Atherosclerosis · 2010
Optimal pharmacologic approach to patients with hypertriglyceridemia and low high-density lipoprotein-cholesterol: randomized comparison of fenofibrate 160 mg and niacin 1500 mg.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Wi Jin, Kim Jong-Youn, Park Sungha, Kang Seok-Min, Jang Yangsoo, Chung Namsik, Shim Won-Heum, Cho Seung-Yun, Lee Sang-Hak
Аннотация
OBJECTIVES: Atherogenic dyslipidemia is emerging as a target of lipid-modifying therapy. However, an optimal pharmacologic approach has not yet been established. The aim of this study is to compare the efficacy and tolerability of the typical doses of fenofibrate and niacin.
METHODS: After an eight-week dietary run-in, 201 patients who had triglyceride (TG) levels of 150-499 mg/dL, high-density lipoprotein-cholesterol (HDL-C) levels of <45 mg/dL and low-density lipoprotein-cholesterol (LDL-C) levels of <130 mg/dL were randomly assigned to one of two treatment groups for 16 weeks: fenofibrate 160 mg or niacin extended release 1500 mg (starting at 500 mg and up-titrated at the fifth and ninth weeks).
RESULTS: One hundred forty patients completed the study. The percent reductions in apoB/A1 were not different between the two groups (-20% and -22% in the fenofibrate and niacin groups, respectively, p=0.47). The effects of the two regimens on HDL-C were similar (24% and 20%, respectively, p=0.22), while fenofibrate reduced TG more than did niacin (-53% and -48%, respectively, p=0.045). Niacin was more effective at lowering LDL-C, Lp (a), and hs-CRP. However, niacin worsened the parameters of glycemic control, whereas fenofibrate improved them. Niacin showed more frequent adverse events including pruritus and skin flushing.
CONCLUSIONS: These two regimens have largely comparable lipid-modifying effects. However, their effects on glucose metabolism and inflammation, and their adverse events need to be considered additionally. Our results underscore more individualized pharmacologic approaches to patients with atherogenic dyslipidemia.
METHODS: After an eight-week dietary run-in, 201 patients who had triglyceride (TG) levels of 150-499 mg/dL, high-density lipoprotein-cholesterol (HDL-C) levels of <45 mg/dL and low-density lipoprotein-cholesterol (LDL-C) levels of <130 mg/dL were randomly assigned to one of two treatment groups for 16 weeks: fenofibrate 160 mg or niacin extended release 1500 mg (starting at 500 mg and up-titrated at the fifth and ninth weeks).
RESULTS: One hundred forty patients completed the study. The percent reductions in apoB/A1 were not different between the two groups (-20% and -22% in the fenofibrate and niacin groups, respectively, p=0.47). The effects of the two regimens on HDL-C were similar (24% and 20%, respectively, p=0.22), while fenofibrate reduced TG more than did niacin (-53% and -48%, respectively, p=0.045). Niacin was more effective at lowering LDL-C, Lp (a), and hs-CRP. However, niacin worsened the parameters of glycemic control, whereas fenofibrate improved them. Niacin showed more frequent adverse events including pruritus and skin flushing.
CONCLUSIONS: These two regimens have largely comparable lipid-modifying effects. However, their effects on glucose metabolism and inflammation, and their adverse events need to be considered additionally. Our results underscore more individualized pharmacologic approaches to patients with atherogenic dyslipidemia.