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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of gemfibrozil and lovastatin treatment on composition and hydrated density distribution of high-density lipoprotein (HDL) were studied in 21 patients with heterozygous familial hypercholesterolemia with the use of HDL density gradient ultracentrifugation. At baseline the patients with familial hypercholesterolemia had a markedly reduced or missing HDL2 subfraction and their HDL3 was more dense with reduced content of cholesteryl ester and increased content of triglyceride compared with HDL of control subjects with normal lipid values. Gemfibrozil and lovastatin caused primarily similar alterations in HDL components in HDL2 and HDL3 subfractions. Both agents increased apolipoprotein AI and apolipoprotein AII concentrations significantly in HDL2, whereas the apolipoprotein changes in HDL3 were relatively smaller. The difference between the effects of these two agents was related to the HDL lipid composition. Gemfibrozil increased the cholesterol concentrations of HDL2 and HDL3 (p less than 0.05 for both), and lovastatin caused significant increases in HDL2 (p less than 0.05) and HDL3 phospholipids (p less than 0.01). The observed similarity of qualitative alterations in HDL subfractions produced by these two agents in patients with familial hypercholesterolemia differs from those reported in other types of hyperlipidemia and is probably a consequence of the basic abnormalities in HDL that are characteristic of familial hypercholesterolemia.
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PMID:Effects of lovastatin and gemfibrozil on high-density lipoprotein subfraction density and composition in patients with familial hypercholesterolemia. 161 16

Gemfibrozil is frequently used for lipid-lowering in familial combined hyperlipidaemia (FCHL) and in other forms of combined hyperlipidaemia. This therapy increases biliary cholesterol saturation, enhancing the risk for gallstone formation. Furthermore, in hypertriglyceridaemia, LDL cholesterol levels often tend to rise. We have explored the possibility that addition of a low dose of cholestyramine to gemfibrozil therapy obliterates these phenomena. Eighteen gallstone-free patients with definite (n = 5) or probable (n = 10) FCHL, or combined hyperlipoproteinaemia (n = 3) were randomized to a 6 week treatment with gemfibrozil, 600 mg b.i.d., or gemfibrozil 600 mg b.i.d. plus 4 g cholestyramine o.d. After 6 weeks the patients were crossed over to the alternative treatment. Plasma lipoproteins and biliary lipids were determined at baseline and at the end of each period. Institution of gemfibrozil treatment resulted in a decrease in plasma cholesterol by 15% (P less than 0.05) and in plasma triglycerides by 47% (P less than 0.05); HDL cholesterol increased by 18% (P less than 0.05). Addition of cholestyramine further decreased plasma and LDL total cholesterol by 9% (P less than 0.05). Total triglycerides and HDL cholesterol did not change. Gemfibrozil treatment was associated with a rise in the relative biliary concentration of cholesterol from 5.6 +/- 0.4 to 6.9 +/- 0.5 molar percent (P less than 0.01), and a parallel decrease in the relative concentration of bile acids, resulting in an increased cholesterol saturation of the bile, from 77 +/- 5 to 90 +/- 6% (P less than 0.05). This change was not observed during the combined therapy (mean cholesterol saturation, 82 +/- 4%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gemfibrozil in familial combined hyperlipidaemia: effect of added low-dose cholestyramine on plasma and biliary lipids. 190 37

Gemfibrozil lowers triglycerides, low density lipoprotein (LDL) and very low density lipoprotein (VLDL) cholesterol. It also promotes a significant increase of high density lipoprotein (HDL) cholesterol. It has been established that normalization of apolipoproteins is an important protective factor against atherosclerosis. The present report examines the effectiveness of 12 months of gemfibrozil treatment on plasma lipids and apolipoproteins in types IIa (VLDL 18 +/- 2 mg cholesterol/dL) and IIb (VLDL 58 +/- 7 mg cholesterol/dL) hypercholesterolemic patients. Gemfibrozil lowered plasma triglycerides, VLDL cholesterol and apolipoprotein B (apoB), increased HDL cholesterol and apoAI levels in both groups, and induced a very substantial reduction in LDL cholesterol in type IIa patients only. Even though HDL particles were enriched in cholesterol, indicating improvement in the reverse cholesterol transport and lower risk of atherosclerosis in both groups, it is important to note that production of cholesterol-poor LDL particles and reduction in LDL cholesterol and the LDL/HDL cholesterol ratio were observed only in the normotriglyceride group (type IIa). Due to the initially elevated concentration of plasma triglycerides and VLDL in type IIb patients and the increased catabolism of VLDL to LDL during gemfibrozil therapy, this drug has a more efficient regulating effect on LDL particles in type IIa compared with type IIb hyperlipidemia.
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PMID:Gemfibrozil therapy in primary type II hyperlipoproteinemia: effects on lipids, lipoproteins and apolipoproteins. 202 87

A subanalysis was performed on data acquired from 67 subjects having serum cholesterol levels of 6.2 mmol/l or above (greater than or equal to 240 mg/dl) and triglyceride levels of 2.25 to 4.00 mmol/l (199-354 mg/dl) (excluding patients with familial hypercholesterolemia), who were participating in a multicenter study comparing lovastatin and gemfibrozil, to evaluate the role of these agents in the treatment of combined hyperlipidemia (type IIb phenotype). In stratum 1 (cholesterol measures of 62.-7.79 mmol/l [240-301 mg/dl]), patients received either lovastatin 20 mg nightly (n = 17) or gemfibrozil 600 mg twice daily (n = 8), and in stratum 2 (cholesterol levels greater than or equal to 7.8 mmol/l [greater than or equal to 302 mg/dl]), patients received either lovastatin 40 mg nightly (n = 23) or gemfibrozil 600 mg b.i.d. (n = 19) for 6 weeks. Low-density lipoprotein (LDL) cholesterol levels were reduced significantly more by lovastatin than by gemfibrozil (stratum 1, -23 versus +1%, stratum 2, -34 versus -12%, respectively). A treatment goal of 4.0 mmol/l (155 mg/dl) for LDL cholesterol was achieved by 59 and 35% of patients receiving lovastatin and by 0 and 11% of patients receiving gemfibrozil in strata 1 and 2, respectively. Gemfibrozil was more effective in reducing triglyceride levels and in increasing high-density lipoprotein (HDL) cholesterol in both strata, although increases in HDL/LDL cholesterol ratios were greater with lovastatin. We conclude that, although lovastatin was more useful in normalizing LDL cholesterol, neither agent was ideal for all patients with combined hyperlipidemia. Further development of treatment regimens is called for in this group of patients.
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PMID:Treatment of combined hyperlipidemia with lovastatin versus gemfibrozil: a comparison study. 207 71

Gemfibrozil, a lipid lowering agent, was administered to two patients with familial hyperlipidaemia and one patient with insulin dependent diabetes mellitus. It was partially effective in familial hyperlipidaemia. It dramatically reduced triglyceride and cholesterol levels in the patient with Type V hyperlipidaemia and insulin dependent diabetes mellitus. Patients with familial and Type V hyperlipidaemias should be given a trial of gemfibrozil therapy.
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PMID:Gemfibrozil in familial and type V hyperlipidaemias. Report of 3 cases. 207 73

Gemfibrozil, like clofibrate, is effective in lowering both serum cholesterol and triglycerides and in increasing high-density lipoproteins. The information available about its effects on biliary lipids is still limited, and conflicting results have been reported. In this study we evaluated the effect of gemfibrozil (1.2 g/day) and clofibrate (2.0 g/day), in a single-blind crossover design for 6 weeks with a 4-week washout period, on the biliary cholesterol saturation index (SI) in stimulated hepatic bile and on the hepatic secretion rate of biliary lipids in patients with hyperlipidemia. Clofibrate increased cholesterol SI (from 1.70 +/- 0.14 to 2.05 +/- 0.24), whereas gemfibrozil decreased it (from 1.70 +/- 0.14 to 1.54 +/- 0.16). The results were not statistically significant. The hepatic secretion rate of cholesterol was significantly (p less than 0.04) increased by clofibrate therapy, whereas it was significantly (p less than 0.04) decreased after gemfibrozil; a significant (p less than 0.04) decrease in the hepatic secretion rate of bile acids, bile acid pool size, and bile acid fecal excretion (p less than 0.04) was also found after gemfibrozil administration. Gemfibrozil interferes extensively with bile acid metabolism, but it does not increase biliary cholesterol secretion, as clofibrate does. These results suggest that gemfibrozil does not seem to increase the risk of gallstone formation in patients with hyperlipidemia.
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PMID:Effect of gemfibrozil administration on biliary lipid secretion in hyperlipidemic patients. A crossover study with clofibrate. 227 44

The efficacy of Gemfibrozil on S. lipid levels was studied in 36 middle aged subjects with type IIA, IIB, IV hyperlipidemia. Gemfibrozil was well tolerated in the dose of 1200 mg/day and no dropouts were attributable to its use. An overall reduction in total cholesterol (39.91%), total triglycerides (71.10%), VLDL triglycerides (62.97%). LDL cholesterol (45.57%) and apolipoprotein B levels (26.83%) were observed at 24 weeks. At the same time HDL cholesterol, and apolipoprotein A levels showed increases by 26.23% and 53.67% respectively. It is concluded that Gemfibrozil is an effective lipid lowering agent. Further long term studies are necessary to determine its optimal dosage and its long term safety in Indian subjects.
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PMID:Gemfibrozil in hyperlipidaemia: an open, single blind trial. 238 Jan 32

Thirteen patients with phenotypic type V hyperlipidemia were treated with either gemfibrozil (Lopid) or a placebo in a randomized, double-blind, crossover study for two 8-week periods. A 4-week baseline period of a low-fat diet preceded the study and served as a dietary control period. A 4-week washout period followed the two 8-week periods. Compared with the placebo phase, gemfibrozil produced a significant reduction in the concentrations of total plasma triglycerides (21.03 vs 5.50 mmol/L) and very low-density lipoprotein triglycerides (14.40 vs 4.59 mmol/L) as well as in total plasma cholesterol levels (10.88 vs 5.62 mmol/L) and very low-density lipoprotein cholesterol (6.66 vs 2.15 mmol/L). Chylomicronemia was virtually abolished by the drug treatment. As expected in treated patients with type V hyperlipidemia, concentrations of low-density lipoprotein cholesterol rose after therapy with gemfibrozil (3.08 mmol/L) as compared with placebo (1.84 mmol/L); high-density lipoprotein cholesterol also increased (0.85 mmol/L after therapy with gemfibrozil, 0.62 mmol/L after placebo). The previously very low values for both of these lipoproteins increased at the same time that the total plasma cholesterol value decreased. We conclude that gemfibrozil is a well-tolerated and effective hypolipidemic agent for the treatment of patients with severe hypertriglyceridemia when used in conjunction with a low-fat diet.
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PMID:The hypolipidemic effects of gemfibrozil in type V hyperlipidemia. A double-blind, crossover study. 268 58

In a 4-year-old boy with steriod-resistant syndrome and extreme hyperlipidemia, an intense pruritic papular eruption developed on the trunk, buttocks, and extensor surface of the extremities. Findings from a skin biopsy specimen were consistent with an eruptive xanthoma. The patient was treated with gemfibrozil (Lopid), a low-fat diet, and antihistamines. Within 1 month pruritus diminished, the cutaneous lesions resolved, and serum lipid levels declined.
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PMID:Eruptive xanthomas in a child with the nephrotic syndrome. 280 50

A randomized double blind, placebo-controlled crossover design was used to determine the efficacy of gemfibrozil and clofibrate in the treatment of familial combined hyperlipidemia and to determine which one of these agents would be more effective. Sixteen patients, 12 men and 4 women, mean age 49.5 years (40-68 yrs), had the entry criteria of increased cholesterol and/or triglyceride with an increase in triglyceride and/or cholesterol in one or more first degree relatives and/or family history of premature cardiovascular disease. Patients received 6 weeks of placebo followed by clofibrate 1000 mg bid or gemfibrozil 600 mg bid for 12 weeks, placebo for 6 weeks and the other drug for 12 weeks. Plasma total cholesterol, triglycerides, HDL-C, LDL-C, apo B and apo A-I were measured every 6 weeks during the study. Gemfibrozil was associated with a significant (P less than 0.05) decrease in plasma triglyceride concentration compared to placebo but it was not significantly different compared to clofibrate. For ease of comparison, the mean value for serum triglycerides during gemfibrozil treatment (average of the 6 and 12 week measurements) was calculated and was 232 +/- 198 mg/dl (mean +/- 1 SD) compared to the average of the placebo treatment values of 381 +/- 410 mg/dl and the average value during the clofibrate treatment period of 217 +/- 178 mg/dl. HDL-C was significantly (P less than 0.05) increased with both drugs and to the same extent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of gemfibrozil and clofibrate on serum lipids in familial combined hyperlipidemia. A randomized placebo-controlled, double-blind, crossover clinical trial. 305 31


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