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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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A patient referred to an endocrinology clinic of a state hospital.

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The capacity of rivers to naturally attenuate trace organic compounds is an important but poorly understood process because the many factors that control attenuation are interrelated and difficult to study in isolation. To better understand the relative importance of chemical (photolysis and sorption) and biological attenuation processes, contaminant removal along a 12-km stretch of the Santa Ana River (SAR) was determined as a function of travel time, distance, and irradiance. Target contaminants included three pharmaceuticals (gemfibrozil, ibuprofen, and naproxen) and their metabolites, and the metabolites of alkylphenol polyethoxylates (APEMs). The APEMs included alkylphenols (APs), short-chain alkylphenol polyethoxylates (APEOs), alkylphenol polyethoxycarboxylates (APECs), and carboxyalkylphenol polyethoxycarboxylates (CAPECs). Overall removals ranged from 50% for APs to 100% for naproxen and increased with distance and time, in many cases following first-order kinetics. For naproxen, which is photolabile, average removals were 20 to 30% more during the day than at night; the nighttime and daytime half-lives were 3 h and 1.7 to 1.9 h, respectively. Comparison of field and laboratory data suggests that approximately 40% of the daytime naproxen removal can be attributed to photolysis with the remainder due to other processes, most likely sorption. For ibuprofen and gemfibrozil, half-lives were 5.4 and 2.7 h, respectively, and laboratory data suggest that biotransformation is the principal attenuating process. The APEM attenuation might be due to sorption and biotransformation; phototransformation may also play a minor role. These data demonstrate that travel times on the order of hours can significantly mitigate the impact of effluent discharge on the water quality of shallow rivers.

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In addition to high concentrations of LDL cholesterol, high levels of triglycerides and low concentrations of HDL cholesterol are now known to be independent risk factors in the development of atherosclerosis. The use of Gemfibrozil, with its LDL cholesterol-reducing, HDL cholesterol-raising, and triglyceride-lowering effects, would thus appear to make good sense for the treatment of lipid metabolism anomalies with no selective elevation of LDL cholesterol; it would thus also appear to be superior to HMG-CoA-reductase inhibitors.

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CI-924 (5'5'-[1,1'-biphenyl]-2,5-diylbis(oxy)]bis [2,2-dimethyl-pentanoic acid]), a lipid lowering agent, was previously shown to be hepatotumorigenic in male and female B6C3F1 mice but not in male and female albino Wistar rats. To determine if the difference between the species in tumorigenic response correlated with the extent of peroxisome proliferation or microsomal changes the effects of CI-924 on liver were characterized in rats and mice. CI-924 doses of 0, 25, 75, and 150 mg/kg were administered in the diet for 4 weeks to B6C3F1 mice and albino Wistar rats. Peroxisomal beta-oxidation activity was significantly increased in all groups at doses of 25 mg/kg or higher and was induced up to 25 times in male rats. Peroxisomal carnitine acyltransferase and acyl-CoA oxidase activities were also increased, with the greatest induction observed in male rats. Catalase activity quadrupled in rats and doubled in mice. Serum liver enzyme activities were unchanged with the exception of 5'nucleotidase which was elevated in mice and decreased in male, but not female, rats. Glutathione S-transferase decreased in the males of both species and glutathione peroxidase increased in the mice. Cytochrome P450 4A1 increased in both species at doses of 25 mg/kg or greater and correlated with increased lauric acid hydroxylation. The high degree of peroxisome proliferation in male rats was unexpected in light of the lack of tumorgenicity demonstrated in a previous 2-year study and these results indicate that early peroxisome proliferation alone is not always a good predictor of hepatocarcinogenicity.

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During treatment with gemfibrozil, plasma TG concentration decreased from 2.83 +/- 0.85 to 2.02 +/- 0.89 mmol L-1 (P < 0.001). All but one patient were shown to have LDL pattern B. The LDL pattern did not change upon treatment with gemfibrozil. The resistance to oxidation, reflected in the lagtime during in-vitro oxidation slightly decreased from 105 +/- 22 to 99 +/- 18 min (P = 0.01). The concentration of autoantibodies against oxidized LDL indicates the rate of LDL oxidation in vivo. This concentration significantly decreased from 14.2 +/- 9.9 to 13.1 +/- 9.2 mg L-1 (P < 0.01).

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Coronary heart disease (CHD) is the leading cause of mortality worldwide. With increasingly urbanized lifestyles in developing countries and the aging populations, the major risk factors for CHD such as obesity, diabetes mellitus, and hypercholesterolemia are likely to increase in the future. In the current report, we reviewed the evidence on the effect of cholesterol lowering using pharmacological agents.

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Using Cox proportional hazards models the crude relative risk for all-cause mortality for the low SOC tertile when compared to the high SOC tertile was 1.23 (95% CI: 0.90-1.68). Adjusting for age, smoking, alcohol and occupation increased the risk slightly to 1.35. Occupation was an effect modifier, since among white-collar workers the corresponding relative risk of the low SOC tertile was 2.27 (95% CI: 1.12-4.59, p = 0.02) and among blue-collar workers the relative risk for all-cause mortality was stable (1.33-1.52) in each SOC tertile. The classic risk factors, smoking and alcohol, showed higher relative risks than the SOC.

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High-density lipoproteins (HDLs) play an important role in the process of reverse cholesterol transport, the pathway by which the cholesterol in extrahepatic tissues is transported through plasma to the liver for recycling or for excretion from the body in bile. The concentration of HDL cholesterol is a powerful inverse predictor of the development of coronary heart disease, leading to a widely held view that HDL protects against the development of atherosclerosis. The mechanism by which HDLs protect is unknown. To date, no studies have been designed specifically to test the proposition that increasing the concentration of HDL cholesterol translates into a reduction in coronary risk. Nevertheless, in a subgroup of the Helsinki Heart Study, it was found that a substantial proportion of the beneficial effect of gemfibrozil was explicable in terms of an increase in the concentration of HDL cholesterol.

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Occurrence of five non-steroidal anti-inflammatory drugs (salicylic acid, ibuprofen, naproxen, indomethacin and diclofenac) and three lipid regulators (bezafibrate, clofibric acid and gemfibrozil) was investigated in wastewater, sewage sludge, and river water of the urban section of the Pearl River at Guangzhou in South China. Behavior and fate of the pharmaceuticals during treatment in two sewage treatment plants (STPs) were also studied in depth by determining concentrations in the influents and effluents at major treatment units and the sewage sludge. Concentrations of the pharmaceuticals in the raw wastewater were mostly at ng L(-1) levels except salicylic acid whose concentrations ranged from 9.6 to 23.3 μg L(-1). No significant amount of the pharmaceuticals was detected in the suspended particulate matter of wastewater and sewage sludge. Salicylic acid, indomethacin, and naproxen were almost completely removed (≥ 99%); gemfibrozil, ibuprofen and bezafibrate were significantly removed (>75%), whereas diclofenac and clofibric acid were removed by 60-70% during treatment in the STPs. Generally, biodegradation was the governing process for elimination of the investigated pharmaceuticals. Anaerobic biodegradation was responsible for most of the removal of diclofenac whereas aerobic biodegradation also played an important role in elimination of the other pharmaceuticals except SA, which was nearly completely removed after the anoxic process. In the Pearl River, the pharmaceuticals were widely detected. Both the concentrations and detection frequency were higher in March 2008 than those in the other seasons, which may be ascribed mainly to less dilution caused by lower precipitation. Besides the STPs, urban canals directly connected with the Pearl River may also be important contributors to the pharmaceutical contamination in the river.

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In addition to the lipid lowering effect, both simvastatin and gemfibrozil also influence the release of PDGF-Band TGF-1 in the neointima after de-endothelialization.

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Gemfibrozil is a widely used drug that elevates plasma HDL and lowers triglycerides and LDL. The mechanism of action of this pharmacological agent on HDL metabolism is not established. Since the liver is the major organ involved in HDL production and removal, we assessed the effect of gemfibrozil on the modulation of apoA-I (a major protein of HDL)-containing particles by a human hepatoblastoma cell line (Hep G2). Incubation of Hep G2 cells with gemfibrozil resulted in the following statistically significant findings: (1) increased accumulation of apoA-I in the medium without affecting uptake of radiolabeled HDL-protein or HDL-apoA-I; (2) accelerated incorporation of [3H]leucine and [35S]methionine into apoA-I; (3) equivalent increases in [3H]leucine incorporation into HDL particles without and with apoA-II (LpA-I and LpA-I+A-II, respectively); (4) equal efflux of fibroblast cholesterol by harvested LpA-I and LpA-I+A-II particles; (5) increased steady state apoA-I mRNA without affecting apoA-I transcription; and (6) increased apoA-I mRNA half-life (2.2-fold). These data indicate that gemfibrozil stabilizes apoA-I mRNA transcripts, resulting in increased translation of functional apoA-I-containing particles capable of effluxing cellular cholesterol, thus defining a major mechanism by which gemfibrozil increases HDL.

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Peroxisome proliferators (PPs) regulate a battery of rodent P450 genes, including CYP2B, CYP2C, and CYP4A family members. We hypothesized that other components of the P450-metabolizing system are altered by exposure to PPs, including NADPH-cytochrome P450 oxidoreductase (P450R), an often rate-limiting component in P450-dependent reactions. In this study, we determined whether exposure to structurally diverse PPs alters the expression of P450R mRNA and protein. Increases in P450R mRNA levels were observed in male and female F-344 rat livers and in male rat kidneys after chronic exposure of the animals to PPs. Paradoxically, under the same treatment conditions in male rats, liver P450R protein levels decreased after exposure to the PPs Wy-14,643 ([4-chloro-6-(2,3-xylidino)pyrimidynylthio]acetic acid) (WY) or gemfibrozil (GEM). The down-regulation of the P450R protein was sex- and tissue-specific in that exposure to PPs led to increases in P450R protein in female rat livers [di-n-butyl phthalate (DBP) only] and male rat kidneys (WY, GEM, DBP). In male wild-type SV129 mice, P450R mRNA levels increased in livers after exposure to WY and diethylhexyl phthalate (DEHP) and in male kidneys after exposure to DEHP. Induction of mRNA by PPs was not observed in the liver or kidneys of mice, which lack a functional peroxisome proliferator-activated receptor alpha (PPAR alpha), the central mediator of the effects of PPs in the rodent liver. In wild-type male mice, P450R protein was decreased in liver after WY and DEHP treatment and in kidneys after WY treatment. The down-regulation of the P450R protein was not observed in PPAR alpha-null mice. These studies demonstrate the complex regulation of P450R expression by PPs at two different levels, both of which are dependent upon PPAR alpha: up-regulation of transcript levels in liver and kidneys and down-regulation of protein levels in male rat and mouse liver by a novel posttranscriptional mechanism.

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In men with CHD and a low high-density lipoprotein cholesterol level, gemfibrozil use was associated with a reduction in major cardiovascular events in persons with diabetes and in nondiabetic subjects with a high fasting plasma insulin level.

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This randomized, parallel-group, multicenter clinical trial compared a newly developed, once-daily, extended-release formulation of gemfibrozil (Lopid SR) and gemfibrozil twice daily (Lopid) in terms of lipid-regulating effects and toxicity. Patients were men and women with elevations of low-density lipoprotein cholesterol and low levels of high-density lipoprotein cholesterol. The trial consisted of a 1-week screening period, an 8-week diet baseline period (Step One Diet), and a 24-week double-blind treatment period (extended-release gemfibrozil 1,200 mg once daily vs gemfibrozil 600 mg twice daily). At the end of the trial, the 2 treatment groups showed comparable improvements in all primary lipid factors: mean percent changes in triglyceride, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were -32, +10 and -10% for extended release (n = 325) and -36, +11 and -10% for twice daily (n = 330). The 90% confidence interval for the relative difference between the treatment means fell within the equivalence bounds of +/- 35% for all 3 factors, demonstrating equivalence of efficacy. Adverse events were reported at low rates and were similarly distributed in frequency and intensity between treatment groups; they were preponderantly mild or moderate, and gastrointestinal effects were the most frequent. The once-daily formulation of gemfibrozil may afford better control of dyslipidemia through improved compliance by patients who have this asymptomatic disease.

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Human pharmaceuticals, like the lipid lowering agent gemfibrozil and the non-steroidal anti-inflammatory drug diclofenac are causing environmental concern. In this study, the marine mussel (Mytilus spp.) was exposed by injection to environmentally relevant and elevated (1 μg/L and 1000 μg/L) concentrations of both compounds and biomarker expression was observed. Gemfibrozil exposure induced biomarkers of stress (glutathione S-transferase and metallothionein) at both concentrations 24h and 96 h after exposure, respectively. Biomarkers of damage (lipid peroxidation (LPO) and DNA damage) were significantly affected, as well as the biomarker for reproduction, alkali-labile phosphate assay, indicating the potential oxidative stress and endocrine disrupting effect of gemfibrozil. Diclofenac significantly induced LPO after 96 h indicating tissue damage. Additionally standard toxicity tests using the marine species Vibrio fischeri, Skeletonema costatum and Tisbe battagliai showed differences in sensitivity to both drugs in the mg/L range. Results indicate a suite of tests should be used to give accurate information for regulation.

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Gemfibrozil may induce a local myositis which, in our patient, precipitated an acute compartment syndrome. One should be alert to symptoms of possible drug-induced myositis in patients receiving gemfibrozil. Extreme caution should be exercised in its use in patients with impaired renal function.

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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 demography of dyslipidemia has changed towards a more complex atherogenic dyslipidemia involving increased levels of LDL cholesterol, in particular highly atherogenic small dense particles, hypertriglyceridemia and low HDL cholesterol, together with increased levels of markers of inflammation, thrombogenesis and endothelial dysfunction. Statins were shown to significantly lower cardiovascular morbidity and mortality, but treated patients are still left with a high residual risk, in particular for those with metabolic syndrome, type 2 diabetes, or low HDL cholesterol levels. Fibrates have been shown to reduce plasma triglycerides and increase HDL cholesterol, while improving inflammation, thrombogenesis and endothelial dysfunction. Clinical trials with fibrates have demonstrated their potential to reduce cardiovascular morbidity and mortality too, often through other mechanisms than those of statins. Combination trials of statins with fibrates have shown a more complete improvement of lipid profile and risk markers than each class separately. In contrast with gemfibrozil, fenofibrate does not interact significantly with the pharmacokinetics of statins, and its combination with statins has been shown to have a low risk of muscular side-effects or liver toxicity. The ACCORD outcome trial is exploring possible benefits of the combination of fenofibrate with statins on morbidity and mortality of patients with type 2 diabetes.

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We included 13 trials involving a total of 16,112 participants. Eleven trials recruited participants with history of coronary heart disease, two trials recruited participants with history of stroke, and one trial recruited participants with a mix of people with CVD. We judged overall risk of bias to be moderate. The meta-analysis (including all fibrate trials) showed evidence for a protective effect of fibrates primarily compared to placebo for the primary composite outcome of non-fatal stroke, non-fatal myocardial infarction (MI), and vascular death (risk ratio (RR) 0.88, 95% confidence interval (CI) 0.83 to 0.94; participants = 16,064; studies = 12; I(2) = 45%, fixed effect). Fibrates were moderately effective for preventing MI occurrence (RR 0.86, 95% CI 0.80 to 0.93; participants = 13,942; studies = 10; I(2) = 24%, fixed effect). Fibrates were not effective against all-cause mortality (RR 0.98, 95% CI 0.91 to 1.06; participants = 13,653; studies = 10; I(2) = 23%), death from vascular causes (RR 0.95, 95% CI 0.86 to 1.05; participants = 13,653; studies = 10; I(2) = 11%, fixed effect), and stroke events (RR 1.03, 95% CI 0.91 to 1.16; participants = 11,719; studies = 6; I(2) = 11%, fixed effect). Excluding clofibrate trials, as the use of clofibrate was discontinued in 2012 due to safety concerns, the remaining class of fibrates were no longer effective in preventing the primary composite outcome (RR 0.90, 95% CI 0.79 to 1.03; participants = 10,320; studies = 7; I(2) = 50%, random effects). However, without clofibrate data, fibrates remained effective in preventing MI (RR 0.85, 95% CI 0.76 to 0.94; participants = 8304; studies = 6; I(2) = 47%, fixed effect). There was no increase in adverse events with fibrates compared to control. Subgroup analyses showed the benefit of fibrates on the primary composite outcome to be consistent irrespective of age, gender, and diabetes mellitus.

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Serum triglyceride concentration was lowered by 49%. Serum high density lipoprotein (HDL) cholesterol concentration was raised by 11% with percentage shift towards the smaller HDL3c subfraction. The low-density lipoprotein cholesterol concentration remained unchanged. The proportion of glucose-intolerant subjects and insulin sensitivity were not altered by gemfibrozil. Plasma PAI-1 activity and fibrinogen levels were unaffected by gemfibrozil. The serum activity of gamma-glutamyltranspeptidase was lowered in all patients.

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Fibric acid derivatives have been demonstrated to reduce circulating lipoprotein and triacylglycerol concentrations and to inhibit hydroxymethylglutaryl CoA reductase, a key regulatory enzyme of cholesterol biosynthesis. This study describes the effect of four fibric acid derivatives on the biosynthesis of isoprenoid products from acetate and mevalonate in Molt-4 cells, a human leukemic T-lymphocyte cell line. The isoprenoids analyzed were cholesterol as well as dolichol and ubiquinone, alternative products of the branched isoprenoid biosynthetic pathway. None of the fibric acid derivatives showed significant effects on the synthesis of cholesterol from acetate or mevalonate and there was little change in the flux of these metabolites into either dolichol and ubiquinone compared to cells grown in drug-free medium. Therefore, in contrast to the reported inhibitory effects of fibric acids on hepatic sterol synthesis in rats and humans and on hydroxymethylglutaryl CoA reductase activity in human nonmalignant lymphocytes, our results show that these drugs do not significantly affect any of the post-reductase enzymes in the branched metabolic pathways leading from acetate to dolichol, ubiquinone and cholesterol in short term culturing of human malignant lymphocytes.

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Interest in the role of fibrates intensified after the publication of the negative results from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, which assessed therapy with fenofibrate plus statins. The evidence for clinical benefit in outcomes with the use of fibrates is heavily weighted on the use of the older fibrates such as gemfibrozil and clofibrate.

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Zomepirac, ibuprofen, gemfibrozil, and compounds A, B, C, and D were incubated in the presence of rat microsomal protein and uridine 5'-diphosphoglucuronic acid (UDPGA), followed by addition of human plasma to evaluate degradation kinetics of the acylglucuronides. As a comparison, authentic acylglucuronide standards of zomepirac, ibuprofen, gemfibrozil, and compounds A, B, C, and D were chemically synthesized and were evaluated for degradation kinetics.

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One questionnaire presented results for three end points of the Helsinki Heart Study as separate drug trials using only absolute differences in events; the other showed the same end points as relative differences. Both questionnaires included a fourth "trial," showing person-years of treatment needed to prevent one myocardial infarction.

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Gemfibrozil is a lipid-regulating agent which is generically classified as a fibric acid derivative, but which exhibits different pharmacological effects from other such drugs. Published data indicate that in patients with all types of dyslipidaemia (except type I) gemfibrozil 800 to 1200 mg/day is particularly effective in reducing total plasma triglyceride concentrations. The reduction in total plasma cholesterol is statistically significant with the most pronounced response occurring in patients with severe hypercholesterolaemia. Gemfibrozil also effectively increases high density lipoprotein cholesterol. In a 5-year double-blind prospective placebo-controlled study in over 4000 male patients with types IIa, IIb and IV primary dyslipidaemia (but without coronary symptoms), gemfibrozil 600mg twice daily significantly reduced the incidence of cardiac events (by 34%) compared with placebo, although overall mortality was not affected. In comparative studies with clofibrate similar reductions in plasma lipid levels have been observed, although these changes tend to be more favorable overall with gemfibrozil. Gastrointestinal symptoms and rash are the only side effects produced more frequently with gemfibrozil than with placebo. Although gemfibrozil is hepatotoxic in male rats, drug-induced pathological liver changes have not been reported in humans. Thus, gemfibrozil is an effective drug indicated for the treatment of severe hypertriglyceridaemia, and in certain patients with severe hypercholesterolaemia who are unresponsive to other standard therapies. In addition, it would appear to reduce the risk of cardiac events in patients with dyslipidaemia, although its effects on overall mortality remain speculative.

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lopid 600 dose 2016-10-04

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 buy lopid abnormalities has not been evaluated in children.

lopid with alcohol 2016-02-04

We present the results of the study of lipid-modulating drugs (pravastatin, atorvastatin, simvastatin, and fibrate gemfibrozil) in complicated coronary heart disease (acute coronary syndrome without ST elevation, chronic heart failure. In acute coronary syndrome buy lopid statins produced a positive effect on some studied parameters, while in heart failure only the safety of short-term therapy with statins was demonstrated.

lopid generic equivalent 2015-12-25

Effects of lowering serum triglyceride levels were investigated among 44 elderly hypertriglyceridemic patients with risk factors for stroke, reduced cerebral perfusion, and a history compatible with symptomatic occlusive cerebrovascular disease. Patients were randomly assigned to either treatment with gemfibrozil, a lipid-lowering agent, or control conditions. Subjects in both groups were instructed to follow a diet recommended for lowering serum lipid levels, while the treatment group was additionally administered 600 mg daily of gemfibrozil. Subjects assigned buy lopid to the treatment group (n = 22) showed significant reductions in serum triglyceride levels (p less than .0005). Control subjects (n = 22) did not show any significant changes in serum triglyceride levels. There were also no significant changes in total cholesterol levels in either group. Analyses of values for mean bihemispheric gray matter cerebral blood flow measured by the xenon 133 inhalation method and cognitive scores tested by the Cognitive Capacity Screening Examination indicated that gemfibrozil-treated patients maintained significantly higher levels of cerebral perfusion and cognitive performance than untreated controls did. Regression analyses for different treatment intervals indicated that both cerebral blood flow and cognition showed linear improvements that correlated directly with the duration of treatment. Lowering triglyceride levels in hyperlipidemic subjects appears to benefit cerebral perfusion and cognitive performance after four to six months.

lopid dose administration 2016-08-18

Cytochrome P450 (CYP) buy lopid 3A4 is considered the most important enzyme in imatinib biotransformation. In a randomized, crossover study, 10 healthy subjects were administered gemfibrozil 600 mg or placebo twice daily for 6 days, and imatinib 200 mg on day 3, to study the significance of CYP2C8 in imatinib pharmacokinetics. Unexpectedly, gemfibrozil reduced the peak plasma concentration (Cmax) of imatinib by 35% (P < 0.001). Gemfibrozil also reduced the Cmax and area under the plasma concentration-time curve (AUC0-∞) of N-desmethylimatinib by 56 and 48% (P < 0.001), respectively, whereas the AUC0-∞ of imatinib was unaffected. Furthermore, gemfibrozil reduced the Cmax/plasma concentration at 24 h (C24 h) ratios of imatinib and N-desmethylimatinib by 44 and 17% (P < 0.05), suggesting diminished daily fluctuation of imatinib plasma concentrations during concomitant use with gemfibrozil. Our findings indicate significant participation of CYP2C8 in the metabolism of imatinib in humans, and support involvement of an intestinal influx transporter in imatinib absorption.

lopid mg 2017-04-22

Gemfibrozil significantly reduced fasting serum triglyceride concentrations (p < 0.001) but buy lopid had no effect on measures of diabetic control. Neither gemfibrozil nor placebo treatment altered insulin sensitivity of glucose or glycerol metabolism during low-dose insulin infusion, but significant falls in both non-esterified fatty acid (NEFA) (p = 0.003) and ketone concentrations (p = 0.002) were observed after treatment with gemfibrozil.

lopid medicine 2015-02-04

Gemfibrozil significantly lowers triglycerides and raises HDL with buy lopid reasonable safety in a pediatric population with metabolic syndrome.

lopid 160 mg 2016-05-08

Gemfibrozil was given at a daily oral buy lopid dose of 600 mg to 28 CAPD patients with serum triglyceride levels higher than 200 mg/dl, after 2 months of low fat low calorie diet. Eleven patients dropped out from the study due to spontaneous withdrawal of the drug or to intercurrent hospitalization. The 17 patients who completed the study showed a significant decrease in serum total (434.6 +/- 207.9 to 237.5 +/- 81.6 mg/dl, p 0.003), VLDL (268.8 +/- 17.8 to 109.2 +/- 66.9 mg/dl, p less than 0.005) and LDL (152.9 +/- 34.6 to 119.2 +/- 30.7 mg/dl, p = 0.004) triglyceride. Serum VLDL cholesterol increased from 108.7 +/- 54.1 to 59.9 +/- 29.0 mg/dl, p = 0.003. Serum HDL cholesterol decreased from 25.4 +/- 4.8 to 35.3 +/- 6.3 mg/dl (p less than 0.001). Apo A1 increased from 117.8 +/- 16.7 to 130.8 +/- 16.7 mg/dl (p less than 0.001) and Apo B increased from 173 +/- 26.7 to 137.8 +/- 21.9 mg/dl (p less than 0.001). No clinical or laboratory side effect was observed in the patients who completed the study. Therefore dropouts were due to the poor patients' compliance rather than to the severity of side effects.

lopid initial dose 2016-09-24

Gemfibrozil or placebo was administered for 3 months to 24 individuals with endogenous hypertriglyceridemia and normal glucose tolerance. Mean ( +/- SEM) fasting plasma triglyceride (TG) concentrations decreased (4.01 +/- 0.55 to 1.34 +/- 0.12 mmol/L; P < 0.001) and high density lipoprotein cholesterol concentrations increased (0.54 +/- 0.03 to 0.67 +/- 0.04 mmol/L; P < 0.001) in gemfibrozil-treated patients, associated with lower (P < 0.01-0.001) plasma free fatty acid and TG concentrations when measured at hourly intervals in response to breakfast (0800 h) and lunch (1200 h). However, day-long plasma glucose and insulin responses to meals in the 2 groups were similar before and after treatment, as were the steady state plasma glucose and insulin concentrations at the end of a 180-min infusion of somatostatin, insulin, and glucose. Thus, marked decreases in both plasma buy lopid TG and free fatty acid concentrations seen in association with gemfibrozil neither enhanced insulin-mediated glucose disposal nor lowered ambient plasma insulin concentrations in patients with endogenous hypertriglyceridemia.

lopid drug classification 2016-02-09

Coronary heart disease is the leading cause of death among patients with non-insulin-dependent diabetes mellitus (NIDDM). NIDDM patients have a high frequency of dyslipidemia, which along with obesity, hypertension, and hyperglycemia may contribute significantly to accelerated coronary atherosclerosis. Because risk factors for coronary heart disease are additive and perhaps multiplicative, even mild degrees of dyslipidemia may enhance coronary heart disease risk. Therefore, therapeutic strategies for management of NIDDM should give equal emphasis to controlling hyperglycemia and dyslipidemia. The National Cholesterol Education Program recently issued guidelines for treatment of hyperlipidemia in adults including diabetic patients. Because of the unique features of diabetic dyslipidemia, however, we suggest that certain modifications in these guidelines be made to meet specific needs of diabetic patients. For example, therapeutic goals for serum cholesterol reduction should be lower in diabetic patients than in nondiabetic subjects. Particular emphasis should be given to weight reduction in NIDDM patients. In some diabetic patients, monounsaturated fatty acids may be a better replacement for saturated fatty acids than carbohydrates. The target for cholesterol lowering should include both very-low-density lipoprotein and low-density lipoprotein (LDL) (non-high-density lipoprotein) rather than LDL alone. To obtain a substantial reduction of cholesterol levels, drug therapy may be required in many patients. However, first-line drugs for nondiabetic patients (nicotinic acid and bile acid sequestrants) may be less desirable in NIDDM patients than hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors buy lopid and even fibric acids. In fact, HMG CoA reductase inhibitors may be the drugs of choice for NIDDM patients with elevated LDL cholesterol and borderline hypertriglyceridemia, whereas gemfibrozil appears preferable for NIDDM patients with severe hypertriglyceridemia.

lopid overdose symptoms 2016-12-13

There is a considerable interest in developing potent and safe hypolipidemic drugs for the prevention and management of coronary heart disease in man. In rodents, many of these hypolipidemic compounds induce hepatomegaly, proliferation of peroxisomes and a polypeptide with an approximate mol. wt. of 80000 in liver cells. In the present study, we have examined 10 hypolipidemic compounds for the induction of peroxisome proliferation associated 80000 mol. wt. polypeptide (polypeptide PPA-80), peroxisomal enzymes and peroxisome proliferation in rat liver, in view of the emerging evidence that hepatic peroxisome proliferators as a class are carcinogenic in rats and mice. All ten compounds, fenofibrate (isopropyl-[4-(p-chlorobenzoyl)2-phenoxy-2-methyl] propionate; LS 2265 (taurine derivative of fenofibrate); bezafibrate (2-(4-(2-[4-chlorobenzamido)ethyl] phenoxy)-methyl propionic acid; gemfibrozil (5-2[2,5-dimethylphenoxy]2-2-dimethylpentanoic acid); methyl clofenapate (methyl-2-[4-(p-chlorophenyl)phenoxy]-2-methyl propionate); DG 5685 (5-[4-phenoxybenzyl]trans-2-(3-pyridyl)1,3-dioxane); DH 6463 (5-[4-phenoxybenzyl] trans-2-(3-pyrimidinyl)-1,3-dioxane); tiadenol(bis[hydroxyethylthio]-7, 10-decane); ciprofibrate (2,-[4-(2,2-dichlorocyclopropyl)-phenoxy]2-methyl propionic acid) and RMI-14,514 ( [5-tetradecycloxy]-2-furancarboxylic acid), produced a marked but variable increase in the activities of peroxisomal enzymes catalase, carnitine acetyltransferase, heat-labile enoyl-CoA hydratase and the fatty acid beta-oxidation system and in the amount of polypeptide PPA-80 as demonstrated by SDS-polyacrylamide gel electrophoresis. The peptide map patterns of polypeptide PPA-80 in liver induced by these compounds were strikingly similar. The ultrastructural studies demonstrate that fenofibrate, ciprofibrate, LS 2265, DG 5685 and DH 6463 can induce proliferation of peroxisomes in liver cells of rats, and further confirm the previous reports of hepatic peroxisome proliferative activity of methyl clofenapate, tiadenol, bezafibrate, gemfibrozil and RMI-14514, as shown morphologically. Whether these structurally unrelated chemicals or their metabolite(s) directly activate the peroxisome specific genes to induce this multi-enzyme system or they exert their action on peroxisomes indirectly by causing fatty acid overload in hepatocytes remains to be elucidated. These chemicals offer a simple and reproducible means of stimulating peroxisomal enzymes in liver and should serve as useful tools, for evaluating the implications of hepatic peroxisome proliferation and in elucidating the mechanism of peroxisome proliferator-induced carcinogenesis. buy lopid

lopid cost 2015-05-27

Immunoglobulin A (IgA) and G (IgG) antibodies to C. pneumoniae were measured using the microimmunofluorescence method. Lipopolysaccharide-containing immune complexes were measured using two antigen buy lopid -specific enzyme immunoassays, the lipopolysaccharide-capture and immunoglobulin M (IgM)-capture methods.

lopid dosage generic 2015-12-06

1. The roles of multidrug resistance-associated protein (Mrp) 2 deficiency and Mrp3 up-regulation were evaluated on the metabolism and disposition of gemfibrozil. 2. Results from in vitro studies in microsomes showed that the hepatic intrinsic clearance (CLint) for the oxidative metabolism of gemfibrozil was slightly higher (1.5-fold) in male TR- rats, which are deficient in Mrp2, than in wild-type Wistar rats, whereas CLint for glucuronidation was similar in both strains. 3. The biliary excretion of intravenously administered [14C]gemfibrozil was significantly impaired in TR-) rats compared with Wistar rats (22 versus 93% of the dose excreted as the acyl glucuronides over 72 h). Additionally, the extent of urinary excretion of radioactivity was much higher in buy lopid TR- than in Wistar rats (78 versus 2.6% of the dose). 4. There were complex time-dependent changes in the total radioactivity levels and metabolite profiles in plasma, liver and kidney, some of which appeared to be related to the up-regulation of Mrp3. 5. Overall, it was demonstrated that alterations in the expression of the transporters Mrp2 and Mrp3 significantly affected the excretion as well as the secondary metabolism and distribution of [14C]gemfibrozil.

lopid 80 mg 2016-02-14

Primary outcome was arterial function assessed by means of endothelial-dependent flow-mediated dilatation (FMD) and small-artery compliance (C2). Secondary buy lopid outcomes included endothelial-independent glyceryl trinitrate-mediated dilatation (GTNMD), large-artery compliance (C1), and levels of lipids, lipoproteins, and oxidized low-density lipoprotein, as well as markers of insulin resistance and inflammation.

lopid reviews 2017-12-19

The purpose of buy lopid the present study was to assess the effect of gemfibrozil on 12 independent coronary heart disease risk factors in patients with primary combined hyperlipidaemia.

lopid gemfibrozil dose 2015-09-12

Niacin ER can help control flushing events while providing favorable effects on lipids and lipoproteins. The generalizability of this analysis may be limited by self-selection and motivation of research subjects, Flonase Coupon Online and further studies of flushing in the clinical practice setting are warranted.

lopid 300 mg 2016-11-17

An assay procedure for diacylglycerol acyltransferase that allows rapid measurement of the activity of this enzyme in isolated hepatocytes is described. The one-step procedure involves permeabilization of the plasma membrane with digitonin and simultaneous measurement of diacylglycerol acyltransferase activity. Digitonin at a concentration of 64 microg/mg of cellular protein was found to be optimal for exposing microsomal diacylglycerol acyltransferase to the components of the assay. The enzyme assay is linear with time up to 4 min and with protein concentrations in the range Aricept Medication Classification 0.25-2.4 mg of cellular protein/assay. It is shown that there is a good correlation of cellular enzyme activity as determined in digitonin-permeabilized hepatocytes with the rate of triacylglycerol synthesis in intact hepatocytes.

lopid dosage instructions 2017-02-23

A randomized double-blind study was carried out with gemfibrozil (600 mg b.i.d.) vs placebo in 20 patients (twelve males and eight females, age 52 +/- 3 years, BMI 24.2 +/- 0.4) suffering from primary hypertriglyceridemia (Fredrickson's type IV). Each group was treated for a 12 week period with gemfibrozil (n = 10) or placebo (n = 10) patients) in a double-blind fashion. Total cholesterol, HDL-cholesterol (HDL-C) and its subfractions (HDL2-C and HDL3-C), blood glucose, Apolipoproteins A1 and B, fibrinogen, plasminogen, factor VII, t-PA:Ag and PAI activity pre- and post-venous occlusion (VO) were determined. In the gemfibrozil-treated group a significant decrease of total cholesterol and triglycerides and a significant Inderal 10mg Dosage increase of HDL-C and HDL2-C were found. During gemfibrozil treatment a significant reduction of factor VII, fibrinogen and plasminogen levels was also observed. After 12 weeks of treatment in the gemfibrozil group the release of t-PA:Ag in response to venous occlusion was significantly higher and plasma PAI activity was significantly lower than in placebo group. Moreover positive correlations between HDL cholesterol and t-PA:Ag post-VO (r = 0.56, P < 0.01) and between HDL2-C cholesterol and t-PA:Ag post-VO (r = 0.59, P < 0.01) and a negative correlation between triglycerides and t-PA:Ag post-VO (r = -0.65, P < 0.01) were found. The data obtained suggest that gemfibrozil, in addition to the well established lipid-regulating effect, appears to have a positive role in the regulation of reverse cholesterol transport and fibrinolytic system.

lopid normal dosage 2015-11-13

Children have been tested and treated for hypercholesterolemia for more than 30 years. Although most treatment regimens have been limited to dietary intervention, statin use is increasing. Statins have been used in children since 1987, but published sources have only reported on small numbers of children with severe hypercholesterolemia. The available data indicates that statins can be useful and well tolerated. New data will Exelon Generic Name be available in the next few years that will lead to the wider use of these drugs. Although statin drugs have proven to be safe in the adult population, physicians will be obliged to follow pediatric patients closely when these agents are widely used in the first few years. The use of highly effective safe drugs such as statins will allow for the assessment of the best time to initiate therapy in younger populations and what benefits may be found over the long term.

lopid maximum dose 2016-06-30

The risks of muscle adverse events related to use of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, increase significantly with the addition of interacting drugs to a patient's therapy. The mechanism for most statin drug interactions involves the cytochrome P-450 system, which provides an indication of which drugs may interact. However, it is difficult to predict the probability of a drug interaction in a given patient because there are individual differences in sensitivity to increased statin drug levels. Drug metabolism studies show simvastatin Levitra Tablets and lovastatin to be especially sensitive to the inhibiting effects of other drugs on the cytochrome P-450 3A4 (CYP3A4) isoenzyme. Atorvastatin metabolism is less affected by inhibitors of this isoenzyme. Case reports, postmarketing surveillance, and clinical trial data demonstrate the clinical effect of CYP3A4 inhibitors on statins. Also, through possible inhibition of statin biliary excretion and glucuronidation, gemfibrozil given concomitantly with rosuvastatin, lovastatin, and simvastatin significantly increases the risk of myopathy and rhabdomyolysis, a potentially life-threatening consequence of statin drug interactions.

lopid user reviews 2015-02-02

The pharmacokinetics and the mechanism of action of Lipitor Dosage Information the antihyperlipaemic compound 2-chloromethyl-5,6,7,8-tetrahydrobenzo(b)thieno[2,3-d]pyrimidin-4(3H)-on e (CAS 89587-03-3, LM-1554) have been studied. Serum concentrations were determined by reverse phase HPLC using methanol : water (60 : 40) as the solvent system. The results of pharmacokinetic studies suggest that the compound LM-1554 is poorly absorbed from the gastrointestinal tract after the oral administration in dogs and rabbits. The volume of distribution (Vd) was found to be low. The poor bioavailability (3-4%) and low volume of distribution of the compound LM-1554 suggest the gastrointestinal tract as the site of action for the antihyperlipaemic activity. This hypothesis is substantiated by the observations that the compound was found active in rabbits only when administered orally and found inactive by the parenteral route. Further, the cholesterol levels were found to increase in blood samples collected from the portal vein after oral administration of cholesterol in coconut oil to rats. This increase was found to be prevented by the compound LM-1554. In conclusion, the compound LM-1554 has a potential to be developed as an antihyperlipaemic agent. The mechanism of action of the compound LM-1554 appears to consist in the inhibition of cholesterol absorption in the gastrointestinal tract.

lopid tablets 600 2016-05-06

We report here that gemfibrozil (GFZ) inhibits axenic and intracellular growth of Legionella pneumophila and of 27 strains of wild-type and multidrug-resistant Mycobacterium tuberculosis in bacteriological medium and in human and mouse macrophages, respectively. At a concentration of 0.4 mM, GFZ completely inhibited L. pneumophila fatty acid synthesis, while at 0.12 mM it promoted cytoplasmic accumulation of polyhydroxybutyrate. To assess the mechanism(s) of these effects, we cloned an L. pneumophila FabI enoyl reductase homolog that complemented for growth an Escherichia coli strain carrying a temperature-sensitive enoyl reductase and rendered the complemented E. coli strain sensitive to GFZ at the nonpermissive temperature. GFZ noncompetitively inhibited this L. pneumophila FabI homolog, as well as M. tuberculosis InhA and E. coli FabI.

lopid 40 mg 2015-01-03

Our study indicated that fibrate therapy might play an important role in reducing the risk of fatal stroke in patients with previous diabetes, cardiovascular disease or stroke. However, it did not have an effect on the incidence of stroke.