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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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Niacin decreased OxPL-apoB levels (median [interquartile range]; 3.5 [2.2-9.2] nM to 3.1 [1.8-7.2] nM, P < .01) and Lp(a) (10.9 [4.6-38.4] to 9.3 [3.1-32.9] mg/dL, P < .01). In contrast, E/S and E/S/N significantly increased OxPL-apoB (3.5 [2.1-7.8] to 4.9 [3.0-11.1] nM, P < .01) and (3.3 [1.9-9.3] to 4.3 [2.6-11.2] nM, P < .01), respectively and Lp(a) (11.5 [6.1-36.4] to 14.9 [6.6-54.6] mg/dL, P < .01) and (11.3 [5.4-43.8] to 11.6 [5.9-52.8] mg/dL, P < .01), respectively. The systematic review of statins and diet demonstrated 23.8% and 21.3% mean increases in OxPL-apoB and 10.6% and 19.4% increases in Lp(a), respectively. However 44.1% and 52.0% decreases in OxPL-apoB and Lp(a), respectively, were present with Lp(a)-lowering therapies.

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VAP-Lp(a)-C and VAP-high density lipoprotein cholesterol (HDL-C) estimated by the VAP technique, Lp(a) mass, oxidized phospholipids on apolipoprotein B-100 (OxPL-apoB) that primarily reflect OxPL on Lp(a), and HDL-C measured by enzymatic methods were measured in 552 hypercholesterolemic patients at baseline and 24 weeks after therapy with niacin monotherapy (N = 118), ezetimibe/simvastatin monotherapy (n = 155), or ezetimibe/simvastatin (10/20 mg) + niacin (to 2 g) (N = 279) in a randomized, double-blind trial.

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Based on 2 studies (n = 83,241), the diagnostic yield of universal screening for FH in childhood is 1.3 to 4.8 cases per 1000 screened. There was no eligible evidence on the benefits or harms of FH screening in childhood. Eight placebo trials of statin drugs (n = 1071, 6-104 weeks) found low-density lipoprotein cholesterol (LDL-C) decreases of 20% to 40%; 1 trial (n = 214) showed a 2.01% decrease in carotid intima-media thickness with statins, compared with 1.02% with placebo (P = .02). Three placebo trials of bile acid-sequestering agents (n = 332, 8-52 weeks) showed LDL-C reductions of 10% to 20%. In 1 trial (n = 248), ezetimibe with simvastatin resulted in greater LDL-C reductions compared with simvastatin alone at 33 weeks (mean, -54.0% [SD, 1.4%] vs -38.1% [SD, 1.4%]). One trial of ezetimibe monotherapy (n = 138) showed mean LDL-C decreases of 28% (95% CI, -31% to -25%) from baseline and negligible change with placebo at 12 weeks. Eighteen studies found statins generally well tolerated. One observational study found lower, but still normal, dehydroepiandrosterone sulfate concentrations in statin-treated males with FH at 10-year follow-up. Bile acid-sequestering agents were commonly associated with adverse gastrointestinal symptoms and poor palatability. There was no eligible evidence on the effect of FH treatment on myocardial infarction or stroke in adulthood.

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Sitosterolemia is inherited in an autosomal recessive manner. Each sib of an affected individual has a 25% chance of being affected, a 50% chance of being an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Carrier testing for at-risk family members and prenatal testing for pregnancies at increased risk are possible if the pathogenic variants in the family have been identified.

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Cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), liver function, renal function, creatine kinase, MMP-2, MMP-9, TIMP-1 were measured at baseline and at 1 month and 3 months post therapy.

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Despite the efficacy of statins in lowering low-density lipoprotein cholesterol (LDL-C) levels, many patients who are at high risk for heart disease with hypercholesterolemia require additional LDL-C level reduction. The cholesterol absorption inhibitor, ezetimibe, has been shown to provide significant incremental reductions in LDL-C levels when co-administered with statins. This study was performed to compare the efficacy and safety of ezetimibe (10 mg) plus response-based atorvastatin titration versus response-based atorvastatin titration alone in the attainment of LDL-C goals in subjects who are at high risk for coronary heart disease (CHD) and are not at their LDL-C goal on the starting dose of atorvastatin.

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A total 363 statin-naïve patients with moderate and high risk of coronary heart disease were consecutively recruited from two hospitals in Shanxi and Henan provinces between October 2008 and June 2009. A standard questionnaire and physical examination were performed at baseline. Atorvastatin (20 mg/day) was administered to patients for 4 weeks. Venous blood samples after an overnight fast were collected before and after treatment for measuring VLDL-C and cholesterol absorption and synthesis markers. In qualitative analyses, the baseline level of cholesterol absorption and synthesis markers and their reduction after atorvastatin treatment were categorized into 3 tertile groups.

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Cholesterol cholelithiasis is one of the most common and costly digestive diseases. Although gallstones are usually asymptomatic and no treatment is generally required, it is imperative to treat symptomatic gallstones with or without complicated conditions. Laparoscopic cholecystectomy is first-line therapy for symptomatic gallstones. By contrast, a cautious study on the natural history of the disease and costs of therapy, indicates that non-surgical treatment of gallstones is currently restricted to a subgroup of patients with mild symptoms or with small radiolucent cholesterol gallstones in a functioning gallbladder. Appropriate selection of patients suitable for medical therapy is therefore of key importance. Oral litholysis with the hydrophilic bile acid ursodeoxycholic acid induces cholesterol desaturation of bile and may lead to gallstone dissolution in patients with small, radiolucent, cholesterol-enriched stones in a functioning gallbladder with a patent cystic duct. Recent studies from experimental animal models and preliminary findings in humans also suggest that blocking intestinal absorption of cholesterol with the powerful, specific, and effective NPC1L1 inhibitor ezetimibe, may offer a novel and exciting strategy for the treatment of cholesterol gallstones. A similar possibility might arise from manipulation of specific nuclear receptors involved in cholesterol and bile acid homeostasis. Current views and perspectives on medicinal treatment of cholesterol gallstone disease are discussed here.

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This is a retrospective study utilizing a comprehensive electronic patient registry to identify all adult HIV-infected patients seen at the Dallas Veterans Affairs (VA) Medical Center during a 4-year period from October 1, 2002 through October 1, 2006.

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The primary aim of this study was to compare the effect of colesevelam HCl in combination with ezetimibe to ezetimibe monotherapy on low-density lipoprotein cholesterol (LDL-C) levels in subjects with primary hypercholesterolemia.

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Statin therapy is widely used and well tolerated by the majority of patients. To further reduce potential adverse effects and to increase efficacy, combined therapy concepts with ezetimibe or niacin are underway.

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ETC-1002 is an oral, once-daily, first-in-class medication being developed to treat hypercholesterolemia.

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Low-density lipoprotein cholesterol (LDL-C) remains the primary target of lipid-lowering therapy. Achieving LDL-C goals as outlined by the National Cholesterol Education Program Adult Treatment Panel III can be difficult with statins alone; therefore, adjunctive therapy is often indicated to reduce cardiovascular risk. Ezetimibe, a potent inhibitor of intestinal cholesterol absorption, has been shown to be safe, tolerable and effective at lowering LDL-C, non-high-density lipoprotein cholesterol and apolipoprotein B, each of which has been correlated with improved clinical outcomes, alone or in combination with a statin. However, because of randomized trials that demonstrated mixed results about atherosclerotic plaque regression via carotid intima-media thickness and a concern about cancer risk, ezetimibe's role in lipid therapy has been questioned. Currently, a large randomized controlled trial is in progress to answer if ezetimibe improves clinical outcomes in patients with high-risk acute coronary syndrome. A smaller trial in patients with chronic kidney disease demonstrated reduced clinical events, including myocardial infarction, stroke and revascularization for patients taking the combination of ezetimibe and simvastatin versus those taking statin or placebo alone. In this paper, we review the trials that have led to the ezetimibe controversy and then discuss the possible role of ezetimibe in specific patient populations until the results of ongoing clinical trials are known.

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Serum samples of 445 CAD subjects participating in a long-term follow-up of the Ludwigshafen Risk and Cardiovascular Health (LURIC) study were analyzed. In addition, samples obtained from a separate randomized parallel three-group study of subjects treated with simvastatin (n=24), ezetimibe (n=24), or their combination (n=24) were studied. Furthermore, samples from the LURIC participants with a loss-of-function mutation (R46L) in the PCSK9 gene (n=19) were analyzed and compared with major allele carriers (n=868).

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Compared to the healthy subjects, hypercholesterolemic patients exhibited lower plasma levels of adiponectin, as well as higher plasma levels of the remaining adipokines. Administration of simvastatin and ezetimibe for 30 days reduced plasma levels of leptin, visfatin, TNF-α, as well as increased plasma levels of adiponectin. The treatment also reduced free fatty acids and C-reactive protein.

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Colesevelam is a safe alternative for those intolerant to other lipid lowering medication. This BAS also provides an option for patients who do not reach their LDL-C goal despite treatment with a statin.

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Ezetimibe lowers serum lipid levels by inhibiting intestinal absorption of dietary and biliary cholesterol. However, the effect of ezetimibe on insulin resistance remains unclear. The aim of the present study was to examine this issue in patients with metabolic syndrome in local-dwelling Japanese, who were not being treated with lipid-lowering drugs.

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Patients (n = 68, 63 ± 9 years, 39% men) were randomly allocated to receive ezetimibe 10/simvastatin 20 mg or simvastatin 80 mg for 6 weeks. Circulating EPCs were measured by flow cytometry before and after the treatment.

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The question whether lipid-lowering treatment is associated with a decrease in cardiovascular morbidity and mortality in patients with chronic kidney disease has been disputed for a while, with recent trials in patients on haemodialysis failing to show benefit. Recently, the long-awaited results of the SHARP (Study of Heart And Renal Protection) trial were published. This randomized trial compared the effects of either simvastatin 20 mg plus ezetimibe 10 mg daily or placebo on the occurrence of a first major vascular event in 9720 patients with chronic kidney disease. There was a 17% relative risk reduction but no benefit on survival. We address our concerns regarding the conclusions drawn from this trial. The trial has a major design flaw by comparing the effects of two different lipid-lowering drugs with placebo. Although the SHARP trial showed that lipid lowering may be beneficial for patients with chronic kidney disease, the clinically as well as economically important question remains unanswered as to whether it was statin therapy and/or ezetimibe that mediated this effect. A great opportunity to investigate superiority, equipoise, or potential inferiority of ezetimibe compared to statins was missed.

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Periprocedural myocardial infarction (MI) is a frequent complication of percutaneous coronary intervention (PCI). Statins might reduce its incidence. The aims of the present study are to assess whether such benefit is a class-effect or whether differences exist between various lipid-lowering strategies and whether cardioprotection is exerted by increasing circulating endothelial progenitor cells (EPCs).

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QRS duration and morphology are associated with poor prognosis in many different populations, but the predictive value, particularly of the risk of sudden cardiac death (SCD), in asymptomatic patients with AS has not been well studied.

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Compared with placebo, ERN increased annual fasting glucose from baseline to 1 year in both those with normal (7.9 ± 15.8 vs 4.3 ± 10.3 mg/dL; P < .001) and impaired fasting glucose (4.1 ± 18.7 vs 1.4 ± 14.9; P < .02) and increased insulin levels. Both effects waned over the next 2 years. There were less consistent effects in those with baseline diabetes. There was an increased risk of progressing from normal to presumed or confirmed impaired fasting glucose (ERN 197/336) cases (58.6%) vs placebo 135/325 cases (41.5%; P < .001) over time, but no difference in diabetes development in the 2 treatment groups except in those with normal fasting glucose at baseline.

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Prescribed ezetimibe often stopped without either a recent lipid value or attainment of optimal, or sometimes minimum, lipid targets. Patients did not always receive parallel intensification of other LMT or a further ezetimibe prescription within 6 months.

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The frequencies of genotypes were as follows: 1735 C/G (46%)>C/C (35%)>G/G (19%), 25342 A/A (97%)>A/C (3%)>C/C (0%) and 27677 T/T (97%)>T/C (3%)>C/C (0%). Serum campesterol levels were significantly higher in the 1735 G/G group than 1735 C/G+C/C group, but lathosterol levels showed no significant differences between the genotypes.

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Consumption of food products enriched with plant sterols and the use of ezetimibe reduce cholesterol absorption in the intestine and effectively reduce low-density lipoprotein (LDL) plasma levels. We evaluated the therapeutic effect of the ezetimibe+plant sterol association in patients with coronary artery disease still not reaching recommended lipid levels despite the use of statins. We performed a prospective open-label study with 41 patients with stable coronary disease and LDL >70 mg/dL. Patients were randomized into four groups for a 6-week treatment: the control (CT) group remained on the same statin therapy, the ezetimibe (EZ) group received 10 mg/day of ezetimibe, the plant sterol (PS) group received spread enriched with 2 g of plant sterols, and the ezetimibe+PS (EZ+PS) group received 10 mg/day EZ +2 g PS. Initial mean LDL level was 97.4 ± 31.1 mg/dL in control group, 105.1 ± 23.1 mg/dL in EZ group, 95.4 ± 27.7 mg/dL in PS group, and 97.0 ± 8.3 mg/dL in EZ+PS group (P > .05). After 6 weeks of treatment, LDL of patients slightly increased in the control group (+8.9%; P > .05) and dropped in EZ group (-19.1%; P = .06), PS group (-16.6%; P = .01), and EZ+PS group (-27.3%; P < .01). Mean LDL levels after treatment were 70.5 ± 17.9 mg/dL in EZ+PS group, lower than the other groups (control was 106.1 ± 34.9 mg/dL, EZ group was 85.0 ± 35.6 mg/dL, and PS was 79.6 ± 29.7 mg/dL) (P = .05 variance analysis factor [ANOVA]). Body weight, body-mass index, and glucose plasma levels did not change significantly after intervention. The combination of PS+ezetimibe was associated with lower LDL levels and suggests beneficial therapeutic effect against major cardiovascular events.

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Intestinal cholesterol absorption is an important regulator of serum cholesterol levels. Ezetimibe is a specific inhibitor of intestinal cholesterol absorption recently introduced into medical practice; its mechanism of action, however, is still unknown. Ezetimibe neither influences the release of cholesterol from mixed micelles in the gut lumen nor the transfer of cholesterol to the enterocyte brush border membrane. With membrane-impermeable Ezetimibe analogues we could demonstrate that binding of cholesterol absorption inhibitors to the brush border membrane of small intestinal enterocytes from the gut lumen is sufficient for inhibition of cholesterol absorption. A 145-kDa integral membrane protein was identified as the molecular target for cholesterol absorption inhibitors in the enterocyte brush border membrane by photoaffinity labeling with photoreactive Ezetimibe analogues (Kramer, W., Glombik, H., Petry, S., Heuer, H., Schafer, H. L., Wendler, W., Corsiero, D., Girbig, F., and Weyland, C. (2000) FEBS Lett. 487, 293-297). The 145-kDa Ezetimibe-binding protein was purified by three different methods and sequencing revealed its identity with the membrane-bound ectoenzyme aminopeptidase N ((alanyl)aminopeptidase; EC; APN; leukemia antigen CD13). The enzymatic activity of APN was not influenced by Ezetimibe (analogues). The uptake of cholesterol delivered by mixed micelles by confluent CaCo-2 cells was partially inhibited by Ezetimibe and nonabsorbable Ezetimibe analogues. Preincubation of confluent CaCo-2 cells with Ezetimibe led to a strong decrease of fluorescent APN staining with a monoclonal antibody in the plasma membrane. Independent on its enzymatic activity, aminopeptidase N is involved in endocytotic processes like the uptake of viruses. Our findings suggest that binding of Ezetimibe to APN from the lumen of the small intestine blocks endocytosis of cholesterol-rich membrane microdomains, thereby limiting intestinal cholesterol absorption.

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A simple, reliable and sensitive liquid chromatography-tandem mass spectrometry method (LC-MS/MS) was developed and validated for quantification of free and total ezetimibe in human plasma. The analyte and internal standard (13C6-ezetimibe) were extracted by liquid-liquid extraction with methyl tert-butyl ether. The reversed-phase chromatographic separation was performed on a Capcell C18 column, and the plasma extract was eluted with a gradient consisting of acetonitrile and 5 mM ammonium acetate. The analyte was detected using negative ionization by multiple reaction monitoring mode. The mass transition pairs of m/z 408.5-->270.8 and m/z 414.5-->276.8 were used to detect ezetimibe and internal standard, respectively. The assay exhibited linear ranges from 0.02 to 20 ng/ml for free ezetimibe and 0.25 to 250 ng/ml for total ezetimibe in human plasma. Acceptable precision and accuracy were obtained for concentrations of the calibration standard and quality control. The validated method was successfully used to analyze human plasma samples for application in a pharmacokinetic study.

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Observational studies suggest a continuous positive relationship between vascular risk and cholesterol without any lower threshold level. We review recent and future clinical trials addressing the question of optimal treatment goals for cholesterol reduction and how these relate to present guidelines. With increasing focus on greater cholesterol reduction, new approaches to lipid-lowering therapy are being developed; we discuss some of these agents including the new statin, rosuvastatin and novel cholesterol transport inhibitors such as ezetimibe.

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Ezetimibe treatment was given to ten patients with diabetes without statin therapy and ten patients with statin therapy. Plasma levels of PCSK9 were examined at baseline and 24 weeks after treatment.

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We randomly assigned eligible patients to receive extended-release niacin, 1500 to 2000 mg per day, or matching placebo. All patients received simvastatin, 40 to 80 mg per day, plus ezetimibe, 10 mg per day, if needed, to maintain an LDL cholesterol level of 40 to 80 mg per deciliter (1.03 to 2.07 mmol per liter). The primary end point was the first event of the composite of death from coronary heart disease, nonfatal myocardial infarction, ischemic stroke, hospitalization for an acute coronary syndrome, or symptom-driven coronary or cerebral revascularization.

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The purpose of this study was to compare the efficacy and tolerability of combination therapy of ezetimibe and atorvastatin in patients with high LDL cholesterol that had not reached the lipid management target value with 10 mg atorvastatin monotherapy, against increasing the dose to 20 mg atorvastatin or switching to 2.5 mg rosuvastatin.

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In patients with asymptomatic AS, LASF was closely related to filling pressure. Higher LASF invariably signifies the maximal LA effort to keep near normal LV filling pressure; lower LASF belongs to a heterogeneous group of patients in which it is much more difficult to depict who have low LA preload or who have intrinsic systolic LA dysfunction.

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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 were determined at baseline and after 6 months of treatment with 10 mg/day ezetimibe.

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In this retrospective, observational study, patients with CHD/CHD risk equivalent on statin therapy were identified during 2004 to 2008 in a US managed care database. Prescribing patterns and effect of switching from statin monotherapy to combination ezetimibe/simvastatin therapy vs uptitration to higher statin dose/potency level and no change from initial statin potency on LDL-C lowering were assessed. Percentage of change from baseline in LDL-C levels and odds ratios for LDL-C goal attainment were estimated with analyses of covariance and logistic regression.

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Recent studies in patients with coronary artery disease (CAD), heart failure, and hypercholesterolemia have demonstrated that treatment with ezetimibe for 4-12 weeks elicits no improvement of endothelial function or other measures of cardiovascular disease risk. In contrast, other studies have reported that ezetimibe improves endothelial function in certain patient buy zetia populations, including those with rheumatoid arthritis, CAD with type 2 diabetes, and metabolic syndrome. However, the statin monotherapy comparator groups in these studies that yielded equivalent reductions in cholesterol were superior, or at least equivalent to, ezetimibe-containing regimens in the improvement of these ancillary endpoints.

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Observational, longitudinal, retrospective, multicenter national study that included consecutive patients of both sexes over 18 years of age referred for dyslipidemia and cardiovascular risk. Information was collected from medical records corresponding to two visits buy zetia in the lipid unit.

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While the optimal lipid-lowering treatment to reduce cardiovascular disease (CVD) risk in elderly patients has not been definitively established, evidence so far indicates that reducing low-density lipoprotein cholesterol (LDL-C) should be a primary goal, as with other patient groups. The VYTELD (VYTorin in the ELDerly) study--a multicenter, 12-week, randomized, double-blind trial--evaluated the efficacy and safety of combination therapy comprised of ezetimibe plus simvastatin (eze/simva) versus atorvastatin in 1289 hypercholesterolemic patients aged ? 65 years. For all prespecified comparisons, patients randomized to eze/simva were found to have significantly greater percentage decreases in LDL-C and were significantly more likely to achieve LDL Anafranil Tablets -C target levels compared with those on atorvastatin monotherapy (p < 0.05 to < 0.001). Also, the proportions of subjects reaching secondary biochemical targets were similarly greater with eze/simva than with atorvastatin monotherapy for all prespecified comparisons (p < 0.01 to < 0.001). Finally, there were no differences in tolerability between the treatments. The authors concluded that in patients aged ≥ 65 years, the eze/simva combination provided significantly greater improvements in key lipid variables, with a larger proportion of subjects reaching target LDL-C compared with atorvastatin monotherapy. Despite these promising short-term results, the longer-term safety and efficacy of combination treatment across diverse populations requires further evaluation.

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Screening can detect FH in children, and lipid-lowering treatment in childhood can reduce lipid concentrations in the short term, with little evidence of harm. There is no evidence for the effect of screening for FH in childhood on lipid concentrations or cardiovascular outcomes in adulthood, or on Cost Sporanox Australia the long-term benefits or harms of beginning lipid-lowering treatment in childhood.

zetia buy 2016-10-02

Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia, insulin resistance, and/or progressive loss of β-cell function. T2DM patients are at increased risk of micro- and macrovascular disease, and are often considered as representing an atherosclerotic coronary heart disease (CHD) risk equivalent. Interventions directed at glucose and lipid level control in T2DM patients may reduce micro- and macrovascular disease. The optimal T2DM agent is one that lowers glucose levels with limited risk for hypoglycemia, and with no clinical trial evidence of worsening CHD risk. Lipid-altering drugs should preferably reduce low-density lipoprotein cholesterol and apolipoprotein B (apo B) and have evidence that the mechanism of action reduces CHD risk. Statins reduce low-density lipoprotein cholesterol and apo B and have evidence of improving CHD outcomes, and are thus first-line therapy for the treatment of hypercholesterolemia. In patients who do not achieve optimal lipid levels with statin therapy, or who are intolerant to statin therapy, add-on therapy or alternative therapies may be indicated. Additional Migraine Medication Topamax available agents to treat hypercholesterolemic patients with T2DM include bile acid sequestrants, fibrates, niacin, and ezetimibe. This review discusses the use of these alternative agents to treat hypercholesterolemia in patients with T2DM, either as monotherapy or in combination with statin therapy.

zetia buy 2015-03-19

Here we report the lipid-lowering effect of rosuvastatin (60 mg/day) associated with ezetimibe (10 mg/day) in a single ARH patient. The sequencing of LDLRAP1 gene showed that the patient was homozygous for the c.432insA mutation. During a 6-month treatment, we observed an 80% reduction of LDL-C and a significant increase of HDL-C and ApoA-I. Some sequence variations in PCSK9 and NPC1L1 genes found in this patient may have contributed to the success of drug treatment Tegretol Xr Online .

zetia buy 2017-04-27

Dyslipidaemia is a major cause of atherosclerotic cardiovascular disease and its progression towards clinical complications, such as acute coronary syndromes and stroke. In August 2016 the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS) issued new joint guidelines for the management of dyslipidaemias. In these new guidelines, the concept of treating patients to a risk-based low-density lipoprotein (LDL) cholesterol target is reinforced. The task force considers LDL cholesterol as the primary target for dyslipidaemia treatment, whereas high-density lipoprotein (HDL) cholesterol is not recommended as a treatment target (based on the failure of HDL cholesterol elevation treatment strategies to reduce cardiovascular risk in recent studies). In patients with a very high risk for cardiovascular events it is recommended to treat to an LDL cholesterol target of less than 70 mg/dl. Moreover, the new guidelines now additionally recommend a > 50% reduction of LDL cholesterol in patients with very high cardiovascular risk patients and baseline levels between 70 and 135 mg/dl as well as in patients with high cardiovascular risk and baseline LDL cholesterol levels between 100 and 200 mg/dl. Statins are recommended as first-line medicinal treatment and the LDL cholesterol goals given imply the more frequent use of maximum tolerated statin therapy, in particular for patients with very high cardiovascular risk. Treatment with ezetimibe in patients with substantially elevated LDL cholesterol levels despite maximum tolerated statin therapy has now received a stronger recommendation (currently IIa recommendation). The guidelines also now include Nexium Dose Child the potential use of the novel proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and a recent ESC/EAS consensus document provides more detailed information on which patients can be considered for treatment with PCSK9 inhibitors, i. e. in particular patients with familial hypercholesterolemia and patients at very high cardiovascular risk who have markedly elevated LDL cholesterol levels despite maximum tolerated statin and ezetimibe therapy.

zetia buy 2015-04-15

The use of lipid-lowering therapy (LLT) in chronic kidney disease (CKD) results in a reduction in atherosclerotic cardiovascular events but not mortality. The risk reduction for patients on dialysis appears to be less than in pre-dialysis CKD. These findings may be due to the higher rate of non-atherosclerotic cardiovascular disease found in end-stage disease. Because of this, the role of LLT is less clear in CKD than in the general population. This review outlines the results of recent trials of LLT, particularly Ezetimibe, and implications for patients with CKD. The evidence in favour of lipid lowering in CKD comes largely from the SHARP study. This study used combined simvastatin and Ezetimibe to reduce cholesterol. Though the benefits of statins are well proven, there is no evidence that Ezetimibe independently reduces cardiovascular events in any population. Data which support the use of Ezetimibe Detrol 1mg Tablet show only that it effectively reduces cholesterol. Surrogate end-point data are contentious. Some studies suggest benefit whilst others suggest off-target effects that question the validity of Ezetimibe in the absence of quality cardiovascular outcome data.

zetia buy 2016-01-14

Quantitative analysis demonstrated that the aortic vessel wall area was significantly larger in patients with familial hypercholesterolemia than in control subjects (123 mm(2) +/- 23 vs 102 mm(2) +/- 18, respectively; P < .007), Aldactone 75 Mg Acne as was vessel wall thickness (1.63 mm +/- 0.28 vs 1.37 mm +/- 0.16, respectively; P < .001). No significant difference was found between mean values of routine serum lipid and lipoprotein parameters.

zetia buy 2015-08-26

Compared with baseline, atorvastatin 40 mg reduced total Bactroban Nasal Cream Dosage and LDL cholesterol (3% and 22%, respectively, P < .05), increased β-sitosterol, campesterol/cholesterol, and β-sitosterol/cholesterol ratios (39%, 47%, and 32%, respectively, P < .05); ezetimibe 10 mg reduced campesterol and campesterol/cholesterol ratio (67% and 70%, respectively, P < .05), and the combined therapy decreased total and LDL cholesterol (22% and 38%, respectively, P < .05), campesterol, β-sitosterol, and campesterol/cholesterol ratio (54%, 40%, and 27%, P < .05). Addition of PS further reduced total and LDL cholesterol by ∼ 7.7 and 6.5%, respectively, in the atorvastatin therapy group and 5.0 and 4.0% in the combined therapy group (P < .05, for all), with no further effects in absorption or synthesis markers.

zetia buy 2015-04-14

In patients with heterozygous familial hypercholesterolaemia, evolocumab administered either 140 mg every 2 weeks or 420 mg monthly was well tolerated and yielded similar Cymbalta Drug Fibromyalgia Medication and rapid 60% reductions in LDL cholesterol compared with placebo.

zetia buy 2016-09-11

Post hoc analysis of two multicenter, 6-week, double-blind, randomized, parallel-group trials assessed age (<65 and ≥ 65 years), gender, and race (white, black, and other) effects on atorvastatin plus ezetimibe versus up-titration of atorvastatin in hypercholesterolemic patients with CHD risk. High CHD risk subjects with low-density Lasix Generic Name And Classification lipoprotein (LDL) cholesterol levels ≥ 70 mg/dL (~1.81 mmol/L) during stable atorvastatin 40 mg therapy were randomized to atorvastatin 40 mg plus ezetimibe 10mg, or up-titrated to atorvastatin 80 mg. Moderately high CHD risk subjects with LDL cholesterol levels ≥ 100 mg/dL (~2.59 mmol/L) with atorvastatin 20mg were randomized to atorvastatin 20mg plus ezetimibe 10mg, or atorvastatin 40 mg.

zetia buy 2015-05-29

Long-term stability of a previously reported formulation (OPT-LCT) consisting of Maisine 35-1 and Labrasol indicated rapid precipitation of ezetimibe. In vitro supersaturation test was carried out for selection of apt polymeric precipitation inhibitor (PPI). Following incorporation of the selected PPI, the precipitates from various formulations were differentiated employing optical microscopy, differential scanning calorimetry (DSC) and X-ray diffraction techniques. The S-SNEDDS was evaluated for globule size distribution. Also, lipid-lowering activity of S-SNEDDS was compared in relation to marketed product and optimized-long chain triglyceride. Subsequently, in situ perfusion studies were carried out for calculating various permeability and absorptivity parameters with specific focus on P-gp and MRP2 inhibition.

zetia buy 2015-06-11

Ezetimibe glucuronide is a substrate of human MRP2. Moreover, etoposide and possibly also its glucuronide are substrates of MRP2. These data demonstrate the functional interplay between transporter-mediated uptake, phase II metabolism and export by hepatic proteins involved in drug disposition.

zetia buy 2016-12-20

In overall AMI patients, high-intensity statin therapy had better clinical outcomes than simvastatin-ezetimibe. However, in patients with high-risk factor, simvastatin-ezetimibe had comparable clinical outcomes to high-intensity statin therapy. Therefore, simvastatin-ezetimibe could be used as an alternative to high-intensity statin therapy in such patients.

zetia buy 2017-07-22

Instead of LDL-cholesterol, non-HDL-cholesterol is proposed as a secondary lipid target when triglyceride level is above 2.3 mmol/L. Non-HDL-cholesterol target values are 0.8 mmol/L higher than those for LDL-cholesterol in the same cardiovascular risk category. Currently, the main issue of lipidology is the degree by which the cardiovascular risk can be reduced with the treatment of residual dyslipidemia that exists under statin therapy. In such a role the examined agents have essentially failed despite their more or less profound effect on HDL-cholesterol and/or non-HDL-cholesterol. The largest loser has been the nicotinic acid. The results of cardiovascular, otherwise controversial fish oil studies cannot be considered convincing because of the administered low doses. In a combination with statin (i) ezetimibe may have role if the LDL-cholesterol target cannot be reached with statin monotherapy, or (ii) fibrates, in case of large increase of triglyceride level, or in less severe hypertriglyceridemia if it is associated with considerable decrease in HDL-cholesterol level. Potential further possibilities are: (i) cholesterol ester transfer protein inhibitors that dramatically raise HDL-cholesterol, while reduce LDL-cholesterol, or (ii) proprotein convertase subtilisin/kexin 9 inhibitors that markedly decrease LDL-cholesterol even on the top of statin.

zetia buy 2017-04-29

In this study, the atorvastatin group showed significant reduction in EFT than in the simvastatin/ezetimibe group. This might be originated from the statin difference. More large, randomized study will be needed to evaluate this statin difference.

zetia buy 2017-09-04

The percent change in LDL cholesterol level from baseline until study completion was statistically greater for the combination of 10 mg ezetimibe + 10 mg atorvastatin compared with increasing atorvastatin to 20 mg (-25.8% vs -15.1%; P < 0.0001). A similar result was observed for ezetimibe + atorvastatin compared with switching to 2.5 mgt rosuvastatin (-25.8% vs 0.8%; P < 0.0001). The proportion of patients who reached the target LDL cholesterol value with the combination of ezetimibe + atorvastatin was significantly higher than increasing atorvastatin and switching to rosuvastatin (78.7%, 41.3%, and 3.1%, respectively). Although 5 serious adverse experiences bearing no relation to the study medications were reported, there were no adverse reactions.

zetia buy 2016-07-15

Dyslipidaemia is a major contributor to the increased risk of heart disease found in people with diabetes. An increase of 1 mmol/L LDL-C is associated with a 1.57-fold increase in the risk of coronary heart disease (CHD) in people with type 2 diabetes. A diagnosis of diabetic dyslipidaemia requiring pharmacological treatment is determined by the person's lipid profile and level of cardiovascular risk.

zetia buy 2017-12-06

We sought to evaluate the achievement of low-density lipoprotein cholesterol (LDL-C) treatment goals in FH patients enrolled in a large national registry.

zetia buy 2016-07-03

The pharmacokinetic parameters (mean ± SD) for total ezetimibe and free ezetimibe following a single dose were: maximum plasma drug concentration (C(max)) 81.56 ± 26.62 and 9.40 ± 6.17 ng/mL; time to reach C(max) (t(max)) 0.93 ± 0.30 and 1.25 ± 1.27 h; elimination half-life (t(½)) 24.32 ± 13.27 and 18.90 ± 9.66 h, and mean area under the plasma concentration-time curve from time zero to the time of the last measurable concentration (AUC(last)) 579.06 ± 241.45 and 126.01 ± 69.01 ng·h/mL, respectively. The pharmacokinetic parameters (mean ± SD) for simvastatin and simvastatin acid following a single dose were: C(max) 11.92 ± 5.50 and 3.37 ± 1.78 ng/mL, t(max) 0.98 ± 0.28 and 3.73 ± 1.68 h, t(½) 4.19 ± 1.81 and 7.65 ± 7.96 h, and mean AUC(last) 33.63 ± 20.41 and 32.50 ± 18.79 ng·h/mL. Higher AUC(last) and AUC from time zero to infinity (AUC(∞)), and lower apparent total body clearance of drug from plasma after oral administration (CL/F) for total ezetimibe and free ezetimibe were observed in female subjects compared with those in male subjects. There were no differences between the pharmacokinetic parameters of simvastatin and simvastatin acid for female and male subjects in the study.

zetia buy 2015-07-06

Coronary artery disease (CAD) is among the leading causes of mortality and morbidity worldwide. Traditional risk markers explain only a proportion of total cardiovascular risk. Thus, development and improvement of early diagnostic strategies and targeted initiation of preventive measures would be of great benefit.

zetia buy 2015-04-15

NPC1L1 (Niemann-Pick C1-like 1), the pharmacological target of the cholesterol-uptake inhibitor ezetimibe, is a transporter localized on the brush border of enterocytes. Although this protein plays a key role in intestinal uptake of sterols, multiple molecular events that underlie intestinal cholesterol absorption have not been fully characterized. Two proteins that might be involved in this process are NPC1 and NPC2 (Niemann-Pick disease type C proteins 1 and 2), which function in the endosomal/lysosomal cholesterol egress pathway and whose deficiency results in NPC (Niemann-Pick type C) disease. The involvement of these proteins in intestinal cholesterol absorption was examined in mutant mice lacking either NPC1 or NPC2. Our data indicate that deficiencies in either protein do not have an effect on cholesterol uptake or absorption. This contrasts with recent results obtained for the fruitfly Drosophila melanogaster, which indicate that a deficiency of NPC1 (dNPC1a being its Drosophila homologue) leads to activation of an NPC1L1 (Drosophila homologue dNPC1b)-independent cholesterol uptake pathway, underscoring fundamental differences in mammalian and non-mammalian cholesterol metabolism.

zetia buy 2016-07-23

Measurement of lipid profile in adults with CKD 1-5: We recommend measuring the lipid profile (T cholesterol, LDL cholesterol, HDL cholesterol and triglycerides) in all adults with newly diagnosed CKD 1-5 (including patients in renal replacement therapy). Monitoring of lipid profile in adults with CKD 1-5: In many cases it is not necessary to regularly monitor the lipid profile. Patients ≥ 50 years with CKD 1-5 ND: We recommend that these patients be treated with a statin (CKD 1-2, evidence level B), and in CKD patients in stages 3-5 ND that a statin or the combination statin/ezetimibe be used (evidence level A). Patients aged 18-49 years with CKD 1-5 ND: We suggest treating these patients with a statin if they also have one or more of the following conditions (evidence level A): known CVD, DM, Prior ischaemic stroke, Estimated 10-year risk of coronary death or non-fatal AMI > 10 % or risk of fatal cardiovascular disease > 5% (SCORE). Patients with CKD stage 5D: We suggest that these patients not be given a statin or started on statin/ezetimibe treatment (evidence level A). Patients who start dialysis and are already being treated with a statin or statin/ezetimibe: We suggest that treatment be continued (evidence level C). Adult kidney transplanted patients: We suggest that these patients be treated with a statin (evidence level B).

zetia buy 2017-04-18

Surrogate outcome trials will be required with lomitapide or mipomersen to confirm their effects in homozygous familial hypercholesterolaemia and clinical endpoint trials will be needed for PCSK9 and CETPIs if these are to be used widely.

zetia buy 2016-08-23

The most recent American College of Cardiology-American Heart Association guidelines recommend high-dose statin therapy for most patients with confirmed atherosclerotic cardiovascular disease (ASCVD) and patients with high cardiovascular risk. There is limited information regarding long-term treatment patterns among these patients.

zetia buy 2017-02-11

It remains undetermined whether the addition of ezetimibe to ongoing statin therapy is more effective than increasing the dose of statin for reducing remnant lipoprotein levels in patients with remnant lipoproteinemia on previous statin treatment. This study examined whether combined ezetimibe and statin therapy resulted in a greater improvement in remnant lipoprotein levels and endothelial function than with the dose of statin in patients with remnant lipoproteinemia on previous statin treatment.

zetia buy 2015-08-07

Overall, 1,741 patients (1.65%) had statin intolerance, and 55,567 patients (52.8%) had high statin adherence. Over a median of 1.9 to 2.3 years of follow-up, there were 4,450 recurrent MIs, 6,250 CHD events, and 14,311 deaths. Compared to beneficiaries with high statin adherence, statin intolerance was associated with a 36% higher rate of recurrent MI (41.1 vs. 30.1 per 1,000 person-years, respectively), a 43% higher rate of CHD events (62.5 vs. 43.8 per 1,000 person-years, respectively), and a 15% lower rate of all-cause mortality (79.9 vs. 94.2 per 1,000 person-years, respectively). The multivariate-adjusted hazard ratios (HR) comparing beneficiaries with statin intolerance versus those with high statin adherence were 1.50 (95% confidence interval [CI]: 1.30 to 1.73) for recurrent MI, 1.51 (95% CI: 1.34 to 1.70) for CHD events, and 0.96 (95% CI: 0.87 to 1.06) for all-cause mortality.

zetia buy 2016-08-20

Since the introduction of HAART, there was a remarkably change in the natural history of HIV disease, leading to a notable extension of life expectancy, although prolonged metabolic imbalances could significantly act on the longterm prognosis and outcome of HIV-infected persons, and there is an increasing concern about the cardiovascular risk in this population. Current recommendations suggest that HIV-infected perons undergo evaluation and treatment on the basis of the Third National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) guidelines for dyslipidemia, with particular attention to potential drug interactions with antiretroviral agents and maintenance of virologic control of HIV infection. While a hypolipidemic diet and physical activity may certainly improve dyslipidemia, pharmacological treatment becomes indispensable when serum lipid are excessively high for a long time or the patient has a high cardiovascular risk, since the suspension or change of an effective antiretroviral therapy is not recommended. Moreover, the choice of a hypolipidemic drug is often a reason of concern, since expected drug-drug interactions (especially with antiretroviral agents), toxicity, intolerance, effects on concurrent HIV-related disease and decrease patient adherence to multiple pharmacological regimens must be carefully evaluated. Often the lipid goals of patients in this group are not achieved by the therapy recommended in the current lipid guidelines and in this article we describe other possibilities to treat lipid disorders in HIV-infected persons, like rosuvastatin, ezetimibe and fish oil.