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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.

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High global consumption rates have led to the occurrence of pharmaceutically active compounds (PhACs) in wastewater. The use of chlorine to disinfect wastewater prior to release into the environment may convert PhACs into uncharacterized chlorinated by-products. In this investigation, chlorination of a common pharmaceutical, the antihyperlipidemic agent gemfibrozil, was documented. Gemfibrozil (2,2-dimethyl-5-(2,5-dimethylphenoxy)pentanoic acid) was reacted with sodium hypochlorite and product formation was monitored by gas chromatography-mass spectrometry (GC-MS). The incorporation of one, two or three chlorine atoms into the aromatic region of gemfibrozil was demonstrated using negative-ion electrospray ionization mass spectrometry (ESI-MS) and tandem mass spectrometry (ESI-MS/MS). Further analysis using (1)H nuclear magnetic resonance (NMR) spectroscopy identified the reaction products as 4'-ClGem (5-(4-chloro-2,5-dimethylphenoxy)-2,2-dimethylpentanoic acid) 4',6'-diClGem (5-(4,6-dichloro-2,5-dimethylphenoxy)-2,2-dimethylpentanoic acid), and 3',4',6'-triClGem (5-(3,4,6-trichloro-2,5-dimethylphenoxy)-2,2-dimethylpentanoic acid), products consistent with electrophilic aromatic substitution reactions. The rapid reaction of gemfibrozil with free chlorine at pH conditions relevant to water treatment indicates that a mixture of chlorinated gemfibrozils is likely to be found in wastewater disinfected with chlorine.

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Fenofibrate (100 microM) produced potent inhibition (48%) of VSMC proliferation at a concentration equivalent to that of its circulating metabolite fenofibric acid, but none of the other drugs produced any significant effect on growth. VSMC derived from graft stenoses were equally sensitive to inhibition as saphenous vein derived controls, in contrast to our previous work which reported that graft stenosis derived VSMC were resistant to growth inhibition by the physiological inhibitor heparin. The antiproliferative effect of fenofibrate was independent of inhibition of cellular cholesterol synthesis or toxicity. Fenofibrate inhibited VSMC growth induced by 15% fetal calf serum, PDGF, and basic fibroblast growth factor to a similar degree, indicating that it is not a specific PDGF antagonist.

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During the past decade, prescriptions for fibrates (particularly fenofibrate) increased in the United States, while prescriptions for fibrates in Canada remained stable.

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Both drugs significantly reduced total cholesterol, calculated low-density lipoprotein (LDL) cholesterol, triglycerides, apolipoprotein B, and fibrinogen (P<0.01 for all calculations, except P<0.05 for fibrinogen with gemfibrozil therapy) and increased high-density lipoprotein (HDL) cholesterol (P<0.01). Neither drug affected Lp(a) lipoprotein, whereas uric acid was reduced only by fenofibrate (P<0.01). The percentage decrease in total cholesterol and LDL cholesterol was greater with fenofibrate than with gemfibrozil (-22% versus -15%, P<0.02; and -27% versus -16%, P<0.02, respectively). In contrast, reductions in levels of triglycerides (-54% versus -46.5%), apolipoprotein B, and fibrinogen, as well as the increase in HDL (+9% for both drugs), showed no significant difference between treatments. Separate analysis of patients with type IIb hyperlipoproteinemia showed essentially the same plasma lipid changes as for the overall group, but with greater modifications in triglyceride and HDL concentrations.

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The major effect of the fibrates on triglycerides is to promote triglyceride-rich lipoprotein catabolism through increased lipoprotein lipase activity. Fibrates also enhance lipolysis of plasma triglycerides by a means different from that of caloric restriction. Their effect on very low-density lipoprotein metabolism also differs from that of nicotinic acid. The effect of fibrate therapy upon low-density lipoprotein-cholesterol concentrations depends upon the patients' overall lipoprotein status. The responsible mechanisms are not understood. In hypertriglyceridemic patients, fibrates often reverse abnormal changes in low-density lipoprotein composition; low-density lipoprotein heterogeneity is reduced and small dense low-density lipoproteins are eliminated, apparently secondary to reduced levels of triglyceride-rich lipoproteins. Kinetic studies indicate that fibrates do not enhance low-density lipoprotein formation rates, thus contradicting the idea that fibrate therapy causes increased low-density lipoprotein cholesterol levels via increased conversion of very low-density lipoprotein to low-density lipoprotein. Though enhanced low-density lipoprotein catabolism in hypertriglyceridemia could occur via several mechanisms, the responsible factors are largely reversed by fibrate therapy. In non-hypertriglyceridemic patients, fibrates may actually enhance the fractional clearance of low-density lipoprotein and thus reduce low-density lipoprotein levels. Fibrate therapy reverses the typical high-density lipoprotein pattern of hypertriglyceridemic patients, producing more high-density lipoprotein2a and less high-density lipoprotein2b. Such treatment also increases high-density lipoprotein cholesterol levels in patients without definite hypertriglyceridemia. Synthesis rates of apolipoproteins AI and AII may be affected by fibrates. The fibrates' major effects on sterol metabolism are interference with cholesterol and bile acid synthesis and increased cholesterol secretion into bile. Although bile saturation increases in most patients, in only a relatively small percentage do gallstones actually develop; super-saturated bile is not sufficient to induce gallstone formation in most patients. Available data strongly imply that fibrates mobilized cholesterol out of tissue pools, perhaps by altering tissue cell membranes to allow cholesterol release from the cell surfaces.

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Patients with diabetes mellitus (DM), Type 1 or 2, with plasma lipid levels exceeding target values (LDL-cholesterol <2.6 mmol/l, triglycerides < 1.7 mmol/l, HDL-cholesterol > 0.9 mmol/l for men and > 1.1 mmol/l for women) were eligible. After 6-12 weeks of diet and glycaemic control, lipid-lowering medication (simvastatin/gemfibrozil/acipimox) was prescribed in steps of incremental dosages and combinations for 30 weeks.

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A total of 1356 subjects with total cholesterol levels >or=239 mg/dL were randomly treated for 5 years (1988-1993) with 1 of these lipid-lowering regimens: low-fat diet, cholestyramine, gemfibrozil, or simvastatin. Participants were divided at baseline into 4 quartiles according to systolic BP level and examined for the percent change in systolic and diastolic BP during the 5 years of treatment.

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Itraconazole, gemfibrozil and their combination markedly raise the plasma concentrations of loperamide. Although not seen in the psychomotor tests used, an increased risk of adverse effects should be considered during concomitant use of loperamide with itraconazole, gemfibrozil and especially their combination.

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Randomized, placebo-controlled, 2.5-year trial comparing patients receiving usual care with patients receiving stepped-care drug therapy.

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Despite the large number of pharmaceutically active compounds found in natural environments little is known about their transport behavior in groundwater, which is complicated by their wide range of physical and chemical properties. The transport behavior of five widely used and often detected pharmaceutical compounds and one lifestyle drug has therefore been investigated, using a set of three column experiments. The investigated compounds were the anticonvulsant carbamazepine, the lifestyle drug caffeine, the antibiotic sulfamethoxazole, the lipid regulator gemfibrozil, and the nonsteroidal anti-inflammatories ibuprofen and naproxen. The columns were filled with three different types of sand. The substrates consisted of artificially prepared iron-coated sand, artificially prepared organic carbon sand (with 5% leaf compost), and natural aquifer sand from Long Point, Ontario (Canada). The experiments were conducted simultaneously under the same hydraulic conditions and with the same input solution of about 1μg·L(-1) of each compound. The transport behavior of the organic compounds differed significantly between both the different columns and the different compounds. A strong correlation was observed between the retardation factors for carbamazepine, gemfibrozil, and ibuprofen and the organic carbon content of the substrate. While the retardation increased with increasing organic carbon content, no direct relationship was observed between the organic carbon content and the removal of these compounds. In contrast, the retardation factors for sulfamethoxazole and naproxen showed no correlation with the organic carbon content but these compounds were significantly removed in the presence of organic matter. The influence of the Fe(3+) surfaces in the iron-coated sand was less significant than expected, with all compounds except for sulfamethoxazole having retardation factors <1.8. Caffeine was so strongly removed during transport through those substrates containing organic carbon that no reliable retardation factor could be determined.

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Nonenzymatic modification of proteins by acyl glucuronides is well documented; however, little is known about their potential to damage DNA. We have previously reported that clofibric acid undergoes glucuronidation-dependent bioactivation to DNA-damaging species in cultured mouse hepatocytes. The aim of this study was to investigate the mechanisms underlying such DNA damage, and to screen chemically diverse carboxylic acid drugs for their DNA-damaging potential in glucuronidation proficient murine hepatocytes. Cells were incubated with each aglycone for 18 h, followed by assessment of compound cytotoxicity using the MTT assay and evaluation of DNA damage using the Comet assay. Relative cytotoxic potencies were ketoprofen > diclofenac, benoxaprofen, nafenopin > gemfibrozil, probenecid > bezafibrate > clofibric acid. At a noncytotoxic (0.1 mM) concentration, only benoxaprofen, nafenopin, clofibric acid, and probenecid significantly increased Comet moments (P < 0.05 Kruskal-Wallis). Clofibric acid and probenecid exhibited the greatest DNA-damaging potency, producing significant DNA damage at 0.01 mM concentrations. The two drugs produced maximal increases in Comet moment of 4.51 x and 2.57 x control, respectively. The glucuronidation inhibitor borneol (1 mM) abolished the induction of DNA damage by 0.5 mM concentrations of clofibric acid and probenecid. In an in vitro cell-free system, clofibric acid glucuronide was 10 x more potent than glucuronic acid in causing DNA strand-nicking, although both compounds showed similar rates of autoxidation to generate hydroxyl radicals. In cultured hepatocytes, the glycation inhibitor, aminoguanidine, and the iron chelator, desferrioxamine mesylate, inhibited DNA damage by clofibric acid, whereas the free radical scavengers Trolox and butylated hydroxytoluene, and the superoxide dismutase mimetic bis-3,5-diisopropylsalicylate had no effect. In conclusion, clinically relevant concentrations of two structurally unrelated carboxylic acids, probenecid and clofibric acid, induced DNA damage in isolated hepatocytes via glucuronidation- dependent pathways. These findings suggest acyl glucuronides are able to access and damage nuclear DNA via iron-catalyzed glycation/glycoxidative processes.

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This study demonstrates suboptimal treatment with statins in patients with type 2 diabetes and cardiovascular risk factors.

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1. To control the bias caused by poor medication compliance in the Helsinki Heart Study three methods were used to measure medication compliance during the total 5 years follow up time: continuous capsule counting, semi-annual urine gemfibrozil analysis and a new method, the digoxin marker at the end of the third and fifth study years. 2. The serum lipid responses to gemfibrozil treatment varied linearly with the level of medication compliance, e.g. the mean change in serum total cholesterol was -11.4% among those whose apparent capsule consumption was greater than or equal to 90% of the scheduled dosage, -11.2% among those who had greater than or equal to 90% positive gemfibrozil analyses and -11.4% among those with good compliance according to both digoxin marker measurements. In contrast the mean serum cholesterol change was only -0.02% if the mean daily capsule count was less than 50%, -1.7% with fewer than 50% positive gemfibrozil analyses and -1.1% if the result was poor in both digoxin marker measurements. 3. Combining the different method findings revealed that the cholesterol changes tended to be small in those groups who had poor compliance classification measured by any of the methods, even if the other results showed good compliance.

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We hypothesized that M1, a metabolite of gemfibrozil, may have antioxidant properties because of its hydroxylated phenol ring, 5-(4-hydroxy-2,5-dimethyl-phenoxy)-2,2-dimethyl pentanoic acid. The susceptibility of low-density lipoprotein (LDL) to oxidative modification was investigated by a method using 2,2-azobis(4-methoxy-2,4-dimethylvaleronitrile [MeO-AMVN]) or Cu2+ as previously reported. Conjugated dienes (CDs), lipid hydroperoxide (LPO), and thiobarbituric acid-reactive substances (TBARS) were measured to evaluate the degree of LDL oxidation. Oxidized LDL (OxLDL), which is used for cytotoxicity studies, was prepared by the dialysis method using Cu2+ as the oxidation inducer. Cytotoxicity induced by OxLDL was studied in J774 macrophages by colorimetric assay using 3-[4,5-dimethyl-thiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT assay). The oxidative modification of LDL was inhibited by M1 in a dose-dependent manner. The antioxidant effect of M1 on LDL oxidation was diminished by dialysis of the LDL incubated with M1 against phosphate-buffered saline (PBS), suggesting that M1 is hydrophilic rather than lipophilic. M1 diminished the cytotoxicity induced by OxLDL, although it was milder versus probucol. These data suggest that this gemfibrozil metabolite has an antioxidant effect on LDL, and thus M1 may contribute to the antiatherogenic effects of gemfibrozil.

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Compared with those in the CRF group, the plasma total cholesterol, triglyceride, low-density lipoprotein cholesterol and very-low-density lipoprotein cholesterol concentrations in the treatment groups were significantly lower with substantially elevated plasma high-density lipoprotein cholesterol and LPL gene expression. No significant differences were noted between different dose groups of Shenshuai Yangzhen.

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We evaluated in a double-blind randomized trial with a double-dummy design in 28 patients with primary hypertriglyceridemia, the effect of gemfibrozil (1200 mg/day) versus Omacor (4 g/day), a drug containing the n-3 fatty acids eicosapentaenoic (EPA) and docosahexaenoic acid (DHA), on lipid and lipoprotein levels, low density lipoprotein (LDL) subfraction profile and LDL oxidizability. Both Omacor and gemfibrozil therapy resulted in a similar significant decrease in serum triglyceride (TG), very low density lipoprotein (VLDL) triglyceride and VLDL cholesterol concentrations and an increase in high density lipoprotein (HDL) and LDL cholesterol concentrations. The increase in LDL cholesterol was due to a significant increase in cholesterol content of the relatively buoyant LDL subfractions LDL1, LDL2 and LDL3, whereas the relative contribution of the dense LDL subfractions LDL4 and LDL5 to total LDL tended to decrease. So, both therapies resulted in a more buoyant LDL subfraction profile, reflected by a significant increase of the value of parameter K (+10.3% on Omacor vs. +26.5% on gemfibrozil therapy, gemfibrozil vs Omacor P>0.05). Cu(2+)-induced oxidation of LDL was measured by continuous monitoring of conjugated dienes. After 12 weeks of Omacor treatment LDL appeared more prone to oxidative modification in vitro than LDL after gemfibrozil treatment, as measured by the significantly decreased lag time, preceding the onset of the lipid peroxidation. In both groups the rate of oxidation did not change with therapy. The amount of dienes formed during oxidation increased significantly on Omacor treatment, but not on gemfibrozil treatment. Plasma thiobarbituric acid reactive substances were higher after Omacor and lower after gemfibrozil treatment, although not significantly. We conclude that both Omacor and gemfibrozil have favorable effects on lipid and lipoprotein concentrations and the LDL subfraction profile. However, Omacor increased the susceptibility of LDL to oxidation, whereas gemfibrozil did not affect the resistance of LDL to oxidative modification in vitro. The clinical relevance of these changes remains to be established in the light of other postulated favorable effects of n-3 fatty acids on the course of cardiovascular disease.

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Rosuvastatin has greater efficacy in lowering LDL cholesterol and non-HDL-cholesterol concentrations than the other statins. It has been shown to enable more patients to reach their LDL cholesterol goals than other statins and to do so with an acceptable safety profile.

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Physicians' views of the effectiveness of lipid lowering drugs and the decision to prescribe such drugs is affected by the predominant use of reduction of relative risk in trial reports and advertisements.

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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 was for the 95% confidence interval (CI) of non-HDL-C to lie entirely below -25% for any rosuvastatin dose.

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Electrokinetic cross membrane extraction of acidic drugs was demonstrated for the first time. The acidic drugs were extracted from an alkaline aqueous donor solution (300 microl), through a thin supported liquid membrane of 1-heptanol sustained in the pores of the wall of a porous hollow fiber, and into an aqueous alkaline acceptor solution (30 microl) present inside the lumen of the hollow fiber by the application of a d.c. electrical potential. The negative electrode was placed in the donor solution, and the positive electrode was placed in the acceptor solution. Optimal extractions were accomplished with 1-heptanol as the supported liquid membrane, with 50 V as the driving force, and with pH 12.0 in both the donor and acceptor solutions, respectively (NaOH). Equilibrium extraction conditions were obtained after 5 min of operation with the whole assembly agitated at 1200 rpm. Eleven different acidic drugs were extracted with recovery values between 8 and 100%, and initial data supported that electrokinetic cross membrane extraction provided repeatable data and linear response between original donor concentration and final acceptor concentration of the acidic model compounds.

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Peripheral lymph lipoproteins were studied in four hyperlipidaemic men before and after 6 weeks of treatment with gemfibrozil, a drug which is known to increase the fractional catabolic rate of very low density lipoproteins (VLDL) by raising lipoprotein lipase activity in peripheral tissues. Decreases in plasma triglycerides of 18-60% (mean, 45%) were accompanied by increases in lymph apolipoprotein (apo) A-I concentration of 30-108% (mean, 66%; P < 0.01), and in lymph cholesterol concentration of 35-100% (mean, 59%; P < 0.05). The additional lymph cholesterol was distributed over a broad range of lipoprotein particle sizes. Effects on plasma apo A-I concentration (mean, +7%) and plasma total cholesterol concentration (-7%) were not statistically significant. No changes were observed in four untreated control subjects. These findings are compatible with the hypothesis that lipolysis of VLDL at the blood-endothelium interface increases the transfer of apo A-I from plasma to interstitial fluids, and thereby promotes cholesterol efflux from cells.

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Drug induced myopathy has been reported with the use of fibric acid derivatives, hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and nicotinic acid. Over the last three decades, hypolipemiants like fibric acid derivatives and statins have been increasingly recognised as causes of rhabdomyolysis and acute renal failure especially during combination therapy and in the presence of underlying renal impairment. We report two cases of bezafibrate-induced rhabdomyolysis in patients with underlying coronary artery disease and pre-existing renal impairment. Both patients developed rhabdomyolysis leading to acute renal failure soon after their hyperlipidaemia treatment was changed from gemfibrozil to bezafibrate. There were no intercurrent illnesses or co-administration of other lipid lowering drugs in both patients. Even though both drugs belong to the same fibric acid derivatives group, these patients developed the complication only after a switchover of therapy.

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Gemfibrozil reduces plasma triglycerides and raises high-density lipoprotein cholesterol (HDL-C) in adults and also reduces the incidence of cardiovascular endpoints in adults. Its efficacy in improving lipid abnormalities has not been evaluated in children.

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Gemfibrozil significantly reduced triglycerides by 44% and increased HDL-cholesterol by 31% without significant change in LDL cholesterol. Before treatment, patients had increased F1 + 2, fibrinogen and IL6, but similar PAI1 compared with the controls, consistent with a hypercoagulable and persistent inflammatory state. Following treatment, F1 + 2 decreased to within the normal range and this reduction correlated with the decrease in triglycerides and inversely with the increase in HDL-cholesterol. A non-significant decrease in fibrinogen was inversely correlated with a significant increase in albumin. However, Lp(a) and PAI1 activity significantly increased whilst insulin and IL6 were unchanged.

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Fenofibrate, bezafibrate, and gemfibrozil reduced plasma low-density lipoprotein cholesterol levels by 22% (P =.009), 14% (P =.042), and 11% (not significant), respectively. Plasma triglyceride levels decreased significantly (24%-36%; P <.05), whereas high-density lipoprotein cholesterol levels rose nonsignificantly after treatment with the 3 fibrates. Except for a 35% increase of apolipoprotein A-I mRNA after fenofibrate administration (P <.05), none of the individual fibrates induced significant changes in the mRNAs tested, although as a group they increased the mRNA for liver carnitine palmitoyltransferase I by 40%(P =.08; marginally significant).

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lopid dosage administration 2017-06-25

Elevated lipid profile (total glyceride, total cholestrol, low-density lipoprotein, and very low-density lipoprotein), lipid peroxidation (MDA), and reduced enzymatic and nonenzymatic antioxidant status coupled with alterations in hematological parameters was observed in the serum of hypercholesterolemic rats when compared with animals on a normal dietCoadministration of methanolic leaf extracts of Talinum triangulare significantly (P < 0.05) restored the elevated serum lipid profile, MDA, and the deranged hematological parameters to near normal.The extract also protected against hypercholesterolemic-induced diminished enzymatic and bnonenzymatic antioxidant status.The activities of the plant extract was dose-dependent and it compared favorably with the standard drug gemfibrozil. Abbreviations used: Lipid peroxidation (MDA), (catalase (CAT), glutathione-S-transferase (GST), superoxide dismutase (SOD), glutathione (GSH), Thrombocytes indices (PLT buy lopid ), Red blood cell (RBC), Packed cell volume (PVC), Mean corpuscular hemoglobin(MCH), Mean corpuscular hemoglobin concentration (MCHC), Total glyceride (TG), Very low density lipoprotein (VLDL), Total cholesterol (TC), Low density lipoprotein (LDL), High density lipoprotein (HDL) and 3-Hydroxy-3-methyl-glutaryl-CoA reductase(HMG-CoA).

lopid 60 mg 2015-09-17

Randomized prospective intervention study buy lopid .

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Outpatient geriatrics clinic in buy lopid a university health system.

lopid 160 mg 2016-06-24

The present study underlines the importance of gemfibrozil, a lipid-lowering drug and an activator of peroxisome proliferator-activated receptor-alpha (PPAR-alpha), in inhibiting the disease process of adoptively transferred experimental allergic encephalomyelitis (EAE), an animal model of relapsing-remitting multiple sclerosis. Clinical symptoms of EAE, infiltration of mononuclear cells, and demyelination were significantly lower in SJL/J female mice receiving gemfibrozil through food chow than those without gemfibrozil. It is noteworthy that the drug was equally effective in treating EAE in PPAR-alpha wild-type as well as knockout mice. Gemfibrozil also inhibited the encephalitogenicity of MBP-primed T cells and switched the immune response from a Th1 to a Th2 profile independent of PPAR-alpha. Gemfibrozil consistently inhibited the expression and DNA-binding activity of T-bet, a key regulator of interferon-gamma (IFN-gamma) expression and stimulated the expression and DNA-binding activity of GATA3, a key regulator of IL-4. Gemfibrozil treatment decreased the number of T-bet-positive T cells and increased the number of GATA3-positive T cells in spleen of donor mice. The histological and immunohistochemical analyses also demonstrate the inhibitory effect of gemfibrozil on the invasion of buy lopid T-bet-positive T cells into the spinal cord of EAE mice. Furthermore, we demonstrate that the differential effect of gemfibrozil on the expression of T-bet and GATA3 was due to its inhibitory effect on NO production. Although excess NO favored the expression of T-bet, scavenging of NO stimulated the expression of GATA-3. Taken together, our results suggest gemfibrozil, an approved drug for hyperlipidemia in humans, may find further therapeutic use in multiple sclerosis.

lopid drug class 2017-04-10

We used Cox regression models to explore the effects of gemfibrozil among overweight subjects with additional coronary risk factors in this hypercholesterolemic male population of 2046 subjects randomized to gemfibrozil and 2035 to placebo. The effect of gemfibrozil was largely confined to overweight subjects: among those with body mass index (BMI) > 26 kg/m2, the net difference in cardiac end points between gemfibrozil and placebo groups was 21 (25 of 1119 versus 46 of 1081), and in those buy lopid with BMI < or = 26 kg/m2, it was 7 (31 of 927 versus 38 of 954). The risk reduction with gemfibrozil was 78% (P = .002) among those with BMI > 26 kg/m2 and dyslipidemia (TG > or = 2.3 mmol/L and HDL cholesterol < 1.08 mmol/L). Among those with BMI > 26 kg/m2 and three or four of the following factors present--smoking, sedentary lifestyle, blood pressure > or = 140/90 mm Hg, or blood glucose > 4.4 mmol/L--the risk reduction was 68% (P = .03).

lopid generic price 2016-06-02

Crude GG was extracted from the urine of volunteers dosed with 600 mg of gemfibrozil, and this material was then purified by reversed-phase high-performance liquid chromatography to yield a white solid. The amphiphilic properties of GG within the bulk aqueous phase were studied by isothermal titration microcalorimetry and 1H-NMR buy lopid spectrometry, whereas those at the aqueous/air interface were studied by surface tensiometry.

lopid cholesterol medication 2017-04-30

There were 2046 dyslipidaemic men in the gemfibrozil group at randomization, 1961 started the extended follow-up; the comparison group comprised 2035 men, and 5 years later 1928 men buy lopid .

lopid 25 mg 2016-07-27

Administration of the HIV PI ritonavir to wild type mice increased plasma triacylglycerols and cholesterol levels and this effect was exacerbated by dosing ritonavir to mice harbouring a disrupted FXR. Dyslipidemia induced by ritonavir associated with a shift in the liver expression of signature genes, Sterol Regulatory Element-Binding Protein (SREBP)-1 and fatty acid synthase. Treating wild type mice with the FXR agonist (chenodeoxycholic acid, CDCA) protected against development of dyslipidemia induced by ritonavir. Administration of ritonavir to ApoE(-/-) mice, a strain that develop spontaneously atherosclerosis, increased the extent of aortic plaques without worsening the dyslipidemia. Treating these mice with CDCA reduced the extent buy lopid of aortic plaques by 70% without changing plasma lipoproteins or the liver expression of signature genes. A beneficial effect on aortic plaques was also obtained by treating ApoE(-/-) mice with gemfibrozil, a PPARα agonist. FXR activation counter-regulated induction of expression/activity of CD36 caused by HIV-PIs in circulating monocytes and aortic plaques. In macrophages cell lines, CDCA attenuated CD36 induction and uptake of acetylated LDL caused by ritonavir. Natural and synthetic FXR ligands reduced the nuclear translocation of SREBP1c caused by ritonavir.

lopid reviews 2016-07-10

A series of 2-aminomethyl-3-aryl-5,6,7,8-tetrahydrobenzo(b)/5,6-dimethylthieno (2,3-d) pyrimidin-4-ones (IX) were prepared by the displacement reaction between various amines and 2-chloromethyl-3-aryl-5,6, 7,8-tetrahydrobenzo(b)/5, 6-dimethylthieno(2, 3-d) pyrimidin-4-ones (VIII), which are obtained by the cyclization of corresponding chloroacetylamino derivatives (VII) under acidic buy lopid condition. Compounds VII were obtained by the interaction of VI and chloroacetylchloride in glacial acetic acid. Compounds VIII were converted to corresponding 2-acetoxymethyl derivatives (X) with potassium acetate in glacial acetic acid. Selected compounds were screened for antihyperlipaemic activity in albino rats, whereby most of these compounds were found to be active. The serum cholesterol and triglyceride lowering activities exhibited by compounds 1 and 3 were found to be comparable to that of gemfibrozil. Compounds 1 and 3 were also found to be safe as indicated by their acute toxicity study.

lopid usual dosage 2016-10-04

High-throughput, automated analytical measurements are desirable in many analytical scenarios, as are rapid sample pre-screening techniques to identify 'positive' samples for subsequent measurements using more time-consuming conventional methodologies (e.g., liquid chromatography/mass spectrometry (LC/MS)). A miniature condensed-phase membrane introduction mass spectrometry (CP-MIMS) probe for the direct and continuous, on- buy lopid line measurement of pharmaceuticals and environmental contaminants in small, complex samples is presented.

lopid capsules 2016-12-25

Pharmaceutical residues are commonly detected micropollutants in the aquatic environment. Biodegradation in sediments is a potentially significant removal process for these compounds in rivers which is constrained by the transfer of water and solutes into the sediment. The aim of this study was to determine the combined effect of flow velocity and sediment dynamics and thus of water-sediment interactions on the attenuation of 6 acidic pharmaceuticals. We carried out experiments with river water and sediment in a bench-scale annular flume at two different hydraulic boundary conditions (flat sediment surface vs moving sediment). The effective biodegradation half-lives of 4 compounds (diclofenac, bezafibrate, ibuprofen, naproxen) were in the range of 2.5 to 18.6 days and were much shorter when the exchange of surface and pore water was fast. For gemfibrozil, a half-life of 10.5 buy lopid d was determined in the experiment with moving sediment, whereas no degradation was observed with flat sediment bed. These findings can be attributed to the limited transfer of water and solutes into the sediment at low flow velocity and flat sediment bed which rapidly induced anaerobic conditions in the sediment. The only compound that was efficiently removed in deeper, anoxic sediment layers was naproxen. The calculated half-life distances in rivers ranged from 53 to 278 km. Our results indicate that it could be favorable to increase the rate of exchange between surface and pore water during river restoration to enhance the attenuation of organic micropollutants like acidic pharmaceuticals.

lopid max dose 2017-01-12

Familial combined hyperlipidemia (FCHL) is a genetic disorder characterized by increases in plasma cholesterol and/or triglyceride, elevated apolipoprotein B, and heterogeneous low density lipoprotein (LDL). To examine the relation between plasma triglyceride concentrations and LDL heterogeneity, buy lopid 13 hypertriglyceridemic FCHL patients with a predominance of small LDL (LDL subclass phenotype B) were treated with gemfibrozil. The distribution of LDL was determined using nondenaturing gradient gel electrophoresis and nonequilibrium density gradient ultracentrifugation. Mean plasma triglyceride levels decreased 55% (p < 0.01) after 3 months of treatment. Mean LDL peak particle size remained small (247 +/- 4 versus 249 +/- 5 A), and the correlation between change in plasma triglyceride concentrations and a change in LDL peak particle size was not significant. Individual changes in LDL flotation rate (Rf) were, however, inversely correlated with changes in triglyceride concentration (R = 0.60, p < 0.05). Although mean LDL Rf increased during treatment (p < 0.005) due to an increase in buoyant LDL, dense LDL remained elevated compared with that of a control population. Thus in FCHL patients, small, dense LDL persists despite decreases in plasma triglyceride concentrations.

lopid with alcohol 2016-07-15

Concentrations and retention of pharmaceutically active substances are crucial for assessing the environmental risk of medication of humans. We hypothesize that environmental introduction concentrations (EICs) of buy lopid drugs in the Mexico City-Mezquital Valley wastewater irrigation system can be estimated using information on water consumption, sales data, and excretion rates. EICs of six acidic and five basic drugs were calculated and compared with concentrations measured in wastewater, irrigation water, soil drainage, and springs by liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS). EICs of trimethoprim, erythromycin, naproxen, ibuprofen, and diclofenac in sewage equaled or exceeded the US FDA action limit of 1mug/L for detailed environmental risk assessment (ERA). Concentrations of clarithromycin, clindamycin, metoprolol, sulfasalazine, bezafibrate, and gemfibrozil were smaller. Calculated EICs of all compounds except metoprolol and clarithromycin were comparable to measured concentrations if excretion rates were considered. Whereas concentrations of basic compounds with positive or neutral charges were effectively reduced during reservoir storage and soil passage, acidic, anionic compounds were hardly retained. Though realistic EICs can be predicted for most substances, large deviations between EICs and measured concentrations in the case of metoprolol illustrate that estimated concentrations cannot substitute for monitoring programs.

lopid renal dosing 2017-07-10

Insulin and its precursors found in increased plasma concentrations in non-insulin-dependent diabetes mellitus (NIDDM) augment synthesis of plasminogen activator inhibitor type 1 (PAI-1) in Hep G2 cells buy lopid in vitro and in rabbit liver in vivo. Reduced endogenous fibrinolysis secondary to increased PAI-1 activity may exacerbate atherogenesis. Recently, the reduction of the coronary heart disease incidence in the Helsinki Heart Study has implicated favorable modulation of endogenous fibrinolysis by gemfibrozil.

lopid 800 mg 2016-12-25

29 patients with primary hypercholesterolemia were treated for 8 weeks each with either bezafibrate (200 mg t.i.d.) or gemfibrozil (600 mg b.i.d.) in a randomized cross-over trial. Compared to placebo bezafibrate was significantly more effective on low density lipoprotein (LDL)-cholesterol (-28% versus -18%) and the LDL/high density lipoprotein (HDL) ratio (-34% versus -24%) by exploratory statistics. There was also a trend for a more marked reduction of bezafibrate on total cholesterol and apoliproprotein B Viagra Buy as well as more pronounced increase in HDL-cholesterol and apolipoprotein A-I. The triglyceride reduction tended to be more extensive with gemfibrozil. Complicance to both drugs was good. No side-effects were observed. The results are considered important with respect to the potential of bezafibrate in reducing the risk of cardiovascular disease.

lopid 600 mg 2016-04-12

Eight type III hyperlipoproteinemic (type III HLP), homozygous E 2/2 patients were enrolled in two periods of long-term diet-gemfibrozil treatment. The combined therapy resulted in highly significant decreases in their low-density lipoprotein cholesterol, very-low density lipoprotein cholesterol, very-low density lipoprotein triglycerides, and increases in their high-density lipoprotein cholesterol during the first treatment period of 24 to 28 months. Type III HLP reasserted itself following an 8-week interruption of gemfibrozil therapy. Resumption of gemfibrozil therapy again lowered the high lipid-lipoprotein concentrations of these patients toward normal. Tuboeruptive xanthomata, palmar Prograf Mg xanthoma, and xanthoma striata palmare subsided with treatment. Follow-up coronary arteriograms performed 2.5 to 3.0 years after initiation of diet-drug treatment showed stabilization of coronary arterial lesions, which was associated with improvement in exercise tolerance.

lopid overdose symptoms 2016-04-24

The plasma concentration-time data of gemfibrozil in 8 male subjects were determined after an oral dose of 600 mg. Two-peak concentrations in plasma were observed. A kind of one-compartment model with two-sites of drug absorption was proposed and used to fit these data. A good agreement between observed and predicted data was found in all subjects with correlation indexes (gamma 2) > 0.99. The corresponding pharmacokinetic parameters were estimated as follows: Tmax1, 1.10 +/- 0.46 h; Tmax2, 2.60 +/- 0.73 h; Cmax1, 13.62 +/- 4.30; Cmax2, 17.22 Flomax Dosage Medication +/- 3.83; T1, 0.06 +/- 0.06 h; T2, 1.42 +/- 0.57 h and T3, 1.79 +/- 0.60 h.

lopid generic 2017-12-20

This study assessed the cost effectiveness of treatments for the primary prevention of coronary heart disease in Spain, which included smoking cessation and reductions in blood cholesterol levels and BP. Cost-effectiveness ratios (measured in terms of US dollars per life-year gained) ranged from 2,608 US dollars to 8,058 US Paracetamol Overdose Died dollars per life-year gained for therapies aimed at smoking cessation, from 7,061 US dollars to 126,990 US dollars per life-year gained for antihypertensive drug treatment, from 15,487 US dollars to 1,689,022 US dollars per life-year gained for the drug treatment of hypercholesterolaemia and from 12,792 US dollars to 149,246 US dollars per life-year gained for cholesterol-lowering diets. In individuals with blood cholesterol levels of 7.7 mmol/L, cost-effectiveness ratios of drug treatment ranged from 33,850 US dollars to 302,088 US dollars. Cost-effectiveness ratios were lower in men than in women for all programmes evaluated. Cost-effectiveness analysis of cholesterol-lowering drugs indicated that lovastatin (HMG-CoA reductase inhibitor) was more cost effective than cholestyramine (bile acid sequestrant) and gemfibrozil (fibrate). Hydrochlorothiazide, propranolol and nifedipine were more cost effective antihypertensive treatments than prazosin and captopril. Cost-effectiveness ratios obtained in this study could be used to develop disease management strategies to facilitate the efficient use of healthcare resources and to reduce costs. When resources for coronary heart disease are limited, available treatments should be selected on the basis of their average and incremental cost-effectiveness ratios.

lopid tab 600mg 2015-12-17

Three fibric acid derivatives, clofibric acid (CFB), bezafibrate (BFB), and gemfibrozil (GFB), mainly used in the treatment of hypertriglyceridaemic or mixed hyperlipidaemic states, have been tested for their ability to modify fatty acid chain elongation and desaturation in vitro. Both endogenous and exogenous (saturated, monounsaturated and Duricef Medication Class polyunsaturated) fatty acid elongations were inhibited by fibrates at concentrations well within the physiological range (IC50 values for GFB were between 0.1 and 0.3 mM). The potency order was GFB > BFB > CFB. Inhibition was not due to an impairment of the activation step from free fatty acids to acyl-CoAs, as palmitoyl-CoA synthetase was only slightly inhibited (IC50 value for GFB = 2.8 mM). Fibrates (GFB) appeared to behave as mixed non-competitive inhibitors with respect to malonyl-CoA when the rate limiting step of elongation, the condensing enzyme, is assayed. Further, delta 6 and delta 5 desaturates were inhibited by the three drugs (GFB > BFB > CFB), although not to the same extent as the elongation system. In contrast, delta 9 desaturase activity was not affected by fibrates.

lopid dosage generic 2016-01-27

This article provides a comprehensive review of 30 years of research on the use of coenzyme Q10 in prevention and treatment of cardiovascular disease. This endogenous Bactrim Uti Dosage antioxidant has potential for use in prevention and treatment of cardiovascular disease, particularly hypertension, hyperlipidemia, coronary artery disease, and heart failure. It appears that levels of coenzyme Q10 are decreased during therapy with HMG-CoA reductase inhibitors, gemfibrozil, Adriamycin, and certain beta blockers. Further clinical trials are warranted, but because of its low toxicity it may be appropriate to recommend coenzyme Q10 to select patients as an adjunct to conventional treatment.