Comparison of Statins in Hypertriglyceridemia

Stein, Evan A.; Lane, Michael; Laskarzewski, Peter M.

doi:10.1016/s0002-9149(98)00041-1

Cited by 353 publications

(159 citation statements)

References 7 publications

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“…Previous data suggested that patients with higher baseline TG levels achieve larger TG reductions with statins. 22 This effect was observed in the present study; however, the differences between the TG strata, although significant, were primarily present at the 20 and 40 mg doses. The small numbers of patients in each treatment group per stratum and the variability of these data make them difficult to interpret with certainty.…”

Section: Discussioncontrasting

confidence: 49%

Effects of simvastatin, an HMG‐CoA reductase inhibitor, in patients with hypertriglyceridemia

Isaacsohn

Hunninghake

Schrott³

et al. 2003

Clinical Cardiology

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SummaryBackground: Patients with elevated levels of serum triglycerides (TG) often have other associated lipid abnormalities (e.g., low levels of high-density lipoprotein cholesterol [HDL-C]) and are at increased risk of developing coronary heart disease. Although the therapeutic benefits of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) in hypercholesterolemic patients have been well established, less is known about the effects of statins in patient populations with hypertriglyceridemia.Hypothesis: The purpose of this study was to evaluate the lipoprotein-altering efficacy of simvastatin in hypertriglyceridemic patients.

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Section: Discussioncontrasting

confidence: 49%

Effects of simvastatin, an HMG‐CoA reductase inhibitor, in patients with hypertriglyceridemia

Isaacsohn

Hunninghake

Schrott³

et al. 2003

Clinical Cardiology

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“…We also observed a similar relationship in non-diabetic patients. Atorvastatin might affect plasma triglyceride levels either through an increased removal of triglyceride rich-lipoproteins or a decreased hepatic secretion of apo B particles such as VLDL in those subjects with excessive production rates or both (17). The IR may affect hypertriglyceridemia greater than effect of atorvastatin.…”

Section: Triglyceride and Insulin Resistancementioning

confidence: 99%

Relationship between Insulin Resistance and Effect of Atorvastatin in Non-diabetic Subjects

Yoshitomi¹,

Ishii

Kaneki³

et al. 2005

JAT

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“…6 Statins, which are often prescribed to lower LDL-C, may also have a mild TG-lowering effect in some patient populations. 7 Fibrates (which include fenofibrate, gemfibrozil, and bezafibrate among others) are the primary treatment for high TG and have a very low frequency of adverse events, 8 but there is significant interindividual variation in response to these drugs. 9 Fibrates bind to transcription factors called PPARs, which then migrate to the nucleus and affect transcription of target genes that are involved in the lipid metabolic pathway.…”

Section: Introductionmentioning

confidence: 99%

The genetic architecture of fasting plasma triglyceride response to fenofibrate treatment

et al. 2008

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Metabolic response to the triglyceride (TG)-lowering drug, fenofibrate, is shaped by interactions between genetic and environmental factors, yet knowledge regarding the genetic determinants of this response is primarily limited to single-gene effects. Since very low-density lipoprotein (VLDL) is the central carrier of fasting TG, identifying factors that affect both total TG and VLDL -TG response to fenofibrate is critical for predicting individual fenofibrate response. As part of the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study, 688 individuals from 161 families were genotyped for 91 single-nucleotide polymorphisms (SNPs) in 25 genes known to be involved in lipoprotein metabolism. Using generalized estimating equations to control for family structure, we performed linear modeling to investigate whether single SNPs, single covariates, SNP -SNP interactions, and/or SNP -covariate interactions had a significant association with the change in total fasting TG and fasting VLDL -TG after 3 weeks of fenofibrate treatment. A 10-iteration fourfold cross-validation procedure was used to validate significant associations and quantify their predictive abilities. More than one-third of the significant, cross-validated SNP -SNP interactions predicting each outcome involved just five SNPs, showing that these SNPs are of key importance to fenofibrate response. Multiple variable models constructed using the top-ranked SNPcovariate interactions explained 11.9% more variation in the change in TG and 7.8% more variation in the change in VLDL than baseline TG alone. These results yield insight into the complex biology of fenofibrate response, which can be used to target fenofibrate therapy to individuals who are most likely to benefit from the drug.

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Comparison of Statins in Hypertriglyceridemia

Cited by 353 publications

References 7 publications

Effects of simvastatin, an HMG‐CoA reductase inhibitor, in patients with hypertriglyceridemia

Effects of simvastatin, an HMG‐CoA reductase inhibitor, in patients with hypertriglyceridemia

Relationship between Insulin Resistance and Effect of Atorvastatin in Non-diabetic Subjects

The genetic architecture of fasting plasma triglyceride response to fenofibrate treatment

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