PubMed · 7475713
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M B Katan. 1995-11-11. Exit trans fatty acids.. https://doi.org/10.1016/s0140-6736(95)91858-2
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BACKGROUND: Combined HMG-CoA reductase inhibitor and fibric acid derivative therapy is often necessary for the effective reduction of concentrations of low-density lipoprotein (LDL) cholesterol and triglycerides in patients with mixed hyperlipidemia; however, the potential risk of myopathy has limited the use of these agents. HYPOTHESIS: This study evaluated long-term safety and efficacy of combined pravastatin and gemfibrozil therapy. METHODS: Eighty-three patients with hyperlipidemia were treated with combined pravastatin and gemfibrozil therapy for a median of 44 months (range 9-78 months). Plasma lipids, serum liver function tests, creatinine, and creatinine kinase (CK) levels were measured every 3 to 4 months. RESULTS: One patient developed myalgia with a normal CK level after 4 months of combination therapy. Three patients had transient elevations in CK levels that ranged from 3 to 5 times the upper limits of "normal" and that returned to normal upon repeat testing. Liver function tests did not change significantly from baseline. In a subset of 26 previously untreated patients, combined pravastatin (mean daily dose 22 mg) and gemfibrozil (mean daily dose 1,154 mg) therapy lowered total cholesterol by 25% (p < 0.001), triglycerides by 53% (p = 0.0001), LDL cholesterol by 14% (p = 0.24), and increased high-density lipoprotein (HDL) cholesterol by 20% (p = 0.012). CONCLUSION: Pravastatin and gemfibrozil therapy is safe and efficacious in patients with mixed hyperlipidemia. The long-term safety results are consistent with other reports on follow-up of shorter duration.
Several studies have reported an inverse relationship between hepatic lipase activity and plasma high density lipoprotein (HDL) cholesterol concentrations. The purpose of the present study was to determine whether genetic and pharmacological variation in hepatic lipase activity alters the distribution of HDL subclasses. Two independent analytical methods (nuclear magnetic resonance and gradient gel electrophoresis) were used to compare HDL subclass distributions in 11 homozygotes for the -514C allele of hepatic lipase and in 6 homozygotes for the -514T allele. Mean hepatic lipase activity was 45 +/- 15 mmol. l(-1). hr(-1) in -514C homozygotes and 20 +/- 7 mmol. l(-1). hr(-1) in -514T homozygotes. Both analytical methods indicated that HDL(2b) was significantly higher and HDL(3a) was significantly lower in -514T homozygotes than in -514C homozygotes. No differences were noted in the other HDL fractions (HDL(2a), HDL(3b), and HDL(3c)). To determine the effects of increased hepatic lipase activity, 20 men were given the synthetic anabolic steroid, stanozolol. Stanozolol treatment increased hepatic lipase activity more than two-fold (38 +/- 18 to 85 +/- 25 mmol. l(-1). hr(-1) ), and markedly reduced the plasma concentrations of the larger HDL subclasses (HDL(2b) and HDL(2a)). The plasma concentrations of the smallest HDL subclasses (HDL(3b) and HDL(3c)) were unchanged by stanozolol treatment. Taken together, these genetic and pharmacological data indicate that variation in hepatic lipase activity has highly specific effects on the distribution of HDL subclasses in the circulation.-Grundy, S. M., G. L. Vega, J. D. Otvos, D. L. Rainwater, and J. C. Cohen. Hepatic lipase activity influences high density lipoprotein subclass distribution in normotriglyceridemic men: genetic and pharmacological evidence.
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