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:
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.
The most common side effects associated with Lopid are:
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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Thirty patients with type II and IV hyperlidemia were studied by a double blind cross over technic. Gemfibrozil at dosages of 1200 mg and 1600 mg a day was compared to 2000 mg daily of clofibrate. The effect of each drug regimen is described for the entire study population and for those who were found to be responders.
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The lipid regulator gemfibrozil (GEM) is one of many human pharmaceuticals found in the aquatic environment. We previously demonstrated that GEM bioconcentrates in blood and reduces plasma testosterone levels in goldfish (Carassius auratus). In this study, we address the potential of an environmentally relevant waterborne concentration of GEM (1.5 microg/l) to induce oxidative stress in goldfish liver and whether this may be linked to GEM acting as a peroxisome proliferator (PP). We also investigate the autoregulation of the peroxisome proliferator-activated receptors (PPARs) as a potential index of exposure. The three PPAR subtypes (alpha, beta, and gamma) were amplified from goldfish liver cDNA. Goldfish exposed to a concentration higher (1500 microg/l) than environmentally relevant for 14 and 28 days significantly reduce hepatic PPARbeta mRNA levels (p<0.001). Levels of CYP1A1 mRNA were unchanged. GEM exposure significantly induced the antioxidant defense enzymes catalase (p<0.001), glutathione peroxidase (p<0.001) and glutathione-S-transferase (p=0.006) but not acyl-CoA oxidase or glutathione reductase. As GEM exposure failed to increase levels of thiobarbituric reactive substances (TBARS), we conclude that a sub-chronic exposure to GEM upregulates the antioxidant defense status of the goldfish as an adaptive response to this human pharmaceutical.
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Subjects were predominantly female (56.2%), with a mean age of 65.1 ± 11.5 years; 93.2% had hypertension; 29.0%, diabetes mellitus; and 10.2%, a history of myocardial infarction. The patients were being treated with lovastatin (84.1%) or gemfibrozil (12.3%)-both at doses below what is recommended-or atorvastatin (1.8%). In patients with high cardiovascular risk, 38.6% achieved goals for low-density lipoprotein cholesterol (LDL-C) levels (<100 mg/dL). Among those at moderate risk, 49.4% reached the target level (< 130 mg/dL). On average, there was a 4.9% reduction in LDL-C. Sex, age, history of cardiovascular disease and/or diabetes mellitus, use of hydrochlorothiazide, and poor therapy adherence were statistically associated with a lack of dyslipidemia control.
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Preliminary results from clinical trials suggest that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors may help prevent acute renal allograft rejection. However, the mechanism for this putative effect of 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors, and whether it is independent of lipid-lowering per SE are unknown.
A 49-year-old woman with chronic renal failure was given gemfibrozil for hyperlipidemia. She developed gemfibrozil-induced myositis which precipitated an acute compartment syndrome, necessitating emergency fasciotomy. The muscle biopsy showed prominent degeneration of the skeletal muscle fibers, associated with moderate chronic inflammatory infiltration. Electron microscopy revealed myofibrillary fragmentation and mitochondrial disorganization. The clinicopathologic features of gemfibrozil-induced myositis appear to be distinct from those of clofibrate-induced muscular syndrome. Extreme caution should be exercised in the use of gemfibrozil in patients with impaired renal function.
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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, and further studies of flushing in the clinical practice setting are warranted.
Familial combined hyperlipidaemia (FCH), characterized by elevated very-low-density lipoprotein (VLDL) and/or low-density lipoprotein (LDL), is associated with an increased prevalence of premature cardiovascular disease. Therefore, lipid-lowering is frequently indicated.
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Hyperlipidemia has been implicated in the pathogenesis of experimental progressive glomerulosclerosis, but its role in human renal injury is controversial. This report describes a 12-yr-old boy presenting with massive proteinuria, hepatomegaly, anemia, severe mixed hyperlipidemia, and progressive renal failure. The initial renal biopsy disclosed large numbers of foam cells that were shown to be monocytes. Evidence is presented suggesting that apoprotein-E2 homozygosity in our patient, together with an 88% reduction in plasma lipoprotein lipase activity associated with severe nephrotic syndrome, is responsible for the atypical clinical features, lipoprotein phenotype III with chylomicronemia, and renal lipidosis. A regimen of dietary lipid restriction, gemfibrozil, and niacin resulted in significant but partial improvement of the dyslipidemia and resolution of the hepatomegaly and ascites. This report stresses the importance of characterizing unique lipid disorders in patients with nephrotic syndrome in order to prescribe effective lipid-lowering strategies. Moreover, the striking resemblance of the clinical and nephrohistologic features of this patient to those occurring in experimental models of coexisting glomerular injury and hyperlipidemia led to the speculation that, in this setting, the hyperlipidemia may contribute to the development of progressive glomerulosclerosis.
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The primary objective of this study was to determine the presence of unregulated organic chemicals in reclaimed water using complementary targeted and broad spectrum approaches. Eleven of 12 targeted human pharmaceuticals, antioxidants, and plasticizers, and 27 tentatively identified non-target organic chemicals, were present in secondary effluent entering tertiary treatment trains at a wastewater treatment plant and two water reclamation facilities. The removal of these compounds by three different tertiary treatment trains was investigated: coagulant-assisted granular media filtration (California Title-22 water, 22 CCR 60301-60357; Barclay ), lime clarification/reverse osmosis (lime/ RO), and microfiltration-reverse osmosis (MF/RO). Carbamazepine, clofibric acid, gemfibrozil, ibuprofen, p-toluenesulfonamide, caffeine, butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), and N-butyl benzenesulfonamide (N-BBSA) were present at low to high nanogram-per-liter levels in Title 22 water. The lime/RO product waters contained lower concentrations of clofibric acid, ibuprofen, caffeine, BHA, and N-BBSA (<10 to 71 ng/L) than their Title 22 counterparts. The MF/RO treatment reduced concentrations to levels below their detection limits, although BHT was present in MF/RO product water from one facility. The presence of the target analytes in two surface waters used as raw drinking water sources and a recharged groundwater was also examined. Surface waters used as raw drinking water sources contained caffeine, BHA, BHT, and N-BBSA, while recharged groundwater contained BHT, BHA, and N-BBSA. Nontarget compounds in recharged groundwater appeared to be attenuated with increased residence time in the aquifer.
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Large-scale intervention trials demonstrate that treatment with statins, the most effective lipid lowering drug class, significantly reduces the risk of coronary heart disease events. Recent evidence suggests that more aggressive LDL cholesterol lowering with newly developed statins may provide greater clinical benefit, even in individuals with moderately elevated serum cholesterol levels. There is increasing evidence that statins exert a myriad of other beneficial pleiotropic effects on the vascular wall, thus altering the course of atherosclerotic disease. In the long-term treatment, non-life-threatening side effects may occur in up to 15% of patients receiving one statin. Significant elevations in the activity of serum aminotransferase and creatine kinase alone or in combination with muscle pain in statin-treated patients should be taken seriously. The combination of the statins with gemfibrozil results in higher rates of drug toxicity. Reports show possible adverse effects of statins on nervous system function including mood alterations, however, statins have also been associated with improvement in central nervous system disorders. Special attention must be paid to the tolerability of the statins in children, elderly and transplant patients. Future clinical studies and surveillance information will warrant long term safety of each member of this class of lipid-lowering agents. New classes of patients with diabetes, metabolic syndrome and renal diseases may have clinical benefits from statins. New upcoming clinical trials will address the fundamental question of whether statin treatment can protect from the natural history of atherosclerotic-related diseases. This will require a more prolonged follow-up (i.e., 10 to 15 years). Finally, the basic understanding of newer pathogenic mechanisms involving the effects of statins on angiogenesis and the nitric oxide pathway should be explored in the clinical setting as well as the study of pathogenic mechanisms by which statins can affect plaque instability.
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patients enrolled in a veterans hospital renal subspecialty clinic.
Triglyceride measurement is not informative on the specificity of the triglyceride-rich lipoproteins present in the plasma because some of these are not atherogenic (chylomicrons, large VLDLs) while others are highly atherogenic (small VLDLs, remnants, IDL...). Statins, in addition to reducing LDL-cholesterol, significantly reduced atherogenic remnant lipoprotein cholesterol levels. 4S, CARE+LIPID, and AFCAPS/TexCAPS studies, suggested enhanced therapeutic potential of statins for improving triglyceride and HDL-cholesterol levels in patients with CHD. A fibrate (gemfibrozil) was shown to reduce death from CHD and non-fatal myocardial infarction in secondary prevention of CHD in men with low levels of HDL-cholesterol (VA-HIT); during the treatment these levels predicted the magnitude of reduction in risk for CHD events.
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Individuals with diabetes require aggressive management of dyslipidaemia as part of an overall management strategy to reduce the risk of cardiovascular disease. Individuals with a previous cardiovascular disease event should be on lipid-lowering therapy, whereas in those who have not had a previous cardiovascular disease event, the decision to use lipid-lowering therapy should be based on lipid levels and the overall risk of a future event. The results of large studies that are currently in progress specifically in people with diabetes should resolve outstanding questions in relation to lipid-lowering therapy in diabetes.
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Gemfibrozil greatly increased the plasma concentration of parent pioglitazone and also inhibited the further metabolism of M-III and M-IV. Careful blood glucose monitoring and dosage adjustments are suggested during coadministration of pioglitazone and gemfibrozil.
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We obtained the first cohort (n = 50,000) dataset from the National Health Insurance Research Database and analyzed the outpatient claim files of the cohort in 2000. The antilipemic drugs were defined as the drug items belonging to the group C10 (serum lipid reducing agents) of the Anatomical Therapeutic Chemical classification system.
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In the published literature, cerivastatin was associated with much larger risks of rhabdomyolysis than other statins. Although only a small percentage of cerivastatin users also took gemfibrozil, approximately half of the case reports of rhabdomyolysis occurred in users of this combination therapy, and a cerivastatin-gemfibrozil interaction was supported by the results of a 3-day pharmacokinetic study. In internal company documents, multiple case reports suggested a drug-drug interaction within approximately 100 days of the launch in 1998; however, the company did not add a contraindication about the concomitant use of cerivastatin and gemfibrozil to the package insert for more than 18 months. Unpublished data available in July 1999 also suggested an increased risk of rhabdomyolysis associated with high doses of cerivastatin monotherapy. In late 1999 and early 2000, company scientists conducted high-quality analyses of the US Food and Drug Administration adverse event reporting system data. These analyses suggested that compared with atorvastatin calcium, cerivastatin monotherapy substantially increased the risk of rhabdomyolysis. To our knowledge, these findings were not disseminated or published. The company continued to conduct safety studies, some of them inadequately designed to assess the risk of rhabdomyolysis, until cerivastatin was removed from the market in August 2001.
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A series of pharmaceutically active compounds including diclofenac, gemfibrozil, ibuprofen, naproxen, 2-propylpentanoic acid, 4-biphenylacetic acid and tolfenamic acid can be reversibly intercalated into a layered double hydroxide, initial studies suggest that these materials may have application as the basis of a novel tuneable drug delivery system.
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Gemfibrozil (GFZ) is a relatively persistent pollutant in surface-water environments and it is rather recalcitrant to biological degradation. The GFZ photochemical lifetimes are relatively short in shallow waters with low levels of dissolved organic carbon (DOC), but they can reach the month-year range in deep and high-DOC waters. The main reason is that GFZ undergoes negligible reaction with singlet oxygen or degradation sensitised by the triplet states of chromophoric dissolved organic matter, which are the usually prevalent photochemical pathways in deep and high-DOC sunlit waters. Nitrate and nitrite scarcely affect the overall GFZ lifetimes, but they can shift photodegradation from direct photolysis to the OH process. These two pathways are the main GFZ phototransformation routes, with the direct photolysis prevailing in shallow environments during summer. Under these conditions the GFZ photochemical lifetimes are also shorter and the environmental significance of photodegradation correspondingly higher. The direct photolysis of GFZ under UVB irradiation yielded several transformation intermediates deriving from oxidation or cleavage of the aliphatic lateral chain. A quinone derivative (2,5-dimethyl-1,4-benzoquinone), a likely oxidation product of the transformation intermediate 2,5-dimethylphenol, is expected to be the most acutely and chronically toxic compound arising from GFZ direct photolysis. Interestingly, literature evidence suggests that the same toxic intermediate would be formed upon OH reaction.
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Twenty-eight normolipidemic men (total plasma cholesterol concentration [TC] < 230 mg/dL [< 6 mmol/L], plasma triglyceride [Tg] < 250 mg/dL [2.75 mmol/L]) with low plasma concentrations of HDL-C were randomly assigned to increasing doses of crystalline niacin (up to 3,000 mg/d) or no drug for 12 weeks, then crossed over to the alternate regimen. Outcome measures included changes in plasma lipoproteins and alimentary lipemia.
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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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Repaglinide metabolism was assessed in vitro (human liver subcellular fractions, fresh human hepatocytes, and recombinant enzymes) and the resulting incubates were analyzed, by liquid chromatography-mass spectrometry (LC-MS) and radioactivity counting, to identify and quantify the different metabolites therein. Chemical inhibitors, in addition to a trapping agent, were also employed to elucidate the importance of each metabolic pathway. Finally, a panel of human liver microsomes (genotyped for UGT1A1*28 allele status) was used to determine the importance of UGT1A1 in the direct glucuronidation of repaglinide.
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Twenty-nine hypercholesterolaemic patients, treated for one year with gemfibrozil but being still hypercholesterolaemic (serum total cholesterol greater than or equal to 6.25 mmol/l) were included in a double-blind trial to evaluate the hypocholesterolaemic effects of gemfibrozil-guar gum combination (GE + GU) vs. gemfibrozil-placebo combination (GE + PL) using a cross-over study design. The patients were treated with gemfibrozil on a constant dosage (range 900-1200 mg/day) during the entire trial. After a 4-week run-in period on GE + PL treatment the patients were randomly allocated to 2 groups: one received GE + GU 15 g/day, and the other GE + PL for 3 months and after that groups were crossed over. Guar gum and placebo were administered as granules taken 3 times a day during meals. Serum total cholesterol was 8.61 +/- 0.17 mmol/l before gemfibrozil therapy, and 7.29 +/- 0.15 mmol/l at the end of the run-in period on GE + PL (P less than 0.01). During the double-blind phase serum total cholesterol values were 6.28 +/- 0.19 mmol/l at the end of the GE + GU treatment period and 7.21 +/- 0.16 mmol/l at the end of the GE + PL treatment period (P less than 0.01). At the end of the GE + GU treatment period serum total cholesterol was 27% lower and LDL-cholesterol 39% lower than before gemfibrozil treatment. A marked improvement (23%) was found in HDL/LDL ratio during GE + GU treatment compared with GE + PL treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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A single dose of TS-PLA-NP and TS II(A) injection was administered to 8 healthy rabbits via the ear-edge vein, at the set time withdrew the blood and prepared. The concentrations of tashinone II(A) in plasma were measured by HPLC with gemfibrozil as the internal standard. The pharmacokinetic parameters of TS-PLA-NP and tashinone II(A) injection were calculated by program DAS2.0.
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One patient developed myalgia with a normal CK level after 4 months of combination therapy. Three patients had transient elevations in CK levels that ranged from 3 to 5 times the upper limits of "normal" and that returned to normal upon repeat testing. Liver function tests did not change significantly from baseline. In a subset of 26 previously untreated patients, combined pravastatin (mean daily dose 22 mg) and gemfibrozil (mean daily dose 1,154 mg) therapy lowered total cholesterol by 25% (p < 0.001), triglycerides by 53% (p = 0.0001), LDL cholesterol by 14% (p = 0.24), and increased high-density lipoprotein (HDL) cholesterol by 20% (p = 0.012).
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Amyloid precursor protein (APP) derivative β-amyloid (Aβ) plays an important role in the pathogenesis of Alzheimer's disease (AD). Sequential proteolysis of APP by β-secretase and γ-secretase generates Aβ. Conversely, the α-secretase "a disintegrin and metalloproteinase" 10 (ADAM10) cleaves APP within the eventual Aβ sequence and precludes Aβ generation. Therefore, up-regulation of ADAM10 represents a plausible therapeutic strategy to combat overproduction of neurotoxic Aβ. Peroxisome proliferator-activated receptor α (PPARα) is a transcription factor that regulates genes involved in fatty acid metabolism. Here, we determined that the Adam10 promoter harbors PPAR response elements; that knockdown of PPARα, but not PPARβ or PPARγ, decreases the expression of Adam10; and that lentiviral overexpression of PPARα restored ADAM10 expression in Ppara(-/-) neurons. Gemfibrozil, an agonist of PPARα, induced the recruitment of PPARα:retinoid x receptor α, but not PPARγ coactivator 1α (PGC1α), to the Adam10 promoter in wild-type mouse hippocampal neurons and shifted APP processing toward the α-secretase, as determined by augmented soluble APPα and decreased Aβ production. Accordingly, Ppara(-/-) mice displayed elevated SDS-stable, endogenous Aβ and Aβ1-42 relative to wild-type littermates, whereas 5XFAD mice null for PPARα (5X/α(-/-)) exhibited greater cerebral Aβ load relative to 5XFAD littermates. These results identify PPARα as an important factor regulating neuronal ADAM10 expression and, thus, α-secretase proteolysis of APP.
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