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.
To present a case of gemfibrozil-induced myositis which precipitated an acute compartment syndrome.
Eight patients completed the study. Three of these patients met the predetermined criterion of a clinically meaningful Lp(a) reduction of 33%. The mean percentage change in Lp(a) was not statistically significant with values of -18.3 +/- 15.4% (p = 0.14, 1-tailed). All patients demonstrated a significant decrease in plasma triglycerides. The mean percentage change was -62.5 +/- 1.8% (p < 0.001, 1-tailed). The mean percentage change in total cholesterol was -12.4 +/- 3.8% (p = 0.007, 1-tailed). Gemfibrozil was considered suspect in five of 16 adverse events reported, but only one of these (dyspepsia) caused withdrawal from the study. For all patients participating in the study no adverse event was characterised as severe.
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Renal dyslipoproteinemia is characterized by the accumulation of intact and partially metabolized triglyceride-rich lipoproteins. Reduced lipolytic enzyme activities may be one of the major pathophysiological mechanisms contributing to a retarded catabolism of these lipoproteins in patients with renal insufficiency.
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The excitation-contraction coupling in skeletal muscle is modulated by nitric oxide via redox status modification of ryanodine receptor on sarcoplasmic reticulum during events that lead to muscle contraction. We have synthesized a derivative of antilipidemic drug, gemfibrozil, in which a NO-donor furoxan moiety is joined to the fibrate by an ester linkage. Aim of the present study was to determine if the NO released from the above compound is capable of influencing the NO-sensible E-C coupling steps in skeletal muscle and if this effect could be potentially utilised for physiopathological studies and pharmaceutical applications. To obtain this goal we decided to study some of the excitation-contraction mechanisms in the presence of NO-releasing derivative of gemfibrozil in skeletal muscle C2C12 cell line.
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We have constructed a large-scale transcriptome database of rat liver treated with various drugs. In an effort to identify a biomarker for interpretation of plasma triglyceride (TG) decrease, we extracted 218 probe sets of rat hepatic genes from data of 15 drugs that decreased the plasma TG level but differentially affected food consumption. Pathway and gene ontology analysis revealed that the genes belong to amino acid metabolism, lipid metabolism and xenobiotics metabolism. Principal component analysis (PCA) showed that 12 out of 15 compounds were separated in the direction of PC1, and these 12 were separated in the direction of PC2, according to their hepatic gene expression profiles. It was found that genes with either large or small eigenvector values in principal component PC 2 were those reported to be regulated by peroxisome proliferator-activated receptor (PPAR)alpha or constitutive androstane receptor (CAR), respectively. In fact, WY-14,643, clofibrate, gemfibrozil and benzbromarone, reported to be PPARalpha activators, distributed to the former, whereas propylthiouracil, omeprazole, phenobarbital, thioacetamide, methapyrilene, sulfasalazine and coumarin did to the latter. We conclude that these identified 218 probe sets could be a useful source of biomarkers for classification of plasma TG decrease, based on the mechanisms involving PPARalpha and CAR.
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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.
Most of the currently available statins and fibric acid derivatives have been implicated in causing complications either in monotherapy or in combination therapy. Adverse events occur more often with the statins that are metabolized via the CYP enzyme system and its 3A4, 2C9 or 2C19 paths. All compounds interfering with the same cytochrome system may either impair or enhance the elimination of statins. Other factors predisposing to adverse effects are age, female sex, renal insufficiency, electrolyte disturbances, infections and trauma. Complications chiefly concern the hepatic function, skeletal muscles and peripheral nerves. The major adverse effect is myopathy, up to rhabdomyolysis with ensuing acute renal insufficiency. Fibrates bind to peroxisome proliferator-activated nuclear receptors alpha, with subsequent stimulation of fatty acid oxidation and reduction in the rate of hepatic lipid generation. Fibrates are associated with a number of adverse effects, including liver enzyme elevations, gastrointestinal side effects and rhabdomyolysis. The combination of statins with fibrates may cause serious complications and should be avoided when possible. In order to prevent or minimize adverse clinical outcomes, patients should be closely monitored and informed of the most common symptoms.
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We studied 45 dyslipidemic abdominally obese men (45.4 +/- 6.2 years of age; body mass index [BMI], 31.3 +/- 3.0 kg/m(2); waist circumference, 103.4 +/- 7.6 cm; total cholesterol, <6.72 mM; triglycerides, > or =1.7 mM but < or =5.65 mM; high density lipoprotein cholesterol, < or =1.2 mM). Each of them followed nutritional recommendations combined with a prescription of gemfibrozil (1200 mg/d) or a placebo for 1 year. After 6 months, a training exercise program was added at a frequency of four sessions of 60 minutes per week at 50% of maximal oxygen uptake.
Hypertriglyceridemia is a common feature of patients with increased blood pressure as well as several rodent models of hypertension. The goal of this study was to evaluate the effects of gemfibrozil on established abnormalities of triglyceride (TG) secretion and TG clearance in the Dahl salt-sensitive rat. Consequently, Dahl salt-sensitive rats received 12 days treatment with gemfibrozil (30 mg/kg/day) or vehicle by p.o. gavage and the following measurements were made: 1) fasting plasma TG levels; 2) TG secretion rate after suppression of TG removal with Triton WR 1339; 3) TG removal rate (half-time of disappearance of prelabeled very low density lipoprotein); and 4) lipoprotein lipase (LPL) activity and mRNA in soleus muscle, fat and liver tissues. Gemfibrozil produced a 50% reduction in fasting plasma TG concentrations, with no effect on TG secretion rate (17 +/- 2 vs. 15 +/- 1 mg/100 g b.wt./hr). The half-time of prelabeled very low density lipoprotein-TG removal was significantly lower in drug-treated animals (3.9 +/- 0.3 vs. 6.1 +/- 0.9 min), and this was associated with a tissue-specific increase in LPL activity in soleus muscle (153 +/- 5 vs. 135 +/- 5 U/g, P < .02). Expression of LPL mRNA, relative to beta-actin mRNA, was similar in both groups of rats. Thus, in this rodent model of hypertension and dyslipidemia, gemfibrozil lowers plasma TG levels by 50% with no effect on TG secretion; the hypotriglyceridemic effect is due mainly to an increase in TG removal rate associated with a post-transcriptional increase in LPL activity in skeletal muscle.
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Some studies have suggested that reductions in plasma cholesterol might be associated with suicidal behaviour. Serotonergic systems are thought to be involved in suicidal ideation and behaviour and links with altered 5-HT1A and 5-HT2A receptors have been proposed. We have therefore examined the effects of cholesterol reduction using gemfibrozil, upon 5-HT2A and 5-HT1A receptor-related behaviours in rats. Rats were treated chronically (57 days) with gemfibrozil (50 mg/kg p.o.) or gum acacia vehicle and challenged sequentially with the 5-HT1A agonist 8-hydroxy-d-n-aminopropyl tetralin, to elicit 5-HT1A syndrome behaviours, and the 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)2-amino-propane to establish their head-shake frequency. Significant cholesterol reduction, within the clinical range, failed to induce any changes in either 5-HT1A or 5-HT2A mediated behaviours. These data suggest that cholesterol reduction fails to induce changes in 5-HT1A and 5-HT2A receptor tone suggesting that the reduction of plasma cholesterol, within the human clinical range, does not result in neuroplasticity of the 5-HT1A and 5-HT2A receptors in rats.
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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.
We retrospectively identified a cohort of patients who initiated a statin or fibrate between January 1, 1998, and December 31, 2007, using a database of a large US health insurer. Patients were followed for the occurrence of hospitalized rhabdomyolysis, determined by clinical review of medical records. Exposure status during the study period was determined by electronic records of statin and fibrate dispensing. Incidence rates (IRs) and incidence rate ratios (IRRs) for various combinations of fibrate and statin exposure were modeled, using Poisson regression.
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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 spectrometry, whereas those at the aqueous/air interface were studied by surface tensiometry.
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To compare the short and long term effectiveness of fish oil, insulin, and gemfibrozil in a non-diabetic patient with severe hypertriglyceridemia.
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6 weeks of atorvastatin, 40 mg/d, or gemfibrozil, 600 mg twice daily, with placebo.
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The hyperlipidemic diet induced a significant increase in total cholesterol; this was prevented by gemfibrozil (P<0.05). The increase in platelet-fibrinogen binding induced by hypercholesterolemia was mildly reduced in the gemfibrozil treated animals. Histological analysis of aortic vascular wall (abdominal aorta at the iliac bifurcation) from hyperlipidemic animals showed early lesions with fibrinogen infiltration; the lesions were reduced in the fibrate-treated animals.
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The objective of this study was to investigate the effect of temperature, oxygen, and organic matter on the removal of selected pharmaceutically active compounds (PhACs) during simulated riverbank filtration (RBF). The behavior of six PhACs (caffeine, carbamazepine, 17-β estradiol [E2], estrone [E1], gemfibrozil, and phenazone) was evaluated by small flow-through column experiments. Results from our study showed that RBF can be used to treat many of the PhACs found in environmental waters. Local conditions at the RBF site, however, can affect the removal of PhACs and should be investigated. Biodegradation and sorption represented the predominant mechanisms involved during the removal of the selected PhACs. All selected PhACs showed limited and slower removal during the winter. Phenazone was highly impacted by the level of oxygen; complete depletion of phenazone below the analytical limit occurred only under aerobic conditions (dissolved oxygen >8 mg L(-1)). Caffeine and E2 were highly impacted by the presence of humic acid in the feed water. Caffeine and E2 were depleted below the detection limit in the presence of humic acid regardless of the temperature and the level of oxygen. E1 was impacted by the different environmental conditions and depletion below the detection limit occurred only during the summer under aerobic conditions. Carbamazepine (10%) and gemfibrozil (<30%) showed limited removal regardless of the different levels of temperature, oxygen and humic acid.
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Spontaneous reports from the National Registry of Drug-Induced Ocular Side Effects, the World Health Organization (WHO), and the Food and Drug Administration were collected on statins and ptosis, diplopia, and ophthalmoplegia.
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Eighteen patients with chronic renal failure (serum creatinine 173-756 mumol/l) and hyperlipidemia were treated with gemfibrozil (1200 mg/day). The drug caused a significant improvement of the dyslipidemia within one week and the effect was progressive during the 28 weeks of treatment. Very-low-density lipoprotein triglycerides and very-low-density lipoprotein cholesterol decreased by about 50% and high-density lipoprotein cholesterol increased by 30%. The lipoprotein changes occurred simultaneously with a significant activation to normal levels of postheparin plasma lipoprotein and hepatic lipases. Opposite effects were observed when gemfibrozil was discontinued and the patients were given placebo. No major harmful effects were observed.
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Leibovitz L-15 medium was superior to RPM11640 in both maintenance and induction of peroxisomal beta-oxidation in cultured rat hepatocytes. Serum was not required for maintenance or induction of beta-oxidation. Cell plating density had only slight effects on maintenance and did not affect induction. Bezafibrate caused time- and dose-related increases in beta-oxidation, as well as increases in catalase, peroxisome volume fraction, and peroxisome number. This system maintained a greater percentage of control beta-oxidation than previously reported, and responded to several hypolipidemics with sizeable increases in activity. The flexibility of this system with respect to serum and cell-plating density facilitates simultaneous studies of cell parameters which are regulated by these variables.
The occurrence of 28 pharmaceuticals and 10 estrogens has been investigated in waters from the lower part of the Llobregat River basin, where the main intakes for production of drinking water for Barcelona (Spain) are located. Sampling was programmed to monitor the same mass of water on its way down the river to reflect inputs from discharges, contribution from subsidiaries plus persistence of the compounds in the surface water. Analysis of pharmaceuticals was performed by off-line solid phase extraction (SPE) followed by liquid chromatography-tandem mass spectrometry with a triple quadrupole analyzer (LC-QqQ-MS/MS). Further analysis by ultra performance liquid chromatography-mass spectrometry with a time-of-flight analyzer (UPLC-TOF-MS) has been proposed and applied for confirmation of several of these target compounds. Estrogens have been analysed by on-line SPE-LC-QqQ-MS/MS. Within the class of pharmaceuticals, 23 out of the 28 compounds investigated, were detected in at least one sample. The highest concentrations were observed for the beta-blockers metoprolol (8042 ng L(-1)) and sotalol (788 ng L(-1)), the antibiotic ofloxacin (1904 ng L(-1)), and the lipid regulator gemfibrozil (1014 ng L(-1)). Within the group of estrogens, only estrone and estrone-3-sulfate were positively identified, with concentrations for the former (0.82-5.81 ng L(-1)) close in some locations to those considered sufficient to induce estrogenic effects in aquatic organisms (1-10 ng L(-1)). As a general pattern, concentration of target compounds increases along the river flow as expected.
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Four previous reports describing rhabdomyolysis in patients on concomitant cerivastatin and gemfibrozil have been cited. Although monotherapy with cerivastatin is well tolerated and has a low frequency of adverse events, the combination with nicotinic acid (i.e., niacin) or a fibric-acid derivative (i.e., gemfibrozil, fenofibrate) may result in severe skeletal muscle toxicity and rhabdomyolysis.
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