A lipid-regulating agent that lowers elevated serum lipids primarily by decreasing serum triglycerides with a variable reduction in total cholesterol.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
Valerates are salts or esters formed from the reaction between valerianic acid and a base, characterized by their tranquilizing and sedative properties, often used in pharmaceuticals and dietary supplements for promoting sleep and reducing anxiety.
A family of isomeric, colorless aromatic hydrocarbon liquids, that contain the general formula C6H4(CH3)2. They are produced by the destructive distillation of coal or by the catalytic reforming of petroleum naphthenic fractions. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
Pentanoic acid, also known as valeric acid, is a carboxylic acid with a 5-carbon chain (C5H10O2), having a distinctive pungent and rancid odor, found in some animals' sweat, certain foods, and produced through wood fermentation.
A fibric acid derivative used in the treatment of HYPERLIPOPROTEINEMIA TYPE III and severe HYPERTRIGLYCERIDEMIA. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986)
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.
A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. It may also be epimerized to UDP iduronic acid, which donates iduronic acid to polysaccharides. In animals, UDP glucuronic acid is used for formation of many glucosiduronides with various aglycones.
An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.
Glycosides of GLUCURONIC ACID formed by the reaction of URIDINE DIPHOSPHATE GLUCURONIC ACID with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and BILIRUBIN metabolism to a more water-soluble compound that can be eliminated in the URINE and BILE.
A large group of cytochrome P-450 (heme-thiolate) monooxygenases that complex with NAD(P)H-FLAVIN OXIDOREDUCTASE in numerous mixed-function oxidations of aromatic compounds. They catalyze hydroxylation of a broad spectrum of substrates and are important in the metabolism of steroids, drugs, and toxins such as PHENOBARBITAL, carcinogens, and insecticides.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Derivatives of carbamic acid, H2NC(=O)OH. Included under this heading are N-substituted and O-substituted carbamic acids. In general carbamate esters are referred to as urethanes, and polymers that include repeating units of carbamate are referred to as POLYURETHANES. Note however that polyurethanes are derived from the polymerization of ISOCYANATES and the singular term URETHANE refers to the ethyl ester of carbamic acid.
Compounds that either share the structure of fibric acid in their molecular arrangement or are considered variants of the fibric acid structure.
A condition of elevated levels of TRIGLYCERIDES in the blood.
Triglycerides are the most common type of fat in the body, stored in fat cells and used as energy; they are measured in blood tests to assess heart disease risk, with high levels often resulting from dietary habits, obesity, physical inactivity, smoking, and alcohol consumption.

A comparison of the use, effectiveness and safety of bezafibrate, gemfibrozil and simvastatin in normal clinical practice using the New Zealand Intensive Medicines Monitoring Programme (IMMP). (1/179)

AIMS: Because of the importance of treating dyslipidaemia in the prevention of ischaemic heart disease and because patient selection criteria and outcomes in clinical trials do not necessarily reflect what happens in normal clinical practice, we compared outcomes from bezafibrate, gemfibrozil and simvastatin therapy under conditions of normal use. METHODS: A random sample of 200 patients was selected from the New Zealand Intensive Medicines Monitoring Programme's (IMMP) patient cohorts for each drug. Questionnaires sent to prescribers requested information on indications, risk factors for ischaemic heart disease, lipid profiles with changes during treatment and reasons for stopping therapy. RESULTS: 80% of prescribers replied and 83% of these contained useful information. The three groups were similar for age, sex and geographical region, but significantly more patients on bezafibrate had diabetes and/or hypertension than those on gemfibrozil or simvastatin. After treatment and taking the initial measure into account, the changes in serum lipid values were consistent with those generally observed, but with gemfibrozil being significantly less effective than expected. More patients (15.8%S) stopped gemfibrozil because of an inadequate response compared with bezafibrate (5.4%) and simvastatin (1.6%). Gemfibrozil treatment was also withdrawn significantly more frequently due to a possible adverse reaction compared with the other two drugs. CONCLUSIONS: In normal clinical practice in New Zealand gemfibrozil appears less effective and more frequently causes adverse effects leading to withdrawal of treatment than either bezafibrate or simvastatin.  (+info)

The effect of peroxisome proliferators on mitochondrial bioenergetics. (2/179)

Peroxisome proliferators are a group of structurally diverse chemicals that cause the proliferation of peroxisomes in rodents. The purpose of this investigation was to test the hypothesis that the shared effect of these compounds on peroxisome proliferation is mediated through a common inhibitory effect on mitochondrial bioenergetics. Freshly isolated rat liver mitochondria were energized with succinate. The effect of the chemicals on mitochondrial bioenergetics was analyzed by monitoring calcium-induced changes in membrane potential and swelling, as well as changes in mitochondrial respiration. Mitochondrial membrane potential was measured with a TPP(+)-sensitive electrode, and swelling was recorded spectrophotometrically. Mitochondrial oxygen uptake was monitored with a Clark-type oxygen electrode. Gemfibrozil and WY-14,643 induced the mitochondrial permeability transition as characterized by calcium-induced swelling and depolarization of membrane potential, both of which were inhibited by cyclosporine A. Fenofibrate, clofibrate, ciprofibrate and diethylhexyl phthalate, on the other hand, caused a direct dose-dependent depolarization of mitochondrial membrane potential. However, the mechanism of membrane depolarization varied among the test chemicals. Bezafibrate and trichloroethylene elicited no effect on succinate-supported mitochondrial bioenergetics. The results of this investigation demonstrate that although most, but not all, peroxisome proliferators interfere with mitochondrial bioenergetics, the specific biomolecular mechanism differs among the individual compounds.  (+info)

Effects of fibrate compounds on expression of plasminogen activator inhibitor-1 by cultured endothelial cells. (3/179)

The consistent positive correlation between triglyceride and plasminogen activator inhibitor-1 (PAI-1) levels in plasma and the fact that very low density lipoprotein (VLDL) induces secretion of PAI-1 from cultured human umbilical vein endothelial cells (HUVECs) and human hepatoblastoma cells have raised the question of whether fibrate treatment, the main effect of which is a profound lowering of plasma concentrations of VLDL, might improve fibrinolytic function by reducing the plasma levels of PAI-1. However, the findings of controlled clinical trials using various fibrate compounds have been discrepant. ECs express PAI-1 under normal conditions in humans. We therefore examined the effects of several fibrate compounds on PAI-1 expression and secretion by cultured HUVECs and the HUVEC-derived cell line EA.hy926. All fibrate compounds examined had significant effects on PAI-1 gene transcription in the EA.hy926 cells. Low concentrations of clofibric acid and bezafibrate increased PAI-1 transcription and secretion, whereas Wy-14643 increased PAI-1 synthesis in a dose-dependent way. In contrast, both fenofibric acid and gemfibrozil markedly decreased PAI-1 transcription and secretion from HUVECs and EA.hy926 cells. Thus, stimulation of the transcriptional activity of the PAI-1 gene by some fibrates is linked to increased secretion of PAI-1 protein by the cells, whereas the opposite effects occur with other fibrate compounds. Whether the different effects on PAI-1 transcription and secretion by ECs in vitro also reflect differences in treatment effects on the regulation of plasma PAI-1 activity in vivo will have to be determined in larger-scale, controlled clinical trials.  (+info)

Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. (4/179)

BACKGROUND: Although it is generally accepted that lowering elevated serum levels of low-density lipoprotein (LDL) cholesterol in patients with coronary heart disease is beneficial, there are few data to guide decisions about therapy for patients whose primary lipid abnormality is a low level of high-density lipoprotein (HDL) cholesterol. METHODS: We conducted a double-blind trial comparing gemfibrozil (1200 mg per day) with placebo in 2531 men with coronary heart disease, an HDL cholesterol level of 40 mg per deciliter (1.0 mmol per liter) or less, and an LDL cholesterol level of 140 mg per deciliter (3.6 mmol per liter) or less. The primary study outcome was nonfatal myocardial infarction or death from coronary causes. RESULTS: The median follow-up was 5.1 years. At one year, the mean HDL cholesterol level was 6 percent higher, the mean triglyceride level was 31 percent lower, and the mean total cholesterol level was 4 percent lower in the gemfibrozil group than in the placebo group. LDL cholesterol levels did not differ significantly between the groups. A primary event occurred in 275 of the 1267 patients assigned to placebo (21.7 percent) and in 219 of the 1264 patients assigned to gemfibrozil (17.3 percent). The overall reduction in the risk of an event was 4.4 percentage points, and the reduction in relative risk was 22 percent (95 percent confidence interval, 7 to 35 percent; P=0.006). We observed a 24 percent reduction in the combined outcome of death from coronary heart disease, nonfatal myocardial infarction, and stroke (P< 0.001). There were no significant differences in the rates of coronary revascularization, hospitalization for unstable angina, death from any cause, and cancer. CONCLUSIONS: Gemfibrozil therapy resulted in a significant reduction in the risk of major cardiovascular events in patients with coronary disease whose primary lipid abnormality was a low HDL cholesterol level. The findings suggest that the rate of coronary events is reduced by raising HDL cholesterol levels and lowering levels of triglycerides without lowering LDL cholesterol levels.  (+info)

Heart rate variability and progression of coronary atherosclerosis. (5/179)

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 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.  (+info)

Bezafibrate as differentiating factor of human myeloid leukemia cells. (6/179)

Bezafibrate belongs to the class of fibric acid derivatives usually used as antihyperlipidemia agents. From the biochemical point of view, these drugs show intriguing properties which leads one to think they may promote a differentiation process in tumour cells. This new pharmacological activity of fibrates could partially depend on the induction of an oxidative stress. To test this hypothesis, the effect of bezafibrate, as well as of clofibric acid and gemfibrozil, on growth, functional and cytochemical characteristics of human leukaemia-derived cell lines HL-60, U-937 and K-562 has been studied in some details. The results show that bezafibrate, gemfibrozil and clofibric acid, do induce differentiation in human myeloid leukaemia cell lines as indicated by several differentiation markers. Moreover fibrates, in dose dependent manner, significantly alter the cell cycle distributions, mainly leading to G0/G1 phase increment and G2/M phase reduction. The differentiating activity of fibrates could have significant implications both for the pharmacotoxicological profile of this class of compounds and for the pathophysiology of neoplastic disease.  (+info)

Activation of the contact system of coagulation does not contribute to the hemostatic imbalance in hypertriglyceridemia. (7/179)

In vitro, triglyceride-rich lipoproteins may act as a surface to initiate the contact system of coagulation. Therefore, we studied the activation of factor XII (FXII), prekallikrein, and FXI and the generation of thrombin in 52 hypertriglyceridemic patients before and after 12 weeks of triglyceride-lowering treatment with gemfibrozil or n-3 polyunsaturated fatty acids. Thrombin generation was assessed by measuring the levels of prothrombin fragment F1+2 and thrombin-antithrombin (TAT) complexes. Contact activation was assessed by measuring FXIIa, kallikrein, and FXIa in complex with their major inhibitor, C1 inhibitor, and FXIa was also determined as part of a complex with alpha(1)-antitrypsin. Triglyceride and cholesterol levels decreased equally in both treatment groups. In the gemfibrozil group, there was a significant decrease in F1+2, while TAT complexes did not change. FXIIa- and kallikrein-C1 inhibitor complexes were elevated in 13% and 9% of the patients before treatment, respectively, and no changes were observed on triglyceride-lowering therapy. Also, no significant changes in regard to FXIa-C1 inhibitor and FXIa-alpha(1)-antitrypsin complexes were seen. FXIa-alpha(1)-antitrypsin complexes were present in 70% of the patients before therapy and were positively correlated with the level of TAT complexes. In conclusion, we did not detect an effect on activation markers of the contact coagulation system in hypertriglyceridemic patients after triglyceride-lowering therapy. Therefore, contact activation is not likely to contribute to the hypercoagulability seen in these patients.  (+info)

Joint effects of an aldosterone synthase (CYP11B2) gene polymorphism and classic risk factors on risk of myocardial infarction. (8/179)

BACKGROUND: The -344C allele of a 2-allele (C or T) polymorphism in the promoter of the gene encoding aldosterone synthase (CYP11B2) is associated with increased left ventricular size and mass and with decreased baroreflex sensitivity, known risk factors for morbidity and mortality associated with myocardial infarction (MI). We hypothesized that this polymorphism was a risk factor for MI. METHODS AND RESULTS: We used a nested case-control design to investigate the relationships between this polymorphism and the risk of nonfatal MI in 141 cases and 270 matched controls from the Helsinki Heart Study, a coronary primary prevention trial in dyslipidemic, middle-aged men. There was a nonsignificant trend of increasing risk of MI with number of copies of the -344C allele. However, this allele was associated in a gene dosage-dependent manner with markedly increased MI risk conferred by classic risk factors. Whereas smoking conferred a relative risk of MI of 2.50 (P=0.0001) compared with nonsmokers in the entire study population, the relative risk increased to 4.67 in -344CC homozygous smokers (relative to nonsmokers with the same genotype, P=0.003) and decreased to 1.09 in -344TT homozygotes relative to nonsmokers with this genotype. Similar joint effects were noted with genotype and decreased HDL cholesterol level as combined risk factors. CONCLUSIONS: Smoking and dyslipidemia are more potent risk factors for nonfatal MI in males who have the -344C allele of CYP11B2.  (+info)

Gemfibrozil is a medication that belongs to a class of drugs called fibrates. It is primarily used to lower elevated levels of triglycerides (a type of fat found in the blood) and increase levels of "good" cholesterol (HDL-C) in the blood.

Gemfibrozil works by reducing the production of triglycerides in the body, increasing the breakdown of fats in the liver, and improving the way the body handles fats and sugar. It is often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or those who have not responded well to other cholesterol-lowering medications, such as statins.

It's important to note that while gemfibrozil can help manage triglyceride and cholesterol levels, it is not a substitute for a healthy lifestyle. Regular exercise, a balanced diet, limiting alcohol consumption, and avoiding smoking are all crucial components of maintaining good cardiovascular health.

As with any medication, gemfibrozil should be taken under the supervision of a healthcare provider, who can monitor its effectiveness and potential side effects. Common side effects of gemfibrozil include stomach pain, diarrhea, and muscle or joint pain. Rare but serious side effects may include liver damage, kidney problems, and an increased risk of gallstones.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

"Valerates" is not a recognized medical term. However, it may refer to a salt or ester of valeric acid, which is a carboxylic acid with the formula CH3CH2CH2CO2H. Valeric acid and its salts and esters are used in pharmaceuticals and perfumes. Valerates can have a sedative effect and are sometimes used as a treatment for anxiety or insomnia. One example is sodium valerate, which is used in the manufacture of some types of medical-grade polyester. Another example is diethyl valerate, an ester of valeric acid that is used as a flavoring agent and solvent.

Xylenes are aromatic hydrocarbons that are often used as solvents in the industrial field. They are composed of two benzene rings with methyl side groups (-CH3) and can be found as a mixture of isomers: ortho-xylene, meta-xylene, and para-xylene.

In a medical context, xylenes may be relevant due to their potential for exposure in occupational settings or through environmental contamination. Short-term exposure to high levels of xylenes can cause irritation of the eyes, nose, throat, and lungs, as well as symptoms such as headache, dizziness, and nausea. Long-term exposure has been linked to neurological effects, including memory impairment, hearing loss, and changes in behavior and mood.

It is worth noting that xylenes are not typically considered a direct medical diagnosis, but rather a potential exposure hazard or environmental contaminant that may have health impacts.

I am sorry for any confusion, but "Pentanoic Acids" is not a recognized medical term or concept. Pentanoic acid, also known as valeric acid, is an organic compound with the formula CH3CH2CH2CH2CO2H. It is a fatty acid with five carbon atoms, and it may have some uses in industry, but it does not have specific relevance to medical definition or healthcare.

Clofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower elevated levels of cholesterol and other fats (lipids) in the blood, specifically low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, while increasing high-density lipoprotein (HDL), or "good" cholesterol. Clofibrate works by reducing the production of very-low-density lipoproteins (VLDL) in the liver, which in turn lowers triglyceride levels and indirectly reduces LDL cholesterol levels.

Clofibrate is available in oral tablet form and is typically prescribed for patients with high cholesterol or triglycerides who are at risk of cardiovascular disease, such as those with a history of heart attacks, strokes, or peripheral artery disease. It is important to note that clofibrate should be used in conjunction with lifestyle modifications, including a healthy diet, regular exercise, and smoking cessation.

Like all medications, clofibrate can have side effects, some of which may be serious. Common side effects include stomach upset, diarrhea, gas, and changes in taste. Less commonly, clofibrate can cause more severe side effects such as liver or muscle damage, gallstones, and an increased risk of developing certain types of cancer. Patients taking clofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working effectively and to monitor for any potential side effects.

Fenofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower levels of cholesterol and other fats (triglycerides) in the blood. Fenofibrate works by increasing the breakdown and elimination of these fats from the body, which can help reduce the risk of heart disease and stroke.

Fenofibrate is available in various forms, including tablets and capsules, and is typically taken once or twice a day with meals. Common side effects of fenofibrate include headache, nausea, and muscle pain. More serious side effects are rare but can include liver damage, kidney problems, and an increased risk of gallstones.

It's important to note that fenofibrate should be used in conjunction with a healthy diet, regular exercise, and other lifestyle changes to manage high cholesterol and triglyceride levels effectively. Additionally, patients taking fenofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working properly and to check for any potential side effects.

Bezafibrate is a medication that belongs to a class of drugs called fibrates. It is primarily used to treat high cholesterol and related conditions, such as hyperlipidemia and mixed dyslipidemia. The medication works by reducing the levels of triglycerides and increasing the levels of "good" cholesterol (HDL) in the blood.

Bezafibrate achieves this effect by activating certain receptors in the body, known as peroxisome proliferator-activated receptors (PPARs), which play a role in regulating lipid metabolism. By binding to these receptors, bezafibrate helps to promote the breakdown of fats and reduce the production of cholesterol in the liver.

It is important to note that bezafibrate should be used in conjunction with lifestyle modifications, such as a healthy diet and regular exercise, to effectively manage high cholesterol and related conditions. Additionally, it may interact with other medications, so it is essential to inform your healthcare provider of all the drugs you are taking before starting bezafibrate therapy.

As with any medication, bezafibrate can cause side effects, including gastrointestinal symptoms such as nausea, diarrhea, and abdominal pain, as well as headaches, muscle cramps, and skin rashes. In rare cases, it may also cause more serious side effects, such as liver or kidney damage, so regular monitoring of liver and kidney function is recommended during treatment.

Overall, bezafibrate is a valuable tool in the management of high cholesterol and related conditions, but it should be used under the guidance and supervision of a healthcare professional to ensure safe and effective use.

Mefenamic Acid is a non-steroidal anti-inflammatory drug (NSAID) commonly used for its analgesic, antipyretic, and anti-inflammatory properties. It works by inhibiting the enzyme cyclooxygenase (COX), which is responsible for prostaglandin synthesis, a key player in pain and inflammation processes.

Mefenamic Acid is primarily used to treat mild to moderate pain, including menstrual cramps, primary dysmenorrhea, post-operative pain, and various types of inflammatory conditions such as rheumatoid arthritis and osteoarthritis.

Common side effects may include gastrointestinal disturbances like nausea, vomiting, diarrhea, or abdominal pain. Long-term use of Mefenamic Acid has been associated with increased risks of cardiovascular events, gastrointestinal ulcers, and bleeding. Therefore, it is essential to follow the recommended dosage and consult a healthcare professional for appropriate usage and potential interactions with other medications.

Uridine Diphosphate Glucuronic Acid (UDP-Glucuronic Acid) is not a medical term per se, but rather a biochemical term. It is a compound that plays an essential role in the detoxification process in the liver. UDP-Glucuronic Acid is a nucleotide sugar derivative that combines with toxins, drugs, and other substances to form glucuronides, which are then excreted through urine or bile. This process is known as glucuronidation, and it helps make the substances more water-soluble and easier for the body to eliminate.

Clofibric acid is the main metabolic product of clofibrate, a medication that belongs to the class of drugs called fibrates. It works by lowering levels of total and LDL (low-density lipoprotein) cholesterol and triglycerides in the blood, while increasing HDL (high-density lipoprotein) cholesterol levels. Clofibric acid is an antihyperlipidemic agent that is used primarily for the treatment of hypertriglyceridemia and mixed dyslipidemia. It may also be used to prevent pancreatitis caused by high triglyceride levels.

Clofibric acid is detectable in the urine and can be used as a biomarker for clofibrate exposure or use. However, it's important to note that clofibrate has largely been replaced by newer fibrates and statins due to its adverse effects profile and lower efficacy compared to these newer agents.

Glucuronides are conjugated compounds formed in the liver by the attachment of glucuronic acid to a variety of molecules, including drugs, hormones, and environmental toxins. This process, known as glucuronidation, is catalyzed by enzymes called UDP-glucuronosyltransferases (UGTs) and increases the water solubility of these compounds, allowing them to be more easily excreted from the body through urine or bile.

Glucuronidation plays a crucial role in the detoxification and elimination of many substances, including drugs and toxins. However, in some cases, glucuronides can also be hydrolyzed back into their original forms by enzymes called β-glucuronidases, which can lead to reabsorption of the parent compound and prolong its effects or toxicity.

Overall, understanding the metabolism and disposition of glucuronides is important for predicting drug interactions, pharmacokinetics, and potential adverse effects.

Aryl hydrocarbon hydroxylases (AHH) are a group of enzymes that play a crucial role in the metabolism of various aromatic and heterocyclic compounds, including potentially harmful substances such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. These enzymes are primarily located in the endoplasmic reticulum of cells, particularly in the liver, but can also be found in other tissues.

The AHH enzymes catalyze the addition of a hydroxyl group (-OH) to the aromatic ring structure of these compounds, which is the first step in their biotransformation and eventual elimination from the body. This process can sometimes lead to the formation of metabolites that are more reactive and potentially toxic than the original compound. Therefore, the overall impact of AHH enzymes on human health is complex and depends on various factors, including the specific compounds being metabolized and individual genetic differences in enzyme activity.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Carbamates are a group of organic compounds that contain the carbamate functional group, which is a carbon atom double-bonded to oxygen and single-bonded to a nitrogen atom (> N-C=O). In the context of pharmaceuticals and agriculture, carbamates are a class of drugs and pesticides that have carbamate as their core structure.

Carbamate insecticides work by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down the neurotransmitter acetylcholine in the synapses of the nervous system. When this enzyme is inhibited, acetylcholine accumulates in the synaptic cleft, leading to overstimulation of the nervous system and ultimately causing paralysis and death in insects.

Carbamate drugs are used for a variety of medical indications, including as anticonvulsants, muscle relaxants, and psychotropic medications. They work by modulating various neurotransmitter systems in the brain, such as GABA, glutamate, and dopamine. Carbamates can also be used as anti- parasitic agents, such as ivermectin, which is effective against a range of parasites including nematodes, arthropods, and some protozoa.

It's important to note that carbamate pesticides can be toxic to non-target organisms, including humans, if not used properly. Therefore, it's essential to follow all safety guidelines when handling or using these products.

Fibric acids, also known as fibric acid derivatives, are a class of medications that are primarily used to lower elevated levels of triglycerides (a type of fat) in the blood. They work by increasing the breakdown and removal of triglycerides from the bloodstream, and reducing the production of very-low-density lipoprotein (VLDL), a type of particle that carries triglycerides in the blood.

Examples of fibric acids include gemfibrozil, fenofibrate, and clofibrate. These medications are often prescribed for people with high triglyceride levels who are at risk for pancreatitis (inflammation of the pancreas) or other complications related to high triglycerides.

Fibric acids may also have a modest effect on raising levels of high-density lipoprotein (HDL), or "good" cholesterol, and lowering levels of low-density lipoprotein (LDL), or "bad" cholesterol, in some people. However, they are generally not as effective at lowering LDL cholesterol as statins, another class of cholesterol-lowering medications.

It's important to note that fibric acids can interact with other medications and may cause side effects such as stomach upset, muscle pain, and an increased risk of gallstones. As with any medication, it's important to use fibric acids under the guidance of a healthcare provider.

Hypertriglyceridemia is a medical condition characterized by an elevated level of triglycerides in the blood. Triglycerides are a type of fat (lipid) found in your blood that can increase the risk of developing heart disease, especially when levels are very high.

In general, hypertriglyceridemia is defined as having triglyceride levels greater than 150 milligrams per deciliter (mg/dL) of blood. However, the specific definition of hypertriglyceridemia may vary depending on individual risk factors and medical history.

Hypertriglyceridemia can be caused by a variety of factors, including genetics, obesity, physical inactivity, excessive alcohol consumption, and certain medications. In some cases, it may also be a secondary consequence of other medical conditions such as diabetes or hypothyroidism. Treatment for hypertriglyceridemia typically involves lifestyle modifications such as dietary changes, increased exercise, and weight loss, as well as medication if necessary.

Triglycerides are the most common type of fat in the body, and they're found in the food we eat. They're carried in the bloodstream to provide energy to the cells in our body. High levels of triglycerides in the blood can increase the risk of heart disease, especially in combination with other risk factors such as high LDL (bad) cholesterol, low HDL (good) cholesterol, and high blood pressure.

It's important to note that while triglycerides are a type of fat, they should not be confused with cholesterol, which is a waxy substance found in the cells of our body. Both triglycerides and cholesterol are important for maintaining good health, but high levels of either can increase the risk of heart disease.

Triglyceride levels are measured through a blood test called a lipid panel or lipid profile. A normal triglyceride level is less than 150 mg/dL. Borderline-high levels range from 150 to 199 mg/dL, high levels range from 200 to 499 mg/dL, and very high levels are 500 mg/dL or higher.

Elevated triglycerides can be caused by various factors such as obesity, physical inactivity, excessive alcohol consumption, smoking, and certain medical conditions like diabetes, hypothyroidism, and kidney disease. Medications such as beta-blockers, steroids, and diuretics can also raise triglyceride levels.

Lifestyle changes such as losing weight, exercising regularly, eating a healthy diet low in saturated and trans fats, avoiding excessive alcohol consumption, and quitting smoking can help lower triglyceride levels. In some cases, medication may be necessary to reduce triglycerides to recommended levels.

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  • Gemfibrozil, sold under the brand name Lopid among others, is a medication used to treat abnormal blood lipid levels. (wikipedia.org)
  • Serum lipids, plasma fibrinogen, whole blood viscosity, plasma viscosity, red cell aggregability and red cell deformability were measured on two baseline samples, separated by 2 weeks of treatment with placebo, and compared with the results obtained after 12 weeks of gemfibrozil (Lopid) 600mg b.d. (iospress.com)
  • It is best not to drink alcohol if you are taking gemfibrozil (Lopid). (camomienoteca.com)
  • Drinking alcohol while taking gemfibrozil (Lopid) can increase your risk of liver problems. (camomienoteca.com)
  • Alcohol can also make gemfibrozil (Lopid) less effective in lowering triglycerides and preventing inflammation of the pancreas. (camomienoteca.com)
  • Lopid is contraindicated in individuals with allergic reaction to gemfibrozil, liver disease, gallbladder disease, severe kidney disease, or when co-administered with repaglinide (Prandin). (buyviagraonliney.com)
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  • Gemfibrozil is contained in the pill Lopid . (allstatins.com)
  • Lopid contains an active ingredient called Gemfibrozil which belongs to a class of drugs called fibrates. (sanfordpharmacy.com)
  • Remember some medicines prevents the full absorption of Lopid as they react with Gemfibrozil . (sanfordpharmacy.com)
  • What is Lopid (Gemfibrozil) prescribed for? (mydrugcenter.com)
  • Generic Lopid ( GEMFIBROZIL ) is a lipid-regulating agent used to lower cholesterol and triglyceride levels in your blood. (rx2go.com)
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  • citation needed] Statin drugs: Concomitant administration of fibrates (including gemfibrozil) with statin drugs increases the risk of muscle cramping, myopathy, and rhabdomyolysis. (wikipedia.org)
  • Gemfibrozil is in a class of lipid-regulating medications called fibrates. (medlineplus.gov)
  • Gemfibrozil belongs to a group of drugs known as fibrates. (familywize.org)
  • Ecotoxicological studies are extensive for gemfibrozil and scarce for other fibrates. (janusinfo.se)
  • Comparative assessment of environmental risk when using the fibrates bezafibrate, fenofibrate and gemfibrozil from a Swedish perspective. (janusinfo.se)
  • Gemfibrozil is a lipid lowering fibrates which increase the low density lipoprotein - cholesterol uptake by the low density lipoprotein - cholesterol receptors. (kembara.co)
  • Gemfibrozil belongs to a class of medicines called fibrates. (mydr.com.au)
  • Fibric acid antilipemic agent that lowers LDL cholesterol more effectively than do older fibrates (ie, clofibrate, gemfibrozil). (medscape.com)
  • Gemfibrozil is used with diet changes (restriction of cholesterol and fat intake) to reduce the amount of cholesterol and triglycerides (other fatty substances) in the blood in certain people with very high triglycerides who are at risk of pancreatic disease (conditions affecting the pancreas, a gland that produces fluid to break down food and hormones to control blood sugar). (medlineplus.gov)
  • Gemfibrozil controls high triglycerides and low HDL, but does not cure them. (medlineplus.gov)
  • Gemfibrozil is a lipid regulating agent which decreases serum triglycerides and very low density lipoprotein (VLDL) cholesterol, and increases high density lipoprotein (HDL) cholesterol. (nih.gov)
  • While modest decreases in total and low density lipoprotein (LDL) cholesterol may be observed with gemfibrozil therapy, treatment of patients with elevated triglycerides due to Type IV hyperlipoproteinemia often results in a rise in LDL-cholesterol. (nih.gov)
  • In the primary prevention component of the Helsinki Heart Study, in which 4081 male patients between the ages of 40 and 55 were studied in a randomized, double-blind, placebo-controlled fashion, gemfibrozil therapy was associated with significant reductions in total plasma triglycerides and a significant increase in high density lipoprotein cholesterol. (nih.gov)
  • This subgroup of Type IIb gemfibrozil group patients had a lower mean HDL-cholesterol level at baseline than the Type IIa subgroup that had elevations of LDL-cholesterol and normal plasma triglycerides. (nih.gov)
  • Gemfibrozil is useful in treating patient with low high density lipoprotein, mixed cases of dyslipidemia ( increase in both plasma triglycerides and increase in cholesterol) and prevention of atheroma. (kembara.co)
  • Gemfibrozil works by blocking the absorption of triglycerides from the intestines and increasing the breakdown of fats in the liver. (overnight-us.net)
  • Gemfibrozil is a medication used in the treatment of high levels of cholesterol and triglycerides in the blood. (overnight-us.net)
  • Gemfibrozil works by inhibiting the synthesis of triglycerides in the liver, which reduces the amount of triglycerides in the blood. (overnight-us.net)
  • Aside from reducing cholesterol levels and managing high triglycerides, gemfibrozil can also be used to help lower elevated aminotransferase, an enzyme that otherwise increases the risk of liver problems. (overnight-us.net)
  • We have investigated the rheological effects of gemfibrozil in 50 patients with angiographically documented but stable peripheral occlusive arterial disease. (iospress.com)
  • The net effects of gemfibrozil were to increase mean plasma viscosity, reduce red cell deformability and aggregation and leave native whole blood viscosity unchanged. (iospress.com)
  • The gemfibrozil-statin interaction was studied at the level of active hepatic uptake as a model for such drug-drug interactions. (aspetjournals.org)
  • Gemfibrozil should be avoided to be used with statin as it may lead to severe myositis. (kembara.co)
  • Risk of rhabdomyolysis (muscle injury) increases when gemfibrozil is used with the statin family of cholesterol-reducing medications: pravastatin (Pravachol), lovastatin (Mevacor), rosuvastatin (Crestor), simvastatin (Zocor), fluvastatin (Lescol), and atorvastatin (Lipitor). (buyviagraonliney.com)
  • Gemfibrozil is pill of type Not a Statin while Lipitor is of Statin type. (allstatins.com)
  • Gemfibrozil increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis. (wikipedia.org)
  • Gemfibrozil is a prescription medicine used to treat high cholesterol and triglyceride levels in adults. (overnight-us.net)
  • As a result, gemfibrozil is a valuable treatment option for those seeking to maintain healthy cholesterol and triglyceride levels, as well as improve overall cardiovascular health. (overnight-us.net)
  • The exact way that gemfibrozil works is unclear, however, it is thought to reduce the amount of triglyceride made in the body. (mydr.com.au)
  • The use of bezafibrate, fenofibrate and gemfibrozil is not considered to pose an environmental risk. (janusinfo.se)
  • if you are taking colestipol (Colestid), take this medication 2 hours before or 2 hours after gemfibrozil. (medlineplus.gov)
  • without knowledge of their own lipid values or double-blind treatment, 60% of patients originally randomized to placebo began therapy with gemfibrozil and 60% of patients originally randomized to gemfibrozil continued medication. (nih.gov)
  • As a long term medication, it is important to lower gemfibrozil cost whenever possible. (familywize.org)
  • Because Gemfibrozil carries a strong risk of interactions with other medications, keep your doctor informed of any changes to your medication schedule. (familywize.org)
  • Pricing is displayed for GEMFIBROZIL , a generic medication. (americaspharmacy.com)
  • Gemfibrozil (GFZ) is a medication of the fibrate category with agonistic effects on PPAR-α and is effective for hypertriglyceridemia and mixed dyslipidemia. (rapamycin.news)
  • Take gemfibrozil at around the same times every day. (medlineplus.gov)
  • Take gemfibrozil exactly as directed. (medlineplus.gov)
  • Continue to take gemfibrozil even if you feel well. (medlineplus.gov)
  • Your doctor will probably tell you not to take gemfibrozil while taking any of these medications. (medlineplus.gov)
  • Your doctor may tell you not to take gemfibrozil. (medlineplus.gov)
  • How do I take Gemfibrozil? (familywize.org)
  • For optimal efficacy, try to take Gemfibrozil at the same time every day. (familywize.org)
  • Do not take Gemfibrozil if you have a history of liver or gall bladder failure. (familywize.org)
  • It is also not known how Gemfibrozil affects unborn fetuses or whether it is transferred into breast milk, so do not take Gemfibrozil if you are pregnant or nursing. (familywize.org)
  • What happens if I take gemfibrozil after I eat? (camomienoteca.com)
  • It is best to take gemfibrozil with the same meals each day, as this helps remind you to take your doses regularly. (camomienoteca.com)
  • In case, you take certain other medications to lower cholesterol like colestipol then take Gemfibrozil 1 hour before. (sanfordpharmacy.com)
  • Hyperlipidemia (Type III) Hypertriglyceridemia (Type IV): Gemfibrozil, though not as effective as niacin (nicotinic acid, a form of Vitamin B3), is better tolerated. (wikipedia.org)
  • Gemfibrozil is used as a therapeutic drug for hyperlipidemia. (phypha.ir)
  • The melting point is 58° - 61°C. Gemfibrozil is a white solid which is stable under ordinary conditions. (nih.gov)
  • The melting point is 58° to 61°C. Gemfibrozil USP is a white or almost white, waxy crystalline solid. (nih.gov)
  • Gemfibrozil increases levels of high density lipoprotein (HDL) subfractions HDL 2 and HDL 3 , as well as apolipoproteins AI and AII. (nih.gov)
  • Moderate reductions in total plasma cholesterol and low density lipoprotein cholesterol were observed for the gemfibrozil treatment group as a whole, but the lipid response was heterogeneous, especially among different Fredrickson types. (nih.gov)
  • Generally gemfibrozil may lead to slight increase in the high density lipoprotein, moderate decrease in low density lipoprotein with marked decreased in plasma very low density lipoprotein. (kembara.co)
  • Typically, when combined with other drugs, such as gemfibrozil, niacin can help to lower levels of harmful low-density lipoprotein (LDL) cholesterol in the blood while raising levels of beneficial high-density lipoprotein (HDL) cholesterol. (overnight-us.net)
  • Gemfibrozil is known to cause allergic reaction in some patients, so contact your doctor immediately if you experience hives, difficulty breathing, or swelling of your face, lips, tongues, or throat. (familywize.org)
  • Gemfibrozil also inhibits the synthesis and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. (wikipedia.org)
  • the mechanism of action is unknown, but gemfibrozil may inhibit lipolysis, the secretion of VLDL, and hepatic fatty acid uptake. (medscape.com)
  • Gemfibrozil will increase the transcription of the gene encoding for the apoprotein apoA1 and apoprotein apoA5 as well as for the lipoprotein lipase. (kembara.co)
  • Gemfibrozil is the generic name for an oral drug used to lower lipid levels. (curecrowd.com)
  • Gemfibrozil comes as a tablet to take by mouth. (medlineplus.gov)
  • Each tablet contains 600 mg gemfibrozil. (nih.gov)
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  • tell your doctor and pharmacist if you are allergic to gemfibrozil, any other medications, or any of the ingredients in gemfibrozil tablets. (medlineplus.gov)
  • Lipazil tablets contain gemfibrozil. (mydr.com.au)
  • In contrast, adding fulvestrant, an Estradiol receptor antagonist, prevents the impact of gemfibrozil on oxidative stress condition, reducing its efficacy to protect the neurons against stress. (phypha.ir)
  • Individuals taking Gemfibrozil or any other prescription medications should talk to their doctors before taking niacin. (overnight-us.net)
  • Gemfibrozil is administered orally, generally taken twice a day. (familywize.org)
  • Gemfibrozil is given orally and gemfibrozil will be excreted via the kidney by metabolizing to glucuronide conjugates. (kembara.co)
  • Lipazil or any other medicine containing gemfibrozil(e.g. (mydr.com.au)
  • Gemfibrozil inhibits the activation of the liver's Cytochrome P450 system and CYP2C8, reducing hepatic metabolism of many drugs, and prolonging their half lives and duration of action. (wikipedia.org)
  • Ensimismados en sus grandezas pasadas, confortados por su valioso patrimonio cultural y lingico, nunca pensaron que el inglacabarborrando al francdel mapa (efectos adversos del gemfibrozilo). (granodesal.com)
  • Gemfibrozil increases HDL subfractions HDL2 and HDL3 as well as apolipoproteins A-I and A-II. (curehunter.com)
  • Gemfibrozil may cause side effects. (medlineplus.gov)
  • What are the possible side effects of taking Gemfibrozil? (familywize.org)
  • Military blue" white-blue colorreplica is a many attention This kind of color can be customized inside (gemfibrozil 300 mg side effects). (granodesal.com)
  • Gemfibrozil Protects Dopaminergic Neurons in a Mouse Model of Parkinson's. (rapamycin.news)
  • If you become pregnant while taking gemfibrozil, call your doctor. (medlineplus.gov)
  • It cannot be excluded that gemfibrozil is persistent, due to the lack of data. (janusinfo.se)
  • Gemfibrozil (GFZ) is a relatively persistent pollutant in surface-water environments and it is rather recalcitrant to biological degradation. (unito.it)
  • Gemfibrozil, used for elevated cholesterol, also is reported to cause memory disorders, as are the more commonly used class of cholesterol drugs, the statins. (camomienoteca.com)
  • Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 μM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 μM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). (aspetjournals.org)
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  • Additionally, gemfibrozil increases levels of HDL ("good") cholesterol in the body, thus further reducing the risk of cardiovascular disease. (overnight-us.net)
  • Results: In gemfibrozil pretreated groups, reduced level of caspase-3 and raised mitochondrial transcription factor A (TFAM) levels were detected. (phypha.ir)
  • Conclusion: Our results indicated the involvement of estradiol receptors in gemfibrozil neuroprotective mechanism, in diminishing oxidative stress-induced damage via reducing caspase-3 and inducing the level of TFAM that plays a crucial role in the mitochondrial biogenesis. (phypha.ir)
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