Statin intolerance limits many patients from achieving optimal low-density lipoprotein cholesterol (LDL-C) concentrations. Current options for such patients include using a lower but tolerated dose of a statin and adding or switching to ezetimibe or other non-statin therapies.
zetia user reviews
The aim of our study was to evaluate the effects of two different statins and a statin/ezetimibe combination on high sensitive C-reactive protein (hsCRP) values, which were given at high doses in the early period of acute coronary syndromes.
zetia prices usa
Tuberculosis (TB) risk might be increased in patients with diabetes by factors other than hyperglycaemia, such as dyslipidaemia. Host lipids are essential energy sources used by mycobacteria to persist in a latent TB state. A potential therapy targeting cholesterol catabolism of mycobacteria has been proposed, but the potential of cholesterol-lowering drugs as anti-TB therapy is unclear. The purpose of this study was to determine the effects of ezetimibe, a 2-azetidinone cholesterol absorption inhibitor, on intracellular mycobacteria survival and dormancy.
No outside funding supported this study. None of the authors report any financial interests or potential conflict of interest with regard to this work. Study concept and design were created by all authors. Data were collected and interpreted by Britt, with input from all authors. The manuscript was written by Britt and revised by all authors.
zetia 10mg tablets
Our patients were referred for suspected homozygous familial hypercholesterolemia. Despite the phenotype, this diagnosis was invalidated and phytosterolemia was confirmed by the identification of mutations in the ABCG5/ABCG8 transporter complex. Plasma PS were analyzed with a mass spectrometric-gas chromatographic procedure. Vascular status was assessed with carotid ultrasonography and completed (for 4 of the 5 patients) with femoral ultrasonography; additional examinations of cardiovascular status included a stress test, determination of coronary calcium score, echocardiography, non-invasive assessment of endothelium-dependent dilatation and coronarography.
zetia usual dosage
The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.
Medical records of children seen in a university pediatric cholesterol clinic between 1998 and 2012 treated with a statin, ezetimibe, or both were reviewed. Aggregate data were obtained to determine the number of children able to reach an LDL-C level of ≤130 mg/dL while on pharmacotherapy. Kaplan-Meier curve and proportional hazard regression analysis were used to examine the propensity for LDL-C levels to stabilize over time while on pharmacotherapy as well as factors affecting this propensity.
The relationship among dietary cholesterol, cholesterol absorption, the metabolism of cholesterol-rich chylomicron remnants and atherosclerosis is complex; however, recent advances have provided insight into the mechanisms involved. Although dietary cholesterol is an independent risk factor for atherosclerosis, the attributable risk is low compared with dietary variables such as the amount and type of fat. Clinical studies have demonstrated that in humans consuming a typical Western-type diet, decreasing the amount of dietary cholesterol intake results in only small changes in low-density lipoprotein (LDL)-cholesterol and little or no change in the ratio of total cholesterol to high-density lipoprotein cholesterol. These findings are better appreciated when all sources of cholesterol entering the intestinal lumen are considered. Only a third of intestinal cholesterol per day is derived from the diet. Cholesterol from endogenous sources, including the bile and intestinal epithelial cells, represents the majority of cholesterol absorbed and subsequently formed into chylomicrons and secreted into the circulation. There is increasing evidence that postprandial lipoproteins are atherogenic, in particular, cholesterol-rich chylomicron remnants. These lipoproteins have the capacity to enter the arterial wall and promote atherogenesis at several stages of development, including the induction of smooth muscle cells and macrophage foam cell formation. Furthermore, enhanced delivery of chylomicron remnants to the liver decreases hepatic LDL-receptor expression, resulting in increased plasma LDL concentrations. Therefore, the inhibition of cholesterol absorption has become an attractive therapeutic target. There is growing genetic and biochemical evidence that intestinal cholesterol absorption is carrier-mediated, which has facilitated the development and characterization of small molecule inhibitors of this process. Ezetimibe, the first of these new compounds, inhibits intestinal absorption of dietary and biliary cholesterol and lowers total and LDL-cholesterol concentrations in plasma. By inhibiting cholesterol absorption, and possibly by reducing the cholesterol content of chylomicrons, ezetimibe may decrease the atherogenic potential of chylomicron remnants.