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Postprandial hyperlipidaemia is known to be a high-risk factor for atherosclerotic disease because of rapid and lasting accumulations of triglyceride-rich lipoproteins and remnants. The Niemann-Pick C1-Like 1 (NPC1L1) protein acts as an intestinal cholesterol transporter and ezetimibe, which inhibits NPC1L1, has been used in patients with hypercholesterolaemia. We investigated effects of ezetimibe on fasting lipid and lipoprotein profiles and postprandial hyperlipidaemia in patients with type IIb hyperlipidaemia.
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Ezetimibe has been reported to inhibit viral entry and to reduce BMI and has been proposed as a novel therapeutic agent for chronic hepatitis C (CHC), potentiating the effects of pegylated interferon and ribavirin (peg-IFN/RBV).
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Lifetime major adverse cardiovascular events (MACE: cardiovascular death, nonfatal myocardial infarction, or stroke), incremental cost per quality-adjusted life-year (QALY), and total effect on US health care spending over 5 years.
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There were 22 women with an age of 42±6.3 years, average disease evolution 7.5±6.6 years, of whom, 18 concluded the study. Right basal CIMT was 0.829±0.1448 vs. final 0.688±0.1453, p<0.003; left CIMT was 0.820±0.1312 vs. 0.724±0.1348, p<0.004. TC 208 mg/dl vs 168 mg/dl, LDL-C 125 mg/dl vs. 72 mg/dl, p=0.0004. CRP 3.12 vs. 2.25 p=0.004. In 2 cases there were gastrointestinal, skin and muscle adverse effects.
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Information from the National Health Insurance Found prescriptions database on pharmacy-claims between October 1, 2012 and September 30, 2013 was analyzed. The authors identified patients who filled prescriptions for fixed or free combinations of simvastatin and ezetimibe and rosuvastatin prescribed for the first time. The subjects have not received antilipemic therapy with similar drugs during the year preceding the study. Using Kaplan-Meier technique, the authors constructed persistence curves with a 95% confidence interval for point estimates calculated on a log scale. Patients who were still persistent at the closing date of the study were considered censored. For the modelling of the curves, the authors used semi-parametric Cox's regression where antihypertensive therapy was the only (categorical) explanatory variable, and the patients taking the fixed combination of simvastatin and ezetimibe were regarded as the reference group.
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Ezetimibe and pravastatin treatment reduced LDL-C (mean ± standard error) to a similar extent (-20.6 ± 4.1 vs. -24.1 ± 4.0 %, respectively; P = 0.4771), while no decrease was observed in the control group. FMD increased significantly after treatment with ezetimibe (from 11.4 ± 5.7 to 16.8 ± 3.6 %; P = 0.022) and with pravastatin (from 13.7 ± 4.9 to 17.5 ± 4.4 %; P = 0.0466), but not in the control group. There were no differences in the endothelial function changes between the two treatment groups.
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Background: Intensive statin therapy was found to reduce thyroid autoimmunity in women with Hashimoto's thyroiditis. No similar data are available for other hypolipidemic agents. Methods: The participants of the study were 16 women with Hashimoto's thyroiditis and coronary artery disease. On the basis of statin tolerance, they were divided into 2 groups. 8 patients who did not tolerate high-dose statin therapy were treated with a statin, the dose of which was reduced by half, together with ezetimibe. The remaining 8 patients tolerating the treatment continued high-dose statin therapy. Plasma lipids, serum levels of thyrotropin, free thyroxine and free triiodothyronine, as well as titers of thyroid peroxidase and thyroglobulin antibodies were measured at the beginning of the study and 6 months later. Results: Replacing high-dose statin therapy with ezetimibe/statin combination therapy increased serum titers of thyroid peroxidase as well as led to an insignificant increase in serum titers of thyroglobulin antibodies. At the end of the study, thyroid peroxidase and thyroglobulin antibody titers were higher in patients receiving the combination therapy than in those treated only with high-dose statin. Conclusions: Our study shows that high-dose statin therapy produces a stronger effect on thyroid autoimmunity than ezetimibe/statin combination therapy.
Ezetimibe significantly improved lipid and lipoprotein profiles from baseline irrespective of apoE epsilon3/epsilon3 or epsilon4 genotype in Hungarian subjects not at cholesterol goals. Limitations of our study include its open-label nature and small sample population, as well as the facts that patients with the epsilon4 allele were not included and data were not collected on initial cholesterol levels, initial statin doses, cholesterol responses to statins, and the safety and tolerability of ezetimibe. Further randomized controlled studies in larger numbers of people followed for longer intervals are warranted to confirm these findings.
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DGE-NET is a novel computational method that predicting drug therapeutic and counter-therapeutic indications by uniquely integrating systems pharmacology with gene expression analysis. DGE-NET correctly predicts various drug-disease indications by linking the biological activity of drugs and diseases at multiple tiers of biological action, and is therefore a useful approach to identifying drug candidates for re-purposing.
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Few clinical studies have focused on the efficacy of lipid-lowering therapies in patients ≥65 years.
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Familial hypercholesterolemia (FH) is a world public health issue because of its high frequency, morbidity, and mortality. FH is characterized by elevated plasma low-density lipoprotein cholesterol (LDL-C) levels and a high risk for premature cardiovascular disease. We report an 8-year-old male with homozygous familial hypercholesterolemia. The clinical and biochemical characteristics of this case were bilateral corneal arcus, xanthomas in several body parts, severe stenosis of the left carotid artery and serum total cholesterol levels of 782.0 mg/dL and 715.0 mg/dL LDL-C. The initial treatment was atorvastatin (40 mg) and ezetimibe (20 mg), with no satisfactory response. LDLR gene was analyzed and homozygosity for c.1055G>A mutation was observed, resulting in an amino acid change from cysteine to tyrosine in codon 352 (p.Cys352Tyr). This mutation is known as Mexico 2 and has only been observed in the Mexican population. Both parents and siblings were carriers of the same mutation, but the paternal grandmother and the father of the index case showed the phenomenon of incomplete penetrance. With the analysis 5 polymorphisms (rs1003723C>T, rs5930A>G, rs688C>T, rs5929T>C and rs5927A>G), a common ancestor for the mutation can be suggested and linkage to TGTCG haplotype.