Cholesterol Lowering Effects of Low-dose Statins in Korean Patients

OBJECTIVE: The aim of this study is to compare cholesterol lowering effects of low dose 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) in Korean patients. METHODS: A total of 909 consecutive patients were enrolled prospectively according to the criteria of National Cholesterol Education Program guidelines. Lipid profiles were obtained before and 2 months after statin therapy. RESULTS: Atorvastatin 10 mg (n=260), lovastatin 20 mg (n=145), pitavastatin 2 mg (n=80), pravastatin 20 mg (n=28), rosuvastatin 5 mg (n=145), and simvastatin 20 mg (n=208) reduced low density lipoprotein (LDL) cholesterol by -41.8+/-11.0%, -33.8+/-12.8%, -39.3+/-10.8%, -31.5+/-8.9%, -48.8+/-12.3%, and -42.8+/-13.5%, respectively. LDL cholesterol less than 130 mg/dL was achieved in 90.3%, 76.9%, 88.5%, 85.2%, 97.2%, and 94.2%, respectively. The reduction of LDL cholesterol by 30% or more was obtained in 84.4%, 60.7%, 81.6%, 63.0%, 93.0%, and 83.5%, respectively. LDL cholesterol less than 70 mg/dL or the reduction by 50% or more was observed in a small portion of patients and was variable according to the different types of statins. CONCLUSION: A low dose statin was enough to manage dyslipidemia in most Korean patients with low to moderate risks and was even effective in a subpopulation of high risk patients.

Influence of Previous Statin Therapy on Cholesterol-Lowering Effect of Ezetimibe

BACKGROUND AND OBJECTIVES: The inhibition of cholesterol absorption by ezetimibe increases cholesterol synthesis. The effect of inhibition of cholesterol synthesis on cholesterol absorption is controversial. The influence of these interactions on cholesterol levels is unknown. We investigated on the extent to which cholesterol levels were affected by the reaction of one pathway to the inhibition of the other pathway. SUBJECTS AND METHODS: This case-controlled study enrolled 198 patients who needed cholesterol-lowering drugs. Ezetimibe (10 mg) was administered to the patients with (n=58) and without on-going statin therapy (n=58). Simvastatin (20 mg) was administered to the patients treated with (n=41) and without ezetimibe (n=41). RESULTS: Ezetimibe without statin lowered the total cholesterol by 13.3+/-8.8% (p<0.001) and the low density lipoprotein-cholesterol (LDL-C) by 18.7+/-15.3% (p<0.001). Ezetimibe added to statin decreased the total cholesterol by 21.1+/-7.7% (p<0.001) and the LDL-C by 29.9+/-12.6% (p<0.001). The total cholesterol and LDL-C were reduced more by ezetimibe in patients with statin therapy than in those without statin therapy (p<0.001 and p<0.001, respectively). The differences in the effect of simvastatin on total cholesterol and LDL-C between the patients with and without ezetimibe showed borderline significance (p=0.10 and p=0.055, respectively). CONCLUSION: A prior inhibition of cholesterol synthesis by statin enhanced the effect of ezetimibe on total cholesterol and LDL-C by 7.8% and 11.2%, respectively. This finding suggests that ezetimibe increased cholesterol synthesis, resulting in a significant elevation of cholesterol levels.

Effect of Short-term Fenofibrate Therapy on Blood Creatinine Levels in Patients with Hypertriglyceridemia / 대한내과학회지

BACKGROUND/AIMS: Previous studies have reported that fenofibrate therapy increases blood creatinine levels. The aim of this study was to evaluate the effect of fenofibrate therapy on the renal function in patients with hypertriglyceridemia and to determine the parameters associated with changes in renal functions. METHODS: This prospective study enrolled 86 hypertriglyceridemic patients (triglycerides > or = 200 mg/dL) who were divided into two groups: the fenofibrate group (n = 43), who received 160 mg of fenofibrate, and the control group (n = 43). Lipid profiles and renal function were measured at the beginning of the study and after 2 months. RESULTS: The estimated glomerular filtration rate (eGFR) decreased in the fenofibrate group (p < 0.001), but did not change in the control group (p = 0.80). Accordingly, the decrease was more pronounced in the fenofibrate group than the control group (-18.6 +/- 8.6 vs. 0.9 +/- 9.6%, respectively; p < 0.001). Changes in serum creatinine (p < 0.001) and blood urea nitrogen (p < 0.005) levels were similar to those of eGFR. In a stepwise linear regression analysis, the percent change in creatinine was independently associated with fenofibrate therapy (r = 0.71; p < 0.001) and old age (r = 0.27; p < 0.05) in all patients. In the fenofibrate group, percent change in creatinine was associated with age (r = -0.51; p < 0.001) and smoking (r = 0.42; p < 0.005), while percent change was associated with body mass index (r = 0.31; p < 0.05) in the control group. Elevation of creatinine by 20% or more was associated with fenofibrate therapy (p < 0.001) and old age (p < 0.005) in all patients, and with old age (p < 0.001) in the fenofibrate group. CONCLUSIONS: Short-term fenofibrate therapy significantly impaired the renal function of hypertriglyceridemic patients, and this effect was more pronounced in elderly patients. This finding suggests that creatinine levels should be followed in patients receiving fenofibrate therapy.

Effect of Fenofibrate Therapy on Blood Creatinine Levels in Patients with Hypertension and Hypertriglyceridemia

OBJECTIVE: Previous studies have reported that fenofibrate therapy increased blood creatinine levels. We investigated the effect of fenofibrate therapy on creatinine levels in patients with hypertension and hypertriglyceridemia. METHODS: This retrospective study included 36 hypertensive patients with hypertriglyceridemia taking fenofibrate for 1-3 years (Fenofibrate group) and 36 control patients with similar age, sex, follow-up duration, creatinine levels, and lipid levels to those of fenofibrate therapy (Control group). RESULTS: Baseline parameters except lipid profiles were similar between the fenofibrate and control groups. Creatinine levels increased in the fenofibrate group (from 0.90+/-0.18 mg/dL to 1.05+/-0.22 mg/dL, p<0.001) and did not change in the control group (from 0.91+/-0.12 mg/dL to 0.92+/-0.14 mg/dL, p=0.39). The elevation was more pronounced in the fenofibrate group than in the control group (0.15+/-0.12 vs. 0.02+/-0.11 mg/dL, p<0.001). Changes in creatinine levels were only associated with fenofibrate therapy (r=0.52, p<0.001) in the stepwise linear regression analysis. CONCLUSION: Fenofibrate therapy for 1-3 years significantly increased creatinine levels in hypertensive patients with hypertriglyceridemia. This finding suggests that follow-up measurement of creatinine level is necessary with fenofibrate therapy.