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Lopid (Gemfibrozil)

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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:

Similar Products:
Pravachol, Mevacor, Zetia, Crestor


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.

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.


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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The in vitro inhibitory effects of gemfibrozil on cytochrome P450 (CYP) 1A2 (phenacetin O-deethylation), CYP2A6 (coumarin 7-hydroxylation), CYP2C9 (tolbutamide hydroxylation), CYP2C19 (S-mephenytoin 4'-hydroxylation), CYP2D6 (dextromethorphan O-deethylation), CYP2E1 (chlorzoxazone 6-hydroxylation), and CYP3A4 (midazolam 1'-hydroxylation) activities were examined using pooled human liver microsomes. The in vivo drug interactions of gemfibrozil were predicted in vitro using the [I]/([I] + K(i)) values. Gemfibrozil strongly and competitively inhibited CYP2C9 activity, with a K(i) (IC(50)) value of 5.8 (9.6) microM. In addition, gemfibrozil exhibited somewhat smaller inhibitory effects on CYP2C19 and CYP1A2 activities, with K(i) (IC(50)) values of 24 (47) microM and 82 (136) microM, respectively. With concentrations up to 250 microM, gemfibrozil showed no appreciable effect on CYP2A6, CYP2D6, CYP2E1, and CYP3A4 activities. Based on [I]/([I] + K(i)) values calculated using peak total (or unbound) plasma concentration of gemfibrozil, 96% (56%), 86% (24%), and 64% (8%) inhibition of the clearance of CYP2C9, CYP2C19, and CYP1A2 substrates could be expected, respectively. In conclusion, gemfibrozil inhibits the activity of CYP2C9 at clinically relevant concentrations, and this is the likely mechanism by which gemfibrozil interacts with CYP2C9 substrate drugs, such as warfarin and glyburide. Gemfibrozil may also impair clearance of CYP2C19 and CYP1A2 substrates, but inhibition of other CYP isoforms is unlikely.

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An integrated database, consisting of 33 trials whose databases were locked up to and including September 16, 2005, was used to examine adverse events and laboratory data.

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The ability of pravastatin, a new hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, to lower plasma lipid levels and modify lipoprotein patterns was compared with that of gemfibrozil in 18 patients with familial hypercholesterolemia who participated in a 16-week, double-blind, parallel trial. Pravastatin proved better than gemfibrozil in lowering total and low-density lipoprotein (LDL) cholesterolemia: -23.6% and -28.2% versus -18.1% and -21.4%, respectively. A significant positive correlation was found between the starting level of serum cholesterol (both total and LDL) and the gemfibrozil-induced reduction (r = 0.72 and 0.69), whereas the hypocholesterolemic effect of pravastatin was apparently independent from pretreatment levels (r = 0.32 and 0.10). Apolipoprotein B concentrations were lowered by 25.4% (pravastatin) and 22.0% (gemfibrozil). Pravastatin and gemfibrozil reduced triglyceride levels by 13.9% and 49.4%, respectively. Both drugs increased the level of high density lipoprotein (HDL) cholesterol, but this change was significant only with gemfibrozil (p less than 0.05). The HDL subfraction structure and distribution were not modified by pravastatin treatment. Gemfibrozil, in contrast, increased HDL3 cholesterol level by 9% because of an enrichment of HDL3 particles in both free cholesterol and cholesteryl esters and lowered the flotation rate of HDL3 (p less than 0.05). LDL particles became smaller after gemfibrozil treatment (diameter: 25.4 +/- 0.3 nm vs 26.1 +/- 0.4 nm, p less than 0.01) and were not modified by pravastatin. This comparison shows a more pronounced efficacy of the HMG CoA reductase inhibitor on total and LDL cholesterol levels, also indicating that pravastatin acts by a single major mechanism, reducing the number of circulating LDL particles. Gemfibrozil may exert additional activities, possibly consequent to the stimulation of very low density lipoprotein catabolism.

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To evaluate the effects of berberine (BBR) on the liver phosphatidate phosphohydrolase (PAP) and plasma lipids in rats fed on high lipogenic and normal diet.

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CFTR Cl- channels may serve as novel and crucial mediators in mouse heart IPC.

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The phytotoxicity of 5 pharmaceuticals detected in Italian rivers, atorvastatin (7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-yl-pyrrol-1-yl]-3,5-dihydroxy-heptanoic acid), gemfibrozil (5-(2,5-dimethylphenoxy)-2,2-dimethyl-pentanoic acid), tamoxifene (2-[4-(1,2-diphenylbut-1-enyl)phenoxy]-N,N-dimethyl-ethanamine), ethinyl estradiol (17-ethynyl-13-methyl-7,8,9,11, 12,13,14,15,16,17-decahydro-6H-cyclopenta[a]phenanthrene-3,17-diol) and sildenafil (methyl-9-propyl-2,4,7,8-tetrazabicyclo[4.3.0] nona-3,8,10-trien-5-one), has been assessed in a laboratory model. The treatment system consists of three main successive sections. The first one includes the phytotoxic evaluation of the single compounds on crops, Lactuca sativa (lettuce), Dacus carota subsp. sativa (carrot), and Lycopersicon esculentum (tomato), until the 10(-9) M, concentration lower then the environmental amounts. The second section includes the phytotoxicity assessment of all the selected chemicals on wild species, Avena fatua (wild oats), Amaranthus retroflexus (redroot pigweed), Lolium perenne (perennial ryegrass), Taraxacum officinale (common dandelion), and Chenopodium album (lambsquarter), at the same concentration as previously used. The third section of the procedure includes the evaluation of the effects of the five pharmaceuticals, at 1 microM and 1 nM environmental concentrations, on the metabolism of L. sativa. The variation of the composition of the photosynthetic pigments, sugars, lipids, phenols, fatty acids and flavonoids in lettuce seedlings exposed to the pollutants in respect to the blank was evaluated. The results of the phytotoxicity assays showed the possibility of a notable impact on the different vegetal communities and evidenced different sensitivity among cultivated and wild species, probably due to the different plant physiology.

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Cerivastatin, but not gemfibrozil significantly reduces RLP-C increase after an oral fat load in combination with a reversal of fat-load induced endothelial dysfunction. The present data imply that lowering of RLP-C, rather than lowering of total TG levels, may contributes to the prevention of endothelial dysfunction after an oral fat load during statin use.

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Two cases of supravalvar aortic stenosis secondary to familial hypercholesterolaemia (type II A hyperlipoproteinaemia) are reported and the role of echocardiography in the diagnosis of this uncommon condition is discussed. The management of these patients is difficult and in one patient the serum cholesterol decreased substantially after treatment with gemfibrozil.

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The occurrence of 15 pharmaceuticals and personal care products in the influent and effluent from the wastewater treatment plant (WWTP) and its receiving water in Beijing, China were determined. Results from the present study confirmed that caffeine, N,N-diethyl-m-toluamide and chloramphenicol were removed at a high rate (>70 % efficiency). In contrast, removal efficiency of the other 12 compounds was quite poor (ranged from -40 % to 58 %). Some compounds in the receiving river were present at higher concentrations compared to those in the WWTP effluent, indicating that sources other than treated effluents are present. The risk to the aquatic environment was estimated by a ratio of measured environmental concentration and predicted no-effect concentration. For those compounds found in the effluent and surface water, mefenamic acid, trimethoprim and gemfibrozil may pose a medium risk to aquatic environment.

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A significant decrease in BP was observed in the 2 upper quartiles of systolic BP (>or=140 mm Hg) and was greater in subjects treated with cholesterol-lowering drugs who also had a greater reduction in plasma levels of low-density lipoprotein cholesterol. The BP decrease was greater in patients treated with statin drugs and, among those treated with antihypertensive drugs, in subjects in the fourth quartile.

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Elevated plasma viscosity is a predictor of atherosclerotic vascular disease and is a potential mechanism by which hypertriglyceridemia increases cardiovascular risk. Previous studies of plasma viscosity reduction in hypertriglyceridemic patients used medications that lowered both triglyceride and fibrinogen levels. Because fibrinogen is a major determinant of viscosity, it is unclear whether triglyceride reduction alone is sufficient to reduce plasma viscosity. The purpose of this study was to determine whether triglyceride-lowering therapy reduces plasma viscosity. This was a prospective study of 24 adult patients with severe hypertriglyceridemia (> or = 5.67 mmol/l). Fasting lipid, total serum protein, fibrinogen, plasma viscosity and serum viscosity levels were measured before and after therapy with 1200 mg/d of gemfibrozil. Triglyceride levels decreased by 70% (P < 0.001). Mean plasma and serum viscosity levels decreased by 0.082 mPa/s (P = 0.003) and 0.086 mPa/s (P = 0.013), respectively. Fibrinogen levels did not change significantly. Triglyceride-lowering therapy reduced plasma and serum viscosity without changes in fibrinogen levels. Since serum samples are deplete of fibrinogen, the serum viscosity reduction observed is corroborative evidence for an independent effect of triglyceride-lowering therapy on plasma viscosity. This observation provides a physiological rationale for triglyceride-lowering therapy in patients at risk for atherosclerotic vascular disease, the chylomicronemia syndrome and pancreatitis.

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The statins (3-hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors) represent drugs of first choice for treatment of hypercholesterolemia. The safety and efficacy of atorvastatin (CAS 134523-00-5), simvastatin (CAS 79902-63-9), lovastatin (CAS 75330-75-7), pravastatin (CAS 81093-37-0) and fluvastatin (CAS 93957-54-1) has been well documented. Statins decrease dose-dependently low-density lipoprotein (LDL) cholesterol as well as coronary events and total mortality. Clinical outcome data indicate that for simvastatin the lowest number of treated patients is needed to prevent one major coronary event (NNT 15). Based on an approximately 30% reduction of LDL (valid surrogate parameter) atorvastatin (5 mg/day) and simvastatin (10 mg/day) are the most potent agents whereas 40 mg of lovastatin or pravastatin and 60 mg of fluvastatin are needed to reach this "therapeutic target". While all statins share the same mode of action their pharmacokinetic properties and their susceptibility to drug interactions differ slightly. Agents inhibiting CYP3A4 (e.g. grapefruit juice, itraconazole, cyclosporine) should be discouraged if a patient is on atorvastatin, lovastatin or simvastatin. Likewise, fluconazole interferes with the CYP2C9-mediated hepatic elimination of fluvastatin. Moreover, coadministration of gemfibrozil should be avoided because it seems to increase the very low risk for statin-induced rhabdomyolysis. Several statins are available and their equieffective doses have been defined. Selection of a particular drug should be primarily based on clinical outcome data. However, costs and in certain situations the pharmacokinetic profile including the interaction potential of the statins should be taken into account.

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The beneficial effect of gemfibrozil in reducing CHD may at least in part depend on a decrease of the rate of LDL oxidation in vivo.

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1. In the present study we have investigated the effects of the relatively low plasma concentrations of gemfibrozil (GFZ) found in clinical practice on the oxygen dissociation curve (ODC) of erythrocytes. 2. ODCs were measured at 30 degrees C and 37 degrees C and at pH 7.4: a) both on HbA solution and erythrocytes incubated in vitro with gemfibrozil and clofibric acid; b) on erythrocytes from healthy volunteers treated with a single oral dose of gemfibrozil. 3. These experiments showed a significant drug-induced shift of the ODC towards lower O2 affinity values without any significant modification of metabolic parameters of erythrocytes such as intracellular pH and intraerythrocytic levels of ATP and DPG. 4. In our experimental conditions gemfibrozil appears to lower both in vitro and in vivo, the partial pressure of oxygen required to give 50% of the haemes saturated with oxygen (P50) of erythrocytes from the control value of 24 +/- 0.5 mm Hg to 29 +/- 0.5 mm Hg (mean +/- s.d.; P < 0.02 by ANOVA). 5. These data clearly indicate that therapeutic doses of gemfibrozil may influence the oxygen transport properties of red cells. This effect could have relevant pharmacological and toxicological implications.

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High-density lipoprotein (HDL) cholesterol, an independent coronary heart disease (CHD) risk factor, is inversely associated with CHD. Whether interventions to increase concentrations of HDL--particularly the HDL2, HDL3, and apolipoprotein A1 subfractions--will reduce the incidence of CHD in high-risk patients is thus an area of intense speculation. Both nonpharmacologic and pharmacologic regimens will raise HDL concentrations. Nonpharmacologic approaches include habitual high-level aerobic exercise and weight loss--both of these somewhat more effective in men than in women--cessation of cigarette smoking, and changing of dietary habits. A number of drugs have been found to elevate HDL cholesterol. These include the bile acid-binding resin cholestyramine, nicotinic acid, gemfibrozil, phenytoin, exogenous estrogens, and alcohol. Terbutaline has also been reported to raise HDL cholesterol. It is not yet known whether, and to what degree, pharmacologic and nonpharmacologic elevation of HDL cholesterol will retard or reverse the progression of atherosclerosis. Conversely, HDL cholesterol is lowered by a broad variety of drugs, including anabolic--androgenic steroids, exogenous progestins, and probucol, which are used therapeutically to reduce low-density lipoprotein (LDL) cholesterol. Some agents used to treat hypertension also reduce HDL cholesterol, especially thiazide diuretics and the beta blockers, with the possible exception of pindolol. In the antiadrenergic class of antihypertensive agents, reserpine and methyldopa lower HDL cholesterol, but the alpha blocker prazosin does not appear to affect HDL cholesterol. The alpha agonist guanabenz has no effect on HDL cholesterol, and the vasodilator carprazidil has been reported to raise HDL cholesterol. In light of these facts, investigations should be undertaken to determine whether the metabolic effects of antihypertensive agents blunt their beneficial effects on CHD.(ABSTRACT TRUNCATED AT 250 WORDS)

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A novel automated analytical scheme for the rapid determination of gemfibrozil in drug dissolution samples is reported. The procedure is based on direct coupling of a low pressure continuous flow technique such as sequential injection analysis (SI) to HPLC. SI performs automated dilution of the samples based on zone sampling and fills on-line the loop of the high pressure injection valve. Rapid separation of the analyte from the samples' matrix can be achieved in less than 1.0 min, by using a short RP monolithic column (25x4.6 mm id) at a flow rate of 2 mL/min. The SI and HPLC parts of the setup operate independently: during HPLC separation the next sample is treated by SI. This way a maximum throughput of 60 samples per hour is achieved allowing the complete analysis of a batch of six dissolution samples within 12-18 min based on the replicates. The proposed method was validated in terms of linearity, LOD and LOQ, precision, selectivity and accuracy. Its applicability was tested during quality control of four validation batches of a gemfibrozil-containing formulation. The results were in good agreement with the HPLC method proposed by the US Pharmacopeia.

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Patients with NIDDM have a two- to fourfold increased risk of macrovascular disease. The constellation of elevated TGs and decreased HDL cholesterol are recognized as risk factors and constitute the major dyslipidemia in NIDDM. We therefore sought to determine if gemfibrozil (600 mg b.i.d.) was effective in correcting the dyslipidemia of NIDDM.

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The effects of gemfibrozil (GFZ), an antihyperlipidemic agent, on the anionic transport of the human red blood cells (RBC) during the oxygenation-deoxygenation cycle were examined. Gemfibrozil clearly plays a role in the modulation of the anionic flux in erythrocytes; in fact it causes a strong increment of anions transport when the RBCs are in the high-oxygenation state (HOS). Such an effect is remarkably reduced in the low-oxygenation state (LOS). With the aim of identifying the dynamics of fibrate action, this effect has been investigated also in human ghost and chicken erythrocytes. These latter, in fact, are known to possess a B3 (anion transporter or Band 3) modified at the cytoplasmic domain (cdb3) which plays a significant role in the metabolic modulation of red blood cells. The results were analyzed taking into account the well-known interactions between fibrates and both conformational states of hemoglobin i.e. the T state (deoxy-conformation) and the R state (oxy-conformation). The effect of gemfibrozil on anionic influx appears to be due to a wide interaction involving a "multimeric" Hb-GFZ-cdb3 macromolecular complex.

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The present study aimed to examine the potential pharmacokinetic drug interaction between valsartan and gemfibrozil. Compared with the control given valsartan (10 mg/kg) alone, the concurrent use of gemfibrozil (10 mg/kg) significantly (p < 0.05) increased the oral exposure of valsartan in rats. In the presence of gemfibrozil, the Cmax and AUC of oral valsartan increased by 1.7- and 2.5-fold, respectively. Consequently, the oral bioavailability of valsartan was significantly higher (p < 0.05) in the presence of gemfibrozil compared with that of the control group. Furthermore, the intravenous pharmacokinetics of valsartan (1 mg/kg) was also altered by pretreatment with oral gemfibrozil (10 mg/kg). The plasma clearance of valsartan was decreased by two-fold in the presence of gemfibrozil, while the plasma half-life was not altered. In contrast, both the oral and intravenous pharmacokinetics of gemfibrozil were not affected by the concurrent use of valsartan. The cellular uptake of valsartan and gemfibrozil was also investigated by using cells overexpressing OATP1B1 or OATP1B3. Gemfibrozil and gemfibrozil 1-O-β glucuronide inhibited the cellular uptake of valsartan with IC50 values (µm) of 39.3 and 20.4, respectively, in MDCK/OATP1B1, while they were less interactive with OATP1B3. The cellular uptake of gemfibrozil was not affected by co-incubation with valsartan in both cells. Taken together, the present study suggests the potential drug interaction between valsartan and gemfibrozil, at least in part, via the OATP1B1-mediated transport pathways during hepatic uptake. Copyright © 2016 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.

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Non-fasting plasma triglyceride (TG) and remnant cholesterol levels, cholesterol content of triglyceride-rich lipoproteins, have been suggested to be an additional cause of cardiovascular diseases; thus, pharmacological TG-lowering with fibrates, activators of PPAR-alpha system, has been linked to risk reduction. Areas covered: This manuscript reviews available evidence on clinical trials involving highly selective PPAR-α agonists (i.e., pemafibrate) and drugs used in the pre-clinical and experimental setting (e.g., WY14,643). Original publications in English were selected, as well as Abstracts of international meetings' presentations. Clinical trials were identified using the database and the EU Clinical Trials Register ( Expert opinion: In addition to the aim of improving lipid profile with fibrates, the interest in new PPAR-α activators stems from the need to overcome some of the clinical problems encountered with dose-dependent adverse events; a rise of plasma creatinine, gallstone formation, drug-drug interactions (i.e. gemfibrozil), and myopathy. New PPAR-α agonists improved TG and HDL-C levels as well as other parameters related to TG metabolism (remnant cholesterol and apoB), without raising liver enzymes. Although the use of fibrates is rated "second choice" by many clinicians, new PPAR-α agonists may offer a more accessible route to the management of hypertriglyceridemia, a frequent clinical condition.

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To better understand the mechanism of action of gemfibrozil on plasma triglycerides, lipoprotein lipase (LPL) concentration was measured in adipose tissue and muscle of 16 hypertriglyceridemic patients before and after treatment with gemfibrozil for 6 weeks. The patients were divided into three groups based on clinical criteria as follows: group 1, hypertriglyceridemia without secondary factors; group 2, hypertriglyceridemia with diabetes; and group 3, hypertriglyceridemia with renal insufficiency. LPL activity, immunoreactive mass, synthetic rate, and mRNA levels were measured in the adipose tissue samples, and LPL activity and mass in the muscle samples. Serum triglyceride levels were decreased by 46% by gemfibrozil, and patients demonstrated no change in diet, weight, or glycohemoglobin during the 6 weeks of treatment. Despite the decrease of blood triglyceride levels, there was no significant change in any measure of LPL either in adipose tissue or muscle. Although several patients demonstrated increases in muscle LPL activity, these changes were inconsistent and not statistically significant. Because there was no significant change in LPL, we conclude that gemfibrozil in these patients decreased circulating triglyceride levels predominantly by decreasing hepatic very-low-density lipoprotein (VLDL) secretion.

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The lipid regulator gemfibrozil (GEM) has been reported to be persistent in conventional wastewater treatment plants. This study investigated the photolytic behavior, toxicity of intermediate products, and degradation pathways of GEM in aqueous solutions under UV irradiation. The results demonstrated that the photodegradation of GEM followed pseudo-first-order kinetics, and the pseudo-first-order rate constant was decreased markedly with increasing initial concentrations of GEM and initial pH. The photodegradation of GEM included direct photolysis via (3)GEM(*) and self-sensitization via ROS, where the contribution rates of degradation were 0.52, 90.05, and 8.38 % for ·OH, (1)O2, and (3)GEM(*), respectively. Singlet oxygen ((1)O2) was evidenced by the molecular probe compound, furfuryl alcohol (FFA), and was identified as the primary reactive species in the photolytic process. The steady-state concentrations of (1)O2 increased from (0.324 ± 0.014) × 10(-12) to (1.021 ± 0.040) × 10(-12) mol L(-1), as the initial concentrations of GEM were increased from 5 to 20 mg L(-1). The second-order rate constant for the reaction of GEM with (1)O2 was calculated to be 2.55 × 10(6) M(-1) s(-1). The primary transformation products were identified using HPLC-MS/MS, and possible photodegradation pathways were proposed by hydroxylation, aldehydes reactions, as well as the cleavage of ether side chains. The toxicity of phototransformation product evaluation revealed that photolysis potentially provides a critical pathway for GEM toxicity reduction in potable water and wastewater treatment facilities.

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A 34-year-old woman presented with acute and progressive pain in the upper abdomen with worsening nausea, vomiting and diarrhoea. Her pain was described as severe, sharp and stabbing, with radiation to her chest and back. The patient's amylase and lipase levels were only mildly elevated. However, triglyceride levels (10,039 mg/dL) were markedly elevated upon presentation and no other causes of acute pancreatitis (e.g. obstruction, alcohol and medication) were identified. The patient was treated with opioids to control her pain and gemfibrozil was initiated to reduce her triglycerides. In addition, the patient received enoxaparin for deep vein thrombosis prevention and insulin for hyperglycaemia which also have been shown to decrease elevated triglycerides. The patient subsequently required antibiotic therapy with piperacillin-tazobactam after developing fever and an elevated white blood cell count. We review the role of adjunctive therapy with heparin and insulin in a patient with recurrent pancreatitis probably because of hypertriglyceridaemia and medication non-compliance.

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Rhabdomyolysis occurring in transplant patients receiving both cyclosporine and the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin has been well documented. The exact mechanism by which this interaction leads to rhabdomyolysis is unknown. Experience with newer agents of the statin drug class in transplant patients is limited. Since the interaction between cyclosporine and HMG-CoA reductase inhibitors involves the CYP3A4 enzyme system, the possibility of amplifying this interaction exists when other drugs affecting the same enzyme system are coprescribed. We describe a case in which a heart transplant recipient stable on a drug regimen that included cyclosporine, simvastatin, and gemfibrozil developed rhabdomyolysis after initiation of the antifungal agent itraconazole.

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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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Photodegradation rates of five pharmaceuticals (gemfibrozil, ibuprofen, ketoprofen, naproxen, and propranolol) and of four estrogens (estriol, estrone [E1], 17beta-estradiol [E2], and 17alpha-ethinylestradiol [EE2]), which are common contaminants in the aquatic environment, were measured in both purified and river water at environmentally relevant concentrations (1-2 microg/L) and different oxygen concentrations. Solutions were irradiated with a xenon arc lamp (765 W/m2; 290 nm < lambda < 700 nm) and analyzed using a high-performance liquid chromatography-tandem mass spectrometry method with electrospray ionization for pharmaceuticals and atmospheric pressure photoionization for estrogens. In river water, half-lives were 4.1 min [corrected] for ketoprofen, 1.1 h [corrected] for propranolol, 1.4 h for naproxen, 2 to 3 h for estrogens, and 15 h for gemfibrozil and ibuprofen. In air-saturated purified water, rates generally were slower except for that of ketoprofen, which reacted with a half-life of 2.5 min. Naproxen, propranolol, and E1 reacted with half-lives of 1.9, 4.4, and 4.7 h, respectively. The EE2, estriol, E2, gemfibrozil, and ibuprofen reacted with half-lives of 28.4, 38.2, 41.7, 91.4, and 205 h, respectively. The presence of oxygen doubled the direct photolysis rates of naproxen and propranolol. In nonautoclaved river water, 80% of E2 rapidly biotransformed to E1 within less than 20 min, whereas all other compounds remained stable over 22 h.

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Median CRP levels at the pravastatin phase, 6 weeks of cerivastatin, and 12 weeks of cerivastatin, were 0.380 mg/dL, 0.403 mg/dL, and 0.364 mg/dL (p = 0.772), respectively. Median BChE activity at the pravastatin phase, 6 weeks of cerivastatin, and 12 weeks of cerivastatin were 0.338 micromol/mL/min, 0.332 micromol/mL/min, 0.33 micromol/mL/min (p = 0.746), respectively. A negative correlation was observed between CRP and BChE at baseline only (r = -0.353, p = 0.032). There was a significant decline in mean TC (p < 0.001) and median LDL (p < 0.001) and a significant increase in mean HDL (p = 0.017) over the three time points. Numerically TG declined, but it was not statistically significant (p = 0.649). No correlations were observed between CRP or BChE and any of the lipids. Gender, aspirin use, and the presence of CHD or diabetes did not affect CRP levels or BChE activity.

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Gemfibrozil, a human pharmaceutical agent, causes hepatomegaly and hepatic peroxisome proliferation in rats, which have been associated with hepatocarcinogenesis. Hamsters are less susceptible than rats to peroxisome proliferation, and no hepatotoxicity has been reported in humans using gemfibrozil. The relationship between hepatic peroxisome proliferation in rodents and human cancer risk is unclear. We investigated the metabolism and excretion of [14C]gemfibrozil in male and female Sprague-Dawley rats and Syrian golden hamsters to better understand species differences in gemfibrozil-induced toxicity. Bile-duct cannulated rats and hamsters excreted 99% and 7 to 20% of a single i.v. gemfibrozil dose in bile, respectively. Cumulative urinary and fecal excretion of gemfibrozil-derived radioactivity after a single oral dose (30 or 2000 mg/kg) were dependent on species and, in rats, on dose. Hamsters excreted 90% of the dose in urine. Rats excreted 55 to 60% of the dose in feces after the low dose and 55 to 70% in urine after the high dose, suggesting possible saturation of biliary excretion. Repeated administration of the low dose to male rats did not alter the routes of excretion compared to a single dose. Major metabolites present in urine and bile were the glucuronide conjugates of gemfibrozil, the 4'-ring hydroxylated metabolite, and the meta-benzoic acid metabolite. The extensive urinary excretion of radioactivity by hamsters and enterohepatic recycling in rats suggests that rats were exposed to a much higher effective dose of gemfibrozil, which may in part explain the previously reported species differences in gemfibrozil-induced toxicity.

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lopid 500 mg 2015-07-09

Considerable amounts of pharmaceuticals are used in human and veterinary medicine, which are not efficiently removed during wastewater and slurries treatment and subsequently entering continuously into freshwater systems. The intrinsic biological activity of these non-regulated pollutants turns their presence in the aquatic environment into an ecological matter of concern. We present the first quantitative study relating the presence of pharmaceuticals and their predicted ecotoxicological effects with human population and livestock units. Four representative Iberian River basins (Spain) were studied: Llobregat, Ebro, Júcar and Guadalquivir. The levels of pharmaceuticals were determined in surface water and sediment samples collected from 77 locations along their stream networks. Predicted total toxic units to algae, Daphnia and fish were estimated for pharmaceuticals detected in surface waters. The use of chemometrics enabled the study of pharmaceuticals for: their spatial distribution along the rivers in two consecutive years; their potential ecotoxicological risk to aquatic organisms; and the relationships among their occurrence and predicted ecotoxicity with human population and animal farming pressure. The Llobregat and the Ebro River basins were characterized as the most polluted and at highest ecotoxicological risk, followed by Júcar and Guadalquivir. No significant acute risks of pharmaceuticals to aquatic organisms were observed. However potential chronic ecotoxicological effects on algae could be expected at two hot spots of pharmaceuticals pollution identified in the Llobregat and Ebro basins. Analgesics/antiinflammatories, antibiotics and diuretics were the most relevant therapeutic groups across the four river basins. Among them, hydrochlorothiazide and gemfibrozil, as well as azithromycin and ibuprofen were widely spread and concentrated pharmaceuticals in surface waters buy lopid and sediments, respectively. Regarding their predicted ecotoxicity, sertraline, gemfibrozil and loratidine were identified as the more concerning compounds. Significantly positive relationships were found among levels of pharmaceuticals and toxic units and population density and livestock units in both surface water and sediment matrices.

lopid dose administration 2017-03-13

Emerging wastewater treatment processes such as membrane bioreactors (MBRs) have attracted a significant amount of interest internationally due to their ability to produce high quality effluent suitable for water recycling. It is therefore important that their efficiency in removing hazardous trace organic contaminants be assessed. Accordingly, this study investigated the removal of trace organic chemical contaminants through a full-scale, package MBR in New South Wales, Australia. This study was unique in the context of MBR research because it characterised the removal of 48 trace organic chemical contaminants, which included steroidal hormones, xenoestrogens, pesticides, caffeine, pharmaceuticals and personal care products (PPCPs). Results showed that the removal of most buy lopid trace organic chemical contaminants through the MBR was high (above 90%). However, amitriptyline, carbamazepine, diazepam, diclofenac, fluoxetine, gemfibrozil, omeprazole, sulphamethoxazole and trimethoprim were only partially removed through the MBR with the removal efficiencies of 24-68%. These are potential indicators for assessing MBR performance as these chemicals are usually sensitive to changes in the treatment systems. The trace organic chemical contaminants detected in the MBR permeate were 1 to 6 orders of magnitude lower than guideline values reported in the Australian Guidelines for Water Recycling. The outcomes of this study enhanced our understanding of the levels and removal of trace organic contaminants by MBRs.

lopid 450 mg 2015-04-19

Evacetrapib is an investigational cholesteryl ester transfer protein inhibitor (CETPi) for reduction of risk of major adverse cardiovascular events in patients with high-risk vascular disease. Understanding evacetrapib disposition, metabolism, and the potential for drug-drug interactions (DDI) may help guide prescribing recommendations. In vitro, evacetrapib metabolism was investigated with a panel of human recombinant cytochromes P450 (CYP). The disposition, metabolism, and excretion of evacetrapib following a single 100-mg oral dose of (14)C-evacetrapib were determined in healthy subjects, and the pharmacokinetics of evacetrapib were evaluated in the presence of strong CYP3A or CYP2C8 inhibitors. In vitro, CYP3A was responsible for about 90% of evacetrapib's CYP-associated clearance, while CYP2C8 accounted for about 10%. In the clinical disposition study, only evacetrapib and two minor metabolites circulated in plasma. Evacetrapib metabolism was extensive. A mean of 93.1% and 2.30% of the dose was excreted in feces and urine, respectively. In clinical DDI studies, the ratios of geometric least squares means for evacetrapib with/without the CYP3A inhibitor ketoconazole were 2.37 for area under the curve (AUC)(0-∞) and 1.94 for C max. There was no significant difference in evacetrapib AUC(0-τ) or C max with/without the CYP2C8 inhibitor gemfibrozil, with ratios of 0.996 and 1.02, respectively. Although in vitro results indicated that both CYP3A and CYP2C8 metabolized evacetrapib, clinical studies confirmed buy lopid that evacetrapib is primarily metabolized by CYP3A. However, given the modest increase in evacetrapib exposure and robust clinical safety profile to date, there is a low likelihood of clinically relevant DDI with concomitant use of strong CYP3A or CYP2C8 inhibitors.

lopid 160 mg 2016-06-07

The use of hypolipidemic drugs has been analyzed in 1,113 patients after myocardial infarction using a questionnaire with data entered from the medical records by spa physicians. 80.1% of patients had total cholesterol values > 5.2 mmol/l; mean value being 6.16 +/- 1.08 mmol/l. Mean values of LDL-cholesterol were 4.05 +/- 0.1 mmol/l, of triglycerides 2.01 +/- 1.14 and of HDL-cholesterol 1.26 +/- 0.61 mmol/l. Hypolipidemic drugs were used only in 16.5% patients with total cholesterol values above 7.0 mmol/l, in 14.4% patients with total cholesterol values 6.2-7.0 mmol/l and in 11.4% of patients with cholesterol values 5 buy lopid .2-6.2 mmol/l. Even some patients with cholesterol more than 8.0 mmol/l were not treated by hypolipidemic drugs. The most frequently used drugs were fibrates (phenofibrate, gemfibrozil)--in 89.5% patients. Statins were used only in 7.5% patients receiving hypolipidemic drugs. Our results show that in contrast to the US and European Recommendations for hypolipidemic drug therapy in patients with CHD, this treatment is still infrequently used by Czech cardiologists and internists. This discrepancy is even more apparent when comparing it with other life prognosis improving drug therapies in this group of patients. Antiplatelet drugs, mainly ASA were used in 85.5% patients, beta-blocking drugs in 59.3% patients and ACE inhibitors in 55.9% patients with left ventricular systolic dysfunction. Thus hypolipidemic therapy in CHD is the key problem of drug therapy in patients after myocardial infarction in the Czech Republic.

lopid 600 dose 2015-02-27

All used fibrates showed a similar, significant efficacy in the treatment of diet-resistant hyperlipidemia, but further studies seem necessary in order to establish the most appropriate guidelines for the management buy lopid of dyslipidemia associated with highly active antiretroviral therapy (HAART).

lopid generic price 2016-11-06

Some mechanisms of the triglyceride-lowering effects of fibrates in patients with hypertriglyceridemia are reviewed. One main effect of the fibrates is the stimulation of lipoprotein lipase activities in plasma as well as in adipose tissue. According to this increase in the degradational activity VLDL catabolism is stimulated, as has been demonstrated for VLDL apo B and VLDL triglycerides. In addition, the composition of hypertriglyceridemic LDL is reverted towards normal. Furthermore, the increased degradation via the nonreceptor pathway is decreased by fibrate treatment, thus lowering the atherogenic potential of triglyceride- buy lopid rich lipoproteins. But additionally the degree of postprandial hypertriglyceridemia is lowered by fibrates.

lopid 300 mg 2015-08-24

The obesity epidemic has now spread worldwide. With increase in weight, there is an increase in dysregulated energy metabolism ultimately leading to dysfunction of multiple organ systems recognized as the metabolic syndrome. Nonalcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease worldwide, and is thought to be the hepatic manifestation of metabolic syndrome. It is a nondiscriminating disease affecting both children and adults and no socioeconomic class is spared. There is a well-defined increase in both liver-related and all-cause mortality. Current projections foresee a continued worsening in prevalence, especially with the increased rate of childhood obesity. Prevention would be the ultimate goal, but with continued trends in obesity, therapeutic options are needed to manage this chronic liver disease and prevent its complications of cirrhosis and even hepatocellular carcinoma. Therapies will buy lopid need to be affordable, tolerable, and safe to be useful on such a large scale. This article will discuss some of the basic understanding of NAFLD, as well as review the currently tested therapies, some novel therapies, and potential future therapeutic options.

lopid reviews 2017-03-26

The removal of commonly used pharmaceuticals (ibuprofen, naproxen, diclofenac, gemfibrozil, carbamazepine, atenolol, metoprolol and trimethoprim) and a biocide (triclosan) in operating wastewater treatment plants in five EU countries has been studied. Under normal operating conditions the acidic drugs and triclosan were partially removed with removal rates varying from ca. 20 to >95%. The highest removal rate was found for ibuprofen and triclosan (>90%) followed by naproxen (80%), gemfibrozil (55%) and diclofenac (39%). Ibuprofen undergoes an oxidative transformation to buy lopid corresponding hydroxy- and carboxy-metabolites, which contributes to its high removal rate. Disturbances in the activated sludge process resulted in lower removal rates for all acidic drugs, mostly for diclofenac (<10% removed) but also for ibuprofen (<60% removed). The treatment of wastewaters by activated sludge usually did not result in any practical removal (<10%) of neutral carbamazepine or basic atenolol, metoprolol and trimethoprim. The removal rates of the investigated drugs and triclosan are discussed in terms of mechanisms responsible for their removal. Discharges of carbamazepine, diclofenac, gemfibrozil, naproxen, triclosan and trimethoprim from WWTPs to the aquatic environment, expressed as the average concentration in the effluent and the daily discharged quantity per person served by WWTPs were assessed.

lopid normal dosage 2015-08-02

This report describes a male patient who was found to have proteinuria at age 31. Renal biopsy showed glomerular hypercellularity with enlarged, lipid-filled endocapillary cells. On subsequent lipid analysis there was elevation of cholesterol buy lopid and triglyceride, with apolipoprotein E genotype E2/E2. The clinical course was complicated by pancreatitis and onset of diabetes. After treatment with gemfibrozil and some improvement of the lipid profile, a second renal biopsy showed marked reduction of the glomerular foam cells, despite an increased level of proteinuria. This case emphasizes the potential role that lipid abnormalities may play in renal dysfunction.

lopid and alcohol 2016-02-02

Low heart rate (HR) variability is associated with increased risk of cardiovascular morbidity and mortality, but the causes and mechanisms of this association are not well known. This prospective study was designed to test the hypothesis that reduced HR variability is related to progression of coronary atherosclerosis. Average HR and HR variability were analyzed in 12-hour ambulatory ECG recordings from 265 qualified patients participating in a multicenter study to evaluate the angiographic progression of coronary artery disease in patients with prior coronary artery bypass surgery and low high-density lipoprotein cholesterol concentrations (<1.1 buy lopid mmol/L). Participants were randomized to receive a placebo or gemfibrozil therapy. The progression of coronary atherosclerosis was estimated by quantitative, computer-assisted analysis of coronary artery stenoses from the baseline angiograms and from repeated angiograms performed an average of 32 months later. The progression of focal coronary atherosclerosis of the patients randomized to placebo therapy was more marked in the tertile with the lowest standard deviation of all normal to normal R-R intervals (SDNN, 74+/-13 ms; mean decrease in the per-patient minimum luminal diameter -0.17 mm; 95% confidence interval [CI], -0.23 to -0.12 mm) than in the middle tertile (SDNN, 107+/-7 ms; mean decrease -0.05 mm; 95% CI, -0.08 to -0.01 mm) or highest tertile (SDNN, 145+/-25 ms; mean change 0.01 mm; 95% CI, -0. 04 to 0.02 mm) (P<0.001 between the tertiles). This association was abolished by gemfibrozil. SDNN was lower (P<0.001) and minimum HR was faster (P<0.01) in the patients with marked progression than in those with regression of focal coronary atherosclerosis. In multiple regression analysis including HR variability, minimum HR, demographic and clinical variables, smoking, blood pressure, glucose, lipid measurements and lipid-modifying therapy, progression of focal coronary atherosclerosis was independently predicted by the SDNN (beta=0.24; P=0.0001). Low HR variability analyzed from ambulatory ECG predicts rapid progression of coronary artery disease. HR variability provided information on progression of focal coronary atherosclerosis beyond that obtained by traditional risk markers of atherosclerosis.

lopid drug interactions 2017-10-23

This work demonstrates for the first time that binding of various compounds within subdomain IB of human serum albumin (HSA) provokes characteristic changes in the near-UV circular dichroism (CD) spectrum of the protein. It can be inferred from the spectroscopic features of difference ellipticity signals and from CD displacement experiments that tyrosine residues located in subdomain IB are the buy lopid source of the observed spectral alterations. It is proposed that inclusion of some ligand molecules (bile acids, dehydroepiandrosterone sulfate, steroidal terpenes, fatty acids, ibuprofen, and gemfibrozil) into the pocket of subdomain IB disrupts the Tyr138-Tyr161 interhelical π-π stacking interaction, which is reflected in the CD spectrum. This phenomenon can be utilized for the CD detection of subdomain IB specific binding of endo- as well as exogenous agents and to study the drug binding associated local conformational adaptation of the HSA molecule.

lopid tablets 2015-08-19

To investigate the therapeutic effect of Shenshuai buy lopid Yangzhen capsule, a preparation of traditional Chinese medicine, on lipid metabolism disorder in rats with chronic renal failure (CRF) and explore its mechanism.

lopid drug class 2017-11-18

To review the efficacy and safety of buy lopid atorvastatin in the treatment of dyslipidemias.

lopid generic 2017-01-30

Information obtained from clinical and laboratory research strongly supports a causal relationship between hyperlipidemia (dyslipidemia) and coronary heart disease (CHD), and provides an impetus to develop strategy for control of dyslipidemia. Some recent developments in the field may include the use of: (1) colestipol-niacin to control hypercholesterolemia and induce regression of coronary atherosclerosis; (2) limited amounts of foods rich in stearic or oleic fatty acids to enhance the appeal of cholesterol-lowering regimen; (3) gemfibrozil or lovastatin to inhibit cholesterol synthetic activity; and (4) gemfibrozil to raise atherosclerosis-protective plasma high-density lipoprotein levels. These and buy lopid other newer developments will stimulate interest in research on dyslipidemia and its control to facilitate primary and secondary prevention of CHD.

lopid drug 2015-09-21

To review the literature investigating increased Arava Reviews lipid concentrations in transplant recipients and the use of lipid-lowering agents in this population.

lopid capsules 2017-05-13

Our investigations indicate that most patients with moderate hypertriglyceridemia have marked defects in the metabolism of Atarax Infant Dosage low-density lipoprotein (LDL) apolipoprotein B. Moreover, these patients have 2 major defects in the metabolism of triglyceride-rich lipoproteins, i.e., an accumulation of remnant lipoproteins (due in part to delayed hepatic clearance) and increased fractional conversion of very-low-density lipoprotein (VLDL) to LDL. Defective triglyceride-rich lipoprotein metabolism has been associated with insulin resistance. Statin therapy in hypertriglyceridemic patients improves the lipoprotein profile by decreasing both LDL cholesterol and remnant lipoproteins. However, statin therapy does not normalize LDL apolipoprotein B metabolism, and high-density lipoprotein (HDL) cholesterol levels remain low. Therefore, consideration may be given to combining a statin with a drug that alters triglyceride metabolism (e.g., fibrate or nicotinic acid) in high-risk patients with hypertriglyceridemia.

lopid tablets 600 2015-11-24

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin Glucophage 5 Mg --lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.

lopid dosage forms 2016-03-06

Markedly increased atherosclerotic wall changes are seen in the carotid Paxil Cr Reviews arteries of patients with hyperlipidaemia after renal transplantation.

lopid 600 dosage 2016-05-14

Physicochemical effects caused by intestinal fluids on drugs in the gastrointestinal (GI) tract can be a contributing factor in food induced changes Bactroban 100 Mg in bioavailability. To identify physicochemical properties of gemfibrozil that may be altered by endogenous and dietary lipids, in vitro studies were conducted in model systems approximating the conditions of the upper GI tract. Factors examined include pH, solubility in bile salt micellar and mixed micellar systems with monoolein and lecithin, effect of fatty acids, dissolution, wetting, and partitioning in triglyceride dispersions. Gemfibrozil was solubilized by glycocholate solutions in a manner typical of other lipids and a three-fold increase in solubility was observed over physiologic concentrations. Addition of increasing amounts of swelling amphiphiles (monoolein, lecithin) to glycocholate solutions resulted in a linear increase in solubility. Fatty acid salts had no effect on gemfibrozil solubilization by micellar solutions. The dissolution rate of gemfibrozil increased slightly in the presence of glycocholate relative to buffer, however, addition of monoolein increased the dissolution rate three-fold. In triglyceride dispersions of mixtures of lipids, monoolein increased the fraction of drug in the micellar subphase, whereas fatty acid reduced it. The results indicate that in the conditions of the fed state gemfibrozil solubility and dissolution could be substantially increased relative to the conditions in the fasted state.

lopid user reviews 2017-01-07

Peroxisome proliferator-activated receptor alpha and gamma Imdur Max Dose (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.