Search

Resume Cet essai clinique randomise, croise, a demontre la securite et l’efficacite d’un dispositif medical de neurostimulation electrique transcutanee rechargeable (TENS) chez des sujets souffrant de douleurs articulaires et musculosquelettiques chroniques. Cette etude montre une diminution de la consommation des antalgiques non morphiniques, des anti-inflammatoires et des antalgiques morphiniques, lorsque l’on compare, sur deux periodes de 28 jours, la prise medicamenteuse a visee antalgique chez les patients lorsqu’ils utilisent le TENS et lorsqu’ils ne prennent que leur traitement antalgique habituel. Le soulagement des douleurs chroniques chez les patients lorsqu’ils utilisent le TENS a egalement ete evalue. Outre la rapidite d’action du TENS au cours de l’application, la remanence de l’effet antalgique semble perdurer plusieurs heures apres l’application, ce qui a pu contribuer a l’epargne therapeutique et a l’attenuation de la gene fonctionnelle occasionnee par les douleurs chroniques au quotidien. Son efficacite, statistiquement et cliniquement significative, rapide et durable, sur le soulagement de la douleur, permettant de diminuer la prise d’antalgiques, son caractere non invasif et sa tolerance, ainsi que sa simplicite d’utilisation, font du dispositif d’electrotherapie rechargeable TENS, teste dans cette etude, une solution antalgique non pharmacologique susceptible d’etre associee ou de remplacer les traitements pharmacologiques dans la prise en charge des douleurs articulaires et musculosquelettiques chroniques.

SummaryAims Guidelines propose additional therapy to statin to treat elevated triglycerides (TG) and low high-density lipoprotein cholesterol (HDLC) in dyslipidemic patients. We evaluated the effects of new fixed-dose combinations (FDC) of fenofibrate/simvastatin on plasma lipids versus simvastatin or fenofibrate monotherapies. Methods Subjects with mixed dyslipidemia at high or very high cardiovascular risk on stable statin therapy for at least 3 months were included in a randomized, double-blind, active-control, parallel-group study. Patients were treated with FDC fenofibrate/simvastatin 145/20 mg or 145/40 mg, simvastatin 20 mg or 40 mg, or fenofibrate 145 mg for 12 weeks. Plasma lipids, C-reactive protein, and cystatin C were measured before and after treatments. Differences in % changes were compared between FDC fenofibrate/simvastatin and monotherapies. Results Significant differences between FDC fenofibrate/simvastatin and simvastatin monotherapies were observed for the % change of TG (LS mean difference [two-sided 95% CI]: −32.2% [−38.6%, −25.8%], P

Background— The Diabetes Atherosclerosis Intervention Study showed that treatment with fenofibrate decreases progression of coronary atherosclerosis in subjects with type 2 diabetes. We determined whether on-treatment plasma lipid concentrations and LDL particle size contribute to the favorable effect of fenofibrate on the progression of coronary artery disease (CAD). Methods and Results— A total of 418 subjects with type 2 diabetes were randomly assigned to 200 mg micronized fenofibrate daily or placebo. The mean follow-up time was 39.6 months. LDL peak particle diameter (LDL size) was determined by polyacrylamide gradient gel electrophoresis from 405 subjects at baseline and at the end of the study. Progression of CAD was measured with quantitative coronary angiography. LDL size increased significantly more in the fenofibrate group than in the placebo group (0.98±1.04 versus 0.32±0.92 nm, P r =−0.16, P =0.002) and decreases in minimum ( r =−0.11, P =0.030) and mean ( r =−0.10, P =0.045) lumen diameter. High on-treatment LDL cholesterol, apolipoprotein B, and triglyceride concentrations were also associated with the progression of CAD. In regression analyses, small LDL size added to the effect of LDL cholesterol and apolipoprotein B on the progression of CAD. Similar associations were observed in the fenofibrate group, whereas in the placebo group, lipoprotein variables were not significantly correlated with the progression of CAD. Conclusions— Changes in LDL size and plasma lipid levels account for part of the antiatherogenic effect of fenofibrate in type 2 diabetes.

The aim of the present study was to investigate the effect of saturated, monounsaturated and polyun-saturated non-esterified fatty acids (NEFA) on lipoprotein fluidity by using the electron spin resonance (ESR) method. The fluidity of the lipid phase of lipoproteins was evaluated by calculating from ESR spectra the S parameter of three different positional isomers of spin-labeled stearic acid incorporated into the lipoprotein. In non-enriched lipoproteins, S values were higher in high-density lipoprotein 3 (HDL3) than in low-density lipoprotein (LDL) indicating that the surface of HDL, was more ordered. Prior incubation of lipoprotein particles with NEFA significantly reduced S values, indicating an increased lipoprotein fluidity as compared with non-supplemented homologous samples. In NEFA-enriched lipoproteins, the modifications in fluidity were shown to be dependent on the structure of the NEFA acyl carbon chains. Medium-chain fatty acids [lauric (12:0) and myristic (14:0) acids] appeared to be better fluidizing molecules as compared with both. shorter [octanoic (8:O) and decanoic (10:0) acids] and longer [palmitic (16:0) and stearic (18:0)acids] homologues. In addition, introducing at least one double bond in the acyl carbon chain significantly increased the ability of NEFA to reduce S as compared with saturated homologues. In both LDL and HDL3, the extent of the modifications of the molecular mobility at the lipoprotein surface was dependent on the final NEFA/lipoprotein ratio. In conclusion, these results suggest that the ability of NEFA to modulate the activity of the cholesteryl ester transfer protein might relate in part to alterations in fluidity at the lipoprotein surface.