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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:
Apo-gemfibrozil, Pms-gemfibrozil

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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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Combinations of gemfibrozil and an HMG, compared with either agent alone, results in improved long-term control of lipid abnormalities in mixed lipid disorders. The low incidence of toxicity permits the use of combination therapy in patients at high risk of atherosclerotic complications.

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Although this double-blind, randomized trial was stopped after 6 months owing to the suspicion of drug interference, we report here on the results of baseline ultrasonographic examinations.

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The ultimate aim in treating hypertension and hyperlipidemia is to reduce cardiovascular mortality and morbidity, especially strokes and coronary events, for example, fatal and nonfatal myocardial infarction and sudden death. Extensive intervention studies in moderate-to-severe hypertension have revealed the significance of antihypertensive therapy in reducing total cardiovascular mortality and morbidity, particularly from cerebrovascular causes. However, the reduction of coronary events has not been equally successful. The situation in mild-to-moderate hypertension is even more disappointing: recent studies, such as the Medical Research Council hypertension trial, the international Prospective Primary Prevention Study in Hypertension, and the Heart Attack Primary Prevention in Hypertensives trial could not demonstrate any benefit from antihypertensive treatment with beta-blockers or diuretics in the prevention of coronary heart disease. The reasons for these negative results are not obvious. However, metabolic side effects associated with certain antihypertensive drugs, which counteract the beneficial effects of blood pressure reduction, are one topic of discussion. For the genesis of atherosclerosis of the coronary vasculature, hyperlipoproteinemia appears to be of greater importance than hypertension and has to be treated simultaneously. Two extensive intervention studies, the Lipid Research Clinics coronary primary prevention trial and the Helsinki Heart Study, showed a significant reduction of coronary events with lipid-lowering treatments with cholestyramine and gemfibrozil, respectively. These findings are in agreement with the results of a recent secondary prevention study, which showed a regression of atherosclerosis in coronary arteries and aortocoronary bypass grafts. Moreover, antihypertensive treatment aimed at a reduction in coronary heart disease has to focus on serum lipids, especially in mild hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

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Obesity and non-insulin-dependent diabetes favor storage of fatty acids in triacylglycerol over oxidation. Recently, individual acyl-CoA synthetase (ACS) isoforms have been implicated in the channeling of fatty acids either toward lipid synthesis or toward oxidation. Although ACS1 had been localized to three different subcellular regions in rat liver, endoplasmic reticulum, mitochondria, and peroxisomes, the study had used an antibody raised against the full-length ACS1 protein which cross-reacts with other isoforms, probably because all ACS family members contain highly conserved amino acid sequences. Therefore, we examined the subcellular location of ACS1, ACS4, and ACS5 in rat liver to determine which isoform was present in peroxisomes, whether the ACSs were intrinsic membrane proteins, and which ACS isoforms were up-regulated by PPAR alpha ligands. Non-cross-reacting ACS1, ACS4, and ACS5 peptide antibodies showed that ACS4 was the only ACS isoform present in peroxisomes isolated from livers of gemfibrozil-treated rats. ACS4 was also present in fractions identified as mitochondria-associated membrane (MAM). ACS1 was present in endoplasmic reticulum fractions and ACS5 was present in mitochondrial fractions. Incubation with troglitazone, a specific inhibitor of ACS4, decreased ACS activity in the MAM fractions 30-45% and in the peroxisomal fractions about 30%. Because the signal for ACS4 protein in peroxisomes was so strong compared to the MAM fraction, we examined ACS4 mRNA abundance in livers of rats treated with the PPAR alpha agonist GW9578. Treatment with GW9578 increased ACS4 mRNA abundance 40% and ACS1 mRNA 25%. Although we had originally proposed that ACS4 is linked to triacylglycerol synthesis, it now appears that ACS4 may also be important in activating fatty acids destined for peroxisomal oxidation. We also determined that, unlike ACS1 and 5, ACS4 is not an intrinsic membrane protein. This suggests that ACS4 is probably targeted and linked to MAM and peroxisomes by interactions with other proteins.

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Fibrates are an important class of drugs for the management of dyslipidemia. This class of drugs is generally well tolerated but is infrequently associated with several safety issues. Fibrates, most likely by an effect mediated by peroxisome proliferator-activated receptor-alpha, may reversibly increase creatinine and homocysteine but are not associated with an increased risk for renal failure in clinical trials. Fibrates are associated with a slightly increased risk (<1.0%) for myopathy, cholelithiasis, and venous thrombosis. In clinical trials, patients without elevated triglycerides and/or low high-density lipoprotein cholesterol (HDL) levels, fibrates are associated with an increase in noncardiovascular mortality. In combination with statins, gemfibrozil generally should be avoided. The preferred option is fenofibrate, which is not associated with an inhibition of statin metabolism. Clinicians are advised to measure serum creatinine before fibrate use and adjust the dose accordingly for renal impairment. Routine monitoring of creatinine is not required, but if a patient has a clinically important increase in creatinine, and other potential causes of creatinine increase have been excluded, consideration should be given to discontinuing fibrate therapy or reducing the dose.

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In selected patients at high risk for pancreatitis, the potential risk of gemfibrozil use during pregnancy may be offset by its benefits in the management of severe hypertriglyceridemia.

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The ingestion of alcohol (Alc) as well as gemfibrozil (Gem), a fibrate drug used to treat hypertriglyceridaemia, may occur on a long-term basis in humans. Since both Alc and Gem can disturb liver function, we assessed the effects of administering Alc together with Gem in Wistar rats.

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To evaluate the incidence and clinical consequences of the use of lovastatin or simvastatin with concomitant CYP3A4 inhibitors and inducers, and with fibrates.

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Compacts of the parent drug and the salts were used to determine Young's modulus of elasticity using beam bending tests. Crystal structures were determined previously from X-ray powder diffraction data.

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

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lopid gemfibrozil dose 2016-01-27

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily. PPAR gamma ligands, which include the naturally occurring PG metabolite 15-deoxy-Delta(12,14)-PGJ(2) (15d-PGJ(2)), as well as thiazolidinediones, have been shown to have anti-inflammatory activity. The PPAR alpha agonists, gemfibrozil, ciprofibrate, and fenofibrate, have an excellent track history as oral agents used to treat hypertriglyceridemia. In the present study, we demonstrate that these PPAR alpha agonists can increase the production of the Th2 cytokine, IL-4, and suppress proliferation by TCR transgenic T cells specific for the myelin basic protein Ac1-11, as well as reduce NO production by microglia. Oral administration of gemfibrozil and fenofibrate inhibited clinical signs of experimental autoimmune encephalomyelitis. More importantly, gemfibrozil Flagyl Overdose was shown to shift the cytokine secretion of human T cell lines by inhibiting IFN-gamma and promoting IL-4 secretion. These results suggest that PPAR alpha agonists such as gemfibrozil and fenofibrate, may be attractive candidates for use in human inflammatory conditions such as multiple sclerosis.

lopid generic price 2017-11-03

To describe the prevalence of prescribing against-label statin-fibrate Augmentin Maximum Dosage combination therapy.

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Eicosapentaenoic acid (EPA) is a triglyceride-lowering agent that reduces circulating levels of the apolipoprotein B (apoB)-containing lipoprotein particles small dense low-density lipoprotein (sdLDL), very-low-density lipoprotein (VLDL), and oxidized low-density lipoprotein (LDL). These benefits may result from the direct antioxidant effects of EPA. To investigate this potential mechanism, these particles were isolated from human plasma, preincubated with EPA in the absence or presence of atorvastatin (active) metabolite, and subjected to copper-initiated oxidation. Lipid oxidation was measured as a function of Allegra Tablet Ingredients thiobarbituric acid reactive substances formation. EPA inhibited sdLDL (IC50 ∼2.0 μM) and LDL oxidation (IC50 ∼2.5 μM) in a dose-dependent manner. Greater antioxidant potency was observed for EPA in VLDL. EPA inhibition was enhanced when combined with atorvastatin metabolite at low equimolar concentrations. Other triglyceride-lowering agents (fenofibrate, niacin, and gemfibrozil) and vitamin E did not significantly affect sdLDL, LDL, or VLDL oxidation compared with vehicle-treated controls. Docosahexaenoic acid was also found to inhibit oxidation in these particles but over a shorter time period than EPA. These data support recent clinical findings and suggest that EPA has direct antioxidant benefits in various apoB-containing subfractions that are more pronounced than those of other triglyceride-lowering agents and docosahexaenoic acid.

lopid usual dosage 2015-11-22

A variety of treatments to lower elevated plasma lipid levels in patients with hyperlipidemia are available. Adverse side effects ranging from mere annoyances to uncommon serious consequences may be associated with dietary modification, recreational physical exercise, and drug intervention. As in other clinical circumstances, risk-to-benefit Zetia Generic Cost ratios must be taken into consideration in the management of hyperlipidemia.

lopid 450 mg 2017-10-02

The bactericidal activity of levofloxacin at therapeutic levels, alone or Copegus 400 Mg in combination with various efflux-pump inhibitors or alkalinizing agents, was studied against Staphylococcus aureus ATCC 25923 in Mueller-Hinton (MH) broth and in a THP-1 monocytic cell model, using intracellular salt medium (ISM) mimicking the phagolysosomal environment, and in cell lysate.

lopid initial dose 2015-03-01

Primary cultures Mysoline 100 Mg of hepatocytes were established from sexually mature male rainbow trout (Oncorhyncus mykiss) and treated with the hypolipidemic drugs gemfibrozil (0.25-1.25 mM), clofibric acid (2.25-3.00 mM), or ciprofibrate (0.25-1.00 mM). Significant dose-related increases in peroxisomal fatty acyl-CoA oxidase (FACO) were seen after exposure for 48 hr to clofibric acid (P < 0.01) and ciprofibrate (P < 0.05) but not gemfibrozil (P = 0.08). Strong correlation was obtained between increased acyl-CoA oxidase activity and the relative amount of peroxisomal bifunctional enzyme (PBE), further supporting evidence of a proliferative effect. These preliminary studies demonstrate that peroxisomal beta-oxidation can be induced in vitro in a primary rainbow trout hepatocyte system.

lopid user reviews 2016-01-27

Severe combined hyperlipidaemia has occasionally been associated with infiltration of tissues in addition to arteries and the skin. We report a woman with Type 2 diabetes mellitus (DM) and severe combined hyperlipidaemia who developed retinal lipid infiltration, resulting in blindness. A 61-year-old woman with Zovirax Max Dose a 15-year history of Type 2 DM was admitted following a two-week history of progressive visual loss. Examination identified lipid infiltration into the retina. Phenotypically she had severe combined hyperlipidaemia with elevated IDL cholesterol and a broad beta band on lipoprotein electrophoresis, raising the possibility of familial dysbetalipoproteinaemia. However, gene sequencing analysis indicated that the patient was homozygous for the E3/E3 allele of the ApoE gene with no mutations detected in either the coding region or intron-exon boundaries. Her lipid profile improved following dietary therapy and gemfibrozil treatment, but this had little effect on either her fundal appearances or her visual acuity. Type 2 DM plays a vital role both in allowing expression of severe combined hyperlipoproteinaemia, in addition to serving as a risk factor for complications such as tissue infiltration.

lopid dosage instructions 2017-11-25

We Altace Drug Classification present clinical data and laboratory findings in a 33-year-old woman with generalized fatigue, a recent 5-kg weight loss, and a papular rash on the extremities as well as a history of diabetes and hypertension.

lopid dose administration 2016-10-15

The occurrence of pharmaceuticals, nonylphenol ethoxylate metabolites, and Diovan Tab other wastewater-derived contaminants in surface waters is a potential environmental concern, especially since the discovery of contaminants with endocrine-disrupting properties. The present study investigated the discharge of emerging contaminants into the Santa Ana River (CA, USA) and their attenuation during river transport and passage through a constructed wetland. Contaminants studied included pharmaceuticals (gemfibrozil, ibuprofen, naproxen, ketoprofen, and carbamazepine) and their metabolites, hormones, the metabolites of alkylphenol polyethoxylates (APEMs), N-butyl benzenesulfonamide (NBBS), and chlorinated tris-propylphosphates (TCPPs). The APEMs included alkylphenols (APs), short-chain AP polyethoxylates (APEOs), AP polyethoxycarboxylates (APECs), and carboxylated APECs (CAPECs). In wastewater treatment plant effluent, APECs and CAPECs represented the dominant APEM fraction (1.8-18.7 microg/L), whereas APEOs and APs contributed only small amounts to the overall APEM concentrations (0.10-0.92 and < or =0.1 microg/L, respectively) except where the effluent was infiltrated into soil (5.2 microg/L). In effluents, ibuprofen and its metabolites, TCPPs, and NBBS were detected regularly (<0.5 microg/L), and the other pharmaceuticals were detected occasionally. Transport in the Santa Ana River for 11 km resulted in the significant attenuation of all contaminants, from 67% for gemfibrozil to 100% for others. Wetland treatment (residence time, 2-4 d) resulted in partial removal of ibuprofen, gemfibrozil, and TCPPs and transformed APEOs to APECs.