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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Primary cultures 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.
Shenshuai Yangzhen capsule can regulate blood lipid levels in rats with renal insufficiency possibly by enhancing LPL gene expression.
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Peroxisome proliferators are a diverse group of chemicals that include several therapeutically used drugs (e.g., hypolipidemic agents), plasticizers and organic solvents used in the chemical industry, herbicides, and naturally occurring hormones. As the name implies, peroxisome proliferators cause an increase in the number and size of peroxisomes in the liver, kidney, and heart tissue of susceptible species, such as rats and mice. Long-term administration of peroxisome proliferators can cause liver cancer in these animals, a response that has been the central issue of research on peroxisome proliferators for many years. Peroxisome proliferators are representative of the class of nongenotoxic carcinogens that cause cancer through mechanisms that do not involve direct DNA damage. The fact that humans are frequently exposed to these agents makes them of particular concern to government regulatory agencies responsible for assuring human safety. Whether frequent exposure to peroxisome proliferators represents a hazard to humans is unknown; however, increased cancer risk has not been shown to be associated with long-term therapeutic administration of the hypolipidemic drugs gemfibrozil, fenofibrate, and clofibrate. To make sound judgments regarding the safety of peroxisome proliferators, the validity of extrapolating results from rodent bioassays to humans must be based on the agents' mechanism of action and species differences in biologic activity and carcinogenicity. The peroxisome proliferator-activated receptor alpha (PPARalpha), a member of the nuclear receptor superfamily, has been found to mediate the activity of peroxisome proliferators in mice. Gene-knockout mice lacking PPARalpha are refractory to peroxisome proliferation and peroxisome proliferator-induced changes in gene expression. Furthermore, PPARalpha-null mice are resistant to hepatocarcinogenesis when fed a diet containing a potent nongenotoxic carcinogen WY-14,643. Recent studies have revealed that humans have considerably lower levels of PPARalpha in liver than rodents, and this difference may, in part, explain the species differences in the carcinogenic response to peroxisome proliferators.
1. The effects in vitro and in vivo of three fibric acid derivatives, clofibrate (CFB), bezafibrate (BFB) and gemfibrozil (GFB) on some enzyme activities related to fatty acid biosynthesis, namely palmitoyl-CoA synthetase and hydrolases (microsomal and cytosolic), NADH and NADPH cytochrome c reductases and acyl-CoA elongases were investigated in guinea-pigs. 2. The three fibrates inhibited acyl-CoA elongation in vitro, irrespective of the substrate of elongation used (saturated, monounsaturated, polyunsaturated) and with an order of potency GFB > BFB > CFB. In the case of GFB, inhibition occurred at concentrations that can be reached in vivo. 3. Microsomal palmitoyl-CoA hydrolase and synthetase were also inhibited in vitro (GFB > or = BFB > CFB), whereas NADH cytochrome c reductase activity was increased by GFB. Nevertheless, the magnitude of changes were lower than those observed in elongation activities. 4. Treatment with fibrates did not produce peroxisomal proliferation in guinea-pigs, as measured by peroxisomal beta-oxidation activity and liver weight/body weight ratio. Nevertheless, fibrates provoked a reduction in plasma cholesterol and triglycerides, at least in GFB- and BFB-treated animals. 5. Fatty acid elongation was significantly modified by GFB treatment in vivo. The remaining enzyme activities studied were only slightly changed by fibrate treatment. 6. Treatment with BFB and to a lesser extent with CFB, increased the relative proportion of MUFA (palmitoleic and oleic acids) in microsomal phospholipids, whereas PUFA (mainly linoleic acid) decreased. GFB behaved differently, increasing palmitic and linoleic acids and decreasing stearic and oleic acids. The latter changes are attributable to an inhibition of elongation activity by GFB. 7. The changes observed after fibrate treatment in both rats and guinea-pigs, as they are not directly related to peroxisome proliferation, could be more reliably extrapolated to man than those observed only in rats.
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This study took place in the Internal Medicine Clinic, Faculty of Medicine, Osmangazi University, Turkey between 2004-2005. This study was carried out on 99 hyperlipidemic and 40 control subjects. Subjects were divided into 2 groups; elderly hyperlipidemic (n=65) and young hyperlipidemic (n=34). In the young and elderly hyperlipidemic subjects of the first group treated only with vit E (600 mg/day) for one month. In the young and elderly hyperlipidemic subjects of the second group were treated only with gemfibrozil (600 mg/twice daily) for one month. The 2 therapies of vit E and gemfibrozil were then combined and applied to the third group of our study. Reduced glutathione (GSH), glutathione peroxidase (GPx), total cholesterol (total chol), serum low density lipoprotein (LDL), high density lipoprotein (HDL), triglyceride (TG), vit E, malondialdehyde (MDA), superoxide dismutase (SOD) levels of the 3 groups were measured.
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Experimental evidence suggests that in addition to hypertension, serum lipids might also accelerate the decline in renal function. We tested this hypothesis in 2702 dyslipidemic middle-aged men without renal disease participating in the Helsinki Heart Study, a coronary primary prevention trial. The decline in renal function was estimated from linear regression slopes based on reciprocals of 10 serum creatinine determinations over the study period. Renal function deteriorated 3% on average during the 5-year study, and hypertension accelerated this change. Subjects with an elevated ratio of low- to high-density lipoprotein cholesterol ( > 4.4) had a 20% faster decline than those with a ratio less than 3.2. Both the contribution of the lipoprotein ratio and the protective effect of high-density lipoprotein cholesterol alone remained significant in multiple regression analyses. In the study of joint effects the contribution of lipids was confined to subjects with simultaneous elevation of blood pressure and lipids. The results suggest that in addition to hypertension, blood lipids also modify the decline in renal function.
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Patients with a diagnosis of type 2 diabetes and either a history of coronary artery disease or at least one other significant cardiovascular risk factor as defined by the American College of Physicians guidelines (i.e., age greater than 55 years, hypertension, left-ventricular hypertrophy, previous cerebrovascular disease, or peripheral arterial disease).
Over one quarter of veterans in the VANCHCS may have metabolic syndrome based on our modified ATP III criteria. We urge screening more veterans with fasting laboratory testing. Computerized screening of a large clinical database can provide an effective strategy to aid clinicians in identifying more patients at risk for cardiovascular disease.
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In this paper, a poly(vinyl chloride) (PVC) membrane electrode is prepared for gemfibrozil, 2, 2-dimethyl-5-(2,5-xylyloxy) valeric acid, based on its ion pair complexes with hexadecyltrioctyl ammonium iodide (HTOA). The membrane composition of the electrode was optimized by using the sequential level elimination method for orthogonal experimental design. The electrode has a Nernstian response range from 2.5 x 10(-5) to 0.1 mol/l with an average slope of 55.3 mV/decade. The limit of detection is 7.1 x 10(-6) mol/l. The electrode responses were not affected by pH in the range 10.0-12.3. A Na2B4O7-Na2CO3 buffer of pH = 11.0 was selected as the background electrolyte solution for potentiometric measurements. The electrode was used for determining gemfibrozil in pharmaceutical preparations with satisfactory results.
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Itraconazole, gemfibrozil and their combination markedly raise the plasma concentrations of loperamide. Although not seen in the psychomotor tests used, an increased risk of adverse effects should be considered during concomitant use of loperamide with itraconazole, gemfibrozil and especially their combination.
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The efficacy of gemfibrozil in the treatment of resistant familial hypercholesterolaemia and type III hyperlipoproteinaemia was evaluated in 26 individuals over a mean period of 16 months. In the untreated state both disorders are associated with a high frequency of coronary heart disease. In the former, gemfibrozil with a bile acid sequestrant reduced plasma cholesterol by 32%, an incremental decrease of 17% compared with sequestrant therapy alone. In type III, plasma cholesterol was reduced by 40% and plasma triglyceride by 70%, while high-density lipoprotein cholesterol increased by 45%. In none of the patients studied did clinical or biochemical side effects occur.
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Eighty-six water samples were collected in early 2009 from Costa Rican surface water and coastal locations for the analysis of 34 pharmaceutical and personal care product compounds (PPCPs). Sampling sites included areas receiving treated and untreated wastewaters, and urban and rural runoff. PPCPs were analyzed using a combination of solid phase extraction and liquid chromatography tandem mass spectrometry. The five most frequently detected compounds were doxycycline (77%), sulfadimethoxine (43%), salicylic acid (41%), triclosan (34%) and caffeine (29%). Caffeine had the maximum concentration of 1.1 mg L(-1), possibly due to coffee bean production facilities upstream. Other compounds found in high concentrations include: doxycycline (74 μg L(-1)), ibuprofen (37 μg L(-1)), gemfibrozil (17 μg L(-1)), acetominophen (13 μg L(-1)) and ketoprofen (10 μg L(-1)). The wastewater effluent collected from an oxidation pond had similar detection and concentrations of compounds compared to other studies reported in the literature. Waters receiving runoff from a nearby hospital showed higher concentrations than other areas for many PPCPs. Both caffeine and carbamazepine were found in low frequency compared to other studies, likely due to enhanced degradation and low usage, respectively. Overall concentrations of PPCPs in surface waters of Costa Rica are inline with currently reported occurrence data from around the world, with the exception of doxycycline.
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Peroxisome proliferator-activated receptor alpha and gamma (PPAR alpha, PPAR gamma) are nuclear transcription factors regulating gene expression in response to their ligands. Initially, PPARs were identified as regulators of gene expression in lipid metabolism and adipogenesis, but recent work has demonstrated PPAR expression in vascular cells and suggests antiinflammatory properties in the vasculature. Since PPAR alpha activators include lipid-lowering fibric acid derivatives and since PPAR gamma can be activated by antidiabetic thiazolidinediones, activation of these receptors might be an intriguing tool to influence atherogenesis in patients with vascular disease. However, there is also evidence that PPAR activators might furnish lesion development under certain circumstances. The following review will focus on these aspects of potential anti- or proatherogenic effects in the vessel wall and discuss potential clinical implications of these findings.
Nonalcoholic fatty liver disease, an entity that includes nonalcoholic steatohepatitis, is typically a benign, indolent condition. However, in a subset of patients, the clinical course may progress to advanced cirrhosis, end-stage liver disease, or hepatocellular carcinoma. Unfortunately, the pathogenesis, natural history, and potential therapies for these disorders remain poorly understood. Identifying patients who should be targeted for potential treatment remains difficult. Liver biopsy should be considered to assess the degree of hepatic inflammation and fibrosis, because physical examination findings, biochemical parameters, and the results of radiographic studies have been shown to correlate poorly with the severity of steatohepatitis and fibrosis. Although there is some evidence suggesting that obesity, diabetes mellitus, older age, and perhaps an aspartate transaminase:alanine aminotransaminase ratio higher than 1 may be predictors of more advanced fibrosis, histology remains the gold standard. Most patients with simple hepatic steatosis appear to follow a benign course and probably do not require aggressive therapy. Conversely, patients with steatohepatitis with extensive inflammation and fibrosis are the patients who are most likely to benefit from effective therapies. The most commonly recommended treatment is weight loss. Existing data suggest that rapid weight loss may promote hepatic inflammation and fibrosis; therefore, gradual weight loss should be recommended. Large, randomized, controlled trials evaluating the long-term histologic impact and clinical outcomes of weight loss strategies are lacking. Potentially promising pharmacologic therapies include insulin-sensitizing oral hypoglycemic agents such as metformin and the thiazolidenediols, antihyperlipidemic agents such as gemfibrozil or 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, vitamin E and other antioxidants, ursodeoxycholic acid, and betaine. As with weight loss, data regarding the efficacy of these pharmacologic options are limited. In addition, there are no widely accepted guidelines to help direct the clinician in the optimal use of these agents in patients with nonalcoholic fatty liver diseases.
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Potencies for the induction of peroxisomal fatty acyl-CoA oxidase (FACO) and microsomal laurate hydroxylase (LH) were determined for clofibric acid (CPIB), ciprofibrate (Cipro) and gemfibrozil (Gem) in primary cultures of rat hepatocytes based on complete concentration-response analysis and determination of theoretical maximum inductive responses for Cipro. CPIB and Cipro each induced FACO and LH in a concentration-dependent manner. Scatchard analysis of the data allowed calculation of EC50 values (mM) of 0.82 and 0.028 (for FACO) and 0.22 and 0.0081 (for LH) for CPIB and Cipro respectively. The EC50 ratios (CPIB/Cipro) were identical (29-fold) for induction of FACO and LH, supporting the concept that these enzymes are induced by CPIB and Cipro through a common mechanism. By comparison, Gem was relatively ineffective as an inducer of FACO and LH. Furthermore, Gem did not antagonize Cipro-mediated enzyme inductions, suggesting that Gem is a peroxisome proliferator of low potency rather than a partial agonist. Based on the potency and time-course profiles observed for induction of FACO and LH, the effects of CPIB, Cipro and Gem on triglyceride (TG) biosynthesis were determined in the cultured rat hepatocytes. Conditions of maximal FACO and LH induction by the drugs did not result in inhibition of TG biosynthesis in the cells. These results support the in vivo evidence which indicates that FACO and LH induction are not causally linked to the hypotriglyceridemic actions of peroxisome proliferating drugs.
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To report a case of rhabdomyolysis in a patient receiving cyclosporine, simvastatin, gemfibrozil, and itraconazole.
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To report a case of rhabdomyolysis possibly due to combination therapy with colchicine and gemfibrozil.
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Acidic pesticide and pharmaceutical contaminants were pre-concentrated and extracted from wastewater samples (500 mL) using solid-phase extraction. Analyte recoveries were 79-96%, with % RSD values in the range, 1.7-7.4%. Analyte identification and quantification were carried out using liquid chromatography-mass spectrometry (LC-MS) with hybrid linear ion trap (LIT) Orbitrap instrumentation. Using a resolution setting of 30,000 FWHM, full-scan MS analysis was performed using heated electrospray ionization (HESI) in negative mode. The high mass resolution capabilities of the Orbitrap MS were exploited for the determination of trace contaminants allowing facile discrimination between analytes and matrix. The dependant scan functions of the Orbitrap MS using higher collisional dissociation (HCD) and LIT MS were evaluated for the confirmation of analytes at trace concentration levels. Mass accuracy for target contaminants using this method was less than 2 ppm. The limits of quantitation (LOQs) were in the range, 2.1-27 ng/L. The inter-day accuracy and precision were measured over a five-day period at two concentrations. The % relative errors were in the range, 0.30-7.7%, and the % RSD values were in the range, 1.5-5.5%. Using this method, 2,4-D, mecoprop, ibuprofen, naproxene and gemfibrozil were identified in several wastewater treatment plants in Ireland.
A 60-year-old black man developed rhabdomyolysis after receiving lovastatin for 14 months. Rhabdomyolysis developed in the absence of other medications previously reported to cause this adverse effect when administered concomitantly with lovastatin. Adverse drug reaction causality algorithms categorized this reaction as either possible or probable.
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Gemfibrozil is long known for its ability to reduce the level of triglycerides in the blood circulation and to decrease the risk of hyperlipidemia. However, a number of recent studies reveal that apart from its lipid-lowering effects, gemfibrozil can also regulate many other signaling pathways responsible for inflammation, switching of T-helper cells, cell-to-cell contact, migration, and oxidative stress. In this review, we have made an honest attempt to analyze various biological activities of gemfibrozil and associated mechanisms that may help to consider this drug for different human disorders as primary or adjunct therapy.
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A series of phenylenebis(oxy)bis[2,2-dimethylpentanoic acid]s have been synthesized and evaluated as potential hypolipidemic agents. Compound 18 (CI-924) was found to be the most potent compound in this series. In rats, compound 18 not only reduced low-density lipoprotein cholesterol but also increased high-density lipoprotein (HDL) cholesterol. Comparative studies in rats indicated 18 produced an equal elevation of HDL cholesterol at one-third of the dose required of gemfibrozil. Structure-activity relationships are discussed.
It was suggested that postprandial lipoproteins (PPLp) may play an important role in atherogenesis. To examine this hypothesis, we studied PPLp metabolism in normolipidemic individuals and hyperlipoproteinemic (HLP) patients on various diets, physical activity programs and hypolipidemic drugs as well as in patients with coronary artery disease (CAD). We used the vitamin A-fat loading test, which labels intestinally derived lipoproteins with retinyl palmitate. Type IV HLP patients demonstrated a severe defect in chylomicron clearance. Type III HLP patients showed severely disordered clearance of chylomicron remnants. Compared to the saturated fatty acid enriched diet, the omega 6 polyunsaturated acid enriched diet reduced chylomicrons and their remnant levels by 56% and 38%, respectively. The diet enriched in omega 3 polyunsaturated acid decreased chylomicrons and their remnant levels by 67% and 53%, respectively. Physical conditioning reduced chylomicron levels by 37%. Gemfibrozil decreased chylomicron levels in type IV HLP patients. Cholestyramine increased chylomicron levels by 88%. Bezafibrate reduced chylomicrons and their remnants levels and increased fasting HDL-C in patients with isolated low HDL-C levels. Continuous prolonged intravenous heparin administration inhibited chylomicron clearance. Normolipidemic patients with CAD had significantly higher plasma levels of chylomicron remnants than matched controls with normal coronary arteries. The studies reported here demonstrate that both chylomicrons and their remnants are present in the plasma of normolipidemic people and more so for hyper- or dyslipidemic patients for a prolonged period of time after fat ingestion. The duration and magnitude of this postprandial lipemia can be regulated or altered by such interventions as diet, physical activity, and drugs. Our case control studies strongly support the hypothesis that PPLp may play a crucial part in atherogenesis, and therefore justify measuring their levels in high risk patients. We believe that in selected patient groups the use of one or more of the interventions mentioned here is warranted.
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