Use of Fenofibrate in the Management of Protease Inhibitor-Associated Lipid Abnormalities
James C. ThomasMaria F. Lopes‐VirellaVictor E. Del BeneJoli D. CervenyKelly TaylorLaura S. McWhorterNanette C. Bultemeier
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Abstract:
Human immunodeficiency virus (HIV) protease inhibitors are associated with several metabolic abnormalities including hypercholesterolemia and hypertriglyceridemia. Fenofibrate is a new lipid-lowering agent for adults with very high triglyceride levels that was administered to two HIV-positive patients who were taking protease inhibitors and developed hypertriglyceridemia. Starting dosages were 134 and 201 mg/day, and were increased to 268 mg/day in both patients. Triglyceride levels decreased from 1450 to 337 mg/dl (76.8%) and from 1985 to 322 mg/dl (83.8%), respectively, after 10 months of therapy. High-density lipoprotein levels increased in both patients.Keywords:
Fenofibrate
Protease inhibitor (pharmacology)
Dose
Fenofibrate
Lipodystrophy
Gemfibrozil
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Fenofibrate
Hyperlipidemia
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Fenofibrate
Differential effects
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Background. Fenofibrate, a peroxisome proliferator-activated receptor-α (PPARα) agonist, is used to treat patients with hypercholesterolemia and hypertriglyceridemia in order to reduce the risk of development of the atherosclerotic cardiovascular disease. However, it exerts pleiotropic effects beyond correcting atherogenic dyslipidemia to treat hypercholesterolemia.Objectives. The aim of this study was to investigate the potential effects of fenofibrate on endothelial function by analyzing the serum nitric oxide (NO) levels in patients with hypertriglyceridemia.Material and Methods. Lipid profiles and serum NO levels were assessed in 56 healthy adults aged 29 to 84 years, before and after 12 weeks of fenofibrate (250 mg/d; n = 30) or placebo (n = 26). Appropriate dietary suggestions for hypertriglyceridemia were made for all patients. This study was randomized, double-blind and placebo-controlled in design.Results. Total cholesterol, low-density lipoprotein (LDL), very low-density lipoprotein (VLDL) and triglyceride levels significantly decreased; high-density lipoprotein (HDL) and NO levels significantly increased after 12 weeks of fenofibrate therapy. We observed a statistically significant correlation between the increase in serum NO levels and decrease in serum triglyceride levels (r = –0.42, p = 0.02) in the fenofibrate group.Conclusion. The positive effect of short-term fenofibrate treatments on vascular endothelial functions in patients with hypertriglyceridemia has been demonstrated by increasing the serum NO levels. Agents such as fenofibrate targeting PPARα-associated signaling pathways show promise as an alternative treatment of vascular dysfunction related to advanced age and hyperlipidemia.
Fenofibrate
Hyperlipidemia
Dyslipidemia
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Human immunodeficiency virus (HIV) protease inhibitors are associated with several metabolic abnormalities including hypercholesterolemia and hypertriglyceridemia. Fenofibrate is a new lipid-lowering agent for adults with very high triglyceride levels that was administered to two HIV-positive patients who were taking protease inhibitors and developed hypertriglyceridemia. Starting dosages were 134 and 201 mg/day, and were increased to 268 mg/day in both patients. Triglyceride levels decreased from 1450 to 337 mg/dl (76.8%) and from 1985 to 322 mg/dl (83.8%), respectively, after 10 months of therapy. High-density lipoprotein levels increased in both patients.
Fenofibrate
Protease inhibitor (pharmacology)
Dose
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Objectives To investigate endothelium-dependent flow-mediated dilatation(FMD) and the serum level of matrix metalloproteinase-2 (MMP-2) in hypertriglyceridemia patients and to study effect of fenofibrate. Methods FMD and serum concentrations of MMP-2 were determined in 30 patients with hypertriglyceridemia and 30 normal controls. Patients with hypertriglyceridemia were treated with fenofibrate. After 8 weeks, transformations of FMD and serum levels of MMP-2 were determined. Results Patients with hypertriglyceridemia caused a marked decrease in endothelium-dependent flow-mediated dilatation (FMD). Compared with control, the serum levels of MMP-2 and tumor necrosis factor-α(TNF-α) were markedly increased in patients. After treatment with fenofibrate for 8 weeks, FMD of the patients were improved. Treated with fenofibrate significantly reduced the elevated levels of MMP-2 and TNF-α. Conclusions These results suggest that patients with hypertriglyceridemia have vascular endothelium dysfunction and the management of fenofibrate can improve the patients' FMD. The protective effect of fenofibrate on endothelial cells maybe relates to reduction of serum MMP-2 level.
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Matrix metalloproteinase 9
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0.05) in patients with hypertriglyceridemia. Conclusions Micronized fenofibrate can improve impaired endothelium-dependent vasodilatation in patients with hypertriglyceridemia. Improving endothelial function may also be the mechanism responsible for the beneficial effects of micronized fenofibrate.
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Introduction: Hypertriglyceridemia is known as an independent risk factor for coronary artery disease (CAD). Fenofibrate that is used for the treatment of hypertriglyceridemia can prevent cardiovascular events in patients with CAD. However, there is little information regarding the vascular effects of fenofibrate on arterial wall stiffness in patients with hypertriglyceridemia and without CAD, diabetes mellitus (DT), and hypertension (HT). The objective of this study is to evaluate the effects of fenofibrate treatment on the arterial stiffness in the patients with pure hypertriglyceridemia.
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We investigated the effects of fenofibrate on C-reactive protein (CRP) levels in patients with hypertriglyceridemia. Patients with a triglyceride level ≥200 mg/dL were randomly assigned to receive either 200 mg of fenofibrate (n=54) or general measures (n=54). A third group of patients with hypercholesterolemia received a statin (n=54). Patients with a CRP level ≥10 mg/L were excluded. CRP levels were measured before and after 2 months of therapy. Fenofibrate did not reduce CRP levels (1.74±1.74 vs. 1.54±1.66 mg/L, P=0.27) nor did general measures (P=0.85). Statin reduced CRP levels (P=0.002). In patients with baseline CRP levels of ≥3 mg/dL, CRP levels were decreased in both the fenofibrate and control groups (P=0.026 and 0.008, respectively). Changes in CRP levels were associated only with baseline CRP levels in both groups (P=0.001 and 0.049, respectively). When all hypertriglyceridemic patients were divided into 2 subgroups according to changes in body weights, CRP levels decreased in patients who reduced their body weight ≥1 kg (n=29, P=0.030), and were not changed in the other patients (n=79, P=0.67). In summary, fenofibrate failed to decrease CRP levels in patients with hypertriglyceridemia. An anti-inflammatory mechanism may not play a significant role in the cardioprotective effect of fenofibrate.
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