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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Of the 2046 dyslipidaemic men initially randomized to gemfibrozil, 2002 survivors entered the 3.5-year follow-up; of the 2035 initial placebo men, 1992 continued to be monitored.
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In the past 3 years, treatment for HIV infection has significantly improved the prognosis for HIV-infected persons. The administration of protease inhibitors for the treatment of HIV infection has had a significant role in the reduction of AIDS-related complications. Recent findings have indicated that protease inhibitors may significantly increase lipids to levels that pose a health risk that may be greater than the illness itself. This article reviews the initial findings of a study that investigated the impact of interventions for the treatment of protease inhibitor-related hyperlipidemia. The purpose of the study was to determine if initiation of interventions based on the National Cholesterol Education Program Guidelines would be effective in lowering protease inhibitor-related hyperlipidemia without disrupting the effectiveness of the HIV therapy. A total of 45 HIV-infected individuals who were taking a protease inhibitor and had abnormally elevated lipids were enrolled into this study. Mean serum cholesterol level prior to initiation of a protease inhibitor regimen was 170 mg/dl as compared to a mean cholesterol at time of enrollment of 289 mg/dl and triglycerides of 879 mg/dl. Interventions included diet and exercise and the prescription of gemfibrozil alone or in combination with atorvatstatin. During the course of the study, overall intervention significantly reduced serum cholesterol level to 201 mg/dl (p. 01) over a study period of ten months. Case studies of five medical events related to hyperlipidemia are included. Currently, 26 participants continue in the study. Sixteen participants discontinued protease inhibitor therapy during the course of the study and thus ended their participation.
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Using the terms lipid-modifying therapy, combination therapy, combination statin-fibrate therapy, and mixed dyslipidemia, a search of PubMed was conducted (completed in April 2007, updated to October 2007) to identify English-language publications and pertinent studies of fibrate combination therapy in patients with mixed dyslipidemia, including those with diabetes or the metabolic syndrome.
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Following a 6-week washout, 32 patients with dysbetalipoproteinemia received rosuvastatin 10 mg, rosuvastatin 20 mg, and pravastatin 40 mg, each for 6 weeks in a randomized, double-blind, three-way crossover design. Patients subsequently entered an 18-week open-label phase in which the rosuvastatin dosage could be increased from 20 mg to a maximum of 40 mg at 6 weekly intervals to reach National Cholesterol Education Program goals for non-high-density lipoprotein cholesterol (non-HDL-C) and optimal triglyceride (TG). Fibrates (except gemfibrozil) could be added if patients were not at goal on rosuvastatin 40 mg. The primary efficacy variable was percent change from baseline in non-HDL-C during the double-blind phase. The prespecified efficacy criterion was for the 95% confidence interval (CI) of non-HDL-C to lie entirely below -25% for any rosuvastatin dose.
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Gemfibrozil significantly lowers triglycerides and raises HDL with reasonable safety in a pediatric population with metabolic syndrome.
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Hyperlipidemia is a major risk factor of cardiovascular diseases. We investigated the utilization ofantilipemic drugs at the outpatient sector within the National Health Insurance in Taiwan.
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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A significant (P < 0.05) increase in lipid profile (total glyceride, total cholestrol, low-density lipoprotein, and very low-density lipoprotein), MDA and reduction (P < 0.05) in enzymatic and nonenzymatic antioxidant status coupled with alterations in hematological parameters was observed in the serum of hypercholesterolemic rats when compared with animals on a normal diet. Coadministration of methanolic leaf extracts of Talinum triangulare or gemfibrozil significantly (P < 0.05) restored the elevated serum lipid profile, MDA, and the deranged hematological parameters to near normal. The extract also protected against hypercholesterolemic-induced diminished enzymatic and nonenzymatic antioxidant status. The activities of the plant extract are dose (250, 500, and 1000 mg/kg) dependent and it compared favorably with the standard drug gemfibrozil.
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patients enrolled in a veterans hospital renal subspecialty clinic.
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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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The authors describe a patient who presented with myoglobinuria after starting cerivastatin-gemfibrozil therapy. Muscle histochemistry revealed ragged-red fibers and cytochrome c oxidase negative (COX) fibers, and biochemistry showed a defect of COX activity. Immunoblot analysis showed a 60% reduction of COX I and COX II polypeptides. Cerivastatin myotoxicity might be related to a depletion of essential metabolites needed to anchor COX subunit I to mitochondrial membrane.
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Gemfibrozil is the most myotoxic fibrate drug commonly used for dyslipidemia, but the mechanism is poorly understood. The current study revealed that gemfibrozil inhibits myoblast differentiation through the regulation of intracellular calcium ([Ca(2+)]i) as revealed in L6 myoblasts by use of laser scan confocal microscopy and flow cytometry using Fluo-4 AM as a probe. Gemfibrozil at 20-400 μM, could regulate [Ca(2+)]i in L6 cells in a biphasic manner, and sustained reduction was observed when the concentration reached 200 μM. Inhibition of L6 differentiation by gemfibrozil was concentration-dependent with maximal effect noted between 200 and 400 μM, as indicated by creatine kinase activities and the differentiation index, respectively. In differentiating L6 myoblasts, gemfibrozil at concentrations below 400 μM led to no significant signs of apoptosis or cytotoxicity, whereas differentiation, inhibited by 200 μM gemfibrozil, was only partially recovered. A good correlation was noted between gemfibrozil concentrations that regulate [Ca(2+)]i and inhibit L6 myoblasts differentiation, and both are within the range of total serum concentrations found in the clinic. These data suggest a potential pharmacodynamic effect of gemfibrozil on myogenesis as a warning sign, in addition to the complex pharmacokinetic interactions. It is also noteworthy that mobilization of [Ca(2+)]i by gemfibrozil may trigger complex biological responses besides myocyte differentiation. Information revealed in this study explores the mechanism of gemfibrozil-induced myotoxicity through the regulation of intracellular calcium.
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Genetically determined and metabolically induced disturbances in lipid metabolism, as manifested in several types of dyslipidemia, have been shown to be causally related to the development of coronary artery disease (CAD). A diversity of clinical and angiographic studies has been made to evaluate the linkage between plasma lipid-control therapy in the development of initial and recurrent cardiovascular events. The plan of treatment invariably begins with a low-fat, low-cholesterol diet before initiation of drug therapy. However, many patients have difficulty in adhering to the low-fat diet. Fortunately, metabolic studies show that foods which contain fats rich in stearic (saturated) and oleic (monounsaturated) fatty acids may be given in limited amounts to boost patients' compliance to a low-fat diet and to prevent their blood lipids from rising to abnormal levels. A bile acid sequestrant (cholestyramine or colestipol) is the first-line drug for control of hypercholesterolemia. Either gemfibrozil or gemfibrozil plus niacin is prescribed to raise high-density lipoprotein (HDL) levels of CAD patients. Approval of two HMG CoA reductase inhibitors, pravastatin and simvastatin, by the FDA gives physicians the additional flexibility of employing a single or a combination drug therapy for optimal control of dyslipidemia. The association of low serum cholesterol level (< 160 mg/dl) with increase in noncardiac mortality has prompted health professionals to consider modifying the universal screening and treatment of serum cholesterol in children and young women and to use hypolipidemic drugs in patients judiciously.
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The effects of ethanolic extract of ginger (200 mg/kg, p.o.) were studied in cholesterol fed rabbits. The marked rise in serum and tissue cholesterol, serum triglycerides, serum lipoproteins and phospholipids that followed 10 weeks of cholesterol feeding, was significantly reduced by the ethanolic ginger extract and results were compared with gemfibrozil, a standard orally effective hypolipidaemic drug. The severity of aortic atherosclerosis as judged by gross grading was more marked in pathogenic, i.e. the hypercholesterolemic group, while animals receiving ginger extract along with cholesterol showed a lower degree of atherosclerosis. The results indicate that ginger is definitely an antihyperlipidaemic agent.
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Peroxisome proliferator activated receptors (PPARs) are a class of nuclear receptors now actively investigated for their involvement in lipid and glucidic metabolism, immune regulation and cell differentiation. Drugs binding and activating PPARs are therefore attracting attention for their potential therapeutic role in various diseases like type 2 diabetes, dyslipidemias, atherosclerosis, obesity (i.e., metabolic syndrome). Agonists of these receptors have been already used in therapeutic protocols: fibrates (PPAR-alpha ligands) are being used in hyperlipidemias, and thiazolidinediones (mainly PPAR-gamma ligands) are being employed as insulin sensitizers. The latter drugs introduction into therapy, however, showed very soon some unwanted effects (hepatotoxicity at first and myocardiotoxicity later on) which confirmed some contradictory data already suggested by pre-clinical trial-experiments. In this study we show that some PPAR ligands impair mitochondrial oxidative metabolism in human liver cell line mainly by deranging NADH oxidation. Intriguingly, the PPAR-gamma ligand ciglitazone caused a dose-dependent inhibition of NADH-cytochrome c reductase that resulted, at a drug concentration of 50 microM, of about 60% (P<0.001), while other PPAR ligands with different receptor affinity - positive controls like clofibrate (0.7 mM), gemfibrozil (0.23 mM) and bezafibrate (1 mM) - reduced the activity of mitochondrial Complex I by about 20% (P<0.01, P<0.01 and P<0.05, respectively). The induced mitochondrial dysfunction imposed a series of metabolic compensatory adaptations characterized by a significant shift to anaerobic glycolysis. These findings underline the undervalued non-genomic effects of PPAR ligands and can provide a better understanding of the pharmacotoxicological profiles of these drugs and of their roles in the therapy of diabetes mellitus.
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In 148 patients, gemfibrozil was started before an HMG was added. The pretreatment total cholesterol level fell from 222 +/- 34 mg/dL to 181 +/- 26 mg/dL (P <.001) on combination therapy. HDL cholesterol level rose from 30 +/- 5 mg/dL to 36 +/- 7 mg/dL (P <.01), triglyceride level fell from 361 +/- 141 mg/dL to 212 +/- 101 mg/dL (P <.03). The ratio of total cholesterol to HDL fell from 7.6 +/- 1. 7 to 5.3 +/- 1.6 (P <.001). In 104 patients an HMG was begun before gemfibrozil was added. Pretreatment total cholesterol level fell from 246 +/- 54 mg/dL to 192 +/- 40 mg/dL on combination therapy (P <.01). HDL level rose from 33 +/- 9 mg/dL to 38 +/- 9 mg/dL (P <.03) and triglyceride level fell from 314 +/- 183 mg/dL to 183 +/- 93 mg/dL (P <.001). The ratio of total cholesterol to HDL fell from 7.9 +/- 3.6 to 5.2 +/- 1.4 (P <.001). In both groups the lipid profile on combination therapy was significantly better than that obtained on single-agent therapy. One episode of myopathy (0.4%) and one episode of aminotransferase level elevation (0.4%) of greater than 3 times upper limit of normal occurred. Both resolved with cessation of therapy without consequence.
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Statins can lower the circulating levels of C reactive protein (CRP). This effect may be relevant because CRP is a predictor of vascular risk. In contrast, the evidence that fibrates lower CRP levels is very limited. The effect of treatment with ciprofibrate (100 mg once daily) was investigated for 8 weeks in 30 patients with primary dyslipidemia. There was a significant (p < 0.01) decrease in median (range) CRP levels by 36.8% from 1.9 mg/L (1.0-6.0 mg/L) to 1.2 mg/L (1.0-5.5 mg/L). Plasma fibrinogen levels were also significantly (p = 0.05) reduced. There was no correlation between the fall in CRP levels and the changes in lipid or fibrinogen levels. These findings support the concept that fibrates, like the statins, lower serum CRP levels. However, fibrates have a different mode of action. Fibrates (with the exception of gemfibrozil) also consistently lower plasma fibrinogen levels. In contrast, the effect of statins on the circulating levels of this coagulation factor remains to be defined. These differences may help in defining the mechanisms responsible for drug-induced changes in the circulating levels of CRP and fibrinogen. A favorable effect on CRP and fibrinogen levels may increase the clinical efficacy of statins and fibrates.
Although less clinical intervention studies have been performed with fibrates than with statins, there are evidences indicating that fibrates may reduce risk of cardiovascular events. The potential clinical benefit of the fenofibrate will be specified by the ongoing Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, which rationale, methods and aims have been just published. Controlled clinical trials show similar or even greater cardiovascular benefits from statins-based therapy in patient subgroups with diabetes compared with overall study populations. Therefore, statins are the drug of first choice for aggressive lipid lowering actions and reducing risk of coronary artery disease in these patients. However, current therapeutic use of statins as monotherapy is still leaving many patients with mixed atherogenic dyslipidemia at high risk for coronary events. A combination statin/fibrate therapy may be often necessary to control all lipid abnormalities in patients with metabolic syndrome and diabetes adequately, since fibrates provide additional important benefits, particularly on triglyceride and HDL-cholesterol levels. Thus, this combined therapy concentrates on all the components of the mixed dyslipidemia that often occurs in persons with diabetes or metabolic syndrome, and may be expected to reduce cardiovascular morbidity and mortality. Safety concerns about some fibrates such as gemfibrozil may lead to exaggerate precautions regarding fibrate administration and therefore diminish the use of the seagents. However, other fibrates, such as bezafibrate and fenofibrate appear to be safer and better tolerated. We believe that a proper co-administration of statins and fibrates, selected on basis of their safety, could be more effective in achieving a comprehensive lipid control as compared with monotherapy.
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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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Sixty four rats were used and classified into two main groups. Group I (treated for 6 weeks): naïve, FF, GF groups and Group II (treated for 14 weeks and drugs were added at the last 6 weeks): Control, high fat diet (HFD) untreated, HFD+FF, HFD+FF+folic acid (FA) and HFD+GF groups. Body weight (BW), liver index (LI), renal perfusion test (RPT), glomerular filtration rate (GFR), serum creatinine (S.cr), plasma homocysteine (Hcy), liver function, non invasive markers of fibrosis and histopathology were done.
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Ten healthy subjects in a randomized cross-over study took gemfibrozil 600 mg or placebo twice daily for 5 days, and on day 3, a single oral dose of 20 mg zafirlukast. The plasma concentrations of zafirlukast were measured for 72 h postdose.
We studied the response of male DBA/2N mouse liver monooxygenases to acute (one-day) and subacute (7-day) exposure to clofibrate, gemfibrozil, and corn oil. The day following a single treatment with clofibrate (200 mg/kg), coumarin 7-hydroxylase (COH) activity decreased significantly (by 70%) with a concomitant decrease in the CYP2A4/5 protein and mRNA levels. The 7-day treatment schedule also decreased COH activity by only by 30%, though the levels of CYP2A4/5 protein and mRNA were still low. Treatment 1 and 7-day with clofibrate decreased 7-pentoxyresorufin O-dealkylase (PROD) activity by 40%. No changes were seen in testosterone 15 alpha-hydroxylase (T15 alpha OH) activity after 1 day of treatment with clofibrate but, after 7 days, it was decreased by 50%. Clofibrate treatment had no significant effects on testosterone 7 alpha-hydroxylase (T7 alpha OH), 7-ethoxyresorufin O-deethylase (EROD), or benzphetamine N-demethylase (BZDM) activities. Gemfibrozil (200 mg/kg) did not alter COH activity or CYP2A4/5 protein content after a single treatment, but a slight decrease was seen in the mRNA level. Treatment for 7 days significantly increased (2.5-fold) the activity and mRNA content but the amount of protein remained unchanged. Gemfibrozil enhanced (2-2.7-fold PROD and EROD (2-2.5-fold) activities by both treatments, whereas T15 alpha OH, T7 alpha OH, or BZDM activities were not significantly affected. Treatment with corn oil for 7 days significantly decreased (65%) COH activity and CYP2A4/5 protein and mRNA levels. PROD (55%) and T15 alpha OH (65%) activities were significantly decreased even after a single dose although injection for 7 days had no effect. Neither of the corn oil schedules had any marked effect on T7 alpha OH, EROD, or BZDM activities. These results demonstrate: 1. a decrease in the expression of CYP2A4/5 gene by clofibrate and corn oil; 2. substantial differences within the CYP2A subfamily in their responses to corn oil, clofibrate, and gemfibrozil; and 3. distinct responses of other xenobiotic metabolizing CYP subfamily enzymes to clofibrate and gemfibrozil.
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Workload and noise increased CHD risk due to increased blood pressure, glucose or body mass index (BMI), separately or combined: the joint effect of workload and MetS defined using these three components yielded an RR of 5.21 (95% CI 2.70 to 10.05). However, when MetS was defined using elevated BMI, high triglycerides and low high-density lipoprotein cholesterol, an RR of 2.19 (95% CI 1.11 to 4.30) among those with MetS only reduced to 1.20 (95% CI 0.61 to 2.35) if concurrently exposed to workload.
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Among the cohort with 46,614 eligible people, 760 patients had ever received antilipemic drugs (prevalence: 1.6%). The group 60-69 years of age had the greatest age-specific prevalence (7.2%), followed by the group over 70 years of age (6.0%). There were more male than female patients, but female patients outnumbered male patients before the age of 49 years. The antilipemic drugs had been prescribed 3,850 times totally with 70,272 defined daily doses (DDDs). On an average, a patient with antilipemic therapy received 5.1 (+/- 4.5) prescriptions of antilipemic drugs in one year and a prescription contained 18.3 (+/- 11.5) DDDs. We measured 4.1 DDDs per 1,000 inhabitants per day for all antilipemic drug use in 2000. The statins and fibrates predominated the antilipemic drug use. While gemfibrozil was most popular in respect of recipients and prescription items, simvastatin had the largest amount of use in unit of DDDs. Diabetes mellitus co-existed in 37.8% of the patients with antilipemic therapy and the standardized morbidity ratio (SMR) was 3.34. The other concomitant diseases included essential hypertension (rate: 48.8%, SMR: 2.40) and other heart disease (rate: 30.7%, SMR: 2.36).
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Low serum levels of high-density lipoprotein (HDL) cholesterol is an independent risk factor for coronary artery disease. Raising HDL cholesterol should be an important therapeutic goal in patients with coronary artery disease. Fibrates can reduce the risk of cardiac events and death from coronary artery disease.
In this study, patients (n=126) with confirmed cases of rhabdomyolysis after cerivastatin administration had their CYP2C8 gene resequenced and the metabolism of cerivastatin by the discovered CYP2C8 variants was assessed in proteins expressed in Escherichia coli.
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