[Acute obstruction of the lower esophagus caused by drug tablets].
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Aged↗
Biomedical subjects
B Jacotot
Publications and source records attributed to B Jacotot.
A multicenter comparison of the effects of simvastatin and fenofibrate therapy in severe primary hypercholesterolemia, with particular emphasis on lipoproteins defined by their apolipoprotein composition.
This multicenter, double-blind, randomized study was designed to compare the effects of simvastatin (20 mg/d and 40 mg/d) and fenofibrate (400 mg/d) on plasma lipids, lipoproteins, apolipoproteins (apo), and lipoprotein particles defined by their apo composition (Lp A-I, Lp A-II:A-I, Lp E:B, Lp C-III:B) in primary hypercholesterolemia. After 6 and 10 weeks of therapy, both drugs lowered plasma cholesterol, low-density lipoprotein (LDL) cholesterol, and apo B. The effect on LDL and apo B was significantly more pronounced for simvastatin (P = .01). Simvastatin increased Lp A-I, but did not change Lp A-II:A-I, while fenofibrate decreased Lp A-I and increased Lp A-II:A-I. Lp E:B and Lp C-III:B were decreased with both drugs, but fenofibrate was significantly more effective in reducing these particles than simvastatin. This study demonstrates that both drugs have beneficial effects on the parameters positively or negatively correlated with the atherosclerotic risk, with simvastatin being more effective in reducing some of them. These results suggest that the drugs led to different structural modifications of the lipoproteins, which would not be revealed by examination of lipoprotein density classes. These differences are probably related to the different mechanisms of action of the agents.
Adolescent↗
[The facts about cholesterol (condensed translation and comments of the common declaration of AHA and NHLBI)].
Many epidemiological and experimental studies have confirmed the continuous positive relationship between serum cholesterol levels and coronary risk. Therapeutic trials have demonstrated that the lowering of serum cholesterol by diet or drugs can lower this coronary risk. The benefits have been shown in men and women, the young and old, in those with a high coronary risk due to raised serum cholesterol and LDL and those with only moderately increased risk. In addition, therapeutic interventions on serum cholesterol are cost-effective. These observations more than justify the present national program of lowering the serum cholesterol.
Age Factors↗
Immuno-metabolic factors in schistosomal hepatic fibrosis modulating atherogenesis.
Clinical expression of atherosclerosis is infrequent among patients with schistosomal hepatic fibrosis (SHF), besides, the latter disease is a disease with many immunological expressions. The aim of the present work was to search for a possible immunological and metabolic interaction which would modulate atherogenic mechanisms. The study was carried out on 31 patients with SHF and 20 non-schistosomal subjects (10 with evident clinical atherosclerosis and 10 without). All investigated subjects were males aged above 40 years, and were subjected to the following: serum lipoprotein pattern, total cholesterol, phospholipids, triglycerides, ApoA, ApoB, IgG, IgM, IgA, C3 + circulating immune complexes (CICs) and passive haemagglutination using S mansoni adult worm antigens. The results showed low levels of blood lipids in patients with SHF especially in those with porto-systemic collaterals; serum levels of IgG and IgM were significantly increased in all patients with SHF, while IgA was only increased in patients with collaterals who in turn showed the least incidence of clinically evident atherosclerosis; serum C3 was increased in patients with clinical atherosclerosis, both schistosomal and non-schistosomal. CICs have been higher in patients with SHF without atherosclerosis while decreased in atherosclerosis patients, both schistosomal and non-schistosomal. Our results may consolidate the view of a protective role of liver affection against atherogenesis as well as the important contribution of the immune mechanisms in this context.
Adult↗
Prevalence of dyslipidemia in liver transplant recipients.
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Adolescent↗
Effect of chronic glucagon administration on lipoprotein composition in normally fed, fasted and cholesterol-fed rats.
Male adult Wistar rats received daily (at 9 a.m. and 5 p.m.) 10 micrograms of zinc-protamine glucagon by subcutaneous injection for 8 days. Plasma cholesterol levels were decreased by 36% in fed rats, 33% in cholesterol-fed rats and by 55% in fasted rats. Lipoproteins were separated into 22 fractions by ultracentrifugation using a density gradient. Glucagon administration decreased the cholesterol content in all lipoproteins except low density lipoprotein (LDL1) (1.006-1.040) and very low density lipoprotein (VLDL) from cholesterol-fed rats. The main decrease (-57 to -81%) was observed in 1.050-1.100 g/mL lipoproteins (LDL2 and HDL2), which contained a large amount of apo E, while HDL3 cholesterol was not affected. Triacylglycerol levels were decreased only in chylomicrons and VLDL (-70%) of fed and cholesterol-fed rats, while plasma and lipoprotein triacylglycerol levels were not changed in fasted rats treated with glucagon. In normally fed rats glucagon administration increased by 42% the fractional catabolic rate of [125I]HDL2 while the absolute catabolic rate appeared to be unchanged. Glucagon seems to be a potent hypolipidemic agent affecting mainly the apo E-rich lipoproteins. Its chronic administration limits lipoprotein accumulation which occurs upon cholesterol feeding.
Animals↗
Lipoprotein particle analysis comparing simvastatin and fenofibrate.
This study compares the effects of fenofibrate and simvastatin in primary hypercholesterolemia, with particular regard to lipoprotein particles, as defined by their apolipoprotein composition: LpAI, LpAII: AI, LpE:B, LpCIII:B. This was a double-blind study in which patients were randomized to 2 groups, one receiving simvastatin 20 mg once daily and the other receiving fenofibrate 200 mg b.i.d., if their total cholesterol and their LDL cholesterol remained above 7.60 mmol/l (300 mg/dl) and 4.95 mmol/l (195 mg/dl) after a 4-week placebo period. Simvastatin dosage was doubled at the end of 6 weeks of therapy if the LDL-cholesterol level remained above 3.55 mmol/l (140 mg/dl). Analyses were done after 6 and 10 weeks of therapy. Apolipoprotein AI was increased significantly only at week 10 with fenofibrate (+7.4%). Simvastatin had a more pronounced effect than fenofibrate on apolipoprotein B. There was a significant difference between drugs at weeks 6 and 10. No change was observed in the LpAII:AI level with simvastatin, whereas fenofibrate increased these particles quite significantly (+13.9 and +22.3%). The drugs had opposite effects on LpAI (+2.5 and +5.6% with simvastatin; -12.8 and -15.1% with fenofibrate). LP E:B (-33.0 and -40.8% with simvastatin; -53.8 and -52.2% with fenofibrate) and LpCIII:B (-23.8 and -31.8% with simvastatin; -35.1 and -43.5% with fenofibrate) were decreased by both drugs, but fenofibrate was significantly more effective in reducing these particles than simvastatin at week 6. This study suggests that both drugs led to different structural modifications of the lipoproteins, which would not be revealed by total apolipoprotein analysis. These differences are probably related to the mechanisms of action of these drugs.
Adolescent↗
Influence of diet on the plasma levels and distribution of ApoA-I-containing lipoprotein particles.
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Adult↗
Effect of simvastatin and fenofibrate on the fatty acid composition of hypercholesterolaemic patients.
1. The effects of simvastatin (one of a new class of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors) and fenofibrate on the fatty acid composition of cholesterol esters, phospholipids and triglycerides of different lipoproteins of 15 patients with primary hypercholesterolaemia were compared in a double-blind study. 2. Fenofibrate (300 mg day-1) increased the relative content of saturated fatty acids of cholesterol esters, phospholipids and triglycerides in VLDL, IDL and HDL. It also increased the relative content of monounsaturated fatty acids of cholesterol esters and phospholipids in all fractions and those of triglycerides in VLDL and IDL. In contrast, it decreased the proportion of polyunsaturated fatty acids of cholesterol esters and phospholipids in all fractions and those of triglycerides in VLDL and IDL. The polyunsaturated/saturated (P/S) ratio was reduced in cholesterol esters and phospholipids in VLDL and in phospholipids in IDL by fenofibrate. The drug significantly increased the 18:1w9/18:2w6 ratio in cholesterol esters and phospholipids in VLDL, LDL and HDL, but produced a non-significant increase in the ratio in IDL. 3. Simvastatin (20 mg day-1) produced a significant decrease in saturated fatty acid and an increase in polyunsaturated fatty acid in triglycerides in VLDL. Simvastatin, in contrast to fenofibrate caused a slight decrease in saturated and monounsaturated fatty acids in the three other lipoprotein fractions, and an increase in polyunsaturated fatty acids. The P/S and 18:1w9/18:2w6 ratios were not modified by simvastatin.
Adult↗
Effect of dietary treatment on the lipid, lipoprotein and fatty acid compositions in type IV familial hypertriglyceridemia.
The effects of a 2-month dietary treatment (1,625 +/- 177 kcal, 40 +/- 2.3% carbohydrate, 35 +/- 3.7% fat, 25 +/- 2% protein, polyunsaturated/saturated fat ratio = 1.02 +/- 0.06) on the overall composition of serum lipids, lipoproteins and the fatty acid composition of cholesterol esters and phospholipids in very low (VLDL), intermediate (IDL), low (LDL) and high (HDL) density lipoprotein in 5 patients with primary familial hypertriglyceridemia type IV were assessed. The data were compared with those for 9 normolipidemic subjects. Treatment decreased serum triglycerides (-52%) and total cholesterol (-12%) due to decrease in free cholesterol (-30%). It produced a significant decrease in all the constituents of VLDL (-58%), but the VLDL remained significantly higher after treatment than those of control subjects. The diet caused a decrease in triglycerides (-16%, -29% and -33%, respectively), and an increase in cholesterol in IDL, LDL and HDL. The IDL level in the treated patients remained significantly higher than in the controls. The LDL cholesterol/HDL cholesterol ratio was unchanged after treatment. The fatty acid compositions of the patients before treatment and the controls were not significantly different. The diet caused a decrease in palmitoleic and oleic acids in the cholesterol ester fraction and an increase in linoleic acid, but this was significant only in VLDL and HDL. The diet decreased the eicosapentaenoic acid but the drop was only significant in IDL and LDL. There was also a decrease in linolenic acid, only significant in IDL. The diet induced only minor changes in the phospholipid fractions. We concluded that a single nutritional regimen can effectively decrease the serum lipids and normalize the lipoprotein composition of type IV hypertriglyceridemic patients.
Adult↗
[Determination of lipoprotein Lp(a). A semi-automatic immuno-turbidimetric method].
A sensitive, accurate, semiautomatic immunoturbidimetric assay for determining Lp(a) levels using a Hitachi 705 apparatus is described. A polyclonal antibody against anti-Lp(a) produced by Immuno-france is used. Studies proved that this test is reliable and that results are well correlated with those obtained by immunonephelometry.
Immunoassay↗
Fluidity changes and chemical composition of lipoproteins in type IIa hyperlipoproteinemia.
The chemical composition and the physical properties of lipoproteins (VLDL, LDL and HDL) were studied in two groups of patients: 14 healthy normolipidemic subjects and 15 type IIa familial hypercholesterolemic patients. The steady-state fluorescence anisotropy rs was estimated in lipoproteins by the fluorescence depolarization of two fluorescent probes: the DPH (1,6-diphenyl-1,3,5-hexatriene) and the TMA-DPH (1,4-trimethylammonium phenyl-6-1,3,5-hexatriene). A structured order parameter S was calculated from the DPH fluorescence anisotropy. The flow activation energies were calculated for LDL and HDL from both groups from the Arrhenius plots (log r DPH versus 1/T). By using TNBS (trinitrobenzene sulfonic acid) as a distance control quencher, the two probes were located in the outer shell of LDL. In HDL, TMA-DPH remained at the surface of the particles, while DPH was more deeply embedded in the lipid core. There was no difference in the physico-chemical properties of VLDL between the two groups studied. DPH fluorescence anisotropies were significantly increased in LDL and HDL from the hypercholesterolemic group compared to the control particles (P less than 0.05 and P less than 0.01, respectively). In LDL this modification of the fluorescence anisotropy can be related to a change in the lipid composition of particles. LDL from hypercholesterolemic patients contained significantly less triacylglycerol (P less than 0.01) and more cholesteryl ester (N.S.). Their cholesteryl ester to triacylglycerol ratio was significantly higher. In HDL, there was no difference in chemical composition between the two groups. The increase in DPH fluorescence anisotropy can be related to the presence of smaller particles in HDL from HC group. No difference was noted in the TMA-DPH fluorescence anisotropy at 37 degrees C in the LDL from the two groups. In contrast, TMA-DPH fluorescence anisotropy in HDL from hypercholesterolemic group was significantly higher than in control HDL. The flow activation energy of DPH was also significantly higher in both LDL and HDL from the hypercholesterolemic group than in control group particles. In both LDL and HDL from the control group, DPH fluorescence anisotropy was negatively correlated with TG/protein and TG/PL ratios and positively correlated with the CE/TG ratio. No correlation was observed between lipid composition and DPH fluorescence anisotropy values in hypercholesterolemic particles. The modification in fluidity parameters, especially the increase in the flow activation energies in LDL and HDL from hypercholesterolemic patients, could lead to a restriction of cholesterol movements in these particles. From a physiological point of view, this could represent a loss of functional capacity.
Adult↗
Effects of dietary fats on the fluidity of human high-density lipoprotein: influence of the overall composition and phospholipid fatty acids.
The present study was undertaken to analyze whether the changes induced by dietary manipulations in the chemical composition of HDL, particularly in total phospholipids, phosphatidylcholine and sphingomyelin fatty acid composition, modified their fluidity. 12 healthy women, aged 26-49 years were studied. They consumed, over periods of 5 weeks, various isocaloric diets, each containing 30% of the calories as fat. 15.6% of the total calories were provided successively by olive oil, soybean oil, corn oil, and milk fats. The HDL fluorescence anisotropy was measured with 1,6-diphenyl-1,3,5-hexatriene (DPH) by fluorescence polarization. The HDL from the monounsaturated diet, olive oil, were the most fluid particles. The HDL fluorescence anisotropy was positively correlated with their free cholesterol percentage and negatively correlated with their triacylglycerol content and their triacylglycerol/phospholipid ratio. Moreover, the HDL fluorescence anisotropy was negatively correlated with the percentage of oleic acid in their total phospholipids and particularly in the phosphatidylcholine. These results suggest that the percentages of triacylglycerol and oleic acid in phospholipids of HDL have a fluidifying effect on these lipoproteins.
Adult↗
Efficacy and safety of simvastatin (alone or in association with cholestyramine). A 1-year study in 66 patients with type II hyperlipoproteinaemia.
The effects and safety of simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, were investigated alone or in association with cholestyramine in 66 patients with hypercholesterolaemia, in a 1-year study. In type IIa hypercholesterolaemia (41 patients), the association was more effective than simvastatin used alone in lowering total cholesterol (37% vs 29%) and LDL-cholesterol (45% vs 37%). In type IIb hypercholesterolaemia (23 patients), the association simvastatin-cholestyramine did not appear more effective than simvastatin used alone. The decrease of apoprotein B was parallel to the LDL-cholesterol decrease. Apoprotein A1 did not change significantly. The long-term safety of simvastatin was good. No lens opacity was noted. The most serious side-effect in our study was myolysis which occurred in two patients with a marked increase in creatine phosphokinase.
Adult↗
[When should hypercholesterolemia patients be diagnosed and treated?].
All prospective epidemiological studies have shown a negative correlation between blood cholesterol level on entering the study and survival in the following years. The same studies have also shown that for a middle-aged man who does not smoke and is neither hypertensive nor diabetic the probability of developing an acute coronary accident increases exponentially with his initial blood cholesterol level. Finally, recent primary prevention studies have provided experimental evidence of the causative role played by hypercholesterolaemia in the genesis of atherosclerosis; they have also led to the conclusion that the reduction of coronary diseases is mainly due to a decrease in blood cholesterol, irrespective of whether this decrease is obtained by diet or drugs. The need for detection and treatment of hypercholesterolaemia therefore is generally accepted. What remains open to discussion and has been the subject of recent consensus conferences is the modalities of detection and the level of blood cholesterol at which diets and drugs should be prescribed.
Adult↗
Effect of simvastatin on plasma lipids, apolipoproteins and lipoprotein particles in patients with primary hypercholesterolaemia.
The effect of treatment with simvastatin, a new HMG-CoA reductase inhibitor, has been investigated in 27 patients with primary hypercholesterolaemia. It produced a significant decrease of cholesterol and phospholipids in plasma, LDL and apolipoprotein B-containing lipoproteins. Plasma apolipoproteins B, C-III and E were also significantly lowered. The concentration of lipoprotein particles recognized by monoclonal antibodies (BL3, BL5 and BL7), associated with atherosclerotic disease, was also lowered by the treatment. Lipoproteins LpA-II:A-I were not changed, while LpA-I, which has been suggested to be the protective fraction of the apo A-I-containing lipoproteins, was slightly and inconsistently increased.
Adolescent↗
[Nicotine gum and lipid profile].
Smoking promotes for atherosclerosis by several mechanisms and particularly its actions on lipid metabolism; nicotine liability is well established. In one patient the use of nicotine-gum was reported to increase total cholesterol and LDL cholesterol. We studied lipid modifications in 14 voluntary students, heavy smokers (greater than 20 cigarettes/day) and nicotine dependent (Fagerström test; score greater than 7). They gave up smoking and received in double blind study either 2 mg nicotine-gum, or placebo-gum (8-12 gums a day for one month). Total and HDL cholesterol (chol.), triglycerides (TG) were measured at day 0, day 30 and day 60. Giving up smoking was ascertained by CO-analyser. At day 30 total chol and TG were unmodified, and HDL chol appeared slightly increased. At day 60 HDL and LDL chol were significantly improved. So in nicotine-dependent smokers, by giving up smoking and receiving 2 mg nicotine-gum, lipid patterns are not worsened but improved.
Adult↗