BACKGROUND:Low HDL-cholesterol, hypertriglyceridemia (HTG) and occurrence of small dense LDL could be involved in increased cardiovascular risk in HIV-infected patients. This study evaluates the effects of fenofibrate and/or Vitamin E on lipoprotein profile. DESIGN:Thirty-six HIV-positive adults with fasting triglycerides (TGs) > or =2 mmol/l and stable antiretroviral therapy (ART) were randomly assigned to receive either micronised fenofibrate (200 mg/day) or Vitamin E (500 mg/day) for a first period of 3 months and the association of both for an additional 3-month period. METHODS AND RESULTS:Total cholesterol, HDL-C, LDL-C, triglycerides, apoA1, apoB, apoCIII, lipoprotein composition, LDL size and LDL resistance to copper-induced oxidation were determined before initiation of fenofibrate or Vitamin E, and 3 and 6 months thereafter. Three months of fenofibrate treatment results in a significant decrease in triglycerides (-40%), apoCIII (-21%), total cholesterol (-14%), apoB (-17%) levels, non-HDL-C (-17%), TG/apoA1 ratio in HDL (-27%) associated with an increase in HDL-C (+15%) and apoA1 (+11%) levels. Moreover, fenofibrate increases LDL size and enhances LDL resistance to oxidation. Three months of Vitamin E supplementation only improves LDL resistance to oxidation and addition to fenofibrate results in a slightly greater effect. CONCLUSION:Fenofibrate therapy improves the atherogenic lipid profile in HIV-positive adults with hypertriglyceridemia.
RCT Entities:
BACKGROUND: Low HDL-cholesterol, hypertriglyceridemia (HTG) and occurrence of small dense LDL could be involved in increased cardiovascular risk in HIV-infectedpatients. This study evaluates the effects of fenofibrate and/or Vitamin E on lipoprotein profile. DESIGN: Thirty-six HIV-positive adults with fasting triglycerides (TGs) > or =2 mmol/l and stable antiretroviral therapy (ART) were randomly assigned to receive either micronised fenofibrate (200 mg/day) or Vitamin E (500 mg/day) for a first period of 3 months and the association of both for an additional 3-month period. METHODS AND RESULTS: Total cholesterol, HDL-C, LDL-C, triglycerides, apoA1, apoB, apoCIII, lipoprotein composition, LDL size and LDL resistance to copper-induced oxidation were determined before initiation of fenofibrate or Vitamin E, and 3 and 6 months thereafter. Three months of fenofibrate treatment results in a significant decrease in triglycerides (-40%), apoCIII (-21%), total cholesterol (-14%), apoB (-17%) levels, non-HDL-C (-17%), TG/apoA1 ratio in HDL (-27%) associated with an increase in HDL-C (+15%) and apoA1 (+11%) levels. Moreover, fenofibrate increases LDL size and enhances LDL resistance to oxidation. Three months of Vitamin E supplementation only improves LDL resistance to oxidation and addition to fenofibrate results in a slightly greater effect. CONCLUSION:Fenofibrate therapy improves the atherogenic lipid profile in HIV-positive adults with hypertriglyceridemia.