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Lopid

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:
Apo-gemfibrozil, Pms-gemfibrozil

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Also known as: Gemfibrozil.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Side effects

The most common side effects associated with Lopid are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

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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A minority of subjects eligible for intensive lipid lowering agreed to participate in a feasibility study, suggesting a potentially large compliance problem for a general lipid-lowering programme in a diabetes clinic. Nevertheless, intensive lipid lowering with drug combinations can attain the recommended target lipid levels in 66% of subjects with diabetes. With this strategy the plasma lipoprotein composition shifts towards a less atherogenic profile. Subjects with diabetes should therefore receive lipid-lowering therapy tailored to reach target levels, rather than standard dosages, in order to reduce atherogenic risk.

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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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Glinides represent a chemically heterogeneous new class of insulin-secreting agents characterized by a rapid onset and short duration of action. They act by closure of the ATP-dependant K channel. Repaglinide, the only glinide available in France, has an equivalent HbA1c lowering effect to conventional sulfonylureas but reduces predominantly postprandial glucose levels. Several studies indicate a decreased risk of hypoglycaemias, particularly nocturnal or in case of a shift or omission of a meal. This drug appears particularly useful in early stage type 2 diabetes or in combination with metformin. The only significant drug-drug interaction concerns gemfibrozil. Due to its hepatic metabolism and biliary elimination, repaglinide can be used in patients with renal insufficiency. Nateglinide has a even shorter duration of action and has almost no effect on fasting plasma glucose levels. For this reason, this drug is only indicated in combination with metformin in the countries where it is licensed. Several experimental data suggest that glinides could preserve B cell function over time better than hypoglycaemic sulfonylureas, and that the improvement of post-prandial glucose levels could exert a long term protective cardiovascular effect.

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Physicians' views of the effectiveness of lipid lowering drugs and the decision to prescribe such drugs is affected by the predominant use of reduction of relative risk in trial reports and advertisements.

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Time-dependent inhibition by gemfibrozil glucuronide is only important for victim drugs eliminated predominantly (>80%) via CYP2C8. Qualitative zoning of OATP1B1 inhibitors based on [I]in/K (i) is valid in drug screening to avoid false negatives. Refinement of the transporter model by incorporating the fraction of drug transported by a particular transporter is recommended.

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Peroxisome proliferator activated receptors (PPARs) are a class of nuclear receptors involved in lipid and glucidic metabolism, immune regulation, and cell differentiation. Many of their biological activities have been studied by using selective synthetic activators (mainly fibrates and thiazolidinediones) which have been already employed in therapeutic protocols. Both kinds of drugs, however, showed pharmacotoxicological profiles, which cannot be ascribed by any means to receptor activation. To better understand these non-receptorial or extrareceptorial aspects, the effect of different PPAR-ligands on the metabolic status of human HL-60 cell line has been investigated. At this regard, NMR analysis of cell culture supernatants was accomplished in order to monitor modifications at the level of cell metabolism. Cell growth and chemiluminescence assays were employed to verify cell differentiation. Results showed that all the considered PPAR-ligands, although with different potencies and independently from their PPAR binding specificity, induced a significant derangement of the mitochondrial respiratory chain consisting in a strong inhibition of NADH-cytochrome c reductase activity. This derangement has been shown to be strictly correlated to the adaptive metabolic modifications, as evidenced by the increased formation of lactate and acetate, due to the stimulation of anaerobic glycolysis and fatty acid beta-oxidation. It is worthy noting that the mitochondrial dysfunction appeared also linked to the capacity of any given PPAR-ligand to induce cell differentiation. These data could afford an explanation of biochemical and toxicological aspects related to the therapeutic use of synthetic PPAR-ligands and suggest a revision of PPAR pathophysiologic mechanisms.

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We have studied, in a prospective blinded fashion, the effects of regular and extended-release gemfibrozil on plasma lipoprotein and apolipoprotein (apo) levels in hypercholesterolemic subjects with decreased high density lipoprotein (HDL) cholesterol (C) levels. Study participants were men and women 19 to 80 years of age with baseline plasma low density lipoprotein (LDL) C levels > or = 4.5 mmol/l (175 mg/dl), HDL-C levels < or = 1.2 mmol/l (45 mg/dl), and triglyceride levels < or = 3.4 mmol/L (300 mg/dl). All subjects were stabilized on a diet for eight weeks prior to entry into two different protocols. In the first protocol 229 subjects were randomized to placebo or extended-release gemfibrozil (1200 mg/day) for 3 months (placebo trial). In the second protocol 655 subjects were randomized to regular or extended-release gemfibrozil (1200 mg/day) for 6 months (equivalency trial). Changes in lipids and apos were stratified by baseline HDL-C levels (< 0.9 mmol/l, and 0.9-12.2 mmol/l). In both studies, treatment with gemfibrozil, either regular or extended-release, was associated with significant (P < 0.05) decreases in plasma very low density lipoprotein (VLDL) C and triglyceride levels of 42-45% and 33-37%, respectively, in subjects with HDL-C level < 0.9 mmol/l, and of 38-47% and 32-39%, respectively, in patients with HDL-C levels of 0.9-1.2 mmol/l. Modest reductions from baseline in directly measured LDL-C levels were observed in both groups (3-6% and 8-9%, respectively). These reductions were less than those observed for calculated LDL-C (7-10% and 11%, respectively). For apo B, reductions were 11-14% and 16-17% in the two groups. HDL-C, apo A-I, and apo A-II levels increased by 15-16%, 5-6%, and 21-25%, respectively, in patients with HDL-C < 0.9 mmol/l, and by 6-7%, 2-3%, and 19-22%, respectively, in patients with HDL-C of 0.9-1.2 mmol/l. These differences in HDL-C levels reached statistical significance in the equivalency trial (P < 0.0001) and were independent of baseline triglyceride levels. Our data indicate that gemfibrozil, either regular or extended-release, is highly effective in lowering plasma triglyceride levels and increases HDL-C levels by approximately 15% in hypercholesterolemic patients with low HDL-C levels (< 0.9 mmol/l). Moreover, this agent lowers VLDL-C somewhat more than triglyceride, resulting in an underestimation of calculated VLDL-C reductions and in an overestimation of calculated LDL-C reductions. This agent also raises apo A-II levels much more than apo A-I levels.

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Abnormal interaction between low density lipoprotein receptors (LDLR) and their ligands, apolipoprotein E and B, causes decreased catabolism of lipoproteins which carry these apolipoproteins (VLDL, IDL and/or LDL) and thereby increased plasma concentrations of these. In familial hypercholesterolemia (FH), abnormal interaction is due to mutations in the LDLR gene, and in type III hyperlipidemia due to mutations in the apo E gene. A few mutations in the apolipoprotein B (apo B) gene have been described, of which the apo B-3,500Arg-Gln seems by far the most frequent, that causes defective binding to normal LDLR. The metabolic disorder associated with these mutations has been named familial defective apolipoprotein B-100 (FDB). The frequency of the apo B-3,500Arg-Gln mutation is particularly high in Central Europe (Switzerland) with lower frequencies south of the Alpes, in Russia and in Scandinavia. We found an incidence of 1/1250 of the mutation in Denmark (III), employing a DNA based assay optimized to allow detection of the mutation in very small amounts of DNA (I). Since other mutations in the receptor binding domain of the apo B-100 have been described, we developed another DNA based assay, employing DGGE technique, to screen for other mutations in the region of amino acid 3,456 to 3,553 (II). However, no other mutations but the apo B-3,500Arg-Gln have so far been detected in Danish hypercholesterolemic patients. In a study of 5 Danish families with FDB (46 heterozygous FDB patients and 57 unaffected relatives) we found that FDB patients had significantly increased mean cholesterol and LDL cholesterol concentrations, but with a wide range of variation and with approximately 30% having cholesterol concentrations below the 95th percentile for the general population (IV). This was confirmed in a compilation of data on 205 FDB patients from the Netherlands, Germany and Denmark (V). In this study we also compared the biochemical and clinical features of FDB with those of 101 Danish FH patients in whome FDB had been ruled out. Our data support, that the LDL cholesterol elevation is less pronounced in FDB than in FH and that the age-specific prevalence of atherosclerotic cardiovascular disease (CVD) is lower in FDB than in FH. In the compiled study of 205 FDB heterozygotes (V), we found that age, gender and genetic variation in the LDLR gene explained a considerable part of the between-individual variation in total and LDL cholesterol. We conducted a prospective study of the lipid lowering effect of pravastatin and gemfibrozil in 30 Danish FDB patients (VI). Together with other, retrospective, studies, we conclude that the cholesterol lowering effect of HMG-coA-reductase inhibitors, anion binding resins and nicotinic acid is fully comparable to that observed when treating FH patients and type IIa hypercholesterolemic patients, without clinical signs of FH.

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Control and streptozotocin-diabetic mice were randomized to receive rosiglitazone (20 mg/kg/day), gemfibrozil (100 mg/kg/day), or compound 3q (3 mg/kg/day) by gavage, or no treatment for a period of 20 weeks. Renal fibrosis was assessed by standard histology and collagen IV immunohistochemistry. Kidney function was assessed by urinary albumin excretion and creatinine clearance.

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Repaglinide is an antidiabetic drug metabolised by cytochrome P450 (CYP) 2C8 and CYP3A4 enzymes. To clarify the mechanisms of observed repaglinide drug interactions, we determined the contribution of the two enzymes to repaglinide metabolism at different substrate concentrations, and examined the effect of fibrates and rifampicin on CYP2C8, CYP3A4 and repaglinide metabolism in vitro. We studied repaglinide metabolism using pooled human liver microsomes, recombinant CYP2C8 and recombinant CYP3A4 enzymes. The effect of quercetin and itraconazole on repaglinide metabolism, and of gemfibrozil, bezafibrate, fenofibrate and rifampicin on CYP2C8 (paclitaxel 6alpha-hydroxylation) and CYP3A4 (midazolam 1-hydroxylation) activities and repaglinide metabolism were studied using human liver microsomes. At therapeutic repaglinide concentrations (<0.4 microM), CYP2C8 and CYP3A4 metabolised repaglinide at similar rates. Quercetin (25 microM) and itraconazole (3 microM) inhibited the metabolism of 0.2 microM repaglinide by 58% and 71%, and that of 2 microM repaglinide by 56% and 59%, respectively. The three fibrates inhibited CYP2C8 (Ki: bezafibrate 9.7 microM, gemfibrozil 30.4 microM and fenofibrate 92.6 microM) and repaglinide metabolism (IC50: bezafibrate 37.7 microM, gemfibrozil 111 microM and fenofibrate 164 microM), but had no effect on CYP3A4. Rifampicin inhibited CYP2C8 (Ki 30.2 microM), CYP3A4 (Ki 18.5 microM) and repaglinide metabolism (IC50 13.7 microM). In conclusion, both CYP2C8 and CYP3A4 are important in the metabolism of therapeutic concentrations of repaglinide in vitro, but their predicted contributions in vivo are highly dependent on the scaling factor used. Gemfibrozil is only a moderate inhibitor of CYP2C8 and does not inhibit CYP3A4; inhibition of CYP-enzymes by parent gemfibrozil alone does not explain its interaction with repaglinide in vivo. Rifampicin competitively inhibits both CYP2C8 and CYP3A4, which can counteract its inducing effect in humans.

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Wastewater treatment plant (WWTP) effluents are important sources of emerging contaminants at environmentally-relevant concentrations. In this study, water samples were collected from a river downstream of two WWTPs to identify practical tracers for tracking wastewater. The results of the study indicate elevated concentrations of Cl(-), nutrients (NH3-N and NO2(-)), the artificial sweetener acesulfame-K (ACE-K), and the pharmaceuticals carbamazepine (CBZ), caffeine (CAF), sulfamethoxazole (SMX), ibuprofen (IBU), gemfibrozil (GEM), and naproxen (NAP) in the river close to the WWTPs that decreased with distance downstream. A correlation analysis using the Spearman Rank method showed that ACE-K, CBZ, GEM, NAP, and Cl(-) were strongly correlated with each other over a 31 km stretch of the river in the study area. The strong correlations of these target compounds indicate that the artificial sweetener ACE-K and the pharmaceuticals CBZ, GEM, and NAP can potentially be used as co-tracers to track wastewater.

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lopid generic equivalent 2016-10-09

Twenty-three patients Micardis Hct Generic Alternative with combined hyperlipidaemia and CHD or a positive family history for both CHD and hyperlipidaemia.

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The occurrence Avelox Iv Cost of low rates of rhabdomyolysis among patients receiving lipid-lowering drugs (LLDs) in randomized clinical trials may be elucidated with population-based studies.

gemfibrozil generic for lopid 2016-07-04

Cytochrome P450 (CYP) 3A4 is considered the most important enzyme in imatinib biotransformation. In a randomized, crossover study, 10 healthy subjects were administered gemfibrozil Tricor Order Forms 600 mg or placebo twice daily for 6 days, and imatinib 200 mg on day 3, to study the significance of CYP2C8 in imatinib pharmacokinetics. Unexpectedly, gemfibrozil reduced the peak plasma concentration (Cmax) of imatinib by 35% (P < 0.001). Gemfibrozil also reduced the Cmax and area under the plasma concentration-time curve (AUC0-∞) of N-desmethylimatinib by 56 and 48% (P < 0.001), respectively, whereas the AUC0-∞ of imatinib was unaffected. Furthermore, gemfibrozil reduced the Cmax/plasma concentration at 24 h (C24 h) ratios of imatinib and N-desmethylimatinib by 44 and 17% (P < 0.05), suggesting diminished daily fluctuation of imatinib plasma concentrations during concomitant use with gemfibrozil. Our findings indicate significant participation of CYP2C8 in the metabolism of imatinib in humans, and support involvement of an intestinal influx transporter in imatinib absorption.

lopid cost 2015-03-16

Certain primary hypertriglyceridemias cause abnormalities in lipoproteins that seemingly predispose patients to coronary heart disease. We examined metabolism of low-density lipoproteins (LDL) in 11 men with both hypertriglyceridemia and coronary heart disease and compared them with that of controls. The LDL turnover was measured during placebo and gemfibrozil therapy. With placebo, LDL-cholesterol level usually was normal, but production and fractional clearance of LDL were high. The LDL composition also was abnormal. Gemfibrozil reduced triglycerides, lowered production and fractional clearance of LDL, and normalized LDL composition. The LDL-cholesterol level usually rose, but generally not Cleocin Where To Purchase to abnormally high levels. Therefore, normalization of LDL metabolism and marked reduction of triglycerides by gemfibrozil suggest benefit to hypertriglyceridemic patients who are at high risk for coronary heart disease. However, when LDL-cholesterol level rises excessively, gemfibrozil may not be sufficient therapy.

lopid dosage generic 2016-10-21

We studied the effect of gemfibrozil on the compositions of VLDL, LDL and distribution of LDL subspecies in type II hyperlipidemic patients. Gemfibrozil significantly lowered serum triglyceride levels in this group of patients who had normal to moderately elevated triglyceride prior to therapy. Gemfibrozil also changed the Lopressor Generic Pictures composition of VLDL by lowering its free cholesterol, cholesterol ester and raising the protein content. In contrast, no measurable changes in LDL chemical composition were found following gemfibrozil therapy. Changes in LDL, however, can be detected using ultracentrifugal and electrophoretic methods. Peak densities of LDL were lowered and LDL subspecies shifted to larger, slower-moving bands on gradient gel electrophoresis in patients receiving gemfibrozil treatment. These results suggest that gemfibrozil treatment resulted in qualitative changes in both VLDL and LDL even in patients with moderately elevated baseline serum triglyceride levels.

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An increased prevalence of plaque (75% of the patients having plaque on one or both sides) was seen in the hyperlipidaemic renal transplant patients in comparison with the control group (16 Crestor Generic Alternative %; P < 0.001). The common carotid intima-media complex was thicker (P < 0.05), and the lumen diameter and the calculated cross-sectional intima-media area were greater (P < 0.01-0.001) in the transplant recipients.

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To provide recommendations for clinicians in the Lipitor Generic Equivalent treatment of refractory mixed hyperlipidemia.

generic lopid side effects 2016-12-14

Statin monotherapy is generally well tolerated, with a low frequency of adverse events. The most important adverse effects associated with statins are myopathy and an asymptomatic increase in hepatic transaminases, both of which occur infrequently. Because statins are prescribed on a long Lipitor Generic Price Canada -term basis, however, possible interactions with other drugs deserve particular attention, as many patients will typically receive pharmacological therapy for concomitant conditions during the course of statin treatment. This review summarizes the pharmacokinetic properties of statins and emphasizes their clinically relevant drug interactions.

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Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. Recently, PPAR activators have been shown to inhibit the production of proinflammatory cytokines in macrophages or vascular smooth muscle cells. It has been reported that tumor necrosis factor-alpha (TNF-alpha) expression is elevated in the failing heart and that TNF-alpha has a negative inotropic effect on cardiac myocytes. Therefore, we examined the effects of PPARalpha and PPARgamma activators on expression of TNF-alpha in neonatal rat cardiac myocytes. Northern blot analysis revealed expression of PPARalpha and PPARgamma mRNA in cardiac myocytes. Immunofluorescent staining demonstrated that both PPARalpha and PPARgamma were expressed in the nuclei of cells. When cardiac myocytes were transfected with PPAR responsive element (PPRE)-luciferase reporter plasmid, both PPARalpha and PPARgamma activators increased the promoter activity. Cardiomyocytes were stimulated with lipopolysaccharide (LPS), and the levels of TNF-alpha in the medium were measured by ELISA. After exposure to LPS, the levels of TNF-alpha significantly increased. However, pretreatment of myocytes with PPARalpha or PPARgamma activators decreased LPS-induced expression of TNF-alpha in the medium. Both PPARalpha and PPARgamma activators also inhibited LPS-induced increase in TNF-alpha mRNA in myocytes. In addition, electrophoretic mobility shift assays demonstrated that PPAR activators reduced LPS-induced nuclear factor-kappaB activation. These results suggest that both PPARalpha and PPARgamma activators inhibit cardiac expression of TNF-alpha in part by antagonizing nuclear factor-kappaB activity and that treatment with PPAR activators may lead to improvement in congestive heart failure.

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This study assessed the cost effectiveness of treatments for the primary prevention of coronary heart disease in Spain, which included smoking cessation and reductions in blood cholesterol levels and BP. Cost-effectiveness ratios (measured in terms of US dollars per life-year gained) ranged from 2,608 US dollars to 8,058 US dollars per life-year gained for therapies aimed at smoking cessation, from 7,061 US dollars to 126,990 US dollars per life-year gained for antihypertensive drug treatment, from 15,487 US dollars to 1,689,022 US dollars per life-year gained for the drug treatment of hypercholesterolaemia and from 12,792 US dollars to 149,246 US dollars per life-year gained for cholesterol-lowering diets. In individuals with blood cholesterol levels of 7.7 mmol/L, cost-effectiveness ratios of drug treatment ranged from 33,850 US dollars to 302,088 US dollars. Cost-effectiveness ratios were lower in men than in women for all programmes evaluated. Cost-effectiveness analysis of cholesterol-lowering drugs indicated that lovastatin (HMG-CoA reductase inhibitor) was more cost effective than cholestyramine (bile acid sequestrant) and gemfibrozil (fibrate). Hydrochlorothiazide, propranolol and nifedipine were more cost effective antihypertensive treatments than prazosin and captopril. Cost-effectiveness ratios obtained in this study could be used to develop disease management strategies to facilitate the efficient use of healthcare resources and to reduce costs. When resources for coronary heart disease are limited, available treatments should be selected on the basis of their average and incremental cost-effectiveness ratios.

gemfibrozil generic for lopid 2017-05-20

The presence of pharmaceutically active compounds (PhACs) in aquatic systems is an emerging environmental issue and poses a potential threat to ecosystems and human health. Unfortunately, current water treatment techniques do not efficiently remove all of the PhACs, which results in the occurrence of such compounds in surface and ground waters. Advanced oxidation/reduction processes (AO/RPs) which utilize free radical reactions to directly degrade chemical contaminants are alternatives to traditional water treatment methods. This study reports the absolute bimolecular reaction rate constants for three pharmaceutical compounds (fibrates), clofibric acid, bezafibrate, and gemfibrozil, with the hydroxyl radical (*OH) and hydrated electron (e(-)(aq)). The bimolecular reaction rate constants for *OH were (6.98 +/- 0.12) x 10(9), (8.00 +/- 0.22) x 10(9), and (10.0 +/- 0.6) x 10(9), and for e(-)(aq) were (6.59 +/- 0.43) x 10(8), (112 +/- 3) x 10(8), and (6.26 +/- 0.58) x 10(8), for clofibric acid, bezafibrate, and gemfibrozil, respectively. Transient spectra were obtained for the intermediate radicals produced by the hydroxyl radical reactions. In addition, preliminary degradation mechanisms and major products were elucidated using (137)Cs gamma-irradiation and LC-MS. These data are required for evaluating the potential use of AO/RPs for the destruction of these compounds in treating water for various purposes.

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Gemfibrozil has no effect on the pharmacokinetics of zafirlukast, indicating that CYP2C8 does not play a significant role in the elimination of zafirlukast.

lopid dosage generic 2015-01-18

In response to gemfibrozil therapy, L162-homozygotes exhibited a 5.5% increase in high-density lipoprotein 2 cholesterol (HDL(2)-C) levels compared with a 50.0% increase among carriers of the V162 allele (P = 0.03).

lopid 600 mg cost 2015-04-25

The results from the present analysis support conclusions from previous meta-analyses that cholesterol lowering is clinically beneficial in patients with CHD or at elevated CHD risk. These results also support the previous finding that non-CHD-related mortality is unrelated to lipid reductions.

lopid generic name 2016-01-08

An optimised and validated method for the determination of pharmaceutical residues in blue mussels (Mytilus spp.) is presented herein, as well as an investigation of the effect of cooking (by steaming) on any potential difference in human exposure risk. Selected pharmaceuticals included two non-steroidal anti-inflammatory drugs (diclofenac and mefenamic acid), an antibiotic (trimethoprim), an anti-epileptic (carbamazepine) and a lipid regulator (gemfibrozil). An in vivo exposure experiment was set up in the laboratory in which mussels were exposed either directly by injection (10 ng) or daily through spiked artificial seawater (ASW) over 96 h. In liquid matrices, pharmaceutical residues were either determined using liquid chromatography–tandem mass spectrometry (LC-MS/MS) directly, or in combination with solid-phase extraction (SPE) for analyte concentration purposes. The extraction of pharmaceuticals from mussel tissues used an additional pressurised liquid extraction step prior to SPE and LCMS/MS. Limits of quantification of between 2 and 46 ng L−1 were achieved for extracted cooking water and ASW, between 2 and 64 μg L−1 for ASW in exposure tanks, and between 4 and 29 ng g−1 for mussel tissue. Method linearities were achieved for pharmaceuticals in each matrix with correlation coefficients of R2>0.975. A selection of exposed mussels was also cooked (via steaming) and analysed using the optimised method to observe any effect on detectable concentrations of parent pharmaceuticals present. An overall increase in pharmaceutical residues in the contaminated mussel tissue and cooking water was observed after cooking.