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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.

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These findings indicate that ezetimibe/simvastatin combination therapy is safe and effective in patients with type 2 diabetes and nonalcoholic fatty liver disease.

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Addition of ezetimibe to ongoing statin therapy was effective in patients with type 2 diabetes. Male sex and baseline LDL-C levels are independent predictors of marked TC reduction by ezetimibe treatment.

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Population-based cohort study.

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Combining low-dose statin and ezetimibe reduces the low-density lipoprotein cholesterol (LDL-C) similar to high-dose statin. However, whether there is a difference in the effect of these 2 lipid-lowering regimes on endothelial function is still controversial.

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Two authors independently extracted and entered data into standardized data sheets and data were analyzed using meta-regression.

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This study demonstrates differential changes in OxPL-apoB and Lp(a) with various lipid-lowering approaches. These changes in OxPL-apoB and Lp(a) may provide insights into the results and interpretation of recent cardiovascular disease outcomes trials.

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There has been recent controversy over failure of ezetimibe to reduce carotid intima-media thickness. Much of this is based on failure to understand important differences among ultrasound phenotypes of atherosclerosis.

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LDL cholesterol (LDL-C) is a well established risk factor for cardiovascular disease. Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds LDL receptors, targeting them for degradation. We therefore assessed the efficacy, safety, and tolerability of AMG 145, a human monoclonal IgG2 antibody against PCSK9, in stable patients with hypercholesterolemia on a statin.

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Ezetimibe treatment decreased "inflammatory" (SAA-containing) HDL3, and may thus have restored the anti-atherogenic function of HDL particles in ESRD patients.

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Absorption of dietary cholesterol in the proximal region of the intestine is mediated by Niemann-Pick C1-like protein (NPC1L1) and is sensitive to the cholesterol absorption inhibitor ezetimibe (EZE). Although a correlation exists between EZE binding to NPC1L1 in vitro and efficacy in vivo, the precise nature of interaction(s) between NPC1L1, EZE, and cholesterol remain unclear. Here, we analyze the direct relationship between EZE analog binding to NPC1L1 and its influence on cholesterol influx in a novel in vitro system. Using the EZE analog [(3)H]AS, an assay that quantitatively measures the expression of NPC1L1 on the cell surface has been developed. It is noteworthy that whereas two cell lines (CaCo-2 and HepG2) commonly used for studying NPC1L1-dependent processes express almost undetectable levels of NPC1L1 at the cell surface, polarized Madin-Darby canine kidney (MDCKII) cells endogenously express 4 x 10(5) [(3)H]AS sites/cell under basal conditions. Depleting endogenous cholesterol with the HMG CoA reductase inhibitor lovastatin leads to a 2-fold increase in the surface expression of NPC1L1, supporting the contention that MDCKII cells respond to changes in cholesterol homeostasis by up-regulating a pathway for cholesterol influx. However, a significant increase in surface expression levels of NPC1L1 is necessary to characterize a pharmacologically sensitive, EZE-dependent pathway of cholesterol uptake in these cells. Remarkably, the affinity of EZE analogs for binding to NPC1L1 is almost identical to the IC(50) blocking cholesterol flux through NPC1L1 in MDCKII cells. From a mechanistic standpoint, these observations support the contention that EZE analogs and cholesterol share the same/overlapping binding site(s) or are tightly coupled through allosteric interactions.

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A total of 25 men with dyslipidaemia and IR were recruited to participate in this double-blind, randomized, crossover, placebo-controlled trial. Participants received 10 mg/day ezetimibe or placebo for periods of 12 weeks each. Intestinal gene expression was measured by quantitative PCR in duodenal biopsy samples collected by gastroduodenoscopy at the end of each treatment.

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Combined therapy with ezetimibe/simvastatin has been shown to improve lipid profile inducing a very rapid reduction of low-density lipoprotein cholesterol levels in clinical trials. In the near future, potential clinical benefits could be observed in the IMPROVE-IT or SHARP trials. Although clinical studies are needed to further confirm safety of ezetimibe/simvastatin therapy, the greater efficacy in lipid-lowering was not associated with the increase of adverse events. Also the possible association between ezetimibe and cancer, which was observed in the SEAS trial, was not confirmed by further studies and meta-analyses. At present, ezetimibe should be considered an effective lipid-lowering agent that can be used in conjunction with simvastatin at the beginning of therapy, or included in the treatment of patients who do not achieve their low-density lipoprotein cholesterol goal with statins alone.

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The molecular mechanisms of cholesterol absorption in the intestine are poorly understood. With the goal of defining candidate genes involved in these processes a fluorescence-activated cell sorter-based, retroviral-mediated expression cloning strategy has been devised. SCH354909, a fluorescent derivative of ezetimibe, a compound which blocks intestinal cholesterol absorption but whose mechanism of action is unknown, was synthesized and shown to block intestinal cholesterol absorption in rats. Pools of cDNAs prepared from rat intestinal cells enriched in enterocytes were introduced into BW5147 cells and screened for SCH354909 binding. Several independent clones were isolated and all found to encode the scavenger receptor class B, type I (SR-BI), a protein suggested by others to play a role in cholesterol absorption. SCH354909 bound to Chinese hamster ovary (CHO) cells expressing SR-BI in specific and saturable fashion and with high affinity (K(d) approximately 18 nM). Overexpression of SR-BI in CHO cells resulted in increased cholesterol uptake that was blocked by micromolar concentrations of ezetimibe. Analysis of rat intestinal sections by in situ hybridization demonstrated that SR-BI expression was restricted to enterocytes. Cholesterol absorption was determined in SR-B1 knockout mice using both an acute, 2-h, assay and a more chronic fecal dual isotope ratio method. The level of intestinal cholesterol uptake and absorption was similar to that seen in wild-type mice. When assayed in the SR-B1 knockout mice, the dose of ezetimibe required to inhibit hepatic cholesterol accumulation induced by a cholesterol-containing 'western' diet was similar to wild-type mice. Thus, the binding of ezetimibe to cells expressing SR-B1 and the functional blockade of SR-B1-mediated cholesterol absorption in vitro suggest that SR-B1 plays a role in intestinal cholesterol metabolism and the inhibitory activity of ezetimibe. In contrast studies with SR-B1 knockout mice suggest that SR-B1 is not essential for intestinal cholesterol absorption or the activity of ezetimibe.

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An 8-year-old boy with a diagnosis of acute MI on January 15, 2012 was admitted to our hospital for further evaluation of the potential cause and treatment. He had severe hypercholesterolemia for the past several years and showed typical signs of FH. Laboratory work-up excluded secondary causes of hypercholesterolemia and a diagnosis of HoFH was made after assessing the lipid profiles of his parents and his relatives. After careful consideration, he was prescribed a combination regime of lipid-lowering therapy. The plasma pro-protein convertase subtilisin/kexin type 9 (PCSK9) levels were also evaluated for him and his family members.

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The ApoE genotype does not predict the efficacy of ezetimibe treatment on serum lipid parameters.

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Because hospitalizations for an increase in serum creatinine level were underestimated, absolute differences may be misleading. Most patients (91%) were prescribed fenofibrate. Serum creatinine levels were measured as part of routine care and were not available for everyone or at predefined times.

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Intestinal cholesterol absorption is a major determinant of plasma low density lipoprotein-cholesterol (LDL-C) concentrations. Ezetimibe (SCH 58235) and its analogs SCH 48461 and SCH 58053 are novel potent inhibitors of cholesterol absorption whose mechanism of action is unknown. These studies investigated the effect of SCH 58053 on cholesterol metabolism in female 129/Sv mice. In mice fed a low cholesterol rodent diet containing SCH 58053, cholesterol absorption was reduced by 46% and fecal neutral sterol excretion was increased 67%, but biliary lipid composition and bile acid synthesis, pool size, and pool composition were unchanged. When the dietary cholesterol content was increased either 10- or 50-fold, those animals given SCH 58053 manifested lower hepatic and biliary cholesterol concentrations than did their untreated controls. Cholesterol feeding increased the relative mRNA level for adenosine triphosphate-binding cassette transporter A1 (ABCA1), ABC transporter G5 (ABCG5), and ABC transporter G8 (ABCG8) in the jejunum, and of ABCG5 and ABCG8 in the liver, but the magnitude of this increase was generally less if the mice were given SCH 58053. We conclude that the inhibition of cholesterol absorption effected by this new class of agents is not mediated via changes in either the size or composition of the intestinal bile acid pool, or the level of mRNA expression of proteins that facilitate cholesterol efflux from the enterocyte, but rather may involve disruption of the uptake of luminal sterol across the microvillus membrane.

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The combination therapy with fenofibrate and ezetimibe substantially reduces concentrations of LDL cholesterol and triglycerides and is safe in a long-term treatment in Japanese patients with combined hyperlipidemia.

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Niemann-Pick C1-like 1 protein (NPC1L1) was recently shown to be the molecular target of the cholesterol absorption inhibitor class of drugs, of which ezetimibe is the first widely used member. Since its discovery, NPC1L1 has also been shown to play a focal physiological role in intestinal absorption of sterols, including plant sterols and cholesterol. Evidence in support of this new metabolic pathway has been garnered not only through human, animal, and cell studies of function but also through the use of human genetics as an approach to study the association of NPC1L1 sequence variation with metabolic and drug-response phenotypes. The example of NPC1L1 shows how the elucidation of a pharmacological target can serve as a means to gain understanding of a key physiological pathway.

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Familial hypercholesterolemia (FH) is an autosomal codominantly inherited disease. The severity of clinical presentation depends on the zygosity of the mutations in the LDLR, APOB, or PCSK9 genes. The homozygous form (HoFH) is associated with high mortality rate by third decade of life, while individuals with HeFH begin to suffer from premature cardiovascular disease in fourth or fifth decade of life. Statin drugs have helped to improve the biochemical profile and life expectancy in HeFH, while they are only minimally effective in HoFH. LDL apheresis remains an effective treatment option in HoFH, though limited by its availability and affordability issues. We present the case that highlights a few novel aspects of clinical and genetic heterogeneity in FH, wherein a child presented with features of both HeFH and HoFH. His clinical picture was that of HoFH; however he responded well clinically and biochemically to pharmacologic treatment only. DNA sequencing showed a novel heterozygous rare splicing variant in the LDLR gene in addition to a relatively high polygenic trait score comprised of LDL-C raising alleles from common polymorphic sites. Interestingly his normolipemic mother showed the same heterozygous mutation. Thus this novel splicing variant in LDLR showed nonclassical co-segregation with the disease phenotype and was associated with a high polygenic trait score comprised of common LDL-C raising polymorphic alleles in the affected proband. Thus it indicates the phenotypic heterogeneity of FH and suggests that secondary causes, such as polygenic factors and possibly as yet undetermined genetic or environmental factors, can exacerbate the metabolic phenotype in an individual who is genotypically heterozygous for FH.

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Kinetics of triglyceride-rich lipoprotein (TRL) apoB-48 and very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL) apoB-100 labeled with a stable isotope were assessed at baseline and at the end of 8 weeks of treatment with 10 mg/d of ezetimibe in 8 men with moderate primary hypercholesterolemia. Data were fit to a multicompartmental model using SAAMII to calculate fractional catabolic rate (FCR) and production rate (PR). Ezetimibe significantly decreased total and LDL cholesterol concentrations by -14.5% and -22.0% (P=0.004), respectively, with no significant change in plasma triglyceride and high-density lipoprotein (HDL) cholesterol levels. Ezetimibe had no significant effect on TRL apoB-48 kinetics and pool size (PS). However, VLDL and IDL apoB-100 FCRs were significantly increased (+31.2%, P=0.02 and +20.8%, P=0.04, respectively) with a concomitant elevation of VLDL apoB-100 PR (+20.9%, P=0.04). Furthermore, LDL apoB-100 PS was significantly reduced by -23.2% (P=0.004), caused by a significant increase in FCR of this lipoprotein fraction (+24.0%, P=0.04).

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This was an analysis of a previously reported 24-week randomized, double-blind study in type IIa/IIb hyperlipidemic patients randomized to treatment with E/S (10/20 mg/day)+N (titrated to 2 g/day) or N (titrated to 2 g/day) or E/S (10/20 mg/day). Samples from a subset of patients (577 of 1220) were available for post hoc analysis of LDL-P and HDL-P by NMR spectroscopy. Increases in HDL-P (+16.2%) and decreases in LDL-P (-47.7%) were significantly greater with E/S+N compared with N (+9.8% for HDL-P and -21.5% for LDL-P) and E/S (+12.8% for HDL-P and -36.8% for LDL-P). In tertile analyses, those with the lowest baseline HDL-P had the greatest percent increase in HDL-P (N, 18.4/7.9/2.1; E/S, 19.3/12.2/5.3; and E/S+N, 26.9/13.8/6.9; all P<0.001). Individuals in the highest tertile of LDL-P had the greatest percent reduction in LDL-P (N, 18.3/23.1/24.6; E/S, 29.7/38.3/41.8; and E/S+N, 44.3/49.0/50.5; all P<0.001).

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SSNMR methods were able to detect interactions between the drug and the silica substrate. Differences between the drug loaded onto silica with two different pore sizes were observed, including differences in hydrogen bonding environment and molecular mobility. These methods should be useful for characterization of similar systems.

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Randomized double blind clinical trial in patients with acute coronary syndrome and low cholesterol level. The simvastatin monotherapy arms LDL-C target was < 70 mg/dl, the comparison arm was simvastatin + ezetimibe. Ezetimibe was assumed to further lower LDL-C by 15 mg/dl and produce an estimated ~ 8 % to 9 % treatment effect. The primary composite end point was CV death, nonfatal myocardial infarction (MI), nonfatal stroke, rehospitalization for unstable angina (UA), and coronary revascularization ( 30 days postrandomization). The targeted number of events was 5,250.

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This was a multi-centre, randomised, double-blind, placebo-controlled parallel group study. Twenty-seven patients (> or = 18 years) with HoS and plasma sitosterol levels > 5 mg/dl who had been taking EZE 10 mg/day for > or = 6 months prior to enrolment received open-label EZE 10 mg/day for the duration of the study and were randomised 1 : 1 to blinded EZE 30 mg/day (4 x EZE 10 mg tablets; n = 13) or placebo (1 x EZE 10 mg tablet and 3 x matching placebo tablets; n = 14) for 26 weeks. Patients were permitted to remain on other ongoing treatments (e.g. bile salt-binding resin, statin and/or low sterol diet). End-points included median per cent between-group changes from baseline in plasma sitosterol, campesterol, lathosterol, low-density lipoprotein (LDL) sterols, LDL cholesterol (LDL-C) measured by gas-liquid chromatography, and Achilles tendon thickness size measured radiographically.

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The recent SHARP trial clearly demonstrated that a reduction in low-density lipoprotein (LDL) cholesterol with a daily regimen of simvastatin plus ezetimibe safely reduced the incidence of major atherosclerotic events in patients with chronic kidney disease (CKD). We aimed to compare the efficacy of and adverse effects from statin uptitration versus statin in combination with ezetimibe since only a few studies have addressed this question.

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The primary outcome was percentage reduction of LDL-C after 6 weeks of randomization. Secondary endpoints included number of patients who achieved National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) LDL-C level and safety and tolerability.

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Two proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, evolocumab and alirocumab, have recently been approved by both the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for the treatment of hypercholesterolemia. These fully human monoclonal antibodies selectively block PCSK9, thus permitting the low-density lipoprotein (LDL) receptor to effectively recycle to the surface of liver cells. The administration of these antibodies leads to robust LDL cholesterol (LDL-C) lowering by 50-60% on top of maximum hypolipidemic treatment. At least 4 randomized, placebo-controlled studies are under way and will address the question of whether the administration of these PCSK9 inhibitors is associated with a significant reduction of cardiovascular events. Because of the high cost associated with the use of these medications it is very important to consider which patients may gain the most benefit, at least until the results of outcome studies are available. In this Consensus paper, 34 clinicians/scientists define 3 groups of patients that should be currently considered as candidates for the use of these novel drugs. These include: 1a. Adults with established cardiovascular disease and LDL-C≥100 mg/dL while on lifestyle modifications and maximally tolerated hypolipidemic treatment, i.e. high-intensity statin + ezetimibe, 1b. Adults with diabetes and established cardiovascular disease or chronic kidney disease or target organ damage and LDL-C ≥100 mg/dL while on lifestyle modifications and maximally tolerated hypolipidemic treatment, i.e. high-intensity statin + ezetimibe, 2. Adults with familial hypercholesterolemia (FH) without established cardiovascular disease and LDL-C ≥130 mg/dL while on lifestyle modifications and maximally tolerated hypolipidemic treatment, i.e. high-intensity statin + ezetimibe (evolocumab is also indicated in children above 12 years with homozygous FH), and 3. Adults at high or very high cardiovascular risk who are statin intolerant and have an LDL-C ≥100 and ≥130 mg/dL, respectively, while on any tolerated hypolipidemic treatment.

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106 patients were included in this analysis, 34 receiving apheresis at study entry and 14 younger than 18 years. The first patient was enrolled on June 28, 2012, and the cutoff date for the analysis was Aug 13, 2015; mean follow-up was 1·7 years (SD 0·63). After 12 weeks, mean LDL cholesterol decreased from baseline by 20·6% (SD 24·4; mean absolute decrease 1·50 mmol/L [SD 1·92]); these reductions were maintained at week 48. 47 of 72 patients not on apheresis at study entry increased evolocumab dosing to every 2 weeks, with an additional mean reduction in LDL cholesterol of 8·3% (SD 13·0; mean absolute decrease 0·77 mmol/L [SD 1·38]; p=0·0001). In a post-hoc analysis, mean reductions in LDL cholesterol in patients on apheresis were significant at week 12 (p=0·0012) and week 48 (p=0·0032), and did not differ from reductions achieved in patients not on apheresis (p=0·38 at week 12 and p=0·09 at week 48). We noted a small reduction (median -7·7% [IQR -21·6 to 6·8]) in lipoprotein(a) at week 12 (p=0·0015), with some additional reduction at week 48 (-11·9% [-28·0 to 0·0]; p<0·0001). HDL cholesterol was increased by a mean of 7·6% (SD 18·1) at week 12 (p<0·0001) and 7·6% (SD 20·6) at week 48 (p=0·0007). Evolocumab was well tolerated; 82 (77%) patients reported treatment-emergent adverse events, which were mostly minor. The most common were nasopharyngitis (14 patients [13%]), influenza (13 [12%]), headache (11 [10%]), and upper respiratory tract infection (11 [10%]). Serious adverse events occurred in 18 (17%) patients, with the most common being cardiovascular events (four patients [4%]). There were no deaths and four positively adjudicated cardiovascular events, one (3%) among patients on apheresis and three (4%) among patients who did not receive apheresis.

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zetia dosage 2015-11-30

There is currently no established treatment for non‑alcoholic fatty liver disease (NAFLD), including its most extreme form, non‑alcoholic steatohepatitis (NASH). Ezetimibe, an inhibitor of Niemann‑Pick C1 Like 1‑dependent cholesterol absorption, improves diet‑induced hyperlipidemia and attenuates liver steatosis and insulin resistance. The aim of the present study was to determine whether ezetimibe treatment is able to inhibit the development of NAFLD, and to elucidate the underlying mechanism, using C57BL/6J (B6) mice maintained on a high‑fat diet. Male B6 mice (20 weeks of age) were divided into the following two groups (n=7 in each group): Mice fed a high‑fat diet for four weeks and mice fed a high‑fat diet with 0.0064% (wt/wt) ezetimibe (5 mg/kg/day) for four weeks. Administration of ezetimibe significantly reduced liver steatosis buy zetia and fibrosis. Ezetimibe reduced serum cholesterol, hepatic fat accumulation and insulin resistance in the liver of mice fed the high‑fat diet. Furthermore, ezetimibe significantly reduced hepatic mRNA expression of Acc1 and Scd1, which are involved in hepatic fatty acid synthesis. Ezetimibe significantly reduced hepatic Cd36 gene expression, upregulation of which is significantly associated with insulin resistance, hyperinsulinemia and increased steatosis. The protein expression of SKP2, a viable therapeutic target in human cancer, was also reduced by ezetimibe. These findings suggest that ezetimibe may be an effective therapy for high fat‑induced NAFLD, including NASH.

zetia online 2016-07-09

Heterozygous familial hypercholesterolaemia is characterised by low cellular uptake of LDL cholesterol, increased plasma LDL cholesterol concentrations, and premature cardiovascular disease. Despite intensive statin therapy, with or without ezetimibe, many patients are unable to achieve recommended target levels of LDL cholesterol buy zetia . We investigated the effect of PCSK9 inhibition with evolocumab (AMG 145) on LDL cholesterol in patients with this disorder.

zetia and alcohol 2016-04-05

Patients at high risk for CHD are more likely to attain LDL-C treatment targets with the usual recommended starting dose of EZE/SIMVA (10 or 20 mg) therapy than with that of atorvastatin (10 mg) or simvastatin ( buy zetia 20 mg) monotherapy.

zetia generic cost 2015-09-05

A retrospective review of lipid profile changes in pediatric patients diagnosed with HoFH seen in our pediatric endocrinology outpatient clinic was performed. HoFH was diagnosed by molecular study buy zetia of these patients and their parents.

zetia generic availability 2017-06-21

Clinical examination, electrocardiography and echocardiography were obtained in asymptomatic patients with mild-to-moderate AS and preserved left ventricular (LV) systolic function, randomized to simvastatin/ezetimibe combination vs. placebo in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. At inclusion, AF was categorized as episodic or longstanding. Rhythm change was assessed buy zetia on annual in-study electrocardiograms. Impact of AF on cardiovascular morbidity and mortality was determined by adjusting for biomarkers, clinical- and echocardiographic covariates.

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Doppler measurements, including E/A, E'/A' and S' were significantly lower in group 3 compared to both groups 1 and 2 but no significant differences were buy zetia noted in chamber sizes or ejection fraction among the groups. Average serum cholesterol was higher in group 3 compared to groups 1 and 2 respectively (495 +/- 305 mg/dl vs. 114 +/- 95 mg/dl and 87 +/- 37 mg/dl; p < 0.01). Myocardial cholesterol content was also higher in group 3 compared to group 2 (0.10 +/- 0.04 vs. 0.06 mg/dl +/- 0.02; p = 0.05). There was significant correlation between S', E'/A', E/E' and serum cholesterol (r2 = 0.17 p = 0.04, r2 = 0.37 p = 0.001 and r2 = 0.24 p = 0.01).

zetia medication guide 2015-02-27

Ezetimibe (E) is a new cholesterol adsorption inhibitor which prevents the adsorption of dietary and biliary cholesterol by binding to a recently described cholesterol transporter. This pilot study was performed to evaluate the safety and the low-density lipoprotein (LDL)-C and C-reactive protein lowering efficacy of atorvastatin (A) and of the association of A plus E in five renal transplant patients with hypercholesterolemia and mild renal functional impairment receiving cyclosporine-A (CsA). Patients received for three periods, each of 3 weeks, A at a dose of 20 mg/day; A at a dose of 10 mg/day and finally, A 10 mg plus E 10 mg daily buy zetia . The medications were well-tolerated and no important clinical or laboratory (muscle enzyme, creatinine clearance and CsA concentration) abnormalities were observed throughout the study period. A alone lead to target LDL-C values only in two of five patients and did not significantly reduce the mean CRP values. The combination of E plus A produced the lowest lipid levels and significantly reduced CRP mean values and allowed all patients to attain target levels of LDL-C: total cholesterol decreased from 240 +/- 42 (mean +/- S.D.) to 171 +/- 34 mg/dl, LDL-C from 129 +/- 32 to 87 +/- 21 mg/dl, plasma triglycerides from 330 +/- 54 to 194 +/- 71 mg/dl and CRP from 6.2 +/- 1.9 to 3.9 +/- 2.4 mg/l (P < 0.05 for all). This pilot study suggests that the co-administration of E and A at 10 mg/day in renal transplant patients receiving CsA is well-tolerated and effective in reducing important cardiovascular risk factors.

zetia maximum dosage 2015-02-02

We buy zetia aimed to determine the efficacy and safety of adding ezetimibe (Ez) to simvastatin (S) in a post-acute coronary syndrome (ACS) population in a prespecified on-treatment analysis.

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Cholesterol, derived from two different sources of endogenous synthesis and diet, is essential for the growth and maintenance of mammalian cells. However, elevated level of serum buy zetia cholesterol is among the associated risk factors for the coronary heart disease. Statins can reduce endogenous sterol synthesis by inhibiting HMG-CoA reductase, whereas cholesterol absorption inhibitors, such as ezetimibe, can block cholesterol uptake from dietary sources by blocking Niemann- Pick C1-like 1 (NPC1L1).

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NPC1L1 may have evolved at two sites (apical membrane of enterocytes and canalicular membrane of hepatocytes buy zetia ) to mediate cholesterol uptake through a clathrin-mediated endocytic process, protecting the body against fecal and biliary loss of cholesterol.

zetia overdose 2015-03-13

The discovery that elevated total cholesterol levels and the subsequent understanding that low-density lipoprotein cholesterol levels are associated with higher risk for cardiovascular disease (CVD) has led to the development of lipid management strategies that seek to reduce the burden of CVD. Although substantive progress has been made in reducing death and cardiovascular events, questions remain regarding the optimal approach to further reduce CVD-associated death and disability. Based on current evidence buy zetia , statins are the clear first-line agents for the management of hyperlipidemia in patients at high risk for cardiovascular events. However, due to the failure of recent clinical trials evaluating antihyperlipidemic drugs, the most appropriate lipid management strategy in patients who cannot tolerate statin therapy or who warrant antihyperlipidemic therapies in addition to statins is a major therapeutic controversy. In this review, we summarize the clinical trial evidence evaluating the efficacy of second-line antihyperlipidemic drug classes for reducing cardiovascular risk, provide recommendations for appropriate use of nonstatin lipid-altering drugs, and identify key areas of future research to support evidence-based lipid management. Given the complexity, magnitude, and burden of CVD, opportunities to improve processes of care and identify new therapeutic options clearly exist.

zetia 5mg dose 2016-02-24

The predominance of small dense low-density lipoproteins (sdLDLs) has been associated with increased cardiovascular risk. The effect of ezetimibe on buy zetia LDL subfraction distribution has not been fully elucidated. This study assessed by gradient gel electrophoresis the effects of ezetimibe alone, simvastatin alone, and their combination on sdLDL subfraction distribution.

zetia tabs 2017-04-15

Familial hypercholesterolemia (FH) is an autosomal dominant genetic disorder. Mutations have been found in at least 3 genes: the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9). We report the first case of FH in an Omani family due to a novel mutation in the LDLR gene. A 9-year-old female was referred to our lipid clinic with eye xanthelasmata and thickening of both Achilles tendons. Evaluation of the lipid profile showed the off treatment total cholesterol of 896 mg/dL (23.2 mmol/L), low-density lipoprotein cholesterol (LDL- buy zetia C) of 853 mg/dL (22.1 mmol/L), APOB of 4.5 g/L, triglyceride of 71 mg/dL (0.8 mmol/L), and high-density lipoprotein cholesterol of 0.74 mmol/L. Genetic analysis of the LDLR gene showed a homozygous frameshift deletion mutation (272delG) at exon 3. The female patient was treated with a combination of rosuvastatin/ezetimibe and LDL apheresis.

zetia drug information 2015-01-06

A population compartment model incorporating input from the gallbladder, consistent with food intake, was developed to account for enterohepatic recirculation. The amount recycled was allowed to vary within a subject and between buy zetia subjects, accommodating variability in bile secretion. The data used consisted of 90 profiles from healthy subjects who received single or multiple doses of ezetimibe 10 or 20 mg. Modeling was carried out using a nonlinear mixed-effect function in the S-PLUS statistical program.

zetia 2 mg 2015-05-10

Ezetimibe, a cholesterol-absorption inhibitor, reduces levels of low-density lipoprotein (LDL) cholesterol when added to statin treatment. However, the effect Imitrex Tabs of ezetimibe on the progression of atherosclerosis remains unknown.

zetia replacement drug 2015-12-04

A total of 32 hypercholesterolaemic type 2 diabetes patients with microalbuminuria, defined as a urinary albumin excretion (UAE) 30 but < 300 mg/g creatinine, were enrolled. Various clinical and laboratory parameters Glucophage Tablets were determined at baseline and after 6 months of treatment with 10 mg/day ezetimibe.

zetia 5 mg 2017-09-12

A total of 136 patients assigned to RSV and 126 Vasaka Syrup to RSV/EZT completed the study protocol. As many as 6.6% of patients in the RSV group experience a major cardiovascular event within 30 days after surgery versus 5.6% in the RSV/EZT group (P = .72). From month 1 to 12 of the follow-up period, primary end point was observed (9 taking RSV vs 2 in the RSV/EZT group [P = .04]). Intensified lipid-lowering therapy with RSV/EZT was associated with a greater decrease in low-density lipoprotein cholesterol levels compared with RSV (75.87 ± 31.64 vs 87.19 ± 31.7, P = .004), while no differential effect on triglyceride, high-density lipoprotein cholesterol or high-sensitivity C-reactive protein levels was noted between groups.

zetia 10mg tablets 2016-05-08

Bodyweight (P < 0.001), body mass index (P < 0.001), systolic blood pressure ( Combivir Pediatric Dose P = 0.003), diastolic blood pressure (P < 0.001), triglycerides (P = 0.002), non-high-density lipoprotein cholesterol (P = 0.001), low-density lipoprotein cholesterol (P < 0.001) and homeostasis model assessment of insulin resistance (P = 0.011) significantly decreased after the observational period. There were no statistically significant differences in the effects of ezetimibe between men and women. Univariate analysis showed that the reduction of homeostasis model assessment of insulin resistance was not associated with the improvement of other metabolic components.

zetia become generic 2016-02-11

Rats were fed diets with and without ezetimibe (5.0 mg/kg), and their lymph was collected after feeding to quantify Cipro Drug Action lymphatic lipid levels. Total cholesterol content in the intestinal mucosa was also measured.

zetia drug cost 2015-11-10

This analysis evaluated changes in prescription patterns for ezetimibe/simvastatin, ezetimibe plus statins, and statin therapies and expected effects on low-density lipoprotein cholesterol (LDL-C) lowering during 2007 to 2008. Accutane Dosage Formula