Simvastatin and proteinuria.
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Biomedical subjects
Publications and source records attributed to P La Belle.
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Patients with non-insulin dependent diabetes mellitus have an increased incidence of coronary artery disease which may, in part, be associated with abnormalities in plasma lipids. In a double-blind, parallel, randomized study, lovastatin and gemfibrozil were compared in 102 diabetic patients with primary hypercholesterolemia; two-thirds of the patients were treated with oral hypoglycemic agents and one-third received diet therapy alone for their diabetes. Mean pretreatment total and low-density lipoprotein (LDL) cholesterol values were 273 and 193 mg/dl, respectively. Lovastatin significantly reduced total, LDL and very low density lipoprotein cholesterol (20, 26 and 28%, respectively) and raised high-density lipoprotein (HDL) cholesterol (14%). Gemfibrozil significantly reduced triglycerides and very low density lipoprotein cholesterol (36 and 41%, respectively) and, to a lesser extent, total cholesterol (9%); it also increased HDL cholesterol (21%). Lovastatin therapy was not associated with a significant change in triglycerides, and gemfibrozil did not significantly lower LDL cholesterol. The decrease in the ratio of total to HDL cholesterol tended to be greater with lovastatin than with gemfibrozil (26.5 and 20.4%, respectively; p = 0.053). Changes in lipid profiles with both agents were of a degree similar to those reported in nondiabetic patients. Neither agent had a clinically important effect on fasting glucose or hemoglobin A1c. Both drugs were well tolerated with the exception of 2 patients treated with gemfibrozil who developed symptoms of cholecystitis.
Hypercholesterolemia may pose a substantial risk for cardiovascular disease. The present investigation was designed to evaluate the safety and efficacy of the cholesterol synthesis inhibitor, lovastatin, in 13 nephrotic patients with 5.6 +/- 0.7 g/24 h of albuminuria. All patients were maintained on a low cholesterol diet throughout the study. After a 4-week placebo period, lovastatin was administered, 20 mg twice daily for 6 weeks. Lovastatin reduced total cholesterol by 27% from 8.6 +/- 0.6 mmol/L (331 +/- 24 mg/dL) to 6.3 +/- 0.4 mmol/L (242 +/- 17 mg/dL) (P less than 0.01), low-density lipoprotein cholesterol by 27%, from 5.8 +/- 0.5 mmol/L (223 +/- 20 mg/dL) to 4.2 +/- 0.6 mmol/L (163 +/- 22 mg/dL) (P less than 0.01), and apolipoprotein B by 29%, from 153 +/- 12 mg/dL to 109 +/- 8 mg/dL to 109 +/- 8 mg/dL P less than 0.01). Triglycerides and very-low-density lipoprotein (VLDL) cholesterol levels were also reduced by 30% and 37%, respectively (P less than 0.01). High-density lipoprotein (HDL) cholesterol, and apolipoproteins A-1 and A-2 were not significantly altered. Renal function and urine protein excretion were not affected by lovastatin. Although one patient developed diarrhea and discontinued treatment before completing 6 weeks of lovastatin, the other 12 patients had no adverse effects. In this short-term study, lovastatin therapy had few side effects and had favorable effects on the lipoprotein profile of nephrotic syndrome patients.