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.
The chemistry, pharmacology, pharmacokinetics, clinical efficacy, dosage and administration, and adverse effects of lovastatin are reviewed. Lovastatin is the first agent marketed in a new class of pharmacologic compounds called the 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors. By competitively inhibiting HMG CoA reductase, the drug disrupts the biosynthesis of cholesterol in hepatic and peripheral cells. This increases the synthesis of low-density-lipoprotein (LDL) receptors and thereby increases the uptake of LDL cholesterol from the plasma. In doses of 20 to 80 mg daily, lovastatin decreases total and LDL cholesterol concentrations 25 to 45%. It also substantially reduces concentrations of triglycerides, very-low-density-lipoprotein (VLDL) cholesterol, and apolipoprotein B and slightly increases high-density-lipoprotein (HDL) cholesterol concentrations. Lovastatin is effective in patients with heterozygous familial and nonfamilial (polygenic) hypercholesterolemia but is ineffective in patients with homozygous familial hypercholesterolemia. It is also effective in combination with bile acid sequestrants, nicotinic acid, and gemfibrozil. Administration of lovastatin once daily in the evening (to enhance compliance) or twice daily is recommended to maximize the drug's cholesterol-lowering effects. Headache and gastrointestinal complaints are the most common adverse effects. Treatment has been withdrawn from 1.9% of patients receiving the drug because of elevated aminotransferase concentrations. The relationship of lovastatin to the development of lens opacities requires further evaluation. Lovastatin is highly effective in the treatment of primary hypercholesterolemia and represents an important therapeutic advance. Safety with long-term use and effect on coronary heart disease remain to be established.
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Human atherosclerotic lesions exhibit increased expression of plasminogen activator inhibitor type-1 (PAI-1) that has been implicated in atherogenesis. Although vascular smooth muscle cells are a predominant source of PAI-1 expression potentially favorable modulation of PAI-1 expression by fibrates has not yet been characterized in these cells. Human aortic smooth muscle cells were exposed to selected growth factors. PAI-1 expression was stimulated most powerfully by TGF-beta (EC50 = 0.2 ng/ml, up to 12-fold increase). Gemfibrozil inhibited basal PAI-1 expression by 23% (p = ns) and TGF-beta-induced PAI-1 expression by 52% (p = 0.017) whereas t-PA and total protein synthesis was not affected. Changes in PAI-1 protein accumulation reflected PAI-1 gene expression attributable to modulation of half-life of PAI-1 mRNA by gemfibrozil. Inhibition by other fibrates was less. Gemfibrozil specifically attenuates TGF-beta-induced PAI-1 expression in human arterial smooth muscle cells. Thus, fibrates are promising agents for normalizing increased PAI-1 expression in arterial walls in patients in whom PAI-1 expression is increased.
Bexarotene (Targretin oral capsules), the first RXR-selective retinoid "rexinoid" approved for all stages of cutaneous T-cell lymphoma (CTCL), had a response rate (RR) of 45% at the optimal dose of 300 mg/m(2) per day in 2 multicenter trials. With hypertriglyceridemia reported at 79%, bexarotene is often administered with lipid-lowering agents (LLAs). Statins (inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase) may modulate class II major histocompatibility class expression and T-cell responses.
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This was a post hoc subgroup analysis in the Veterans Affairs High-Density Lipoprotein Intervention Trial, a randomized double-blind trial of gemfibrozil versus placebo in 2,531 men with coronary disease, HDL-C levels of 40 mg/dL or less (< or =1.0 mmol/L), low-density lipoprotein cholesterol levels of 140 mg/dL or less (< or =3.6 mmol/L), and a range of triglyceride values. Moderate CRI is defined as estimated glomerular filtration rate (GFR) of 30 to 59.9 mL/min/1.73 m2 at baseline. Multivariate regression was used to calculate rates of decline in estimated GFR for individuals administered gemfibrozil or placebo, controlling for prospectively determined potential confounders.
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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.
The presence of PPARα and PPARγ has been evaluated by real-time-PCR in Graves' disease (GD) and control cells in primary culture. Furthermore, we have tested the role of PPARα and PPARγ activation on CXCL9 and CXCL11 secretion in GD and control cells after stimulation of these chemokines secretion with IFNγ and TNFα.
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In this prospective 1-year study, 48 heart transplant recipients with moderate hypercholesterolemia were randomized to therapy with gemfibrozil 600 mg twice daily (n = 17), simvastatin 10 mg daily (n = 13), and cholestyramine 4 gm twice daily (n = 18). Detailed lipoprotein analysis was performed at baseline and after 3, 6, and 12 months of treatment.
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Immediately after renal transplantation we randomly allocated (proportioned 2:1:2) patients to: 1) simvastatin (10 mg/day, n=53), 2) simvastatin placebo plus gemfibrozil (dose adjusted for renal function, n=36), and 3) simvastatin placebo (n=52).
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of selected studies were then stratified using a rating system devised to determine the quality of results using the scientific evidence provided for them. Combination fibrate and statin therapy can be more effective in achieving optimal lipid levels than just fibrate or statin therapy alone without significant side effects as long as gemfibrozil is not used in therapy.
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A 39-year-old Hispanic man arrived at the emergency department with complaints of abdominal pain, nausea, and vomiting over one day. A computed tomography scan of the abdomen revealed peripancreatic inflammatory changes surrounding the tail of the pancreas, consistent with pancreatitis. Pertinent laboratory test values on admission were as follows: triglyceride concentration, 5366 mg/dL; total cholesterol concentration, 555 mg/dL; amylase concentration, 131 units/L; lipase concentration, 51 units/L; serum glucose concentration, 253 mg/dL; and serum sodium concentration, 128 mmol/L. The patient was diagnosed with hypertriglyceridemia-induced pancreatitis. On hospital day 1, the patient was given nothing by mouth and received a 1-L bolus dose of 0.9% sodium chloride injection, followed by a continuous infusion of 0.9% sodium chloride injection at a rate of 125 mL/hr. Subcutaneous heparin 5000 units every eight hours, sliding-scale regular insulin, and gemfibrozil 600 mg twice daily were initiated. On hospital day 2, the patient's triglyceride concentration decreased to 2962 mg/dL, and his blood glucose concentration was 147 mg/dL. Subcutaneous insulin detemir 25 units daily was ordered, and sliding-scale insulin was continued. Due to continued elevated triglyceride levels, the patient was transitioned from subcutaneous insulin to an i.v. insulin infusion at 0.1 unit/kg/hr in addition to an infusion of 5% dextrose. On hospital day 5, the patient's triglyceride concentration decreased to 717 mg/dL; the insulin-dextrose infusion was discontinued. The patient was discharged on hospital day 6.
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This retrospective analysis was conducted at a publicly funded teaching institution whose predominant patient population consists of Hispanics and Asians. A computer-generated report was used to identify outpatients who received a prescription for maximum-dose simvastatin or atorvastatin between January 1, 2002, and January 1, 2004. Data evaluated included demographic information; metabolic syndrome elements; coronary heart disease (CHD) risk equivalents; clinical characteristics placing patients at very high risk of having a CHD event; 10-year Framingham risk score; documentation of hepatotoxicity, myalgia, myositis, or rhabdomyolysis during maximum-dose therapy; concomitant medication during maximumdose therapy; relevant laboratory test values; and physician response to biochemical abnormalities or adverse events associated with maximum-dose therapy.
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Among participants of all four groups, unadjusted and adjusted mean concentrations of total cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B, but not triglycerides, decreased significantly. Among participants with prediabetes and normoglycemia, unadjusted and adjusted mean concentrations of high-density lipoprotein cholesterol increased significantly. Adjusted mean log-transformed concentrations of triglycerides decreased in adults with undiagnosed diabetes and prediabetes. During 2005-2008, unadjusted concentrations of apolipoprotein B ≥80 mg/dl were observed in 72.8% of participants with diagnosed diabetes, 87.9% of participants with undiagnosed diabetes, 86.6% of participants with prediabetes, and 77.2% of participants with normoglycemia. The unadjusted use of cholesterol-lowering medications rose rapidly, especially among participants with diabetes (from ~1% to ~49%, P <0.001). The use of fenofibrate, gemfibrozil, and niacin rose significantly only among adults with diagnosed diabetes (from ~2% to ~8%, P = 0.011).
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Using the prices of gemfibrozil that were negotiated by the VA, gemfibrozil was cost saving. Using drug prices found outside the VA, a quality-adjusted life-year saved by gemfibrozil therapy cost between $6300 and $17 100.
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These results confirm the hypothesis that a glucuronide conjugate of a relatively nonpolar xenobiotic, such as gemfibrozil, behaves as an amphiphile in aqueous solution. The implications of this observation include a likely basis for the previously observed concentration-dependence in the degradation rate of the acyl glucuronides of 2-phenylpropionic acid, as well as identifying a possible broader contributory effect to the structural dependencies in biliary choleresis of different glucuronide conjugates of xenobiotics.
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Pharmaceuticals, including the lipid regulator gemfibrozil and the non-steroidal anti-inflammatory drug diclofenac have been identified in waste water treatment plant effluents and receiving waters throughout the western world. The acute and chronic toxicity of these compounds was assessed for three freshwater species (Daphnia magna, Pseudokirchneriella subcapitata, Lemna minor) using standardised toxicity tests with toxicity found in the non-environmentally relevant mid mg L(-1) concentration range. For the acute endpoints (IC(50) and EC(50)) gemfibrozil showed higher toxicity ranging from 29 to 59 mg L(-1) (diclofenac 47-67 mg L(-1)), while diclofenac was more toxic for the chronic D. magna 21 d endpoints ranging from 10 to 56 mg L(-1) (gemfibrozil 32-100 mg L(-1)). These results were compared with the expression of several biomarkers in the zebra mussel (Dreissena polymorpha) 24 and 96 h after exposure by injection to concentrations of 21 and 21,000 μg L(-1) corresponding to nominal concentrations of 1 and 1000 μg L(-1). Exposure to gemfibrozil and diclofenac at both concentrations significantly increased the level of lipid peroxidation, a biomarker of damage. At the elevated nominal concentration of 1000 μg L(-1) the biomarkers of defence glutathione transferase and metallothionein were significantly elevated for gemfibrozil and diclofenac respectively, as was DNA damage after 96 h exposure to gemfibrozil. No evidence of endocrine disruption was observed using the alkali-labile phosphate technique. Results from this suite of biomarkers indicate these compounds can cause significant stress at environmentally relevant concentrations acting primarily through oxidation pathways with significant destabilization of the lysosomal membrane and that biomarker expression is a more sensitive endpoint than standardised toxicity tests.
To evaluate whether initiation of a fibrate or statin increases the risk of hospitalization for gastrointestinal bleeding in warfarin users.
When pravastatin (40 mg/day) was co-administered with gemfibrozil (600 mg, b.i.d., 3 days) to man, the AUC of pravastatin increased approximately 2-fold. We have clarified that OATP1B1 is a key determinant of the hepatic uptake of pravastatin in humans. Thus, we hypothesized that gemfibrozil and the main plasma metabolites, a glucuronide (gem-glu) and a carboxylic acid metabolite (gem-M3), might inhibit the hepatic uptake of pravastatin and lead to the elevation of the plasma concentration of pravastatin. Gemfibrozil and gem-glu inhibited the uptake of (14)C-pravastatin by human hepatocytes with K(i) values of 31.7 microM and 15.7 microM, respectively and also inhibited pravastatin uptake by OATP1B1-expressing Xenopus laevis oocytes with K(i) values of 15.1 microM and 7.6 microM. Additionally, we examined the biliary transport of pravastatin and demonstrated that pravastatin was transported by MRP2 using both human canalicular membrane vesicles (hCMVs) and human MRP2-expressing vesicles. However, gemfibrozil, gem-glu and gem-M3 did not affect the biliary transport of pravastatin by MRP2. Considering the plasma concentrations of gemfibrozil and gem-glu in humans, the inhibition of OATP1B1-mediated hepatic uptake of pravastatin by gem-glu would contribute, at least in part, to the elevation of plasma concentration of pravastatin by the concomitant use of gemfibrozil.
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The effect of a single intrajejunal dose of gemfibrozil (600 mg) on the plasma pharmacokinetics and biliary excretion of a single intrajejunal dose of rosuvastatin (20 mg) was investigated by using a multichannel catheter positioned in the distal duodenum-proximal jejunum in 8 healthy volunteers. Bile and plasma samples were collected every 20 minutes for 200 minutes, with additional plasma samples being drawn for up to 48 hours. Gemfibrozil did not affect the bioavailability of rosuvastatin, although it increased the apparent absorption phase during the initial 200 minutes (AUC(plasma,200min)) by 1.56-fold (95% confidence interval, 1.14-2.15). The interaction was less pronounced in this single-dose study than in a previous report when gemfibrozil was administered repeatedly; nevertheless, the interaction coincided with the highest exposure to gemfibrozil. The plausible reason why the interaction in this investigation was only minor is the low exposure to gemfibrozil (and its metabolites), suggesting that the total plasma concentration of gemfibrozil needs to be above 20 µM to affect the disposition of rosuvastatin. This study demonstrates the value of monitoring the plasma pharmacokinetics of the inhibitor, and not only the drug under investigation, to improve the mechanistic interpretation.
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Contamination of natural aquatic environments with human-use pharmaceuticals poses a significant potential threat to local ecosystems. However studies of the risk assessment of this contamination are limited, in part because currently the environmental concentration prediction is logistically and technically difficult to perform. In this study, 1) a strategic method to determine occurrence and risk of pharmaceutical compounds in an aquatic environment is proposed, and 2) this method is applied to study ten human-use pharmaceuticals in Taiwan's Sindian river, which traverses and supplies drinking water for Taipei, a major metropolitan center. In river-water samples collected over a three-week period, concentrations of NSAIDs (acetaminophen, diclofenac, ibuprofen, naproxen, and ketoprofen), steroids (estrone, 17alpha-ethinylestradiol and 17beta-estradiol), the anti-hypertensive agent propranolol, and the lipid regulator gemfibrozil were found at ng/L to microg/L levels; night-time concentrations were often doubled or even greater, compared to day-time levels. With the exception of the estrogens, predicted environmental concentrations (PECs) of the target pharmaceuticals agreed well with measured environmental concentrations (MECs).
Triglycerides (TGs) are now considered an independent risk factor for cardiovascular disease (CVD). When TGs are elevated, lipoprotein metabolism is altered, which increases CVD risk. Patients with elevated TGs and low high-density lipoprotein are at particularly high risk of CVD. TGs are often associated with other CVD risk factors, such as obesity, insulin resistance, diabetes mellitus, low HDL cholesterol, lifestyle factors, and changes in lipoprotein size and density. Elevated TGs remain an independent risk even when controlling for the other factors and are a greater risk for women than men. Treatment of elevated TGs in clinical trials has been shown to reduce CVD events, cardiac deaths, and total mortality.
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Mechanism-based inhibition of cytochrome P450 involves the bioactivation of the drug to a reactive metabolite, which leads to cytochrome inhibition via various mechanisms. This is generally seen in the Phase I of drug metabolism. However, gemfibrozil (hypolipidemic drug) leads to mechanism-based inhibition after generating glucuronide conjugate (gemfibrozil acyl-β-glucuronide) in the Phase II metabolism reaction. The mechanism involves the covalent binding of the benzyl radical (generated from the oxidation of aromatic methyl group in conjugate) to the heme of CYP2C8. This article deals with the development of a 2D QSAR model based on the inhibitory potential of gemfibrozil, its analogues and corresponding glucuronide conjugates in inhibiting the CYP2C8-catalysed amodiaquine N-deethylation. The 2D QSAR model was developed using multiple linear regression analysis in Accelrys Discovery Studio 2.5 and helps in identifying the descriptors, which are actually contributing to the inhibitory potency of the molecules studied. The built model was further validated using leave one out method. The best quantitative structure activity relationship model was selected having a correlation coefficient (r) of 0.814 and cross-validated correlation coefficient (q(2)) of 0.799. 2D QSAR revealed the importance of volume descriptor (Mor15v), shape descriptor (SP09) and 3D matrix-based descriptor (SpMax_RG) in defining the activity for this series of molecules. It was observed that volume and 3D matrix-based descriptors were crucial in imparting higher potency to gemfibrozil glucuronide conjugate, as compared with other molecules. The results obtained from the present study may be useful in predicting the inhibitory potential (IC50 for CYP2C8 inhibition) of the glucuronide conjugates of new molecules and compare with the standard gemfibrozil acyl-β-glucuronide (in terms of pIC50 values) in early stages of drug discovery and development.
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We tested the hypothesis that gemfibrozil has a differential effect on low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subclass distributions and postprandial lipemia that is different in subjects classified as having LDL subclass pattern A or LDL pattern B who do not have a classic lipid disorder. Forty-three normolipemic subjects were randomized to gemfibrozil (1,200 mg/day) or placebo for 12 weeks. Lipids and lipoproteins were determined by enzymatic methods. The mass concentrations of lipoproteins in plasma were determined by analytic ultracentrifugation and included the S(f) intervals: 20 to 400 (very LDL), 12 to 20 (intermediate-density lipoprotein), 0 to 12 (LDL), and HDL(2) mass (F(1.20) 3.5 to 9.0) and HDL(3) mass (F(1.20) 0 to 3.5). Postprandial measurements of triglycerides and lipoprotein(a) were taken after the patients consumed a 500 kcal/M(2) test meal. Treatment with gemfibrozil, compared with placebo, significantly reduced fasting plasma triglycerides (difference from placebo +/- SE; -50.2 +/- 20.6 mg/dl, p = 0.02), total cholesterol (-16.4 +/- 7.5 mg/dl, p = 0.04), apolipoprotein B (-16.1 +/- 5.5 mg/dl, p = 0.006), very LDL mass of S(f) 20 to 400 (-50.8 +/- 24.1 mg/dl, p = 0.02), S(f) 20 to 60 (-17.5 +/- 8.5 mg/dl, p = 0.05), S(f) 60 to 100 (-16.2 +/- 8.1 mg/dl, p = 0.05), and increased peak S(F) (0.48 +/- 0.27 Svedberg, p = 0.08). Gemfibrozil reduced the postprandial triglyceride level significantly at 3 (p = 0.04) and 4 (p = 0.05) hours after the test meal. A significantly different subclass response to gemfibrozil was observed in those with LDL pattern A versus B. Those with LDL pattern B had a significantly greater reduction in the small LDL mass S(f) 0 to 7 (p = 0.04), specifically regions S(f) 0 to 3 (p = 0.009) and S(f) 3 to 5 (p = 0.009). In conclusion, normolipemic subjects with either predominantly dense or buoyant LDL respond differently to gemfibrozil as determined by the changes in LDL subclass distribution. Thus, treatment with gemfibrozil may have additional antiatherogenic effects in those with LDL pattern B by decreasing small dense LDL that is not apparent in those with pattern A.
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Fenofibrate, bezafibrate, and gemfibrozil reduced plasma low-density lipoprotein cholesterol levels by 22% (P =.009), 14% (P =.042), and 11% (not significant), respectively. Plasma triglyceride levels decreased significantly (24%-36%; P <.05), whereas high-density lipoprotein cholesterol levels rose nonsignificantly after treatment with the 3 fibrates. Except for a 35% increase of apolipoprotein A-I mRNA after fenofibrate administration (P <.05), none of the individual fibrates induced significant changes in the mRNAs tested, although as a group they increased the mRNA for liver carnitine palmitoyltransferase I by 40%(P =.08; marginally significant).
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There were 1,116,805 patients who initiated statin and/or fibrate therapy, with 2.4 million person-years of observation. Seventy cases of hospitalized rhabdomyolysis were confirmed. Adjusted analyses showed a persistent increased risk of rhabdomyolysis with combination therapy, while statin and fibrate therapy alone showed similar, nonsignificant increases in risk. The adjusted IRR for a statin and fenofibrate was 3.26 (95% CI 1.21 to 8.80), while the adjusted IRR for a statin and gemfibrozil was 11.93 (95% CI 3.96 to 35.93) versus statin therapy alone. The individual IRs for statin monotherapy ranged from 0.00 to 3.34 per 100,000 person-years. The number needed to harm was lower for combination statin-gemfibrozil therapy (2753) compared with that for statin therapy alone (454,545).
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Gemfibrozil monotherapy of hyperlipidemia may predispose to rhabdomyolysis with acute renal failure. Patients using gemfibrozil should be cautioned regarding strenuous exertion, dehydration, and the need for prompt evaluation of myalgias.
To study the effects of gemfibrozil treatment on LDL particle size, density distribution, and composition in NIDDM patients.
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Thirty-eight renal allograft recipients who had persistent hyperlipidemia and stable renal function 27.8 +/- 18.2 months after renal transplantation were treated with gemfibrozil. Gemfibrozil therapy resulted in a decrease in the levels of total cholesterol (TC; 297.6 +/- 41.0 mg/dl to 249.2 +/- 43.7 mg/dl, -16.3%; p < 0.0001), triglyceride (TG; 231.9 +/- 116.8 to 125.7 +/- 58.4 mg/dl, -45.8%, p < 0.0005), and LDL-cholesterol (LDL-C; 203.8 +/- 37.4 to 174.5 +/- 42.5 mg/dl, -14.4%; p = 0.001), which were sustained for 29.1 +/- 16.0 months. Comparison of sequential lipid profiles between gemfibrozil-treated individuals and untreated hyperlipidemic controls matched for age, sex, time after transplantation, and the degree of hyperlipidemia, showed that gemfibrozil-treated patients had lower levels of TC (239.9 +/- 39.5 vs. 272.8 +/- 34.1 mg/dl; p < 0.005), TG (125.7 +/- 26.6 vs. 167.3 +/- 69.0 mg/dl; p < 0.05), and LDL-C (160.2 +/- 41.3 vs. 185.3 +/- 26.6 mg/dl; p < 0.05) on serial follow-up. No significant side-effect was observed with gemfibrozil therapy. Our data showed that gemfibrozil was a safe and effective drug for the treatment of hyperlipidemia in renal allograft recipients, which could reduce these patients's long-term cardiovascular risks.
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Statin/fibrate combinations are frequently used to treat mixed dyslipidemia. However, these combinations may cause life-threatening drug interactions (e.g. rhabdomyolysis) possibly induced by modifications of cytochrome P450 isozyme activities. Some statins are also transported by P-glycoprotein (Pgp) and may act as inhibitors of this drug efflux pump. So far, nothing is known about possible Pgp modulating effects of fibrates. We tested whether gemfibrozil, fenofibrate, fenofibric acid, and bezafibrate inhibit Pgp in vitro using a calcein acetoxymethylester (calcein-AM) uptake assay and confocal laser scanning microscopy with bodipy-verapamil as substrate in L-MDR1 cells, which overexpress human Pgp. In uptake assays in cells with (L-MDR1) and without (LLC-PK1) human Pgp we also investigated whether these compounds are transported by Pgp. Intracellular concentrations were measured by liquid chromatography tandem mass spectrometry. Of the tested fibrates, only fenofibrate increased calcein-AM uptake into cells indicating an inhibition of Pgp mediated transport by this compound. The potency of fenofibrate (mean+/-SD: 7.1+/-3.2 microM), evaluated by calculating the concentration needed to double baseline fluorescence (f2), was similar to that of simvastatin (5.8+/-1.5 microM), lovastatin (10.1+/-1.0), and verapamil (4.7+/-0.8 microM). For simvastatin and fenofibrate Pgp inhibition was confirmed with confocal laser scanning microscopy. Fenofibrate, fenofibric acid, gemfibrozil, and bezafibrate showed no difference in the cellular uptake between LLC-PK1 and L-MDR1, indicating that the tested fibrates are not Pgp substrates. In conclusion, this study demonstrates that fenofibrate inhibits Pgp in vitro with a potency similar to simvastatin.
Recent studies, abstracts, reviews, and consensus statements published in the English-language literature were identified through searches of MEDLINE (1966-January 2002), International Pharmaceutical Abstracts (1970-January 2002), and PharmaProjects (1990-January 2002) using the search terms fenofibrate, fibrates, hyperlipidemia, hypertriglyceridemia, and dyslipidemia.
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Large randomized, controlled clinical trials of lovastatin and gemfibrozil for heart disease prevention have reported statistically significantly lower melanoma incidences in persons receiving these medications. Results of in vitro animal model and human case-control studies also suggest that statins and fibrates may reduce the risk of melanoma.
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