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Tricor

Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes. Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Other names for this medication:

Similar Products:
Lipitor, Lopid, Zocor, Crestor, Zetia, Mevacor

 

Also known as:  Fenofibrate.

Description

Tricor is the medication of high quality, which is taken in treatment of high triglyceride levels and high cholesterol with diet changes.

The target of this perfect remedy is the treatment of high triglyceride levels and high cholesterol with diet changes.

Tricor is also known as Fenofibrate, Fenofibric acid, Lipicard, Lofibra, Lipanthyl, Fenocor-67.

Tricor is acting by increasing enzyme which breaks down fats in the blood. It is fibrate (lipid-lowering agent).

Generic name of Tricor is Fenofibrate.

Brand names of Tricor are Tricor, Tricor, Antara, Triglide, Lofibra, Lipofen.

Dosage

Tricor can be taken once a day. Take Tricor capsules orally with water at the same time every day, with food.

If you are taking colestipol (such as Colestid) or cholestyramine (such as Questran) while using Tricor you should take these medicines at least 1 hour after using Tricor or 4-6 hours before using Tricor.

Follow low-fat diet, low-cholesterol.

If you want to achieve most effective results do not stop taking Tricor suddenly.

Overdose

If you overdose Tricor and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. 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 Tricor 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 Tricor if you are allergic to its components.

Do not take Tricor if you're pregnant or you plan to have a baby, or you are a nursing mother. Tricor can ham your baby.

Be careful with Tricor if you suffer from liver cirrhosis, hepatitis, severe kidney disease, gallbladder disease, diabetes, kidney, liver, heart disease, hypothyroidism.

Be careful with Tricor if you are taking such medicines as blood thinner (warfarin (such as Coumadin)); fluvastatin (such as Lescol), cholesterol-lowering medicines (lovastatin (such as Mevacor), simvastatin (such as Zocor), cerivastatin (such as Baycol), pravastatin (such as Pravachol), atorvastatin (such as Lipitor), cyclosporine (such as Gengraf, Neoral, Sandimmune).

If you experience drowsiness and dizziness while taking Tricor you should avoid any activities such as driving or operating machinery.

Avoid alcohol.

Elderly people should be very careful with Tricor.

Keep low-cholesterol and low-fat diet.

Do not stop taking Tricor suddenly.

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A randomized, double-blind, placebo-controlled study was undertaken in 20 hypertriglyceridemic men [plasma triglyceride (TG), >2.3 mM] with low levels (<0.9 mM) of high-density lipoprotein cholesterol (HDL-C) to investigate the ability of micronized fenofibrate (Tricor or Lipidil; 200 mg/day) to affect atherogenic and thrombogenic plasma risk factors in the fed and fasted state. Each patient underwent (a) 4 weeks of dietary stabilization, (b) 8 weeks of treatment with fenofibrate or placebo, (c) a 5-week washout period, and (d) 8-weeks of treatment with the alternative medication. An oral fat-loading test (1 g fat/kg body weight) was carried out after both treatment periods. Before treatment, patients had a mean (+/- SD) total plasma TG of 3.31+/-0.93 mM; total C, 5.75+/-0.89 mM; HDL-C, 0.71+/-0.09 mM; and low-density lipoprotein (LDL)-C, 3.40+/-0.68 mM. Compared with placebo, fenofibrate reduced fasting TG levels by 36%, and triglyceride-rich lipoprotein (TRL, d<1.006 g/ml) -TG, and TRL-C levels by approximately 40%. In the postprandial state, fenofibrate reduced total TG, TRL-TG, TRL-C, TRL-apoC-III, and TRL-apoE levels by -35% (all values of p<0.01). Fasted and fed HDL-C and apoA-I levels were increased -10%, and total cholesterol/HDL cholesterol ratios were decreased -15% by fenofibrate. No significant differences were observed in mean LDL-C and LDL-apoB levels. A 6% increase in the LDL-C/LDL-apoB ratio during fenofibrate treatment indicated a shift to larger, more buoyant LDL particles. A small, but statistically significant (p<0.01) increase was observed in fasted and fed Lp(a) levels during fenofibrate treatment. Hemostatic parameters were not significantly affected by fenofibrate, except for a 12-15% decrease (p<0.05) in fibrinogen levels in the fasted and fed state, and a significant increase (43%; p<0.05) in fasting levels of plasminogen activator-inhibitor-1. These data demonstrate that micronized fenofibrate is highly effective, in both the fed and fasted state, in reducing TRL lipids and apolipoproteins, and in reducing plasma fibrinogen levels of men with an atherogenic lipoprotein profile.

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University clinic and laboratory.

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Treatment of ARPE-19 cells with fenofibric acid significantly reduced the increment of permeability and the breakdown of the ARPE-19 cell monolayer induced by D-glucose, 25 mmol/l, and IL-1β, 10 ng/ml, in a dose-dependent manner. This effect was unrelated to changes in the content of tight junction proteins. Fenofibric acid prevented the activation of AMPK induced by IL-1β and the hyperpermeability induced by IL-1β was blocked by silencing AMPK.

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This trial compares the efficacy of administering a combination of ezetimibe plus fenofibrate as an alternative to statin monotherapy for the treatment of dyslipidemia. In this randomized, unblinded crossover study, 43 patients with documented hypercholesterolemia requiring pharmacotherapy were randomized to receive six weeks of either a combination of 10 mg of ezetimibe plus 160 mg of fenofibrate (combination) or 10 mg of atorvastatin monotherapy (atorvastatin). The primary endpoint was the percentage reduction of low-density lipoprotein cholesterol (LDL-C).

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Several proprotein convertase subtilisin kexin type 9 (PCSK9) mutations lead to familial hypercholesterolemia by virtue of its role as a negative modulator of the low-density lipoprotein receptor (LDLr). Here, we uncover that upon dietary challenge, the down-regulation of the LDLr is also a key mechanism by which PCSK9 modulates the hepatic production of apolipoprotein-B-containing lipoproteins. Thus, adenoviral-mediated overexpression of PCSK9 in 24-h fasted mice results in massive hyperlipidemia, due to a striking increase in very-low-density lipoprotein (VLDL) triglycerides and apolipoprotein B100 hepatic output. Similar studies in LDLr (-/-) mice demonstrate that PCSK9-mediated alteration of VLDL output in the fasted state requires the LDLr. This increased production of VLDL was associated with a concomitant reduction of intrahepatic lipid stores as well as a lack of down-regulation of peroxisome proliferator-activated receptor-alpha activity and target genes expression. Finally, we show that PCSK9 hepatic expression is inhibited by the hypotriglyceridemic peroxisome proliferator-activated receptor-alpha agonist fenofibrate. In summary, the negative modulation of LDLr expression by PCSK9, which decreases plasma LDL clearance, also promotes an overproduction of nascent VLDL in vivo upon fasting.

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Treatment for periods of 6 weeks each with the following consecutive treatments: CoQ10 150 mg/day, PUFA 3000 mg/day, fenofibrate 200 mg/day, PUFA 3000 mg/day + fenofibrate 200 mg/day, PUFA 3000 mg/day + CoQ10 150 mg/day, fenofibrate 200 mg/day + CoQ10 150 mg/day, and finally, fenofibrate 200 mg/day + PUFA 3000 mg/day + CoQ10 150 mg/day.

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Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary cholesterol without affecting the absorption of fat-soluble nutrients. Following oral administration, ezetimibe is rapidly absorbed and extensively metabolised (>80%) to the pharmacologically active ezetimibe-glucuronide. Total ezetimibe (sum of 'parent' ezetimibe plus ezetimibe-glucuronide) concentrations reach a maximum 1-2 hours post-administration, followed by enterohepatic recycling and slow elimination. The estimated terminal half-life of ezetimibe and ezetimibe-glucuronide is approximately 22 hours. Consistent with the elimination half-life of ezetimibe, an approximate 2-fold accumulation is observed upon repeated once-daily administration. The recommended dose of ezetimibe 10 mg/day can be administered in the morning or evening without regard to food. There are no clinically significant effects of age, sex or race on ezetimibe pharmacokinetics and no dosage adjustment is necessary in patients with mild hepatic impairment or mild-to-severe renal insufficiency. The major metabolic pathway for ezetimibe consists of glucuronidation of the 4-hydroxyphenyl group by uridine 5'-diphosphate-glucuronosyltransferase isoenzymes to form ezetimibe-glucuronide in the intestine and liver. Approximately 78% of the dose is excreted in the faeces predominantly as ezetimibe, with the balance found in the urine mainly as ezetimibe-glucuronide. Overall, ezetimibe has a favourable drug-drug interaction profile, as evidenced by the lack of clinically relevant interactions between ezetimibe and a variety of drugs commonly used in patients with hypercholesterolaemia. Ezetimibe does not have significant effects on plasma levels of HMG-CoA reductase inhibitors commonly known as statins (atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin), fibric acid derivatives (gemfibrozil, fenofibrate), digoxin, glipizide, warfarin and triphasic oral contraceptives (ethinylestradiol and levonorgestrel). Concomitant administration of food, antacids, cimetidine or statins had no significant effect on ezetimibe bioavailability. Although coadministration with gemfibrozil and fenofibrate increased the bioavailability of ezetimibe, the clinical significance is thought to be minor considering the relatively flat dose-response curve of ezetimibe and the lack of dose-related increase in adverse events. In contrast, coadministration with the bile acid binding agent colestyramine significantly decreased ezetimibe oral bioavailability (based on area under the plasma concentration-time curve of total ezetimibe). Hence, ezetimibe and colestyramine should be administered several hours apart to avoid attenuating the efficacy of ezetimibe. Finally, higher ezetimibe exposures were observed in patients receiving concomitant ciclosporin, and ezetimibe caused a small but statistically significant effect on plasma levels of ciclosporin. Because treatment experience in patients receiving ciclosporin is limited, physicians are advised to exercise caution when initiating ezetimibe in the setting of ciclosporin coadministration, and to carefully monitor ciclosporin levels.

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The present work was aimed at formulating a SMEDDS (self-microemulsifying drug delivery system) of fenofibrate and evaluating its in vitro and in vivo potential. The solubility of fenofibrate was determined in various vehicles. Pseudoternary phase diagrams were used to evaluate the microemulsification existence area, and the release rate of fenofibrate was investigated using an in vitro dissolution test. SMEDDS formulations were tested for microemulsifying properties, and the resultant microemulsions were evaluated for clarity, precipitation, and particle size distribution. Formulation development and screening was done based on results obtained from phase diagrams and characteristics of resultant microemulsions. The optimized formulation for in vitro dissolution and pharmacodynamic studies was composed of Labrafac CM10 (31.5%), Tween 80 (47.3%), and polyethylene glycol 400 (12.7%). The SMEDDS formulation showed complete release in 15 minutes as compared with the plain drug, which showed a limited dissolution rate. Comparative pharmacodynamic evaluation was investigated in terms of lipid-lowering efficacy, using a Triton-induced hypercholesterolemia model in rats. The SMEDDS formulation significantly reduced serum lipid levels in phases I and II of the Triton test, as compared with plain fenofibrate. The optimized formulation was then subjected to stability studies as per International Conference on Harmonization (ICH) guidelines and was found to be stable over 12 months. Thus, the study confirmed that the SMEDDS formulation can be used as a possible alternative to traditional oral formulations of fenofibrate to improve its bioavailability.

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Outpatient university-affiliated cardiology clinic.

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Aim of the study was to assess effect of fenofibrate on lipid blood composition, markers of inflammation and the state of vascular wall in patients with type 2 diabetes mellitus (DB2). We randomized 73 patients with DB2 in 2 groups. Patients of group one (n = 34) in addition to hypoglycemic and lipid lowering therapy with statins received fenofibrate (145 mg/day), patients of control group (n = 38) received standard therapy. We assessed effect of selected therapy on lipids, endothelium dependent vasodilatation (EDVD) in a test with reactive hyperemia of brachial artery, intimaAmedia thickness of common carotid arteries, levels of CAreactive protein (CRP) and uric acid, parameters of stiffness of arterial wall. At the end of the study we found in the fenofibrate group significant lowering of mean levels of total cholesterol, low density lipoprotein cholesterol, CRP, uric acid. We also noted more significant elevation of EDVD, improvement of parameters of arterial wall thickness. The use of fenofibrate in a daily dose 145 mg in patients with DB2 at the background of traditional hypoglycemic, antihypertensive, and lipid lowering therapy corrects effectively lipid disturbances and normalizes function of endothelium and parameters of vascular wall stiffness. This substantially decreases risk of vascular complications of DB2.

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The aim of this study was to compare the action of fenofibrate on monocyte cytokine release between patients with isolated mixed dyslipidemia and dyslipidemia coexisting with prediabetic states in relationship with its metabolic actions.We compared 96 primary mixed dyslipidemic patients and 29 age-, sex- and weight-matched control subjects with normal lipid profile. Depending on glucose metabolism, dyslipidemic patients were allocated into one of three treatment groups: isolated dyslipidemia, dyslipidemia coexisting with impaired fasting glucose (IFG) and dyslipidemia coexisting with impaired glucose tolerance (IGT). Lipid profile, fasting and 2-h post-glucose load plasma glucose levels, HOMA and monocyte release of interleukin-1beta and MCP-1 were assessed at baseline and after 30 and 90 days of micronized fenofibrate treatment (267 mg/daily). Compared to monocytes from control subjects, monocytes of dyslipidemic patients released a greater amounts of interleukin-1beta and MCP-1. MCP-1 release was higher in the IFG group than in the remaining groups of dyslipidemic patients. In all groups of dyslipidemic patients, micronized fenofibrate reduced monocyte release of interleukin-1beta and MCP-1, and this effect was stronger in prediabetic subjects. Fenofibrate treatment also decreased HOMA in IFG and IGT patients, fasting plasma glucose in IFG subjects and 2-h post-glucose load plasma glucose in IGT patients. The observed differences between the studied groups regarding fenofibrate action on glucose homeostasis and cytokine release suggest that fibrate therapy may bring particular benefits to persons with metabolic syndrome.

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We investigated the effect of fenofibrate on lipoprotein(a)levels in hypertriglyceridemic patients and the parameters relating to its effect. Patients with a triglyceride level >/=300 mg/dL or with a triglyceride level >/=200 mg/dL and a high density lipoprotein cholesterol level

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Reported associations between liver enzymes and mortality may not hold true in type 2 diabetes, owing to a high prevalence of non-alcoholic fatty liver disease, which has been linked to cardiovascular disease and mortality in its own right. Our study aimed to determine whether alanine aminotransferase (ALT) or γ-glutamyl transferase (GGT) levels predict mortality in type 2 diabetes, and to examine possible mechanisms.

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Phospholipid transfer protein (PLTP) plays an important role in the metabolism of plasma high density lipoprotein. The mouse gene encoding PLTP and its promoter region has been cloned in our laboratory. The present study was conducted to functionally analyze the transcriptional regulation of the mouse PLTP gene. The results indicated that DNA sequences between -245 and -69 were responsible for the full promoter activity and binding motifs for transcription factor Sp1 and AP-2 within this functional promoter region were synergistically essential for the basal transcription. The transcriptional activity of this gene was significantly increased by chenodeoxycholic acid and fenofibrate, suggesting that transcription factor farnesoid X-activated receptor (FXR) and peroxisome proliferator-activated receptor (PPAR) are likely involved in the transcriptional regulation. DNA sequence analysis suggests that DNA sequences from -407 to -395 and from -393 to -381 are homologous to the recognition motifs of FXR, and those from -859 to -847 and from -309 to -297 are similar to the potential binding motif for PPAR. These findings provide a molecular basis for further investigation of the physiological function and regulation of the PLTP gene in mice.

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Fish oil has been shown to reduce serum triglyceride (TG) concentrations. In HIV-infected patients on antiretroviral therapy, high TG concentrations likely contribute to increased risk of cardiovascular disease. AIDS Clinical Trials Group A5186 examined the safety and efficacy of fish oil plus fenofibrate in subjects not achieving serum TG levels < or =200 mg/dL with either agent alone.

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The prochiral carbonyl group of fenofibrate (isopropyl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methyl propionate) is reduced during its metabolism giving rise to a chiral secondary alcohol, "reduced fenofibric acid." Chiral and diastereomeric HPLC methods have been developed for the determination of its enantiomeric composition and these have been applied to the measurement of the "reduced fenofibric acid" enantiomers in urine of rats, guinea pigs, dogs, and human volunteers given [14C]fenofibrate. In the three animal species, the reduction is markedly enantioselective for the (-)-isomer, the enantiomeric ratios (-/+) being 95:5. This was not due to differences in the excretion of the enantiomers, since when racemic "reduced fenofibric acid" was given to rats it was recovered in the urine with the same enantiomeric composition as the dose form. In humans the ratio was 52:48 showing the lack of stereoselectivity of reduction in this species.

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Baseline and year 2 renal status were examined in relation to clinical and biochemical characteristics. Outcomes included total cardiovascular disease (CVD), cardiac and non-cardiac death over 5 years.

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Combinations of statins and fibrates may be increasingly prescribed to achieve lipid goals in high-risk patients and those with other cardiovascular risk factors, such as mixed dyslipidemia. The purpose of this retrospective cohort study was to compare rates of hospitalization for specific diagnoses in a cohort of new users of statins or fibrates, using claims data from a large United States health insurer. New users of statin, fibrate, or statin-fibrate therapy from 2004 to 2007 were identified; followed for hospitalization with rhabdomyolysis, renal impairment, hepatic injury, or pancreatitis; and confirmed by medical record review. Incidence rates (IRs) were compared across categories of fibrate or statin use, with adjusted IR ratios estimated using Poisson regression. A total of 584,784 patients initiated statins or fibrates. The IR of rhabdomyolysis in statins was 3.30 per 100,000 patient-years; the adjusted IR ratio for statin-fenofibrate combinations compared to statins alone was 3.75 (95% confidence interval 1.23 to 11.40). The IRs of renal impairment and pancreatitis in statins were 108.87 per 100,000 patient-years and 45.76 per 100,000 patient-years, respectively; the adjusted IR ratios for statin-fenofibrate combinations compared to statins alone were 1.47 (95% confidence interval 1.12 to 1.93) and 2.87 (95% confidence interval 2.05 to 4.02), respectively. The IR of hepatic injury with statins was 8.57 per 100,000 patient-years, with no risk difference between exposure groups. In conclusion, the risk for rhabdomyolysis was low, although higher in patients newly treated with statin-fibrate concurrent therapy than those treated with either as monotherapy. The risk for pancreatitis was higher in patients treated with fenofibrate, whether in combination with statins or alone.

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Many patients who receive statin therapy for hyperlipidemia-such as patients with diabetes mellitus and metabolic syndrome--have residual cardiovascular risk. These patients often have dyslipidemia, including low levels of HDL cholesterol and elevated levels of triglycerides and small, dense LDL. For such patients, combination treatment with statins and fibrates is a potentially useful strategy to improve lipid and lipoprotein profiles and reduce cardiovascular risk. However, statin-fibrate combination regimens have potential adverse effects on skeletal muscle, including myopathy. To date, no large-scale, prospective, randomized, controlled trial has evaluated the safety and efficacy of statin-fibrate combination therapy; one such trial is underway but will not report data until 2010. Until then, clinicians need to consider pharmacokinetic, pharmacodynamic, metabolic, pathophysiologic and other factors that can increase the systemic exposure of statins and/or fibrates and hence heighten the risk of toxic effects on muscles, as well as data from clinical trials and recommendations of consensus panels to optimize the safety of such combination regimens. On the basis of currently available data, fenofibrate or fenofibric acid is the fibrate of choice when used in combination with a statin because each is, in theory, associated with a lower risk of myopathy than gemfibrozil.

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Permeability increased following the administration of simvastatin (by 20%; P = 0.01), atorvastatin (by 22%; P = 0.001), fenofibrate (by 16%; P = 0.02), and quinapril (by 13%; P = 0.04) like for aspirin (P < 0.001). Turbidity analysis showed that administration of any of the drugs was associated with higher maximum absorbancy, suggesting thicker fibers, and shorter fibrinolysis time (P < 0.001). Post-treatment reduction in lysis time correlated with an increase in clot porosity in all the groups (r from 0.42 to 0.61; P from 0.01 to 0.001).

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We performed a systematic screening among hypercholesterolaemic outpatients attending a lipid clinic. The heterozygote subjects were followed up during more than one year and, in some of them, we compared the efficiency of cholesterol-lowering drugs belonging to the different classes: fibrate and statine.

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After a 4-week washout period, dyslipidemic patients were randomized to either micronized fenofibrate (n = 64) or atorvastatin (n = 72).

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Fenofibrate can reduce the degree of liver fibrosis in mice induced by CCl4. The mechanism may involve up-regulation of PPARa, inhibition of the inflammatory response, and enhancement of SOD antioxidant activity.

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Before treatment, post-prandial phase was characterized by an increase in triglycerides (3.7 +/- 1 mmol/L at baseline vs. 4.2 +/- 1, 6.5 +/- 1, 6.6 +/- 2, and 5.3 +/- 2 mmol/L after 2, 4, 6, and 8 h), a decrease in FMV (4.3 +/- 2% at baseline vs. 2.8 +/- 1, 2.2 +/- 1, and 1.3 +/- 1% after 2, 4, and 6 h), and an increase in ICAM and VCAM. After fenofibrate there was a significant reduction in fasting triglycerides (3.7 +/- 1.3 vs. 2.1 +/- 0.8 mmol/L), ICAM (480 +/- 113 vs. 269 +/- 65 ng/mL) and VCAM (1821 +/- 570 vs. 1104 +/- 376 ng/mL), and an increase in FMV (4.3 +/- 2 vs. 7.1 +/- 2%). Post-prandially triglycerides increased (2.1 +/- 1 at baseline vs. 2.4 +/- 2 and 3.6 +/- 1 mmol/L after 4 and 6 h), FMV decreased (7.1 +/- 2 at baseline vs. 5.8 +/- 2, 5.5 +/- 2, 5.9 +/- 2, 6.4 +/- 2% after 2, 4, 6, and 8 h), and there was an increase of ICAM and VCAM. Before therapy post-prandial changes in FMV had an inverse correlation with the changes in triglycerides (r = -0.34; P < 0.05) and ICAM (r = -0.66; P < 0.001).

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Scopus and MEDLINE databases were searched (up to October 15, 2014) to identify RCTs investigating whether fibrates lower plasma PAI-1 concentration or activity. A random-effects model and the generic inverse variance method were used for quantitative data synthesis. Sensitivity analyses were conducted using the one-study remove approach. Random-effects meta-regression was performed to assess the impact of potential moderators on the estimated effect sizes.

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Although FIELD did not show a significant benefit with fenofibrate for major coronary events (the primary outcome), there was significant reduction in total cardiovascular events (relative risk reduction [RRR] 11%, p = 0.035 vs. placebo). The clinical benefits of fenofibrate treatment were greater in patients with marked mixed dyslipidemia (elevated triglycerides >or=200 mg/dL and low plasma levels of HDL-C), features of the metabolic syndrome commonly observed in patients with type 2 diabetes, with a RRR of 27%, p = 0.005. These data are consistent with evidence from other fibrate trials showing increased treatment benefits in patients with metabolic syndrome or type 2 diabetes and mixed dyslipidemia. The FIELD study also provided promising data for microvascular benefits with fenofibrate, specifically on the need for laser treatment for diabetic retinopathy, progression of albuminuria, and prevention of diabetes-related lower-limb amputation.

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In at least some patients who experience marked HDL-C decrease when given a combination of fenofibrate and rosiglitazone, this severe adverse effect is the result of a drug interaction between the 2 pharmaceutical agents and is not reproduced by the administration of either drug singly.

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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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Six asymptomatic patients with no grossly evident gait abnormality, treated by CRPSF for a posterior pelvic disruption, were included in the study (SG). A control group (CG) of six healthy volunteers was created. All participants completed the 12-Item Short Form Health Survey version 2 (SF-12v2), the Majeed Pelvic Score (MPS), and the Iowa Pelvic Score (IPS). In addition, the participants' gait was analyzed.

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The prevalence of statins' pDDIs was high in our study, mostly in the therapy before admission, with only a small number of pDDIs resulting in clinical outcome.

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Diabetic retinopathy (DR) is one of the leading risk factors and causes of blindness worldwide. Tight glucose and blood pressure control has been shown to significantly decrease the risk of development as well as the progression of retinopathy and represents the cornerstone of medical management of DR. The two most threatening complications of DR are diabetic macular edema (DME) and proliferative diabetic retinopathy (PDR). Photocoagulation is standard treatment for both DME and PDR. However, some patients suffer permanent visual loss despite therapy. Treatment with fibrates first showed reduction in hard exudates, an effect subsequently shown with statins in short term studies, in particular two randomized studies in patients with macular edema. In the FIELD study which pre-specified microvascular outcomes, fenofibrate reduced laser treatment for DME or PDR by 31%:164 (3.4%) patients on fenofibrate vs. 238 (4.9%) on placebo (p<0.001). In the ophthalmology sub-study of FIELD, the composite exploratory endpoint of 2-step progression of ETDRS retinopathy grade, macular edema or laser treatment was significantly reduced by 34%: 53 (11.1%) patients on fenofibrate vs. 75 (16.1%) on placebo (p=0.022). Conversely, there was no reduction in laser treatment or reduced progression of retinopathy in two large scale studies of statins where cardiovascular events were significantly reduced. Neither class of lipid-lowering drugs consistently improved visual acuity. In the ACCORD-EYE study, the combination of fenofibrate and simvastatin reduced by 40% the rate of progression of diabetic retinopathy compared with simvastatin alone. Other studies are needed to establish the place of lipid lowering drugs in the treatment of macular edema and the prevention of vision loss.

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Drug release from mesoporous silica systems has been widely investigated in vitro using USP Type II (paddle) dissolution apparatus. However, it is not clear if the observed enhanced in vitro dissolution can forecast drug bioavailability in vivo. In this study, the ability of different in vitro dissolution models to predict in vivo oral bioavailability in a pig model was examined. The fenofibrate-loaded mesoporous silica formulation was compared directly to a commercial reference product, Lipantil Supra®. Three in vitro dissolution methods were considered; USP Type II (paddle) apparatus, USP Type IV (flow-through cell) apparatus and a USP IV Transfer model (incorporating a SGF to FaSSIF-V2 media transfer). In silico modelling, using a physiologically based pharmacokinetic modelling and simulation software package (Gastroplus™), to generate in vitro/in vivo relationships, was also investigated. The study demonstrates that the in vitro dissolution performance of a mesoporous silica formulation varies depending on the dissolution apparatus utilised and experimental design. The findings show that the USP IV transfer model was the best predictor of in vivo bioavailability. The USP Type II (paddle) apparatus was not effective at forecasting in vivo behaviour. This observation is likely due to hydrodynamic differences between the two apparatus and the ability of the transfer model to better simulate gastrointestinal transit. The transfer model is advantageous in forecasting in vivo behaviour for formulations which promote drug supersaturation and as a result are prone to precipitation to a more energetically favourable, less soluble form. The USP IV transfer model could prove useful in future mesoporous silica formulation development. In silico modelling has the potential to assist in this process. However, further investigation is required to overcome the limitations of the model for solubility enhancing formulations.

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Glucocorticoids (GCs) are well-known anti-inflammatory compounds, but they also inhibit cell proliferation depending on cell type. Similarly, peroxisome proliferator-activated receptors (PPARα, PPARδ, and PPARγ) also possess anti-proliferation properties beyond their canonical roles as metabolic mediators. In the present study, we investigated the potential additive or synergistic inhibitory effects on cancer cell proliferation by simultaneous application of fenofibrate and budesonide, agonists for PPARα and glucocorticoid receptor, respectively. We observed differential effects on cell proliferation in A549 and SK-MES-1 lung cancer cells by budesonide and fenofibrate. Fenofibrate inhibited cell proliferation in both TP53 wild type and deficient lung cancer cells. The anti-proliferation effect of budesonide in TP53 wild type A549 cells was abolished in SK-MES-1 cells that do not have wild type TP53 protein. An additive effect against cell proliferation by budesonide and fenofibrate combination was observed only in TP53 wild type A549 cancer cells. Analysis of cell cycle distribution and cyclin profile indicated that the inhibition of cell proliferation was associated with G1 cell cycle arrest. The suppression of NF-κB activity and ERK signaling may contribute to the inhibition of cell proliferation by budesonide and or fenofibrate. The additive inhibitory effect on cell proliferation by budesonide and fenofibrate combination suggests that the same or greater therapeutic effect could be achieved with reduced dosage and side effects when the two compounds are applied simultaneously.

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tricor tabs 2017-02-16

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a macrophage-synthesized lipase that is primarily bound to small electronegative low-density lipoproteins (LDLs). Lipoprotein-associated phospholipase A2 oxidatively modifies LDL and generates the proinflammatory byproducts oxidized fatty acids (ox-FAs) and lysophosphatidylcholine. Fenofibrate reduces Lp- buy tricor online PLA2 mass; however, it remains unknown whether the anti-inflammatory effects of fenofibrate are related to changes in LDL subclasses.

tricor cholesterol medicine 2016-05-26

Peroxisome proliferator buy tricor online -activated receptors (PPARs) may modulate in vitro the vascular production of vasoactive peptides such as endothelin-1 (ET-1). Thus, we investigated in vivo the interaction between PPARs and ET-1 in deoxycorticosterone acetate (DOCA)-salt rats that overexpress vascular ET-1.

tricor medication fenofibrate 2017-10-04

Irrigation with reclaimed water is becoming a common practice in arid- and semi-arid regions as a consequence of structural water resource scarcity. This practice can lead to contamination of the vadose zone if sewage-derived contaminants are not removed properly. In the current work, we have characterized soils from the Guadalete River basin ( buy tricor online SW Spain), which are often irrigated with reclaimed water from a nearby wastewater treatment plant and amended using sludge. Physico-chemical, mineralogical and hydraulic properties were measured in soil samples from this area (from surface up to 2 m depth). Emerging contaminants (synthetic surfactants and pharmaceutically active compounds, or PhACs) were also determined. Synthetic surfactants, widely used in personal care products (PCPs), were found in a wide range of concentrations: 73-1300 μg kg(-1) for linear alkylbenzene sulfonates (LAS), 120-496 μg kg(-1) for alkyl ethoxysulfates (AES), 19-1090 μg kg(-1) for alcohol polyethoxylates (AEOs), and 155-280 μg kg(-1) for nonylphenol polyethoxylates (NPEOs). The presence of surfactant homologues with longer alkyl chains was predominant due to their sorption capacity. A positive correlation was found between LAS and AEOs and soil organic carbon and clay content, respectively. Out of 64 PhACs analyzed, only 7 were detected occasionally (diclofenac, metoprolol, fenofibrate, carbamazepine, clarithromycin, famotidine and hydrochlorothiazide), always at very low concentrations (from 0.1 to 1.3 μg kg(-1)).

tricor brand communications 2016-05-16

There are accepted the lipid levels goals in all world, which are needed to achievement in primary and secondary prevention. Despite efficacy of current standards of care (including achievement of LDL-C, blood pressure and blood sugar goals), patients with atherogenic dyslipidemia (DLP) (high TG levels, low HDL-C, high apolipoprotein B and small dense LDL-particles), which is common in patients with diabetes melitus (DM), metabolic syndrome or cardiovascular diseases (KVD), remain exposed to a high residual risk of major cardiovascular events and microvascular complications. Statin therapy does not adequately address vascular risk asociated with elevated buy tricor online triglycerides (TG) and low HDL-C levels. As ACCORD lipid trial last time shows, the addition of lipid-modifying activity of fenofibrate to statin therapy benefited only certain subgroups of patients at increased cardiometabolic risk.

tricor 48mg tablets 2017-08-26

A low serum level of high-density lipoprotein (HDL)-cholesterol is an buy tricor online independent risk factor for coronary heart disease (CHD). Fibrates, particularly gemfibrozil, have been shown to raise HDL-cholesterol levels and reduce the incidence of CHD. The literature on fibrate cost effectiveness is quite limited.

tricor 40 mg 2017-09-03

These results show that CoQ supplementation may improve blood pressure and long-term glycaemic control in subjects with type buy tricor online 2 diabetes, but these improvements were not associated with reduced oxidative stress, as assessed by F2-isoprostanes.

tricor generic equivalent 2017-06-17

Optimal cardiovascular risk reduction in patients exhibiting the lipid triad requires integrated pharmacotherapy to normalize LDL-C, HDL buy tricor online -C, TGs, and potentially lipoprotein(a). Ongoing studies may provide definitive evidence of the impact of niacin plus statins on cardiovascular outcomes.

tricor 145 mg 2015-03-10

In addition to inhibiting cholesterol biosynthesis, statins increase the conversion of linoleic acid to its derivatives, in particular to arachidonic acid, both in vivo and in vitro. Desaturases are the rate-limiting enzymes in this metabolic process and statins markedly enhance delta5 desaturase activity. To evaluate the delta5 desaturase gene expression and the transcription factors involved, THP-1 cells (a monocytic cell line) were incubated with 5 microM simvastatin for different time periods. The activity of the enzyme, evaluated as product/precursor ratio in the metabolic pathway (starting from [1-(14)C] linoleic acid), increased in treated cells with respect to controls after 24 h, whereas, mRNA levels of the delta5 desaturase increased after 12 h of incubation with simvastatin. Fatty acid desaturase genes are regulated by both sterol regulatory element binding proteins (SREBPs) and peroxisome proliferators activated receptors (PPARs). Both PPARalpha (WY 14643 and fenofibrate) and PPARgamma (ciglitazone) agonists did not affect linoleic acid conversion and the delta5 desaturase activity at any time considered (8-48 h), but they increased the delta5 desaturase mRNA levels, after 48 h; only fenofibrate showed a synergistic effect with simvastatin at this time, with a concomitantly increase in PPARalpha expression and beta-oxidation. Simvastatin alone increased SREBP-1 levels with respect to controls, starting from 8 h of incubation, whereas PPARalpha and linoleic acid beta-oxidation (a PPARalpha mediated process) were not affected after 48 h of incubation. These results taken together suggest that SREBP-1 is involved in the early regulation of delta5 desaturase gene by simvastatin buy tricor online , in THP-1 cells.

tricor 125 mg 2015-11-21

Treatment with the 3-drug regimen was associated with a significant reduction in triglyceride levels compared with simvastatin monotherapy. However, there was not a significant incremental reduction in triglyceride levels when nicotinic acid was added to the 2-drug treatment, suggesting that the buy tricor online triglyceride-lowering effect of fenofibrate + nicotinic acid is not cumulative. To obtain clinically meaningful responses, particularly for the treatment of elevated HDL-C, higher doses of nicotinic acid might be required.

tricor 135 mg 2015-04-04

Population-based cohort buy tricor online study.

tricor 345 mg 2017-04-02

Ten of 16 patients (63%) treated with fenofibrate achieved a 30% reduction in triglyceride levels or LDL/HDL ratio reduction < 5 compared to 2 of 17% in the placebo group (p = 0.015). Triglyceride levels were significantly reduced in the fenofibrate group (-31%) versus placebo (+1.3%, p = 0.003). In compliant patients (n = 25) there was also a significantly greater increase in HDL cholesterol levels in the fenofibrate group (+19.9%) compared to placebo (-4.7%, p = 0.001). Changes in measured creatinine clearance were not significantly different between the buy tricor online groups and there were no serious adverse effects of treatment.

tricor 67 mg 2016-01-22

Ursodeoxycholic acid (UDCA) is currently the only available pharmacological treatment for asymptomatic primary biliary cirrhosis (aPBC). Fibrates may be useful for treating aPBC patients who exhibit incomplete responses to UDCA. The mechanism of action of such fibrates involves the regulation of the expression of various kinds of lipids and proteins through the activation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha ), which increases the phospholipid output into the bile and reduces the cytotoxicity of hydrophobic bile acids. Among these fibrates, the binding activity of fenofibrate to PPAR-alpha is stronger than that of bezafibrate. Because the majority of PBC patients exhibit a slow progression of their disease, and since the administration of UDCA plus fibrate buy tricor online may further delay the liver deterioration, cardiovascular risk factors, such as dyslipidemia may thus have a bigger impact on the long-term survival of PBC patients. The aim of this study was to evaluate the effects of fenofibrate in patients with aPBC who are refractory to UDCA and to simultaneously compare the effectiveness of fenofibrate with that of bezafibrate.

tricor cost 2016-10-13

Predefined monoclonal antibodies (Mabs) were used in an immunoenzymometric assay to study the immunochemical heterogeneity of lipoproteins and to search for potential epitopes with pathological importance. By measuring apolipoprotein B (apo B) epitopes in patients with and without angiographically documented coronary artery disease and in patients with type IIa hyperlipoproteinemia, we have found that both types of patients have a significant increase in Apo B-containing particles specifically recognized by one Mab (BL3). We have also observed that the effects of fenofibrate on type IIa patients vary greatly buy tricor online depending on the plasma concentrations of various Apo B-containing lipoproteins. The greatest effects occurred in patients with epitopes recognized by BL3. Lastly, by sequential precipitation of specific epitopes by BL3, we have obtained evidence that the residual epitope(s) may be related to one or more lipoprotein particles.

tricor generic medication 2015-11-12

We have compared serum levels of adiponectin in 199 non-obese FCHL patients (BMI 25.96+/-3.7), 116 normolipaemic (NL) non-affected relatives (BMI 24.4+/-4.0) and 192 controls (BMI 28.0+/-7.4). In a subgroup of FCHL patients, changes in adiponectin levels after treatment with atorvastatin (n=22) or fenofibrate (n=26) were also evaluated. FCHL patients as well as their NL relatives showed lower serum adiponectin levels compared to controls (9.7+/-5.4 microg/mL, 10.7+/-5.3 microg/mL and 17.3+/-13.7microg/mL, respectively; p<0.0001 for all comparisons). After controlling for confounders, the strongest association with hypoadiponectinemia was observed with family history of FCHL, followed by HDL-C (negatively) and age (positively). These variables jointly explained 15% of the total variance of serum adiponectin levels. After 24-week of treatment, adiponectin was increased by 12.5% (p<0.05) by atorvastatin and was reduced by 10% by fenofibrate, resulting buy tricor online in a treatment difference of 22.5% in favor of atorvastatin (p<0.017).

tricor 200 mg 2017-04-25

The effects of fenofibrate on C-reactive protein (CRP) are Paxil 75 Mg under debate. We investigated the effect of fenofibrate on CRP levels and the variables determining changes.

tricor 500 mg 2017-06-05

FFB particles formed within the nanosize range from Group I gradually increased with time but decreased with increasing stirring rates. However, the mean size of FFB formed by B series was as low as 200 nm, which was smaller than that of A series at three stirring rates. The release rate from both groups obviously increased with increasing stirring rate. However, incomplete release was observed for S and N in Tween 20 series Lasix 2 Mg , whereas a faster release rate and complete release were observed for Tween 80 series with an insignificant difference among them. Results of pharmacokinetic study demonstrated that the highest-ranked area under the curve and Cmax values were for Q(SMEDDS) and B2(solution), respectively. The relative bioavailability of Q(SMEDDS) with respect to Tricor was enhanced by about 1.14-1.22-fold.

tricor 45 mg 2015-12-31

Small dense (sd)-low-density lipoprotein (LDL) is a potent atherogenic Ilosone Gel Topico lipoprotein. The overall atherogenicity of this lipoprotein can be precisely assessed by quantifying sd-LDL rather than by measuring the LDL size. We studied the effects of representative lipid-lowering agents (statin and fibrate) on sd-LDL-cholesterol (C) in patients with type 2 diabetes.

tricor tablets 2015-01-25

This was a retrospective observational study in which data was collected from case notes of patients started on fibrates (n = 118, 2002-2008) in the lipid clinic at Good Hope Hospital and pre/post-fibrate lipid and LFT values Plavix 81 Mg were obtained. All biochemistry was performed on the Roche P-Unit using supplied reagents. Statistical analyses included t tests and regression analyses (factorised when quartiles were compared).

tricor mg 2015-08-01

In subjects with obesity, diabetes and coronary artery disease, circulating levels of leptin increased while that of adiponectin is decreased. In this study we have investigated effects of physiological and pharmacological weight reduction on leptin and adiponectin mRNA expression. Wistar rats were fed either standard laboratory chow for 16 weeks (chow-fed) or given a fat-enriched, glucose-enriched diet (diet-fed) for 8 weeks. After 8 weeks, diet-fed group was subdivided into three subgroups, namely, an untreated obese, or were returned to chow diet, or treated with fenofibrate for further 8 week. After 16 weeks, compared with chow-fed group, diet-fed rats had significantly higher body weight, epididymal fat pad mass, and plasma levels of insulin, leptin, adiponectin, non-esterified fatty acids and triglycerides (P<0.001, for all). Moreover, untreated obese rats had significantly (P<0.01, for both) raised levels of Ob mRNA but reduced adiponectin mRNA levels in epididymal fat pads compared with chow- Glucotrol Brand Name fed group. These changes were corrected by chronic removal of the high-energy diet and fenofibrate treatment. These findings indicate that physiological or pharmacological lowering of body weight together with circulating plasma lipids play a significant role in leptin and adiponectin synthesis and metabolism.

tricor 48 mg 2017-10-03

The Diabetes Atherosclerosis Intervention Study showed that treatment with fenofibrate decreases progression of coronary atherosclerosis in subjects with type 2 diabetes. We determined whether on-treatment plasma lipid concentrations and Coumadin Pills LDL particle size contribute to the favorable effect of fenofibrate on the progression of coronary artery disease (CAD).

tricor order forms 2015-07-25

PEG-b-PCL in ACN assembles with fenofibrate into drug-loaded polymeric micelles with the addition of water and the Cymbalta Capsules subsequent removal of a negative ACN-water azeotrope.

tricor overdose 2016-05-14

To assess the efficacy of fenofibrate and statin dual therapy versus a double or equivalent dose of statin monotherapy.

tricor medication 2016-08-25

The results from the characterization and solubility studies showed that formulations containing mixed glycerides were highly efficient SNEDDS as they had higher solubility of the drug and produced nanosized droplets. The dispersion studies confirmed that SNEDDS (containing polar mixed glycerides) can retain >98% drug in solution for >24 hours in aqueous media. The in vivo pharmacokinetics parameters of SNEDDS formulation in comparison with pure drug showed significant increase in C max and AUC0- t , ~78% and 67%, respectively. The oral BA of fenofibrate from SNEDDS in rats was ~1.7-fold enhanced as compared with the BA from pure drug.

tricor online 2015-06-09

Alirocumab 150 mg every 4 weeks produced maximal LDL-C reductions of 47% in combination with placebo and 54% to 57% in combination with ezetimibe or fenofibrate. The oral lipid-lowering therapies appear to increase PCSK9 levels, leading to increased alirocumab clearance. Although the duration of effect was modestly diminished with alirocumab plus ezetimibe/fenofibrate versus placebo, the effect was less than observed in trials with background statins, and it would not preclude the use of alirocumab every 4 weeks in patients taking these nonstatin lipid-lowering therapies concomitantly.

medication tricor 2016-09-14

Diabetic dyslipidaemia, among the main factors contributing to vascular risk in type 2 diabetes, is characterized by hypertriglyceridaemia, low HDL-cholesterol and increased prevalence of small dense LDL particles. Because fibrates have positive effects on triglycerides, HDL-cholesterol and LDL particle size, they may be an appropriate treatment for diabetic dyslipidaemia. Statins have been shown to diminish significantly the risk for coronary disease in patients with type 2 diabetes, and so what are the real effects of fibrates on cardiovascular risk in type 2 diabetes?

tricor dose 2017-01-25

We observed 60 patients with CP accompanied by MS, of whom 30 patients received standard therapy complex CPs (comparison group), 30--received Creon (microspheres of pancreatin) and Tricor (fenofibrate) in the combined treatment (observation group). In assessing the effectiveness of therapies used in clinical and advanced laboratory and instrumental studies.

tricor reviews 2015-11-18

Urine was collected from 26 healthy adults before and after treatment with fenofibrate (145 mg/day for 6 weeks). Excretions of betaine, N,N-dimethylglycine, free choline, myo-inositol, taurine, trimethylamine-N-oxide, carnitine, and acetylcarnitine were measured by liquid chromatography with mass spectrometric detection.