aim of our study was to evaluate the effects of two different statins and a statin/ezetimibe combination on high sensitive C-reactive protein (hsCRP) values, which were given at high doses in the early period of acute coronary syndromes.

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Tuberculosis (TB) risk might be increased in patients with diabetes by factors other than hyperglycaemia, such as dyslipidaemia. Host lipids are essential energy sources used by mycobacteria to persist in a latent TB state. A potential therapy targeting cholesterol catabolism of mycobacteria has been proposed, but the potential of cholesterol-lowering drugs as anti-TB therapy is unclear. The purpose of this study was to determine the effects of ezetimibe, a 2-azetidinone cholesterol absorption inhibitor, on intracellular mycobacteria survival and dormancy.

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No outside funding supported this study. None of the authors report any financial interests or potential conflict of interest with regard to this work. Study concept and design were created by all authors. Data were collected and interpreted by Britt, with input from all authors. The manuscript was written by Britt and revised by all authors.

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Our patients were referred for suspected homozygous familial hypercholesterolemia. Despite the phenotype, this diagnosis was invalidated and phytosterolemia was confirmed by the identification of mutations in the ABCG5/ABCG8 transporter complex. Plasma PS were analyzed with a mass spectrometric-gas chromatographic procedure. Vascular status was assessed with carotid ultrasonography and completed (for 4 of the 5 patients) with femoral ultrasonography; additional examinations of cardiovascular status included a stress test, determination of coronary calcium score, echocardiography, non-invasive assessment of endothelium-dependent dilatation and coronarography.

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The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.

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Medical records of children seen in a university pediatric cholesterol clinic between 1998 and 2012 treated with a statin, ezetimibe, or both were reviewed. Aggregate data were obtained to determine the number of children able to reach an LDL-C level of ≤130 mg/dL while on pharmacotherapy. Kaplan-Meier curve and proportional hazard regression analysis were used to examine the propensity for LDL-C levels to stabilize over time while on pharmacotherapy as well as factors affecting this propensity.

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The relationship among dietary cholesterol, cholesterol absorption, the metabolism of cholesterol-rich chylomicron remnants and atherosclerosis is complex; however, recent advances have provided insight into the mechanisms involved. Although dietary cholesterol is an independent risk factor for atherosclerosis, the attributable risk is low compared with dietary variables such as the amount and type of fat. Clinical studies have demonstrated that in humans consuming a typical Western-type diet, decreasing the amount of dietary cholesterol intake results in only small changes in low-density lipoprotein (LDL)-cholesterol and little or no change in the ratio of total cholesterol to high-density lipoprotein cholesterol. These findings are better appreciated when all sources of cholesterol entering the intestinal lumen are considered. Only a third of intestinal cholesterol per day is derived from the diet. Cholesterol from endogenous sources, including the bile and intestinal epithelial cells, represents the majority of cholesterol absorbed and subsequently formed into chylomicrons and secreted into the circulation. There is increasing evidence that postprandial lipoproteins are atherogenic, in particular, cholesterol-rich chylomicron remnants. These lipoproteins have the capacity to enter the arterial wall and promote atherogenesis at several stages of development, including the induction of smooth muscle cells and macrophage foam cell formation. Furthermore, enhanced delivery of chylomicron remnants to the liver decreases hepatic LDL-receptor expression, resulting in increased plasma LDL concentrations. Therefore, the inhibition of cholesterol absorption has become an attractive therapeutic target. There is growing genetic and biochemical evidence that intestinal cholesterol absorption is carrier-mediated, which has facilitated the development and characterization of small molecule inhibitors of this process. Ezetimibe, the first of these new compounds, inhibits intestinal absorption of dietary and biliary cholesterol and lowers total and LDL-cholesterol concentrations in plasma. By inhibiting cholesterol absorption, and possibly by reducing the cholesterol content of chylomicrons, ezetimibe may decrease the atherogenic potential of chylomicron remnants.

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zetia 5mg dose 2015-01-24

Using patient data from a large, national, administrative claims database, this retrospective observational study evaluated the efficacy of EZE/SMV in lowering LDL-C values and achieving LDL-C target values in newly initiating users and compared the results with those from several Generic Glucotrol Xl statin monotherapies.

zetia statin medication 2016-03-13

At present, literally no one disputes hyperlipoproteinaemia and dyslipidemia (HLP and DLP) treatment as a rational therapeutic Abilify High Dose approach in the prevention of cardiovascular diseases (CVD). This approach is in line with the current principles of evidence-based medicine (EBM) and is sufficiently evidenced particularly by the results of large intervention studies. Nevertheless! When the results of the recent studies are critically appraised, these by no means are (mostly, there, obviously, are exceptions) as conclusive as the studies conducted in 1980s and 1990s. Consequently, positive results are being sought in subanalyses, subgroup evaluations and multiple-study metaanalyses. This paper is not intended as a critique of new drugs. These certainly are developed to be safe, effective and well-tolerated. However, the newer studies suffer from a range of issues: the populations studied are already very well managed, it is not possible to compare against placebo and sometimes, let us be honest, the trial design itself is problematic (often it is an uncritical effort to treat as wide as possible range of patients as well as new groups of patients who might not be suitable for the given treatment). Certainly, we should not start disputing the well-evidenced hypotheses and seek alternatives to the long-established arguments and approaches as a consequence to some less convincing studies. We must not overlook the most robust results of statin studies as well as 'positive' studies with other hypolipidemics. There is no doubt that the effect ofstatins on LDL-cholesterol represents a significant move towards cardiovascular disease prevention. Despite this, we currently recognise with increased intensity that this very effective and well-evidenced treatment has its limits and that a high proportion of patients dies or are faced with cardiovascular diseases even though they are treated with a correct dose ofa statin and a target LDL-C level is achieved. This remaining risk (represents more than 50% ofevents) has been termed 'RESIDUAL RISK'. The issue of residual risk is crucial in patients with type 2 diabetes mellitus (DM2T) or in all patients with HDL-C-low DLP. As was repeatedly emphasised, a statin will be a cornerstone of pharmacological treatment of a DLP. However, a question arises what to combine it with. The most convincing data exist for niacin (combination of niacin with laropiprant minimising the incidence of unwanted flushes). We surely should not marginalize other hypolipidemics used mainly in combinations: resin and ezetimibe to treat LDL-C, niacin, fibrates and possibly omega-3-fatty acids to manage the residual risk (HDL and TG). Last but not least we should not forget non-pharmacological treatment as the pivotal treatment approach in all patients.

zetia drug prices 2015-02-01

Hypoglycaemic and lipid-lowering therapies may have a role in the treatment of NAFLD/NASH but large scale Prednisone Yellow Pills endpoint trials remain to be performed.

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Of 134 Abilify High Dosage 168 patients taking SMV, 11 929 (8.9%) switched to other statins or SMV/EZE. The mean age of switching patients was 54 years (standard deviation, 9 years), 61% were men, 50% were high risk, and 30% were moderate risk. The mean time to switch among new starters of SMV (n = 3379) was 77 days. Forty percent (n = 4772) of the total switches occurred among those taking the lower doses (5, 10, and 20 mg) of SMV. Most patients switched from SMV to SMV/EZE (60.5%), followed by atorvastatin (17.3%), rosuvastatin (10.1%), lovastatin (8.6%), pravastatin (2.9%), and fluvastatin (0.7%). Similarly, most patients switching from higher doses of SMV switched to SMV/EZE (52.5%), followed by atorrestatin (21.1%) and rosuvastatin (10.1%). Overall, 55.6% (758 of 1362) of patients were at ATP III goal at the time of switch from SMV (across all doses; n = 758), and 56.1% (292 of 521) of those taking lower doses were at goal at time of switch. A majority (69.9%) of patients who were at goal and switched from SMV (across all doses) were switched to SMV/EZE, and 61.6% of those at lower doses of SMV switched to the combination drug. Of patients who were not at goal at switch (n = 604), 73.3% attained ATP III LDL-C goal after switch. The mean percent LDL-C reduction that was needed to attain LDL-C goal at switch from SMV (n = 604) was 18.1%.

zetia medication generic 2015-11-11

Ezetimibe, a cholesterol-absorption inhibitor, significantly lowers low-density lipoprotein cholesterol (LDL-C) when administered in addition to statin treatment. The effect of ezetimibe on the incidence and progression of vascular disease is elusive. The objective Seroquel Starting Dose of the study was to examine the effects of fluvastatin plus ezetimibe on lipoprotein subfractions in patients with type 2 diabetes and/or coronary heart disease.

zetia generic price 2017-05-02

The pharmacologic regulation of lipid metabolism in patients with dyslipidemia is unequivocally associated with significant reductions in risk for cardiovascular morbidity and mortality. A number of therapeutic drug classes have been developed in an effort to ever more precisely and intensively modulate lipid metabolism. Statins, fibrates, ezetimibe, and niacin exert their effects via different mechanisms and afford physicians the opportunity to beneficially impact multiple pathways in patients. When used alone or in combination, these drugs decrease risk for the development and progression of atherosclerotic disease. There are strong clinical trial data to support of the use of lipid-lowering therapies in the settings of both primary and secondary prevention Hytrin Overdose . This article (1) discusses the mechanisms of action of antilipidemic medications, (2) reviews dosing regimens and the pharmacokinetic differences among drugs of the same class, (3) assesses risk for drug interactions, and (4) reviews the clinical trial evidence used to support the use of particular antilipidemic medications in specific physiologic settings. The incidence of dyslipidemia is rising worldwide. This trend portends an ever-growing need for the aggressive and judicious use of different antilipidemic medication(s) in patients at risk for all forms of atherosclerotic vascular disease.

zetia y alcohol 2017-08-15

A comprehensive (PubMed) search Inderal Capsules was performed to identify relevant publications up to May 2007.

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Despite important advances in the management of hypercholesterolemia in recent decades, many patients with lipid disorders remain unidentified or undertreated and so continue to have unfavorable levels of low-density lipoprotein (LDL) cholesterol and an increased risk for coronary events. The statins--which inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis--have proved to be the most powerful pharmacologic agents for lowering serum lipids, and newer statins offer even Yog Shallaki Tablets greater efficacy than the agents introduced 10 to 15 years ago. Studies have shown that rosuvastatin, in late-stage development, is a very potent agent for the treatment of primary hypercholesterolemia, and that relatively low doses decrease LDL cholesterol levels to a greater extent than do similar doses of pravastatin, simvastatin, or atorvastatin as evaluated in separate clinical trials. Pitavastatin, in phase II trials, also has promise as a more potent drug than currently available statins. Because neither of these drugs has been approved for use in the United States, clinical trial results should be considered preliminary. In the future, agents that combine the actions of statins and nicotinic acid may achieve still greater LDL cholesterol reductions. Drugs that lower lipids via mechanisms other than inhibition of HMG-CoA reductase also offer promise. The newest addition to the roster of lipid-regulating agents is ezetimibe, a cholesterol absorption inhibitor that has been approved for use either alone or in combination with a statin. Agents in development include bile acid transport inhibitors and inhibitors of acyl CoA:cholesterol acyltransferase. More research will be needed to determine the full clinical potential of such approaches to the management of hypercholesterolemia.

zetia generic alternative 2015-10-09

This study was an open-label, randomized, controlled study. Type 2 diabetes patients with high levels of low-density lipoprotein (LDL) cholesterol (>100 mg/dL) were randomized to receive ezetimibe/simvastatin or atorvastatin.

zetia medication dosage 2017-05-27

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.

zetia usual dosage 2017-07-26

At baseline, the patient had elevated low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC), and Lp(a) (306 nmol/L) levels and low high-density lipoprotein cholesterol (HDL-C) levels. Early initiation of combination therapy with a statin and niacin extended release (ER) titration was started. After 3 months, despite progressive weight gain caused by dietary indiscretion, LDL-C decreased by 24% and TG and TC levels reached goal. Lp(a) levels did not change. Niacin ER titration continued, pravastatin was maximized, and ezetimibe 10 mg daily was started. Despite dramatic 9-month weight gain (68 lb total), LDL-C and HDL-C reached goal and Lp(a) levels decreased by 33% (204 nmol/L) after niacin ER maximization.