Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long term use of lipid-lowering drugs in the treatment of patients with hyperlipoproteinaemia is aimed at reducing plasma concentrations of known atherogenic lipoproteins with a favourable effect on lipid deposition in the arterial wall. A less common aim is to prevent the adverse sequelae of hyperchylomicronaemia in patients with severe hypertriglyceridaemia. The decision to begin drug therapy should be made only after the exclusion of secondary factors and after an adequate trial of diet has failed to produce acceptable concentrations of plasma lipids and lipoproteins. The bile acid sequestrants (cholestyramine and colestipol), nicotinic acid, fenofibrate and inhibitors of hydroxymethylglutaryl coenzyme A (HMG CoA) reductase (e.g. lovastatin or simvastatin) are the most effective drugs for use in patients with primary hypercholesterolaemia; these agents reduce plasma concentrations of total and LDL-cholesterol by 15 to 45%. For those patients with concurrent hypertriglyceridaemia, nicotinic acid, lovastatin or simvastatin, or fenofibrate are the preferred drugs for initial use; bile acid sequestrants frequently exacerbate hypertriglyceridaemia in these patients. Fibric acid derivatives (e.g. clofibrate, gemfibrozil, bezafibrate or fenofibrate) are all effective in the therapy of patients with type III hyperlipoproteinaemia, as is nicotinic acid and I have found lovastatin to be effective also. Gemfibrozil or nicotinic acid are the most effective agents to use in the treatment of patients with severe hypertriglyceridaemia who are at increased risk of abdominal pain and pancreatitis. Combined therapy with drugs which have different mechanisms of action can be effectively used in the treatment of patients with severe hypercholesterolaemia or combined hyperlipidaemia; for the former group, combinations which use bile acid sequestrants, HMG CoA reductase inhibitors and nicotinic acid are the most effective.
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PMID:An overview of lipid-lowering drugs. 307 24

Elevated levels of serum cholesterol have long been associated with an increased risk of both the occurrence and the progression of coronary atherosclerosis. The use of dietary therapy to reduce elevated lipid labels has received widespread attention, but like other therapy requiring behavioral modification has met with only partial success in most patients. Little wonder that drugs which lower lipids have been utilized to supplement the effect of diet in hyperlipidemia subjects. Currently available hypolipidemic agents are far from ideal in their effectiveness and lack of side effects, so the search for more potent, safer drugs has been intense. This paper reports on the use of one such agent, gemfibrozil; and its comparison with clofibrate and placebo. Gemfibrozil (CL719, 2,2-dimethyle-5-(2,5 xylyloxy) valeric acid is a substituted phenoxy alkyl acid which has been shown to decrease lipids in hyperlipidemia subjects. A short term study using 1200 mg of gemfibrozil daily demonstrated reduction in total serum cholesterol, triglyceride and apo B levels, and a concomitant rise in HDL cholesterol levels. A long term study of the effect so gemfibrozil showed that the drug had a more pronounced effect on triglyceride then cholesterol, that it had few side effects and the effect was sustained. A recent study from New Zealand demonstrated that gemfibrozil, compared to placebo, lowered plasma cholesterol, triglyceride and VLDL levels and raised HDL levels.
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PMID:Hyperlipoproteinemia, atherosclerosis and gemfibrozil. 695 55

The effects of gemfibrozil on serum lipids and apolipoproteins were investigated in 60 male survivors of myocardial infarction (MI) (age range 29-48 years, mean 44). Fifteen had normal serum cholesterol (less than or equal to 7.0 mmol/l) and triglyceride (less than or equal to 1.7 mmol/l) levels, but most had low levels of high density lipoprotein (HDL) cholesterol (less than 1.00 mmol/l). Ten had type II A, 27 type II B and 8 type IV hyperlipidaemia. A double-blind placebo-controlled cross-over design was used with 3-month treatment periods. Gemfibrozil was given in daily doses of 1200 mg. The drug was well tolerated and there were no drop-outs attributable to its use. In all subjects, gemfibrozil reduced the mean serum total cholesterol by 17% and triglycerides by 54% and increased HDL cholesterol by 16%. The percentage HDL cholesterol of total cholesterol increased from 14 to 19%. The changes were similar in patients with normal serum cholesterol and triglyceride values and in those with classical hyperlipidaemias. In contrast, the changes during placebo treatment corresponded to those in healthy male untreated controls who were followed simultaneously. Apoprotein A-I remained unchanged, but A-II increased by 20% during gemfibrozil treatment. It is concluded that gemfibrozil corrects effectively dyslipidaemias in male MI patients but further long-term studies are warranted.
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PMID:Gemfibrozil in the treatment of dyslipidaemias in middle-aged male survivors of myocardial infarction. 701 Sep 29

Although combination therapy using 3-hydroxy-3-methylglutaryl coenzyme A (HMG-Co-A) reductase inhibitors and fibrates is efficacious in combined hyperlipidemia, such treatment has been associated with myopathy. For this reason, we studied the effects of fluvastatin and gemfibrozil, alone or in combination, on muscle. A total of 21 patients with combined hyperlipidemia were recruited who were matched for age, body mass index, and baseline levels of total cholesterol, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglycerides, creatine phosphokinase, and myoglobin. Patients were randomized to three groups for 6-week treatment with fluvastatin at 40 mg/day, gemfibrozil at 600 mg twice daily, or a combination of the two drugs. Parameters for muscle damage were rises in levels of serum creatine phosphokinase and myoglobin compared with pre-exercise levels; these were assessed 1 hr and 8 hr after a 45 min lean body mass standardized ergometer test, which was performed before and after treatment in all patients. Biopsies from the quadriceps muscle were taken 48 hr after each test. Fluvastatin lowered total cholesterol and LDL-C by 23% and 35%, respectively (p < 0.01), with no effects on triglycerides and HDL-C. Gemfibrozil lowered triglycerides by 40% (p < 0.01) but did not lower total cholesterol or LDL-C significantly. The combination therapy decreased total cholesterol, LDL-C, and triglycerides by 28%, 29%, and 39%, respectively (p < 0.05). Pre-exercise creatine phosphokinase and myoglobin levels were not affected by treatment in any group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of combined hyperlipidemia with fluvastatin and gemfibrozil, alone or in combination, does not induce muscle damage. 760 87

The aim of this study was to determine the effect of gemfibrozil, compared with lovastatin, in patients with high levels of lipoprotein(a) and on plasma lipid profile. Twenty-seven nondiabetic patients with high levels of plasma lipids and lipoprotein(a), 19 male and eight female, aged 37-68 (mean +/- S.D. 54.2 +/- 7.5) years, were randomly assigned to 2 weeks of treatment with gemfibrozil 600 mg twice daily (14 pts.) or lovastatin 40-80 mg once daily (13 pts.). Patients had fasting plasma total cholesterol levels > or = 6.2 mmol/l, low-density lipoprotein > 4.14 mmol/l and lipoprotein(a) > 0.62 mmol/l. All patients but one had triglycerides > 2.82 mmol/l. There were no statistical differences between both groups in terms of age, sex, clinical diagnosis and previous medication. After 3 months of treatment, gemfibrozil reduced triglycerides (47.9% vs. 24.5%; P < 0.001), very low density lipoprotein (43.9% vs. 24.6%; P < 0.05), lipoprotein(a) (25.3% vs. 4.9%; P < 0.05) and increased high-density lipoprotein (34.4% vs. 11%; P < 0.01) more than lovastatin. Gemfibrozil and lovastatin reduced comparably total cholesterol (21.4% vs. 29.0%; P = NS) and low-density lipoprotein (26.5% vs. 37.3%; P = NS). The plasma levels of high-density lipoprotein and lipoprotein(a) were unchanged significantly by lovastatin. In conclusion, besides well-known efficacy in hyperlipidemia treatment, gemfibrozil also increased high-density lipoprotein and reduced lipoprotein(a), which may have important epidemiologic implications.
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PMID:Effect of gemfibrozil versus lovastatin on increased serum lipoprotein(a) levels of patients with hypercholesterolemia. 777 89

Thirty-eight renal allograft recipients who had persistent hyperlipidemia and stable renal function 27.8 +/- 18.2 months after renal transplantation were treated with gemfibrozil. Gemfibrozil therapy resulted in a decrease in the levels of total cholesterol (TC; 297.6 +/- 41.0 mg/dl to 249.2 +/- 43.7 mg/dl, -16.3%; p < 0.0001), triglyceride (TG; 231.9 +/- 116.8 to 125.7 +/- 58.4 mg/dl, -45.8%, p < 0.0005), and LDL-cholesterol (LDL-C; 203.8 +/- 37.4 to 174.5 +/- 42.5 mg/dl, -14.4%; p = 0.001), which were sustained for 29.1 +/- 16.0 months. Comparison of sequential lipid profiles between gemfibrozil-treated individuals and untreated hyperlipidemic controls matched for age, sex, time after transplantation, and the degree of hyperlipidemia, showed that gemfibrozil-treated patients had lower levels of TC (239.9 +/- 39.5 vs. 272.8 +/- 34.1 mg/dl; p < 0.005), TG (125.7 +/- 26.6 vs. 167.3 +/- 69.0 mg/dl; p < 0.05), and LDL-C (160.2 +/- 41.3 vs. 185.3 +/- 26.6 mg/dl; p < 0.05) on serial follow-up. No significant side-effect was observed with gemfibrozil therapy. Our data showed that gemfibrozil was a safe and effective drug for the treatment of hyperlipidemia in renal allograft recipients, which could reduce these patients's long-term cardiovascular risks.
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PMID:Hyperlipidemia after renal transplantation: treatment with gemfibrozil. 793 22

Eleven men with hypoalphalipoproteinemia (HPAL; fasting plasma high density lipoprotein (HDL) cholesterol level of < 0.9 mmol/l), mild hypertriglyceridemia (HTG; triglycerides (TG) level of 1.75-7.5 mmol/l) and a normal calculated LDL cholesterol level (< 3.7 mmol/l) participated in a randomized, double-blind, double-placebo, crossover trial to compare the effect of two drugs, lovastatin (40 mg once daily) and gemfibrozil (600 mg twice daily), on clearance of postprandial lipoproteins. A 2-week washout period separated drug treatment periods of 6 weeks each. Ten subjects completed each treatment period. After ingestion of a vitamin A fat load, plasma, chylomicron and non-chylomicron retinyl palmitate (RP) and TG responses (areas under curves) were reduced in all subjects on gemfibrozil therapy and in 7 on lovastatin therapy. There was close correlation between change in fasting TG (but not fasting HDL-cholesterol) and change in postprandial RP areas on gemfibrozil but not lovastatin therapy. Postheparin lipoprotein lipase (LPL) and hepatic lipase (HL) activities were increased by gemfibrozil therapy while only a mild elevation in LPL activity alone was seen on lovastatin therapy. These data indicate that improvement in HTG is the main feature associated with improvement in postprandial lipemia and this is likely due to LPL-mediated enhancement of lipolytic hydrolysis. Gemfibrozil is more effective than lovastatin in attenuating postprandial lipemia in the HPAL/HTG syndrome.
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PMID:Effect of gemfibrozil and lovastatin on postprandial lipoprotein clearance in the hypoalphalipoproteinemia and hypertriglyceridemia syndrome. 831 63

The effect of gemfibrozil on postprandial lipoprotein metabolism was investigated in a 12-week, randomized, double-blind, placebo-controlled trial in 20 non-insulin-dependent diabetic patients with moderate hypertriglyceridemia. The patients were given a meal containing 78 g of fat and 345,000 units of vitamin A to label chylomicrons and their remnants. Plasma obtained at various times during the fat-load test was separated into six fractions by gradient-density ultracentrifugation. Gemfibrozil reduced the postprandial triglyceride response, measured as the area under the time-dependent concentration curve, on average by 32% in whole plasma, by 38% in the Svedberg flotation unit (Sf) 1,100-3,200 chylomicron fraction, by 36% in Sf 400-1,100 chylomicrons, and by 38% in the Sf 60-400 lipoproteins. Retinyl palmitate, a measure of intestinally derived particles, was reduced in plasma by 34%, in Sf 1,100-3,200 by 46%, in Sf 400-1,100 by 44%, and in Sf 60-400 by 37%. All these reductions were significant in comparison with the placebo group. Particles with Sf < 60 were not significantly affected. In contrast to earlier observations in healthy subjects, no significant negative correlations existed between postprandial lipemia and high density lipoprotein cholesterol or the postheparin lipoprotein lipase activity. The reduction of the potentially atherogenic chylomicron remnants may decrease the risk of atherosclerosis in non-insulin-dependent diabetes mellitus, a hypothesis that awaits testing in prospective studies.
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PMID:Gemfibrozil reduces postprandial lipemia in non-insulin-dependent diabetes mellitus. 842 63

Hyperlipidemia associated with non-insulin-dependent diabetes mellitus (NIDDM) and insulin resistance is characterized by high triglyceride levels; raised levels of total low-density lipoprotein (LDL), which is made up of small, dense, cholesterol-rich particles; low levels of high-density lipoprotein (HDL); and glycosylation of apolipoproteins. Optimal drug therapy for this lipid profile is controversial. To test whether a fibrinic acid derivative (gemfibrozil) or a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (lovastatin) would produce better results in these patients, a crossover study was performed. Gemfibrozil 600 mg twice daily and, after a washout period, lovastatin 20 to 40 mg twice daily were administered to nine patients with NIDDM. Gemfibrozil significantly decreased triglyceride, very-low-density lipoprotein (VLDL), and intermediate-density lipoprotein (IDL) levels, the total cholesterol:HDL ratio, and the IDL plus VLDL;HDL ratio, and significantly increased levels of HDL, HDL2, and HDL3. Lovastatin significantly decreased levels of total cholesterol, calculated LDL, directly measured LDL, IDL, total triglycerides, VLDL, and the ratios of LDL:HDL, total cholesterol:HDL, and directly measured LDL:HDL and significantly increased total HDL and HDL3 levels. Gemfibrozil was significantly more effective than lovastatin in raising total HDL and HDL3 levels and in lowering the IDL plus VLDL:HDL ratio. Lovastatin was significantly more effective than gemfibrozil in lowering total cholesterol, LDL, directly measured LDL, and the LDL:HDL and directly measured LDL:HDL ratios. In the absence of malignant hypertriglyceridemia, an HMG-CoA reductase inhibitor, rather than a fibrinic acid derivative, is indicated for the treatment of patients with dyslipidemia associated with NIDDM and insulin resistance.
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PMID:A comparison of lovastatin, an HMG-CoA reductase inhibitor, with gemfibrozil, a fibrinic acid derivative, in the treatment of patients with diabetic dyslipidemia. 859 42

Hyperlipidemia is a common side-effect of oral retinoid treatment, which sometimes interferes with long-term therapy. To evaluate the safety and efficacy of the lipid-lowering drug gemfibrozil on retinoid-associated hyperlipidemia, we studied the clinical response and the plasma lipoprotein levels in 22 acitretin-treated (0.25-0.75 mg/kg) patients mainly suffering from psoriasis. Gemfibrozil or placebo was given in a double-blind cross-over fashion to 14 patients, who after 8 weeks of acitretin therapy and dietary advice exhibited hyperlipidemia (triglyceride levels > or = 50% above baseline and/or > or = 2.0 mmol/l). Serum triglycerides remained high (3.7 +/- 2.4 mmol/l) during placebo treatment but were reduced after 8 weeks of gemfibrozil treatment (p < 0.01). The total cholesterol level decreased slightly (p < 0.05) during gemfibrozil treatment, but the LDL/HDL ratio did not change significantly. No untoward effects of gemfibrozil on acitretin dose-response and clinical side-effects were noted. Gemfibrozil thus appears useful in patients prone to retinoid-induced hyperlipidemia unresponsive to dietary treatment and acitretin dose reductions.
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PMID:Effects of gemfibrozil (Lopid) on hyperlipidemia in acitretin-treated patients. Results of a double-blind cross-over study. 861 57


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