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Lopid (Gemfibrozil)

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Lopid is an effective medication which helps to fight with high levels of serum triglycerides. Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.

Other names for this medication:

Similar Products:
Pravachol, Mevacor, Zetia, Crestor


Also known as:  Gemfibrozil.


Lopid target is to fight against high levels of serum triglycerides.

Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.

Generic name of Lopid is Gemfibrozil.

Brand name of Lopid is Lopid.


Take Lopid tablets orally.

Take Lopid twice a day with water at the same time.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Lopid suddenly.


If you overdose Lopid and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lopid overdosage: arthralgia, muscle pain, vomiting, abdominal cramps, diarrhea, nausea.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Protect from light and humidity. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lopid are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lopid if you are allergic to Lopid components.

Do not take Lopid if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not use potassium supplements or salt substitutes.

Be careful with Lopid if you are taking cholesterol-lowering medications (statins) such as atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor); and repaglinide (Prandin), anticoagulants ('blood thinners') such as warfarin (Coumadin).

Be careful with Lopid if you suffer from or have a history of kidney, liver, gallbladder disease.

Do not stop taking Lopid suddenly.

lopid medication

Low heart rate (HR) variability is associated with increased risk of cardiovascular morbidity and mortality, but the causes and mechanisms of this association are not well known. This prospective study was designed to test the hypothesis that reduced HR variability is related to progression of coronary atherosclerosis. Average HR and HR variability were analyzed in 12-hour ambulatory ECG recordings from 265 qualified patients participating in a multicenter study to evaluate the angiographic progression of coronary artery disease in patients with prior coronary artery bypass surgery and low high-density lipoprotein cholesterol concentrations (<1.1 mmol/L). Participants were randomized to receive a placebo or gemfibrozil therapy. The progression of coronary atherosclerosis was estimated by quantitative, computer-assisted analysis of coronary artery stenoses from the baseline angiograms and from repeated angiograms performed an average of 32 months later. The progression of focal coronary atherosclerosis of the patients randomized to placebo therapy was more marked in the tertile with the lowest standard deviation of all normal to normal R-R intervals (SDNN, 74+/-13 ms; mean decrease in the per-patient minimum luminal diameter -0.17 mm; 95% confidence interval [CI], -0.23 to -0.12 mm) than in the middle tertile (SDNN, 107+/-7 ms; mean decrease -0.05 mm; 95% CI, -0.08 to -0.01 mm) or highest tertile (SDNN, 145+/-25 ms; mean change 0.01 mm; 95% CI, -0. 04 to 0.02 mm) (P<0.001 between the tertiles). This association was abolished by gemfibrozil. SDNN was lower (P<0.001) and minimum HR was faster (P<0.01) in the patients with marked progression than in those with regression of focal coronary atherosclerosis. In multiple regression analysis including HR variability, minimum HR, demographic and clinical variables, smoking, blood pressure, glucose, lipid measurements and lipid-modifying therapy, progression of focal coronary atherosclerosis was independently predicted by the SDNN (beta=0.24; P=0.0001). Low HR variability analyzed from ambulatory ECG predicts rapid progression of coronary artery disease. HR variability provided information on progression of focal coronary atherosclerosis beyond that obtained by traditional risk markers of atherosclerosis.

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The effects of gemfibrozil on plasma prekallikrein, kallikrein inhibitors, kininogen and plasma lipids were investigated in 31 male subjects having either type IIA or IIB dyslipidaemia. During gemfibrozil use, plasma prekallikrein and kininogen were increased significantly while kallikrein inhibitors increased only slightly. Total cholesterol and triglycerides decreased while HDL cholesterol was increased. Changes in prekallikrein and HDL cholesterol were correlated, whereas no other significant correlations between changes in lipid and kinin parameters were seen. The observed changes in prekallikrein and kininogen possibly indicate a shift in the thrombo-haemorrhagic balance in favour for increased fibrinolysis. If so, the effects of gemfibrozil in prevention and management of atherosclerosis would not be solely due to correlation of the dyslipidaemia but also to protection against the accelerated coagulation tendency seen in type II dyslipidaemia.

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Gemfibrozil was given as 600 mg tablets twice a day for 12 months to a group of middle-aged non-diabetic men with moderate HTG. Patients served as their own controls, because the treatment period was preceded by a single-blinded 2-month placebo phase. Gradient gel electrophoresis subfractionation of HDL was performed and glucose tolerance was defined according to World Health Organization criteria. The insulin sensitivity was assessed by the insulin-modified minimal model method. Plasma PAI-1 was assayed as activity.

lopid 500 mg

The aim of this study was to investigate the safety and efficacy of combined treatment with fluvastatin (F) and gemfibrozil (G) in hypercholesterolemic renal transplant recipients (RTR). Ten hypercholesterolemic (total cholesterol [TC] > 220 mg/dl) RTR (7 men) with mean age 44 years (range 25-56 years) who remained hypercholesterolemic after 3 months of treatment (period A) with fluvastatin (40 mg/d) continued taking the same dose of F plus G (600 mg/dl) for another 3-month period (B). Serum total cholesterol, high density lipoprotein cholesterol (HDL-C), LDL cholesterol (LDL-C), triglyceride, serum creatinine (creatinine phosphokinase (CPK), serum glutamic-oxaloacetic transaminase (SGOT), and serum glutamate pyruvate transaminase (SGPT) were measured before treatment and at the end of periods A and B. Mean TC levels were 360.30 +/- 62.42 mg/dl, 324.10 +/- 100.53 mg/dl, 270.80 +/- 67.77 mg/dl; mean LDL-C levels were 259.33 +/- 71.43 mg/dl, 219.60 +/- 81.31 mg/dl, 189.70 +/- 65.51 mg/dl; mean HDL-C levels were 37.10 +/- 11.68 mg/dl, 39.80 +/- 13.21 mg/dl, 41.00 +/- 12.94 mg/dl; mean triglyceride levels were 354.60 +/- 183.29 mg/dl, 349.30 +/- 242.94 mg/dl, 207.00 +/- 85.35 mg/dl before treatment and at the end of periods A and B, respectively. There was a statistically significant fall of serum TC (P = 0.002), LDL-C (P = 0.016), and triglyceride (P = 0.029) levels at the end of periods A and B. Kidney and liver function did not change. F and G combined treatment is safe and useful in patients who do not respond satisfactorily to monotherapy with F. Gemfibrozil augments the effect of F on TC, LDL-C, and triglyceride levels.

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We included three randomised trials with 170 participants. Ninety participants were randomised to the Chinese herbal medicines groups and 80 to the comparator groups with numbers ranging from 50 to 60 participants per trial. The duration of treatment varied from four to six weeks. All the included trials were conducted in China and published in Chinese. Overall, the risk of bias of included trials was unclear. There were no outcome data in any of the trials on death from any cause, cardiovascular or cerebrovascular events, health-related quality of life, or costs.Three different herbal medicines, including Zhusuan Huoxue decoction, Huoxue Huayu Tongluo decoction, and Chushi Huayu decoction were evaluated. All three trials investigating Chinese herbal medicines treatment alone (two studies) or in combination with gemfibrozil (one study) reported results on serum triglyceride (TG) in favour of the herbal treatment. We did not perform a meta-analysis due to significant clinical heterogeneity between the studies.No relevant differences in adverse effects occurred and no serious adverse events were noted.

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The three subtypes of peroxisome proliferator activated-receptors (PPARalpha, delta and gamma) control the storage and metabolism of fatty acids. Treatment of rats with the PPARalpha ligand ciprofibrate increases serum gastrin concentrations, and several lines of evidence suggest that non-amidated gastrins act as growth factors for the colonic mucosa. The aim of the present study was to investigate the expression of PPARs and the effect of PPAR ligands on gastrin production and cell proliferation in human colorectal carcinoma (CRC) cell lines. mRNAs for all three PPAR subtypes were detected by PCR in all CRC cell lines tested. The concentrations of progastrin, but not of glycine-extended or amidated gastrin, measured by radioimmunoassay in LIM 1899 conditioned media and cell extracts were significantly increased by treatment with the PPARalpha ligand clofibrate. Similar increases in progastrin were seen following treatment with the PPARalpha ligands ciprofibrate and fenofibrate, but not with bezafibrate, gemfibrozil or Wy 14643. The PPARgamma agonist rosiglitazone had no significant effect on progastrin production. The PPARalpha ligand clofibrate also stimulated proliferation of the LIM 1899 cell line. We conclude that some PPARalpha ligands increase progastrin production by the human CRC cell line LIM 1899, and that clofibrate increases proliferation of LIM 1899 cells. These studies have revealed a relationship between PPARs and gastrin, two regulatory molecules implicated in the pathogenesis of CRC.

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Fifty eight patients with primary dysli pidemia were recruited for a 12-week treatment. Forty two patients were allocated to be treated with statins (20 mg): 24 with simvastatin and 18 with pravastatin. Sixteen patients received gemfibrozil in a dose of 900 mg daily. Using enzyme, colorimetric, turbidimetric, immunoenzyme and chromogenic substrate methods, we studied the following laboratory parameters: 1) lipid parameters - total cholesterol, LDL and HDL cholesterol, triglycerides, apoli poprotein A-I, apoli poprotein B, anticardioli pin antibodies and lipid indices; 2) hemostasis, fibrinolysis and blood rheology parameters - platelet count, ADP-induced platelet aggregation, fibrinogen, platelet factor 4,antithrombin III activity, alpha2-anti plasmin concentrations, alpha2-macroglobulin, alpha1-antitripsin, plasma viscosity and hematocrit.

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In VA-HIT, a population with low HDL-C and LDL-C, high Lp-PLA(2) independently predicted CV events that were reduced by gemfibrozil.

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Aggressive treatment of atherosclerotic risk factors can substantially reduce stroke risk in patients with a history of stroke or transient ischemic attack. Data from several recent large clinical trials provide convincing evidence of benefit for a number of specific therapies directed at this population. The authors recommend treatment with ramipril alone or perindopril plus indapamide regardless of blood pressure, provided there is no contraindication. For patients already taking a different angiotensin- converting enzyme (ACE) inhibitor, the authors do not routinely switch agents. The authors recommend use of simvastatin 40 mg per day in patients with a total cholesterol level of 135 mg/dL or greater, provided no contraindication exists. The authors also recommend consideration of gemfibrozil in patients with isolated low high- density lipoprotein levels. In patients with diabetes mellitus, tight glycemic control has not been shown to reduce macrovascular complications such as stroke, but does reduce microvascular complications. However, diabetics should receive especially aggressive treatment of other vascular risk factors. There is no role for post-menopausal hormone replacement therapy in prevention of stroke. Weight loss for overweight patients, regular exercise, and a diet rich in fruits, vegetables, cereals, and fish, as well as low in fat and cholesterol, should be a standard recommendation for this group of patients. Treatment with folic acid, B(6), and B(12) for patients with elevated homocysteine appears rational, though this is unproven. However, there is no benefit to vitamin E, vitamin C, or beta-carotene supplementation. Smokers should stop. For every 43 smokers who quit, one stroke is prevented. Moderate consumption of alcohol (one to two drinks a day) may be beneficial, but heavy alcohol use (more than five drinks a day) increases stroke risk.

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Treatment with gemfibrozil modifies acyl composition of hepatic microsomal phosphatidylcholine and phosphatidylethanolamine in guinea-pigs. Palmitic (16:0) and palmitoleic (16:1) fatty acids are increased, and stearic (18:0) and oleic (18:1) are decreased; further, while linoleic acid [18:2 (n-6)] is increased by gemfibrozil treatment, the other constituents of the n-6 fatty acids family, including arachidonic acid [20:4 (n-6)], are decreased. As gemfibrozil is a potent inhibitor of fatty acid elongation in vitro (Sánchez et al., FEBS Lett 300: 89-92, 1992), the inhibition of this enzyme system by gemfibrozil treatment could be responsible for the observed results in vivo. These changes in fatty acid composition are accompanied by a decrease in serum lipids and, more important, are independent of peroxisomal proliferation.

lopid reviews

The evaluation of drug disposition properties of chemical entities in drug discovery research typically involves the conduct of pharmacokinetic studies in rodents that requires blood sampling over several time points, preferably without disrupting the physiological status of the animals. Several blood withdrawal methods have been employed throughout the industry, yet these methods have not been comprehensively evaluated with regard to their effects on pharmacokinetic profiles of the drug investigated to recommend best practices.

lopid capsules

In a university hospital setting, 48 patients with uncomplicated gallstones and a serum level of low-density lipoprotein cholesterol greater than 130 mg/dL were randomly assigned to open-label treatment with bezafibrate (400 mg/d), fenofibrate (200 mg/d), gemfibrozil (900 mg/d), or placebo for 8 weeks before elective cholecystectomy. Serum samples for lipid determinations were obtained at baseline and before surgery. A liver specimen was obtained at operation, and the relative levels of messenger ribonucleic acid (mRNA) for the wild and truncated forms of PPAR(alpha), acyl coenzyme A oxidase, liver carnitine palmitoyltransferase I, apolipoprotein A-I, and stearoyl coenzyme A desaturase were determined.

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The study was conducted using an open, randomized, two-period crossover design with a 1-week washout interval. Plasma samples were obtained over a 24-h period. Plasma gemfibrozil concentrations were analyzed by liquid chromatography coupled to tandem mass spectrometry (LC-MS-MS) with negative ion electrospray ionization using multiple reaction monitoring (MRM). From the gemfibrozil plasma concentration vs time curves, the following pharmacokinetic parameters were obtained: AUClast, AUC(0-inf) and Cmax.

lopid renal dosing

Bexarotene (Targretin oral capsules), the first RXR-selective retinoid "rexinoid" approved for all stages of cutaneous T-cell lymphoma (CTCL), had a response rate (RR) of 45% at the optimal dose of 300 mg/m(2) per day in 2 multicenter trials. With hypertriglyceridemia reported at 79%, bexarotene is often administered with lipid-lowering agents (LLAs). Statins (inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase) may modulate class II major histocompatibility class expression and T-cell responses.

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Hypertriglyceridaemia is a well known risk factor for acute pancreatitis. Hypertriglyceridaemia may be primary in origin or secondary to alcohol abuse, diabetes mellitus, pregnancy or use of drugs. In this case report, the cause of acute pancreatitis was tamoxifen. We report on a patient with tamoxifen-induced acute pancreatitis and hypertriglyceridaemia who was successfully treated with insulin infusion and long-term gemfibrozil.

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Combination therapy with simvastatin and gemfibrozil often did not meet ATP III standards. A higher risk of serious adverse events results from combining these drugs, and systems to improve adherence to guidelines may improve the safety of treating dyslipidemic patients.

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Gemfibrozil therapy retarded the progression of coronary atherosclerosis and the formation of bypass-graft lesions after coronary bypass surgery in men with low HDL cholesterol as their main lipid abnormality.

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The liver plays an important role in the disposition of acyl glucuronides by determining their extent of formation, biliary excretion, and efflux into blood. Thus, both intrahepatic and extrahepatic exposure to these reactive polar conjugates depends on the efficiency of hepatic transport mechanisms, which may be shared with other nonbile acid organic anions. Using the isolated perfused rat liver preparation, the hepatic disposition of the acyl glucuronide, 1-O-gemfibrozil-beta-D-glucuronide, was examined in the presence of the organic anion dibromosulfophthalein (DBSP). Using a recirculating system, livers were perfused for 90 min with an erythrocyte-free perfusion medium containing 1% (w/v) albumin and 1-O-gemfibrozil-beta-D-glucuronide (3 microM) alone (n = 6) or with DBSP (200 microM, n = 7). The glucuronide was avidly taken up by the liver, excreted into bile, and hydrolyzed within the liver to its aglycone, gemfibrozil. DBSP significantly (P <.05) lowered the conjugate's mean hepatic clearance (8.98-5.17 ml/min), intrinsic clearance (44.0-17.7 ml/min), and fraction eliminated in bile (72. 8-48.7% of the dose), while increasing perfusate gemfibrozil concentrations (0.52-0.92 microM at 90 min). Furthermore, DBSP significantly (P <.05) lowered the ratio of intrahepatic to unbound perfusate concentrations of 1-O-gemfibrozil-beta-D-glucuronide (139. 0-35.0) and showed a trend to lower the ratio of bile to intrahepatic concentrations (111.3-76.2, P =.05). Thus, the study demonstrated that DBSP inhibited both the sinusoidal uptake and canalicular transport of 1-O-gemfibrozil-beta-D-glucuronide, suggesting that the hepatic membrane transport of acyl glucuronides is carrier mediated and shared with other organic anions.

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In patients with advanced CKD, atorvastatin is associated with improvement in dyslipidemia and small-artery stiffness, but not endothelial function. Gemfibrozil improves dyslipidemia, but has no effect on arterial function.

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The dyslipidaemia of chronic renal disease could contribute to a hypercoagulable state by activation of blood coagulation and/or impairment of fibrinolysis, thereby increasing cardiovascular disease (CVD) risk.

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Induction with HFD for 10 weeks caused significant (p < 0.05) increase in % body wt, BMI, LEE indices; serum glucose, triglyceride, LDL, VLDL, cholesterol, free fatty acid, ALT, AST; tissue TBARS, nitrate/nitrite levels; different fat pads and relative liver weight; and significant decrease in food intake (g and kcal), serum HDL and tissue glutathione levels in HFD control rats. Treatment with B. ceiba extract and Gemfibrozil significantly attenuated these HFD induced changes, as compared to HFD control. The effect of B. ceiba 200 and 400 mg/kg was more pronounced in comparison to Gemfibrozil.

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Male Sprague Dawley rats were fed a purified 10 kcal% from fat diet for 56 days and assigned to diet alone (control) or diet plus oral administration of gemfibrozil (34 mg/kg), metformin (500 mg/kg), rosiglitazone (3 mg/kg), taurine (520 mg/kg), or vitamin E (200 mg/kg).

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Our purpose was to investigate whether gemfibrozil would lower triglycerides and raise HDL-C with minimal adverse effects in a pediatric population with metabolic syndrome.

lopid with alcohol

We obtained data on incident melanomas from 20 of 36 qualifying randomized controlled trials (12 statin trials and eight fibrate trials), with a total of 70,820 participants. A total of 127 melanomas occurred among the 39,426 participants in the statin trials (59 among the 19,872 statin group participants and 68 among the 19,554 control group participants). A total of 27 melanomas occurred among the 31,394 participants enrolled in the fibrate trials (seven among the 12,324 fibrate group participants and 20 among the 19,070 control group participants). Overall, incidence of melanoma was not statistically significantly associated with the use of either statins (OR = 0.87, 95% CI = 0.61 to 1.23) or fibrates (OR = 0.45, 95% CI = 0.20 to 1.01). In a subgroup analysis by drug, only lovastatin use (in one trial) was statistically significantly associated with lower incidence of melanoma (OR = 0.52, 95% CI = 0.27 to 0.99).

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The average retention times of gemfibrozil and tashinone II(A) were 10.5 and 14.5 min, respectively. The half-life was prolonged from 2. 573 h of free tashinone II(A) to 4. 117 h and MRT(0-infinity) from 2.585 h to 6.033 h. The max concentration of tashinone II(A) was reduced from 0.21 to 0.134 mg/L.

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In a randomized crossover study, 11 healthy subjects ingested gemfibrozil 600 mg, itraconazole 100 mg (first dose 200 mg) or both, or placebo twice daily for 5 days, and on day 3, 10 mg montelukast. Plasma concentrations of montelukast, gemfibrozil, itraconazole and their metabolites were measured up to 72 h.

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In the approach to lipid-related risk factors for cardiovascular diseases, serum high density lipoprotein-cholesterol (HDL-C) levels bear a particular significance as this lipoprotein is considered to be an antiatherogenic factor mainly, but not only, because of its influence and impact on reverse cholesterol transport. Hence the need and requirement to consider serum HDL-C levels for both primary and secondary prevention of cardiovascular disease. A particularly important aspect is the association of the 'low HDL syndrome' with the metabolic syndrome. These factors force us to consider serum HDL-C level as a therapeutic target by itself, or even in association with low density lipoprotein-cholesterol (LDL-C) levels when the latter are increased. This review stresses the aspects connecting serum HDL-C levels and cardiovascular risk, and looks at the populations that should be considered amenable to therapeutic management because of low serum HDL-C levels. We review therapeutic strategies, both pharmacological and nonpharmacological. The aim of this review is to present therapeutic management recommendations for correcting the proportion of cardiovascular risk that is attributable to changes in HDL-C. Serum HDL-C levels of >40 mg/dL must be a therapeutic target in primary and secondary prevention. This goal is particularly important in patients with low serum HDL-C levels and ischemic heart disease (IHD) or its equivalents, even if the therapeutic target for serum LDL-C levels (<100 mg/dL) has been achieved. The first choice for this clinical condition is fibric acid derivates. The same therapeutic option should be considered in patients without IHD with low serum HDL-C levels and high cardiovascular risk (>20%), hypertriglyceridemia, type 2 diabetes mellitus, or metabolic syndrome.

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Compared with placebo, atorvastatin significantly decreased low-density lipoprotein (-52%), triglyceride (-30%), and oxidized low-density lipoprotein levels (-41%; P < 0.0001). Gemfibrozil significantly decreased triglyceride levels (-40%) and increased high-density lipoprotein levels (+20%; P < 0.0001). Neither atorvastatin nor gemfibrozil had a significant effect on markers of insulin resistance or inflammation. There was no significant change in FMD, GTNMD, or C1 with either atorvastatin or gemfibrozil. There was improvement in C2 with atorvastatin (+1.1 mL/mm Hg x 100) compared with placebo (P = 0.024), but not with gemfibrozil compared with placebo.

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Bezafibrate belongs to the class of fibric acid derivatives usually used as antihyperlipidemia agents. From the biochemical point of view, these drugs show intriguing properties which leads one to think they may promote a differentiation process in tumour cells. This new pharmacological activity of fibrates could partially depend on the induction of an oxidative stress. To test this hypothesis, the effect of bezafibrate, as well as of clofibric acid and gemfibrozil, on growth, functional and cytochemical characteristics of human leukaemia-derived cell lines HL-60, U-937 and K-562 has been studied in some details. The results show that bezafibrate, gemfibrozil and clofibric acid, do induce differentiation in human myeloid leukaemia cell lines as indicated by several differentiation markers. Moreover fibrates, in dose dependent manner, significantly alter the cell cycle distributions, mainly leading to G0/G1 phase increment and G2/M phase reduction. The differentiating activity of fibrates could have significant implications both for the pharmacotoxicological profile of this class of compounds and for the pathophysiology of neoplastic disease.

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Previously, we demonstrated that when two human hepatoma cell lines, Hep3B and HepG2, were exposed to gemfibrozil, a hypolipidemic drug, a 2-fold induction in apolipoprotein A-I (apoA-I) mRNA levels resulted. To determine if mRNA stabilization was responsible for the changes in apoA-I mRNA levels, the half-lives for apoA-I mRNA were measured in the presence of actinomycin D with and without gemfibrozil. These experiments revealed no differences in stability. However, nuclear run-off assays indicated that the transcription rate of the apoA-I gene was increased 2-fold in gemfibrozil-treated cells. Transient transfection experiments also indicated that the induction of apoA-I mRNA level in response to gemfibrozil is mediated at the transcriptional level. We have identified two copies of the "drug-responsive element" (DRE) in the apoA-I promoter region that may be responsible for the increase in apoA-I transcriptional activity by gemfibrozil. Using gel mobility shift assays with a synthetic DRE oligonucleotide, we have demonstrated that exposure of Hep3B and HepG2 cells to gemfibrozil resulted in strong induction of a protein-DNA complex. The formation of this complex is highly sequence-specific as indicated by the DNA competition experiments. The drug-inducible nuclear proteins bind to the DRE of the human apoA-I gene with an apparent Kd of 4.1 nM. Methylation interference experiments have localized the contact sites of nuclear factors to the DRE region. Southwestern blot analyses have identified two groups of drug-inducible nuclear proteins with molecular masses of approximately 30 and 15 kDa. When a copy of synthetic DRE oligonucleotide was inserted upstream of the thymidine kinase promoter and luciferase reporter construct, a significant 2-fold induction in luciferase activity was observed in the presence of gemfibrozil following transient transfection of two human hepatoma cell lines, HepG2 and Hep3B. However, a plasmid containing one copy of mutated apoA-I-DRE oligomer did not confer responsiveness to gemfibrozil treatment. Furthermore, pGL2 (apoA-I -250 mutant DRE), which carried an internal mutation of the DRE in the human apoA-I proximal promoter region, showed no increase in luciferase activity in response to gemfibrozil. These results implicate protein-DNA interactions at the DRE region in the transcriptional induction of human apoA-I gene expression by gemfibrozil.

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lopid overdose symptoms 2017-08-04

We report four cases of rhabdomyolysis and severe, disabling myopathy associated with HMG CoA reductase-inhibitor therapy. Patient developed symptoms following the addition of roxithromycin to combination lipid-lowering therapy with simvastatin and gemfibrozil. Patients 2 and 3 buy lopid online became symptomatic after developing acute on chronic renal impairment while taking simvastatin. The muscle biopsy of patient 3 revealed a necrotizing myopathy and the presence of inclusion bodies. Patient 4 developed symptoms within 4 weeks of starting cerivastatin monotherapy. The four cases illustrate the importance of considering the potential for drug interactions and making appropriate dosage adjustments for renal insufficiency in patients receiving HMG CoA reductase therapy.

lopid drug classification 2016-01-25

Cohort characteristics included age 63 ± 7 years, 92% men, 43% with previous myocardial infarction, systolic blood pressure 139 ± 17 mm Hg, triglycerides 168 ± 81 mg/dL and buy lopid online high-density lipoprotein cholesterol 34 ± 6 mg/dL. The mean number of metabolic syndrome components decreased from 2.2 ± 0.9 to 1.5 ± 1.1, P < 0.001, and metabolic syndrome prevalence decreased from 38% to 18% (P < 0.001) for the entire cohort. In the lifestyle intervention and placebo group, the mean number of metabolic syndrome components decreased from 2.2 ± 0.9 to 1.9 ± 1.1 (P = 0.01), and prevalence of metabolic syndrome decreased from 44% to 30% (P = 0.15). A far more marked change was observed with lifestyle intervention and pharmacologic therapy: abnormal metabolic components decreased from 2.2 ± 0.9 to 1.0 ± 1.0 (P < 0.001), and prevalence of metabolic syndrome decreased from 32% to 6% (P < 0.001).

lopid maximum dose 2015-07-14

Oxidation of low-density lipoprotein is believed to be an important step in the pathogenesis of buy lopid online atherosclerosis. The purpose of the present study was to determine whether antibody against oxidized low-density lipoprotein, reported to be associated with the progression of carotid atherosclerosis, is predictive of cardiac death and nonfatal myocardial infarction.

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This review will concentrate on more recent evidence on the prevention of coronary heart disease and hypertension. With the evidence from lipid-lowering regimes using cholestyramine or gemfibrozil, it is clear that cardiovascular mortality can be reduced by relatively short interventions (years rather than decades). This is surprising in a disease with a long incubation period. We are also on the threshold of much more powerful intervention with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors. Follow-up of the very large number of subjects screened for the Multiple Risk Factor Intervention Trial study showed that the relation between serum cholesterol and risk is linear, with no hint of a "safe" level or threshold. This is borne out with the data from rural Chinese, who show the same trend, albeit at levels of risk that are 4% of those of Western populations. The suggestion that low cholesterol levels increase cancer risk appears to result from an artifact. The best dietary interventions for cholesterol lowering are still unresolved, with recent interest in fish oil and olive oil. On the background of raised cholesterol (most Western levels could be regarded as biologically abnormal), cigarette smoking assumes very great importance. Recent evidence from the U.S. Nurses survey points out a two- or threefold increase in risk from as few as four cigarettes per day. With other risk factors the relative risk increases buy lopid online 20-fold. These data are particularly important given that young girls in the United Kingdom and United States currently smoke more than boys.(ABSTRACT TRUNCATED AT 250 WORDS)

lopid 450 mg 2015-05-30

To study changes of HDL buy lopid online subfractions and their regulation during gemfibrozil treatment in hypertriglyceridaemia.

lopid generic equivalent 2015-02-10

The effect of the L162V polymorphism at the PPARA locus buy lopid online on CV risk depends on the presence of DM/IR. Among subjects treated with gemfibrozil, the V162 allele was associated not only with reduced CV risk in subjects with DM/IR, but also with significantly increased CV risk in the absence of these traits, identifying this genetic variant as a potential marker for predicting which subjects may have a favorable response to fibrate therapy.

lopid 200 mg 2015-12-30

We used the VA computerized clinical database and modified Adult Treatment Panel III (ATP III) criteria of fasting blood glucose (FBG) >or=110 mg/dL, blood pressure >or=130/>or=85, triglyceride >or=150 mg/dL, high-density lipoprotein cholesterol (HDL-C) <40 mg/dL (men) or <50 mg/dL (women), but body mass index (BMI) >or=30 in lieu of waist circumference >102 cm (40 inches) for men and 88 cm (35 inches) for women. We also accepted current pharmacotherapy for diabetes as buy lopid online qualifying for elevated fasting blood sugar (FBS); current therapy with niacin, gemfibrozil, or fenofibrate for elevated triglyceride concentrations; and recent use of multiple International Classification of Diseases, 9(th) Revision (ICD-9) codes for hypertension for elevated blood pressure.

lopid dosage instructions 2015-12-26

A large-scale toxicogenomcis database has now been constructed in the Toxicogenomics Project in Japan (TGP). To facilitate the analytical procedures for such large-scale microarray data, we developed a simple one-dimensional score, named TGP1 which expresses the trend of the changes in expression of biomarker genes as a whole. To evaluate the usefulness of the TGP1 score, microarray data of rat liver and rat hepatocytes deposited in the TGP database were scored for three biomarker gene sets, i.e., carcinogenesis-related, PPARalpha-regulated and glutathione depletion-related gene sets. The TGP1 scoring system gave reasonable results, i.e., the scores for carcinogenesis-related genes were high in omeprazole-, chlorpromazine-, hexachlorobenzene-, sulfasalazine- and Wy-14,643-treated rat livers, that for PPARalpha-regulated genes were high in clofibrate-, Wy-14,643-, gemfibrozil-, benzbromarone- and aspirin-treated rat livers as well as rat hepatocytes, and for glutathione deficiency-related genes were high in omeprazole-, bromobenzene-, acetaminophen- and coumarin-treated rat liver. We concluded that the TGP1 score is useful for surveying the expression changes in multiple biomarker gene sets for a large-scale toxicogenomics database, which would reduce the buy lopid online time of doing conventional multivariate statistical analysis. In addition, the TGP1 score can be applied to screening of compatible biomarker gene sets between rat liver and rat hepatocytes, like PPARalpha-regulated gene sets, which will allow us to develop an appropriate in vitro system for drug safety assessment in vivo.

lopid initial dose 2017-07-11

Combined hyperlipidemia results from overproduction of hepatically synthesized apolipoprotein B in very low-density lipoproteins in association with reduced lipoprotein lipase activity. Thus, this condition is typically characterized by concurrent elevations in total cholesterol and triglycerides with decreased high-density lipoprotein cholesterol. High levels of apolipoprotein B-containing lipoproteins, most prominently carried by low-density lipoprotein (LDL) particles, are an important risk factor for coronary heart disease. Statin therapy is highly effective at lowering LDL cholesterol. Despite the benefits of statin treatment for lowering total and LDL cholesterol, many statin-treated patients still have initial or recurrent coronary heart disease events. In this regard, combined therapy with statins and fibrates is more effective in controlling atherogenic dyslipidemia in patients with combined hyperlipidemia than either drug alone. Furthermore, statins and fibrates activate PPARalpha in a synergistic manner providing a molecular rationale for combination treatment in coronary heart disease. Endothelial dysfunction associated with cardiovascular diseases may contribute to insulin resistance so that there may also be additional beneficial metabolic effects of combined statin/fibrates therapy. However, there has been little published evidence that combined therapy is synergistic or even better than monotherapy alone in clinical studies. Therefore, there is a great need to study the effects of combination therapy in patients. When statins are combined with gemfibrozil therapy, this is more likely to be accompanied by myopathy. However, this limitation is not observed when fenofibrate, bezafibrate, or ciprofibrate are used in combination therapy. buy lopid online

lopid capsules 2015-11-17

The literature for the last seven years was reviewed in terms of the effect of the various fibric acid derivatives on blood lipid and lipoprotein levels. The criteria for review resulted in a greater focus on three of the newer fibric acid derivatives: bezafibrate, ciprofibrate, fenofibrate. In type II A hyperlipoproteinemia, all fibric acid derivatives produce modest reductions in total plasma cholesterol and low-density lipoprotein cholesterol. The evidence suggests that bezafibrate, ciprofibrate, and fenofibrate may produce greater reductions in low-density lipoprotein cholesterol than those usually observed with clofibrate and gemfibrozil. All fibric acid derivatives produce modest reductions in triglycerides and modest increases in high-density buy lopid online lipoprotein cholesterol in type II A hyperlipoproteinemia. In type II B hyperlipoproteinemia, the low-density lipoprotein cholesterol lowering effect of fibric acid derivatives is generally less than that observed in type II A hyperlipoproteinemia. In type II B hyperlipoproteinemia, there is a mean decrease in low-density lipoprotein cholesterol for all patients studied. However, there is a considerable interpatient variation ranging from significant decreases to significant increases in low-density lipoprotein cholesterol. Further studies are required to assess whether the low-density lipoprotein cholesterol lowering effect is greater with the newer fibric acid derivatives. All fibric acid derivatives produce clinically significant decreases in triglyceride levels in type II B. There is also an associated increase in high-density lipoprotein cholesterol. In type IV hyperlipoproteinemia, all fibric acid derivatives produce clinically significant reductions in triglyceride. There is also an associated increase in high-density lipoprotein cholesterol and generally also an increase in low-density lipoprotein cholesterol levels. The available data do not suggest a clinically significant difference in the hypotriglyceridemic effect of the various fibric acid derivatives in type IV hyperlipoproteinemia. The lipid-altering effects of the various fibric acid derivatives were usually less in those studies that contained placebo and dietary controls. Additional controlled clinical trials are needed to accurately discriminate the relative lipid-and lipoprotein-altering effects of the various fibric acid derivatives.

lopid dosage administration 2017-02-18

We report a case of pedal tuberoeruptive xanthomatosis associated with ethanol-induced type Vhyperlipoproteinemia that was controlled with diet, withdrawal from ethanol use, and the buy lopid online fibric acid derivative gemfibrozil.

lopid medication dosage 2017-06-13

We have investigated the role of steroid hormones as coronary risk factors in the Helsinki Heart Study population of dyslipidemic middle-aged men. We compare here the effects of gemfibrozil and placebo on the serum levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), their metabolite androstanediol glucuronide (3 alpha-AdiolG), androstenedione, cortisol, testosterone, and sex-hormone binding globulin (SHBG) in non-smokers. We also examined the associations between steroid and lipoprotein levels in both treatment groups. Compared with placebo gemfibrozil treatment was associated with significant elevations of the mean levels of DHEA 10.2 vs 8.0 nmol/l; P < 0.005, of DHEAS 8.0 vs 5.8 mumol/l; P < 0.001, of 3 buy lopid online alpha AdiolG 18.3 vs 8.4 nmol/l; P < 0.001, of androstenedione 5.7 vs 5.1 nmol/l; P < 0.02, and of cortisol 426 vs 358 nmol/l; P < 0.001. The mean SHBG levels decreased from 46.4 to 41.7 nmol/l; P = 0.03 with gemfibrozil treatment. No difference was found in testosterone levels 17.7 vs 18.8 nmol/l; P = 0.11, or the ratio of testosterone/SHBG 0.45 vs 0.43; P = 0.23. Positive correlations were found between high density lipoprotein-cholesterol and DHEAS (r = 0.267; P < 0.01) and DHEA (r = 0.282; P < 0.01) levels and negative correlations between low density lipoprotein-cholesterol and 3 alpha-AdiolG (r = -0.400; P < 0.001) and cortisol (r = -0.281; P < 0.01) levels in the gemfibrozil group. Our results indicate that gemfibrozil treatment increases the production and turnover of adrenal androgens and cortisol, and suggest that activation of the adrenocortical function and increased metabolism of androgens are related to the improved lipoprotein pattern during gemfibrozil treatment.

lopid dosage 2016-09-22

A sewage lagoon serving the small municipality of Lakefield in Ontario, Canada was monitored in the summer, fall and winter to determine removals of carbamazepine, trimethoprim, sulfamethoxazole, ibuprofen, gemfibrozil, triclosan, sucralose, HHCB and AHTN. Concentrations of these compounds in untreated and treated wastewater were estimated by deploying POCIS and SPMD passive samplers in the sewage lagoon. Passive samplers were also deployed at several points upstream and downstream of the point of discharge from the lagoon into the Otonabee River. LC-MS/MS and GC buy lopid online -MS were utilized to determine the concentrations of pharmaceuticals and personal care products (PPCPs) and sucralose, an artificial sweetener. Among PPCPs sampled by POCIS, the highest estimated concentration in untreated wastewater was ibuprofen sampled during the fall, at an estimated concentration of 60.3 ng/L. The estimated average concentration of sucralose was 13.6 ng/L in the untreated wastewaters. Triclosan, HHCB and AHTN in SPMDs were highest during fall season, at 30, 1677 and 109 ng/L, respectively. For all compounds except gemfibrozil, carbamazepine and sucralose, removals were highest in the summer (83.0 to 98.8%) relative to removals in the fall (48.4 to 91.4%) and winter (14.0 to 78.3%). Finally, the estimated concentrations of carbamazepine, sulfamethoxazole, triclosan and HHCB were compared with predicted values obtained through application of the WEST® modeling tool, with a new model based on the River Water Quality Model No. 1 and extended with dynamic mass balances describing the fate of chemicals of emerging concern subject to a variety of removal pathways. The model was able to adequately predict the fate of these four compounds in the lagoon in summer and winter, but the model overestimated removals of three of the four test compounds in the fall sampling period. This lagoon was as effective at removing PPCPs as many conventional WWTPs, but removals were better during the summer.

lopid 25 mg 2016-10-25

Two-step stacking of organic anions by sweeping and micelle to solvent stacking (MSS) using cationic cetyltrimethylammonium micelles in co-electroosmotic flow (co-EOF) capillary zone electrophoresis (CZE) is described. The co-EOF condition where the direction of the EOF is the same as the test anions was satisfied by positive dynamic coating of a fused silica capillary with hexadimethrine bromide. The strategy was as follows. After conditioning the capillary with the background solution (BGS), a micellar solution (MS) was injected before the sample solution (S). The BGS, MS and S have similar conductivities. Voltage was applied at negative polarity. The analytes in the micelle-free S zone were swept by micelles from the MS. The swept analytes were brought by the micelles to the MSS boundary where the second stacking step was induced by the presence of organic solvent in the BGS. Finally was the separation of concentrated analytes by CZE. The effect of electrolyte concentration in the S, injection time of the MS and the S and surfactant concentration in the MS were studied. A 20-29, 17-33 and 18-21 times increase in peak height sensitivity was obtained for the test hypolipidaemic drugs (gemfibrozil, fluvastatin and atorvastatin), non-steroidal anti-inflammatory drugs (diflunisal, naproxen, ketoprofen, indoprofen and indomethacin), and herbicides (mecoprop and fenoprop), respectively. The LODs (S/N=3) were from 0.05 to 0.55 μg/mL. The intraday and interday repeatabilities (%RSD Lexapro Suggested Dosage , n=12) in terms of retention time, corrected peak area, and peak heights was less than 3.6, 8.9, and 10.8%, respectively. The application of sweeping and MSS in co-EOF CZE together with a simple extraction procedure to a waste water sample spiked with the test herbicides was also demonstrated.

lopid 60 mg 2016-09-18

A non smoking male patient 42 years old complained of pain in the calves after exercise and Diamox Sequels Generic had a low 'high density'-lipoprotein (HDL) cholesterol serum concentration. Angiography of the leg vessels revealed no abnormalities. Treatment with simvastatin and gemfibrozil did not affect HDL cholesterol concentrations. Blood tests of relatives made familial hypo-alpha-lipoproteinaemia unlikely. It appeared that the patient had used anabolic steroids; these increase hepatic lipase activity leading to a higher metabolism of HDL and reduced HDL cholesterol levels.

lopid drug information 2017-01-28

The consistent positive correlation between triglyceride and plasminogen activator inhibitor-1 (PAI-1) levels in plasma and the fact that very low density lipoprotein (VLDL) induces secretion of PAI-1 from cultured human umbilical vein endothelial cells (HUVECs) and human hepatoblastoma cells have raised the question of whether fibrate treatment, the main effect of which is a profound lowering of plasma concentrations of VLDL, might improve fibrinolytic function by reducing the plasma levels of PAI-1. However, the findings of controlled clinical trials using various fibrate compounds have been discrepant. ECs express PAI-1 under normal conditions in humans. We therefore examined the effects of several fibrate compounds on PAI-1 expression and secretion by cultured HUVECs and the HUVEC-derived cell line EA.hy926. All fibrate compounds examined had significant effects on PAI-1 gene transcription in the EA.hy926 cells. Low concentrations of clofibric acid and bezafibrate increased PAI-1 transcription and secretion, whereas Wy-14643 increased PAI-1 synthesis in a dose-dependent way. In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells. Thus, stimulation of the transcriptional activity of the PAI-1 gene by some fibrates is linked to increased secretion of PAI-1 protein by the cells, whereas the opposite effects occur with other fibrate compounds. Vasotec 50 Mg Whether the different effects on PAI-1 transcription and secretion by ECs in vitro also reflect differences in treatment effects on the regulation of plasma PAI-1 activity in vivo will have to be determined in larger-scale, controlled clinical trials.

lopid 80 mg 2015-03-29

A randomized, double-blind 12 week study to compare lovastatin (20-80 mg/day) and gemfibrozil (600 mg b.i.d.) was performed in 59 patients with primary hypercholesterolemia. Resincholestyramine was started on week 12, at a dose of 8-16 g/day Protonix Capsule for the next 12 weeks in any patient whose LDL-cholesterol exceeded 165 mg/dl at week 12.

lopid starting dose 2017-07-23

Treatment with pravastatin reduced the combined risk of fatal and nonfatal myocardial infarction by 31%. Cardiovascular death overall fell by 32% and the need for coronary revascularisation procedures was reduced by 37%. All of these endpoint benefits were statistically significant. Because there was no increase in non-cardiovascular mortality, the reduction in death from any cause also proved to be statistically significant (p = 0.051 by log rank test and p = 0.037 Amalaki Capsules after adjustment for baseline risk factors).

lopid 600 dosage 2015-09-13

This is a case report that describes a 67-year-old woman with mixed hyperlipidemia and diabetic nephropathy. She was initially prescribed a combination of simvastatin plus gemfibrozil by her general practitioner (GP). When referred to our cardiovascular unit, we further diagnosed the patient to have mixed hyperlipidemia and rhabdomyolysis. Because of concerns with her chronic kidney disease (CKD), we temporarily stopped all her drug treatments and started insulin treatment for her type 2 diabetes (T2D). A month later when her T2D was stabilised, we prescribed atorvastatin and an omega-3 fatty acid ethyl ester supplement to treat her hypertriglyceridemia. Within two months her blood lipids were within the recommended range. In patients with stage 3-5 CKD, it is not advisable to prescribe the fibrate gemfibrozil, particularly in combination with a statin that is metabolised predominantly in the kidneys. To minimise adverse events without compromise Seroquel Therapeutic Dose on efficacy, we used a combination of omega-3 fatty acid ethyl esters, which are not metabolised in the kidneys, with a statin that is minimally metabolised in the kidneys for the treatment of her hyperlipidemia.

lopid tab 600mg 2017-05-26

In response to the 1-year intervention program, men showed significant reductions in body weight, BMI, waist circumference, and in the partial volume of visceral and abdominal subcutaneous AT measured from two abdominal computed tomography scans performed at lumbar vertebra (L)2 to L3 and L4 to L5 levels. No change Crestor Reviews in waist-to-hip ratio was observed. Changes in visceral AT were strongly correlated with changes in body weight, BMI, and waist circumference (0.83 < r < 0.85; p < 0.001). However, a weak association was noted between waist-to-hip ratio and changes in visceral AT (r = 0.40; p < 0.05). There was no change in slopes or in intercepts before and after treatment in the relationships between volume or area of abdominal AT and anthropometric markers.

lopid reviews 2017-07-23

Our goal was to further define the role of LPL gene polymorphisms in coronary heart disease (CHD) risk. We determined the frequencies of three LPL polymorphisms (D9N, N291S, and S447X) in 899 men Paxil 10 Mg from the Veterans Affairs HDL Intervention Trial (VA-HIT), a study that examined the potential benefits of increasing HDL with gemfibrozil in men with established CHD and low high density lipoprotein cholesterol (HDL-C; < or =40 mg/dl), and compared them with those of men without CHD from the Framingham Offspring Study (FOS). In VA-HIT, genotype frequencies for LPL D9N, N291S, and S447X were 5.3, 4.5, and 13.0%, respectively. These values differed from those for men in FOS having an HDL-C of >40, who had corresponding values of 3.2% (P = 0.06), 1.5% (P < 0.01), and 18.2% (P < 0.01). On gemfibrozil, carriers of the LPL N9 allele in VA-HIT had lower levels of large LDL (-32%; P < 0.01) but higher levels of small, dense LDL (+59%; P < 0.003) than did noncarriers. Consequently, mean LDL particle diameter was smaller in LPL N9 carriers than in noncarriers (20.14 +/- 0.87 vs. 20.63 +/- 0.80 nm; P < 0.003). In men with low HDL-C and CHD: 1) the LPL N9 and S291 alleles are more frequent than in CHD-free men with normal HDL-C, whereas the X447 allele is less frequent, and 2) the LPL N9 allele is associated with the LDL subclass response to gemfibrozil.

lopid renal dosing 2017-03-03

Following a 6-week washout, 32 patients with dysbetalipoproteinemia received rosuvastatin 10 mg, rosuvastatin 20 mg, and pravastatin 40 mg, each for 6 weeks in a randomized, double-blind, three-way crossover design. Patients subsequently entered an 18-week open-label phase in which the rosuvastatin dosage could be increased from 20 mg to a maximum of 40 mg at 6 weekly intervals to reach National Cholesterol Education Program goals for non-high-density lipoprotein cholesterol (non-HDL-C) and optimal triglyceride (TG). Fibrates (except gemfibrozil) could be added if patients were not at goal on rosuvastatin 40 mg. The primary efficacy variable was percent change from baseline in non-HDL-C during the double-blind phase. The prespecified efficacy criterion Vasotec 5 Mg was for the 95% confidence interval (CI) of non-HDL-C to lie entirely below -25% for any rosuvastatin dose.

lopid generic price 2017-04-11

Disruption of the murine mdr2 gene leads to the complete absence of biliary phospholipids. We tested the hypothesis that the increase in biliary phospholipid output induced by fibrates is mediated via induction of the hepatic Lexapro Generic Reviews mdr2 gene and its encoded product, the P-glucoprotein canalicular flippase. Increased levels of mdr2 mRNA were observed in the liver of mice treated with different fibrates: ciprofibrate, 660+/-155% (as compared with control group); clofibrate, 611+/-77%; bezafibrate, 410+/-47%; fenofibrate, 310+/-52%; gemfibrozil, 190+/-25% (P <0.05 compared with control group). Induction of expression of the mdr gene family was specific to the mdr2 gene. Two- to three-fold increases in P-glycoprotein immunodetection were evident on the canalicular plasma-membrane domain of clofibrate- and ciprofibrate-treated mice. Biliary phospholipid output increased from 4.2+/-1.2 nmol/min per g of liver in the control group to 8.5+/-0.6, 7.1+/-2.9 and 5.8+/-2.5 in ciprofibrate-, clofibrate- and bezafibrate-treated mice respectively (P <0.05 compared with control group). Moreover, a significant correlation between biliary phospholipid output and the relative levels of mdr2 mRNA was found (r=0.86; P <0.05). In treated animals, bile flow as well as cholesterol and bile acid outputs remained unchanged. Our findings constitute the first evidence that pharmacological modulation of biliary lipid secretion mediated by fibrates can be related to the overexpression of a specific liver gene product, the mdr2 P-glycoprotein, and are consistent with the hypothesis that the mdr2 P-glycoprotein isoform plays a crucial role in the secretion of biliary phospholipid.

lopid 10 mg 2015-04-19

Wastewater samples from the secondary clarifier of two treatment plants were spiked in the microgram-to-tens-of-microgram per liter range with diuron (herbicide), ibuprofen and diclofenac (anti-inflammatory drugs), sulfamethoxazole and erythromycin (antibiotics), bezafibrate and gemfibrozil (lipid regulators), atenolol (β-blocker), carbamazepine (anti-epileptic), hydrochlorothiazide (diuretic), caffeine (stimulant) and N-acetyl-4-amino-antipiryne, a metabolite of the antipyretic drug dypirone. They were subsequently ozonated in continuous flow using 1.2L lab-scale bubble columns. The concentration of all spiking compounds was monitored in the outlet stream. The effects of varying ozone input, expressed as energy per unit volume, and water flow rate, and of using single or double column were studied in relation to the efficiency of ozone usage and the ratio of pollutant depletion. The ozone dosage required to treat both wastewaters with pollutant depletion of >90% was in the 5.5-8.5 mg/L range with ozone efficiencies greater than 80% depending on the type of wastewater and the operating conditions. This represented 100-200 mol of ozone transferred per mole of pollutant removed. Direct and indirect environmental impacts of ozonation were assessed according to Life Cycle Assessment, a technique that helped identify the most effective treatments in terms of potential toxicity reduction, as well as of toxicity reduction per unit mass of greenhouse-gas emissions, which were used as an indicator of environmental efficiency. A trade-off between environmental effectiveness (toxicity reduction) and greenhouse-gas emissions was observed since maximizing toxicity removal led to higher greenhouse-gas emissions, due to the latter's relatively high ozone requirements. Also, there is an environmental trade-off between effectiveness and efficiency. Our results indicate that an efficient use of ozone was not compatible with a full pollutant removal.

lopid normal dosage 2016-11-12

IR type 2 DM induced by administering streptozotocin (90 mg/kg, i.p.) in neonatal rat model. IR type 2 DM rats at 6-week age treated for 8 weeks with (1) gemfibrozil (140 mg/kg od) and (2) gemfibrozil (70 mg/kg bid) + metformin (60 mg/kg bid). At the end, risk parameters like MMP-9, IL-10 and adiponectin were evaluated by ELISA kits.

lopid dosage forms 2016-06-09

Gemfibrozil, not fenofibrate, down-regulates systemic glucose level and glycogen storage in the liver dependent on PPARα, suggesting its potential value for treatment of dyslipidemia with concurrent diabetes or high glucose levels.