A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
Substances used to lower plasma CHOLESTEROL levels.
A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
Azetidines are saturated, organic compounds containing a 4-membered ring with two carbon atoms and two nitrogen atoms (one as a secondary amine), which can be found in certain pharmaceuticals and natural substances, although they are less common than other cyclic amines.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
7-carbon saturated monocarboxylic acids.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).
Mevalonic acid is a crucial intermediate compound in the HMG-CoA reductase pathway, which is a metabolic route that produces cholesterol, other steroids, and isoprenoids in cells.
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
'Fluorobenzenes' are aromatic hydrocarbons consisting of a benzene ring substituted with one or more fluorine atoms, characterized by the presence of the highly electronegative fluorine atom(s) that influence the compound's chemical reactivity and physical properties.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
Phosphoric or pyrophosphoric acid esters of polyisoprenoids.
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.
Therapy with two or more separate preparations given for a combined effect.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/1310)

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.  (+info)

Involvement of tyrosine phosphorylation in HMG-CoA reductase inhibitor-induced cell death in L6 myoblasts. (2/1310)

Our previous studies have shown that the HMG-CoA reductase (HCR) inhibitor (HCRI), simvastatin, causes myopathy in rabbits and kills L6 myoblasts. The present study was designed to elucidate the molecular mechanism of HCRI-induced cell death. We have demonstrated that simvastatin induces the tyrosine phosphorylation of several cellular proteins within 10 min. These phosphorylations were followed by apoptosis, as evidenced by the occurrence of internucleosomal DNA fragmentation and by morphological changes detected with Nomarski optics. Simvastatin-induced cell death was prevented by tyrosine kinase inhibitors. The MTT assay revealed that the addition of mevalonic acid into the culture medium partially inhibited simvastatin-induced cell death. Thus, these results suggested that protein tyrosine phosphorylation might play an important role in the intracellular signal transduction pathway mediating the HCRI-induced death of myoblasts.  (+info)

In vitro effects of simvastatin on tubulointerstitial cells in a human model of cyclosporin nephrotoxicity. (3/1310)

To investigate the possibility that 3-hydroxy-3-methylglutaryl CoA (HMGCoA) reductase inhibitors ameliorate renal disease via direct effects on the tubulointerstitium, primary cultures of human proximal tubule cells (PTC) and renal cortical fibroblasts (CF) were exposed for 24 h to simvastatin (0.1-10 micromol/l) under basal conditions and in the presence of 1,000 ng/ml of cyclosporin (CsA), which we have previously shown to promote in vitro interstitial matrix accumulation at least partially via activation of local cytokine networks. Simvastatin, in micromolar concentrations, engendered cholesterol-independent inhibition of CF and PTC thymidine incorporation and cholesterol-dependent suppression of PTC apical Na+/H+ exchange (NHE) (ethylisopropylamiloride-sensitive apical 22Na+ uptake). Similarly, CF secretion of insulin-like growth factor-I (IGF-I) and IGF binding protein-3 were depressed, whereas CF collagen synthesis ([3H]proline incorporation) and PTC secretion of the fibrogenic cytokines, transforming growth factor-beta1, and platelet-derived growth factor were unaffected. A lower concentration (0.1 micromol/l) of simvastatin did not affect any of the above parameters under basal conditions but completely prevented CsA-stimulated CF collagen synthesis (control, 6.6 +/- 0.6; CsA, 8.3 +/- 0.6; CsA+simvastatin, 6.2 +/- 0.5%; P < 0.05) and IGF-I secretion (89.5 +/- 16.6, 204.7 +/- 57.0, and 94.6 +/- 22.3 ng. mg protein-1. day-1, respectively; P < 0.05). The results suggest that simvastatin exerts direct cholesterol-dependent and -independent effects on the human kidney tubulointerstitium. HMGCoA reductase inhibitors may ameliorate interstitial fibrosis complicating CsA therapy via direct actions on human renal cortical fibroblasts.  (+info)

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). (4/1310)

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)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (5/1310)

Our understanding of the factors that regulate the secretion of apoB100 lipoproteins remains incomplete with considerable debate as to the role, if any, for cholesterol ester in this process. This study examines this issue in primary cultures of hamster hepatocytes, a species in which both cholesterol and apoB100 metabolism are very similar to man. Addition of oleate to medium increased the mass of triglyceride and cholesterol ester within the hepatocyte and also increased the secretion of triglycerides, cholesterol ester, and apoB100 into the medium. Next, the responses of hamster hepatocytes to addition of either an HMG-CoA reductase inhibitor (lovastatin) or an acyl-CoA cholesterol acyltransferase inhibitor (58-035) to the medium, with or without added oleate, were determined. Effects of either agent were only evident in the oleate-supplemented medium in which cholesterol ester mass had been increased above basal. If oleate was not added to the medium, neither agent reduced apoB100 secretion; equally important, over the 24-hour incubation, neither agent, at the concentration used, produced any detectable change in intracellular cholesterol ester mass. However, in contrast to the estimates of mass, which were unchanged, under the same conditions radioisotopic estimates of cholesterol ester synthesis were markedly reduced. Any conclusion as to the relation of cholesterol ester mass to apoB100 secretion would therefore depend on which of the 2 methods was used. Overall, the data indicate a close correlation between the mass of cholesterol ester within the hepatocyte and apoB100 secretion from it and they go far to explain previous apparently contradictory data as to this relation. More importantly, though, taken with other available data, they indicate that the primary response of the liver to increased delivery of lipid is increased secretion rather than decreased uptake. These results point, therefore, to a hierarchy of hepatic responses to increased flux of fatty acids and increased synthesis of cholesterol that in turn suggests a more dynamic model of cholesterol homeostasis in the liver than has been appreciated in the past.  (+info)

Effect of long term simvastatin administration as an adjunct to ursodeoxycholic acid: evidence for a synergistic effect on biliary bile acid composition but not on serum lipids in humans. (6/1310)

BACKGROUND: Stimulated bile acid synthesis preferentially utilises newly synthesised cholesterol, raising the possibility that combination of simvastatin (an inhibitor of cholesterol synthesis) with ursodeoxycholic acid (UDCA; a stimulator of bile acid synthesis) may result in reduced bile acid synthesis and greater enrichment of the pool with UDCA than that achieved with UDCA treatment alone. AIMS: To investigate the effect of simvastatin and UDCA given alone and in combination on serum and biliary lipid and biliary bile acid composition. METHODS: Eighteen patients with primary non-familial hypercholesterolaemia were studied during treatment with simvastatin 20 mg/day, UDCA 10 mg/kg/day, and a combination of the two drugs. Each regimen was given in random order for three months following a three month lead in period. RESULTS: Simvastatin significantly reduced serum low density lipoprotein (LDL) cholesterol but biliary cholesterol concentration remained unchanged. Combination of the two drugs had no synergistic effect on serum cholesterol concentration, but significantly increased the proportion of UDCA in the bile acid pool from 35% during UDCA to 48% during combination treatment (p<0.04). CONCLUSIONS: Results showed that: (1) simvastatin reduces serum LDL cholesterol but has no effect on biliary cholesterol concentration, supporting the concept that newly synthesised cholesterol is not the preferential source for biliary cholesterol; and (2) combination of simvastatin with UDCA has the predicted effect of enhancing the proportion of UDCA in the pool. This effect may be of benefit in the treatment of cholestatic liver diseases.  (+info)

Role of tyrosine phosphorylation of phospholipase C gamma1 in the signaling pathway of HMG-CoA reductase inhibitor-induced cell death of L6 myoblasts. (7/1310)

Our previous studies have shown that the HMG-CoA reductase (HCR) inhibitor (HCRI), simvastatin, kills L6 myoblasts by involving Ca2+ mobilization from the Ca2+ pool in the cells but not by influx from extracellular space. More recently, we found that HCRI induced tyrosine phosphorylation of several cellular proteins, followed by apoptotic cell death of L6 myoblasts. The present study was aimed to elucidate the molecular target(s) of these tyrosine phosphorylations induced by HCRI and demonstrated that simvastatin induces tyrosine phosphorylation of phospholipase C (PLC) gamma1. This tyrosine phosphorylation of PLC-gamma1 caused the increment of the intracellular inositol triphosphate (IP3) levels in L6 myoblasts. Pretreatment of the cells with herbimycin A, a specific inhibitor of protein tyrosine kinase, inhibited a simvastatin-induced increase in IP3 level in the cells as well as tyrosine phosphorylation of PLC-gamma1. Interestingly, pretreatment of the cells with U-73122, a specific inhibitor of PLC, prevented simvastatin-induced cell death. Thus, these results strongly suggest that simvastatin-induced tyrosine phosphorylation of PLC-gamma1 plays, at least in part, an important role for the development of simvastatin-induced cell death.  (+info)

Inhibition of thrombin generation by simvastatin and lack of additive effects of aspirin in patients with marked hypercholesterolemia. (8/1310)

OBJECTIVES: To assess the effects of aspirin compared with simvastatin on thrombin generation in hypercholesterolemic men, and to establish whether the reduction of elevated blood cholesterol by simvastatin would affect the action of aspirin on thrombin formation. BACKGROUND: Aspirin inhibits thrombin formation, but its performance is blunted in hypercholesterolemia. By virtue of altering lipid profile, statins could be expected to influence thrombin generation. METHODS: Thirty-three men, aged 34 to 61 years, with minimal or no clinical symptoms, serum total cholesterol >6.5 mmol/liter and serum triglycerides <4.6 mmol/liter, completed the study consisting of three treatment phases. First, they received 300 mg of aspirin daily for two weeks (phase I), which was then replaced by simvastatin at the average dose of 24 mg/d for three months (phase II). In phase III, aspirin, 300 mg/day, was added for two weeks to simvastatin, the dose of which remained unchanged. Thrombin generation was assessed: 1) in vivo, by measuring levels of fibrinopeptide A (FPA) and prothrombin fragment 1+2 (F1+2) in venous blood; and 2) ex vivo, by monitoring the rates of increase of FPA and F1+2 in blood emerging from standardized skin incisions of a forearm. A mathematical model was used to describe the kinetics of thrombin formation at the site of microvascular injury. RESULTS: Two-week treatment with aspirin had no effect on thrombin markers in vivo, while ex vivo it depressed the total amount of thrombin formed, though not the reaction rate. After simvastatin treatment, serum cholesterol decreased by 31% and LDL cholesterol by 42%, while thrombin generation became markedly depressed. In venous blood, FPA was significantly reduced. Concomitantly, the initial thrombin concentration and total amount of thrombin generated decreased significantly. Addition of aspirin to simvastatin (phase III) had no further effect on any of these parameters. CONCLUSIONS: In men with hypercholesterolemia, lowering serum cholesterol level by a three-month simvastatin treatment is accompanied by a marked reduction of thrombin generation both at basal conditions in venous blood and after activation of hemostasis by microvascular injury. Once blood cholesterol became reduced, adding aspirin to simvastatin did not enhance dampening of thrombin formation.  (+info)

Simvastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. It works by inhibiting HMG-CoA reductase, an enzyme that plays a key role in the production of cholesterol in the body. By reducing the amount of cholesterol produced by the liver, simvastatin helps to lower the levels of LDL (low-density lipoprotein) or "bad" cholesterol and triglycerides in the blood, while increasing HDL (high-density lipoprotein) or "good" cholesterol.

Simvastatin is used to prevent cardiovascular diseases such as heart attacks and strokes in individuals with high cholesterol levels, particularly those who have other risk factors such as diabetes, hypertension, or a history of smoking. It is available in various strengths and forms, and is typically taken orally once a day, usually in the evening.

Like all medications, simvastatin can cause side effects, ranging from mild to severe. Common side effects include headache, muscle pain, and gastrointestinal symptoms such as nausea, constipation, or diarrhea. Rare but serious side effects may include liver damage, muscle breakdown (rhabdomyolysis), and increased risk of diabetes. It is important to follow the dosage instructions carefully and inform your healthcare provider of any pre-existing medical conditions or medications you are taking, as these may affect the safety and efficacy of simvastatin.

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as statins, are a class of cholesterol-lowering medications. They work by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. By blocking this enzyme, the liver is stimulated to take up more low-density lipoprotein (LDL) cholesterol from the bloodstream, leading to a decrease in LDL cholesterol levels and a reduced risk of cardiovascular disease.

Examples of HMG-CoA reductase inhibitors include atorvastatin, simvastatin, pravastatin, rosuvastatin, and fluvastatin. These medications are commonly prescribed to individuals with high cholesterol levels, particularly those who are at risk for or have established cardiovascular disease.

It's important to note that while HMG-CoA reductase inhibitors can be effective in reducing LDL cholesterol levels and the risk of cardiovascular events, they should be used as part of a comprehensive approach to managing high cholesterol, which may also include lifestyle modifications such as dietary changes, exercise, and weight management.

Anticholesteremic agents are a class of medications that are used to lower the levels of cholesterol and other fats called lipids in the blood. These medications work by reducing the production of cholesterol in the body, increasing the removal of cholesterol from the bloodstream, or preventing the absorption of cholesterol in the digestive tract.

There are several types of anticholesteremic agents, including:

1. Statins: These medications work by blocking a liver enzyme that is necessary for the production of cholesterol. Examples of statins include atorvastatin, simvastatin, and rosuvastatin.
2. Bile acid sequestrants: These medications bind to bile acids in the digestive tract and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which in turn lowers cholesterol levels. Examples of bile acid sequestrants include cholestyramine and colesevelam.
3. Nicotinic acid: Also known as niacin, this medication works by reducing the production of very low-density lipoproteins (VLDL) in the liver, which are a major source of bad cholesterol.
4. Fibrates: These medications work by increasing the removal of cholesterol from the bloodstream and reducing the production of VLDL in the liver. Examples of fibrates include gemfibrozil and fenofibrate.
5. PCSK9 inhibitors: These are a newer class of medications that work by blocking the action of a protein called PCSK9, which helps regulate the amount of cholesterol in the blood. By blocking PCSK9, these medications increase the number of LDL receptors on the surface of liver cells, which leads to increased removal of LDL from the bloodstream.

Anticholesteremic agents are often prescribed for people who have high cholesterol levels and are at risk for heart disease or stroke. By lowering cholesterol levels, these medications can help reduce the risk of heart attack, stroke, and other cardiovascular events.

Lovastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. It works by inhibiting HMG-CoA reductase, an enzyme that plays a crucial role in the production of cholesterol in the body. By reducing the amount of cholesterol produced in the liver, lovastatin helps to decrease the levels of low-density lipoprotein (LDL) or "bad" cholesterol and triglycerides in the blood, while increasing the levels of high-density lipoprotein (HDL) or "good" cholesterol.

Lovastatin is available in both immediate-release and extended-release forms, and it is typically taken orally once or twice a day, depending on the dosage prescribed by a healthcare provider. Common side effects of lovastatin include headache, nausea, diarrhea, and muscle pain, although more serious side effects such as liver damage and muscle weakness are possible, particularly at higher doses.

It is important to note that lovastatin should not be taken by individuals with active liver disease or by those who are pregnant or breastfeeding. Additionally, it may interact with certain other medications, so it is essential to inform a healthcare provider of all medications being taken before starting lovastatin therapy.

Azetidines are a class of organic compounds that contain a 4-membered saturated ring with two carbon atoms and two nitrogen atoms. The general structure of an azetidine is R-CH2-CH2-N-R', where R and R' can be hydrogen atoms or any other organic substituents.

Azetidines are relatively rare in nature, but they have attracted significant interest in the field of medicinal chemistry due to their unique structure and potential as building blocks for drug design. Some azetidine-containing compounds have been developed as drugs for various therapeutic indications, such as antibiotics, antivirals, and anti-inflammatory agents.

It's worth noting that the term 'azetidines' can also refer to the class of pharmaceutical compounds that contain an azetidine ring in their structure.

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.

Heptanoic acid, also known as enanthic acid, is an organic compound with the formula CH3(CH2)5COOH. It is a fatty acid with a 7-carbon chain, and it is a colorless liquid that is slightly soluble in water and fully miscible with ether and ethanol.

Heptanoic acid is not typically considered a medical term, as it is not a substance that is directly related to human health or disease. However, like other fatty acids, heptanoic acid can be metabolized in the body for energy and used in various physiological processes. Abnormal levels of certain fatty acids, including heptanoic acid, may be associated with various medical conditions, such as metabolic disorders or genetic diseases that affect fatty acid metabolism.

It's important to note that Heptanoic Acid is not a common term in medicine, and it's more related to chemistry and biochemistry fields.

Hypercholesterolemia is a medical term that describes a condition characterized by high levels of cholesterol in the blood. Specifically, it refers to an abnormally elevated level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, which can contribute to the development of fatty deposits in the arteries called plaques. Over time, these plaques can narrow and harden the arteries, leading to atherosclerosis, a condition that increases the risk of heart disease, stroke, and other cardiovascular complications.

Hypercholesterolemia can be caused by various factors, including genetics, lifestyle choices, and underlying medical conditions. In some cases, it may not cause any symptoms until serious complications arise. Therefore, regular cholesterol screening is essential for early detection and management of hypercholesterolemia. Treatment typically involves lifestyle modifications, such as a healthy diet, regular exercise, and weight management, along with medication if necessary.

Pravastatin is a medication that belongs to a class of drugs called statins, which are used to lower cholesterol levels in the blood. Specifically, pravastatin works by inhibiting HMG-CoA reductase, an enzyme involved in the production of cholesterol in the liver. By reducing the amount of cholesterol produced, pravastatin helps to decrease the levels of low-density lipoprotein (LDL) or "bad" cholesterol and increase the levels of high-density lipoprotein (HDL) or "good" cholesterol in the blood.

Pravastatin is used to prevent cardiovascular diseases such as heart attacks and strokes, particularly in people with high cholesterol levels, diabetes, or other risk factors for heart disease. It is available in tablet form and is typically taken once daily. As with any medication, pravastatin should be taken under the supervision of a healthcare provider, who will determine the appropriate dosage based on the individual's medical history and current health status.

Mevalonic acid is not a term that is typically used in medical definitions, but rather it is a biochemical concept. Mevalonic acid is a key intermediate in the biosynthetic pathway for cholesterol and other isoprenoids. It is formed from 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) by the enzyme HMG-CoA reductase, which is the target of cholesterol-lowering drugs known as statins.

In a medical context, mevalonic acid may be mentioned in relation to certain rare genetic disorders, such as mevalonate kinase deficiency (MKD) or hyperimmunoglobulinemia D and periodic fever syndrome (HIDS), which are caused by mutations in the gene encoding mevalonate kinase, an enzyme involved in the metabolism of mevalonic acid. These conditions can cause recurrent fevers, rashes, joint pain, and other symptoms.

"Pyrroles" is not a medical term in and of itself, but "pyrrole" is an organic compound that contains one nitrogen atom and four carbon atoms in a ring structure. In the context of human health, "pyrroles" often refers to a group of compounds called pyrrol derivatives or pyrrole metabolites.

In clinical settings, "pyrroles" is sometimes used to refer to a urinary metabolite called "pyrrole-protein conjugate," which contains a pyrrole ring and is excreted in the urine. Elevated levels of this compound have been associated with certain psychiatric and behavioral disorders, such as schizophrenia and mood disorders. However, the relationship between pyrroles and these conditions is not well understood, and more research is needed to establish a clear medical definition or diagnostic criteria for "pyrrole disorder" or "pyroluria."

Fluorobenzenes are a group of organic compounds that consist of a benzene ring (a cyclic structure with six carbon atoms in a hexagonal arrangement) substituted with one or more fluorine atoms. The general chemical formula for a fluorobenzene is C6H5F, but this can vary depending on the number of fluorine atoms present in the molecule.

Fluorobenzenes are relatively stable and non-reactive compounds due to the strong carbon-fluorine bond. They are used as starting materials in the synthesis of various pharmaceuticals, agrochemicals, and other specialty chemicals. Some fluorobenzenes also have potential applications as refrigerants, fire extinguishing agents, and solvents.

It is worth noting that while fluorobenzenes themselves are not considered to be particularly hazardous, some of their derivatives can be toxic or environmentally harmful, so they must be handled with care during production and use.

LDL, or low-density lipoprotein, is often referred to as "bad" cholesterol. It is one of the lipoproteins that helps carry cholesterol throughout your body. High levels of LDL cholesterol can lead to a buildup of cholesterol in your arteries, which can increase the risk of heart disease and stroke.

Cholesterol is a type of fat (lipid) that is found in the cells of your body. Your body needs some cholesterol to function properly, but having too much can lead to health problems. LDL cholesterol is one of the two main types of cholesterol; the other is high-density lipoprotein (HDL), or "good" cholesterol.

It's important to keep your LDL cholesterol levels in a healthy range to reduce your risk of developing heart disease and stroke. A healthcare professional can help you determine what your target LDL cholesterol level should be based on your individual health status and risk factors.

Cholesterol is a type of lipid (fat) molecule that is an essential component of cell membranes and is also used to make certain hormones and vitamins in the body. It is produced by the liver and is also obtained from animal-derived foods such as meat, dairy products, and eggs.

Cholesterol does not mix with blood, so it is transported through the bloodstream by lipoproteins, which are particles made up of both lipids and proteins. There are two main types of lipoproteins that carry cholesterol: low-density lipoproteins (LDL), also known as "bad" cholesterol, and high-density lipoproteins (HDL), also known as "good" cholesterol.

High levels of LDL cholesterol in the blood can lead to a buildup of cholesterol in the walls of the arteries, increasing the risk of heart disease and stroke. On the other hand, high levels of HDL cholesterol are associated with a lower risk of these conditions because HDL helps remove LDL cholesterol from the bloodstream and transport it back to the liver for disposal.

It is important to maintain healthy levels of cholesterol through a balanced diet, regular exercise, and sometimes medication if necessary. Regular screening is also recommended to monitor cholesterol levels and prevent health complications.

Polyisoprenyl phosphates are a type of organic compound that play a crucial role in the biosynthesis of various essential biomolecules in cells. They are formed by the addition of isoprene units, which are five-carbon molecules with a branched structure, to a phosphate group.

In medical terms, polyisoprenyl phosphates are primarily known for their role as intermediates in the biosynthesis of dolichols and farnesylated proteins. Dolichols are long-chain isoprenoids that function as lipid carriers in the synthesis of glycoproteins, which are proteins that contain carbohydrate groups attached to them. Farnesylated proteins, on the other hand, are proteins that have been modified with a farnesyl group, which is a 15-carbon isoprenoid. This modification plays a role in the localization and function of certain proteins within the cell.

Abnormalities in the biosynthesis of polyisoprenyl phosphates and their downstream products have been implicated in various diseases, including cancer, neurological disorders, and genetic syndromes. Therefore, understanding the biology and regulation of these compounds is an active area of research with potential therapeutic implications.

Lipids are a broad group of organic compounds that are insoluble in water but soluble in nonpolar organic solvents. They include fats, waxes, sterols, fat-soluble vitamins (such as vitamins A, D, E, and K), monoglycerides, diglycerides, triglycerides, and phospholipids. Lipids serve many important functions in the body, including energy storage, acting as structural components of cell membranes, and serving as signaling molecules. High levels of certain lipids, particularly cholesterol and triglycerides, in the blood are associated with an increased risk of cardiovascular disease.

Niacin, also known as vitamin B3 or nicotinic acid, is a water-soluble vitamin that is essential for human health. It is a crucial component of the coenzymes NAD (nicotinamide adenine dinucleotide) and NADP (nicotinamide adenine dinucleotide phosphate), which play key roles in energy production, DNA repair, and cellular signaling.

Niacin can be obtained from various dietary sources, including meat, poultry, fish, legumes, whole grains, and fortified foods. It is also available as a dietary supplement and prescription medication. Niacin deficiency can lead to a condition called pellagra, which is characterized by symptoms such as diarrhea, dermatitis, dementia, and, if left untreated, death.

In addition to its role in energy metabolism and DNA repair, niacin has been shown to have potential benefits for cardiovascular health, including lowering LDL (low-density lipoprotein) cholesterol and triglyceride levels while raising HDL (high-density lipoprotein) cholesterol levels. However, high-dose niacin therapy can also have adverse effects, such as flushing, itching, and liver toxicity, so it should be used under the guidance of a healthcare professional.

Rhabdomyolysis is a medical condition characterized by the breakdown and degeneration of skeletal muscle fibers, leading to the release of their intracellular contents into the bloodstream. This can result in various complications, including electrolyte imbalances, kidney injury or failure, and potentially life-threatening conditions if not promptly diagnosed and treated.

The process of rhabdomyolysis typically involves three key components:

1. Muscle injury: Direct trauma, excessive exertion, prolonged immobilization, infections, metabolic disorders, toxins, or medications can cause muscle damage, leading to the release of intracellular components into the bloodstream.
2. Release of muscle contents: When muscle fibers break down, they release various substances, such as myoglobin, creatine kinase (CK), lactate dehydrogenase (LDH), aldolase, and potassium ions. Myoglobin is a protein that can cause kidney damage when present in high concentrations in the bloodstream, particularly when it is filtered through the kidneys and deposits in the renal tubules.
3. Systemic effects: The release of muscle contents into the bloodstream can lead to various systemic complications, such as electrolyte imbalances (particularly hyperkalemia), acidosis, hypocalcemia, and kidney injury or failure due to myoglobin-induced tubular damage.

Symptoms of rhabdomyolysis can vary widely depending on the severity and extent of muscle damage but may include muscle pain, weakness, swelling, stiffness, dark urine, and tea-colored or cola-colored urine due to myoglobinuria. In severe cases, patients may experience symptoms related to kidney failure, such as nausea, vomiting, fatigue, and decreased urine output.

Diagnosis of rhabdomyolysis typically involves measuring blood levels of muscle enzymes (such as CK and LDH) and evaluating renal function through blood tests and urinalysis. Treatment generally focuses on addressing the underlying cause of muscle damage, maintaining fluid balance, correcting electrolyte imbalances, and preventing or managing kidney injury.

Combination drug therapy is a treatment approach that involves the use of multiple medications with different mechanisms of action to achieve better therapeutic outcomes. This approach is often used in the management of complex medical conditions such as cancer, HIV/AIDS, and cardiovascular diseases. The goal of combination drug therapy is to improve efficacy, reduce the risk of drug resistance, decrease the likelihood of adverse effects, and enhance the overall quality of life for patients.

In combining drugs, healthcare providers aim to target various pathways involved in the disease process, which may help to:

1. Increase the effectiveness of treatment by attacking the disease from multiple angles.
2. Decrease the dosage of individual medications, reducing the risk and severity of side effects.
3. Slow down or prevent the development of drug resistance, a common problem in chronic diseases like HIV/AIDS and cancer.
4. Improve patient compliance by simplifying dosing schedules and reducing pill burden.

Examples of combination drug therapy include:

1. Antiretroviral therapy (ART) for HIV treatment, which typically involves three or more drugs from different classes to suppress viral replication and prevent the development of drug resistance.
2. Chemotherapy regimens for cancer treatment, where multiple cytotoxic agents are used to target various stages of the cell cycle and reduce the likelihood of tumor cells developing resistance.
3. Cardiovascular disease management, which may involve combining medications such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, and statins to control blood pressure, heart rate, fluid balance, and cholesterol levels.
4. Treatment of tuberculosis, which often involves a combination of several antibiotics to target different aspects of the bacterial life cycle and prevent the development of drug-resistant strains.

When prescribing combination drug therapy, healthcare providers must carefully consider factors such as potential drug interactions, dosing schedules, adverse effects, and contraindications to ensure safe and effective treatment. Regular monitoring of patients is essential to assess treatment response, manage side effects, and adjust the treatment plan as needed.

The double-blind method is a study design commonly used in research, including clinical trials, to minimize bias and ensure the objectivity of results. In this approach, both the participants and the researchers are unaware of which group the participants are assigned to, whether it be the experimental group or the control group. This means that neither the participants nor the researchers know who is receiving a particular treatment or placebo, thus reducing the potential for bias in the evaluation of outcomes. The assignment of participants to groups is typically done by a third party not involved in the study, and the codes are only revealed after all data have been collected and analyzed.

... is contraindicated with pregnancy, breastfeeding, and liver disease. Pregnancy must be avoided while on simvastatin ... "Simvastatin - Drug Usage Statistics". ClinCalc. Retrieved 7 October 2022. Pedersen TR, Tobert JA (December 2004). "Simvastatin ... the patent for simvastatin had expired by 2004.[citation needed] Simvastatin was initially marketed by Merck & Co under the ... later to be named simvastatin). In 1994, publication of the results of the Scandinavian Simvastatin Survival Study (4S) ...
A follow-up of treatment with simvastatin for up to eight years was published in 2000. Ten years after the start of the 4S ... The Scandinavian Simvastatin Survival Study (also known as the 4S study), was a multicentre, randomized, double-blind, placebo- ... After 5.4 years, compared to the group that were given placebo, the simvastatin group demonstrated a 35% reduction in LDL-C and ... The objective of the study was to assess the effect of a cholesterol-lowering drug called simvastatin on mortality and ...
... simvastatin acid, it was significantly higher (~60%). Thus, the increased bioavailability of active simvastatin acid ... However, for simvastatin the point estimate of Cmax, AUC0-t and AUC0-∞ for Ln-transformed data were significantly lower (~25%) ... Three of the groups of 200 received only aspirin, simvastatin or thiazide respectively; Three groups received two of the three ... Polycap combines 100 milligrams of aspirin, with simvastatin (a generic version of Zocor, the cholesterol-lowering statin; 20 ...
Simvastatin and pravastatin appear to have a reduced incidence of side-effects. A comparison of simvastatin, pravastatin, and ... and simvastatin. Combination preparations of a statin and another agent, such as ezetimibe/simvastatin, are also available. The ... Researchers tested simvastatin, later sold by Merck as Zocor, on 4,444 patients with high cholesterol and heart disease. After ... Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE (July 2007). "Simvastatin is associated with a reduced incidence of dementia ...
... when simvastatin is used with amiodarone. This interaction is dose-dependent with simvastatin doses exceeding 20 mg. This drug ... "Information on Simvastatin/Amiodarone". Food and Drug Administration. Archived from the original on 21 September 2008. ... Ciclosporin Digoxin Flecainide Procainamide Quinidine Sildenafil Simvastatin Theophylline Warfarin In 2015, Gilead Sciences ... combination especially with higher doses of simvastatin should be avoided. Excretion is primarily via the liver and the bile ...
Flores NA (September 2004). "Ezetimibe + simvastatin (Merck/Schering-Plough)". Current Opinion in Investigational Drugs. 5 (9 ... and simvastatin (Zocor). Red yeast rice extract, one of the fungal sources from which the statins were discovered, contains ... Vytorin is drug that combines the use simvastatin and ezetimibe, which slows the formation of cholesterol by every cell in the ...
Statins (predominantly simvastatin) have been trialled in combination with fibrates to manage dyslipidemia in patients who also ... Scandinavian Simvastatin Survival Study Group (November 1994). "Randomised trial of cholesterol lowering in 4444 patients with ... June 2011). "The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease ( ... Early results comparing atorvastatin to simvastatin demonstrated that atorvastatin appeared more potent and with fewer side ...
"Metabolomics reveals amino acids contribute to variation in response to simvastatin treatment". PLOS ONE. 7 (7): e38386. doi: ... "Enteric Microbiome correlates with response to simvastatin treatment". PLOS ONE. 6 (10): e25482. doi:10.1371/journal.pone. ... "Lipidomics analysis of variation in response to simvastatin in the cholesterol and pharmacogenetics study". Metabolomics. 6 (2 ...
The combination niacin/simvastatin was approved by the FDA in 2008. Subsequently, large outcome trials using these niacin and ... "Drug Approval Package: Simcor (Niacin/Simvastatin) NDA #022078". U.S. Food and Drug Administration (FDA). 31 July 2008. ... "Drugs.com, Abbott Receives FDA Approval for Simcor (Niaspan / simvastatin), a Novel Combination Medicine for Comprehensive ... Extended release niacin was combined with lovastatin (Advicor), and with simvastatin (Simcor), as prescription drug ...
"Annotation of CPIC Guideline for simvastatin and SLCO1B1". PharmGKB. Barbarino, Julia M.; Whirl-Carrillo, Michelle; Klein, Teri ... and SLCO1B1 rs4149056 and myopathy in patients taking simvastatin CPIC guidelines are published in the journal Clinical ...
"Pharmacokinetic interactions between simvastatin and setipiprant, a CRTH2 antagonist". European Journal of Clinical ...
Examples of statins include atorvastatin, lovastatin, rosuvastatin, and simvastatin. They are used in the treatment of ...
April 2008). "Simvastatin with or without ezetimibe in familial hypercholesterolemia" (PDF). N. Engl. J. Med. 358 (14): 1431-43 ...
However, people can also combine ezetimibe with either simvastatin or atorvastatin and other agents on their own, for somewhat ... As of 2006[update] some published information for comparing rosuvastatin, atorvastatin, and ezetimibe/simvastatin results is ... 2003). "Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses ( ... The main competitors to rosuvastatin are atorvastatin and simvastatin. ...
Heart Protection Study Scandinavian Simvastatin Survival Study Myat, Aung; Gershlick, A. H.; Gershlick, Tony (2012). Landmark ...
"Simvastatin augmentation for recent-onset psychotic disorder: A study protocol". BBA Clinical. 4: 52-58. doi:10.1016/j.bbacli. ...
As cancer appeared more frequently in patients treated with simvastatin-ezetimibe combination therapy in one clinical trial, it ... SEAS Investigators) (September 2008). "Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis". The New ...
Concomitant use with cholesterol medications such as lovastatin or simvastatin. Hypersensitivity to clarithromycin or any ...
Vytorin (ezetimibe/simvastatin) tablets can cause steatorrhea in some people. Some studies have shown that stool lipids are ...
Moreyra, Abel E. (23 May 2005). "Effect of Combining Psyllium Fiber With Simvastatin in Lowering Cholesterol". Archives of ...
Liu S, Uppal H, Demaria M, Desprez PY, Campisi J, Kapahi P (December 2015). "Simvastatin suppresses breast cancer cell ... Glucocorticoids as potent suppressors of selected components of the SASP Statins such as simvastatin, that can reduce the ...
The study compared a combination of simvastatin and niacin with antioxidant vitamin therapy. Using angiography, coronary artery ... Heart Protection Study Scandinavian Simvastatin Survival Study "HDL-Atherosclerosis Treatment Study". American College of ... "Simvastatin and Niacin, Antioxidant Vitamins, or the Combination for the Prevention of Coronary Disease". New England Journal ... stenosis progressed when using placebo or antioxidant alone, and regressed with the combination of simvastatin and niacin. The ...
Robins, Douglas N. (September 2007). "Alopecia Universalis: Hair Growth following Initiation of Simvastatin and Ezetimibe ...
LCT has supported trials in ambroxol, exenatide, simvastatin, liraglutide, and others. In October, the institute announced a ...
"Simvastatin protects bladder and renal functions following spinal cord injury in rats". Journal of Inflammation. Subach, BR; ...
The statins lovastatin, mevastatin, and simvastatin precursor monacolin J, are fungal isolates. Additional fungal isolates that ...
... is a precursor to simvastatin and has potential neuroprotective activities.[unreliable medical source?] It can be ...
IDL Composition and Angiographically Determined Progression of Atherosclerotic Lesions During Simvastatin Therapy.' ...
2008). "Simvastatin vs therapeutic lifestyle changes and supplements: randomized primary prevention trial". Mayo Clin. Proc. 83 ...
The increased cholesterol levels are due to simvastatin's effect on the expression of different genes. Simvastatin increases ... Simvastatin is a known inhibitor of HMG-CoA reductase, and most importantly is able to cross the blood-brain barrier. It has ... It is still unknown if simvastatin will improve the behavioural or learning deficits in SLOS. Antioxidants are those which ... For individuals that show no residual DCHR7 activity, such as those homozygous for null alleles or mutations, simvastatin ...
Simvastatin is contraindicated with pregnancy, breastfeeding, and liver disease. Pregnancy must be avoided while on simvastatin ... "Simvastatin - Drug Usage Statistics". ClinCalc. Retrieved 7 October 2022. Pedersen TR, Tobert JA (December 2004). "Simvastatin ... the patent for simvastatin had expired by 2004.[citation needed] Simvastatin was initially marketed by Merck & Co under the ... later to be named simvastatin). In 1994, publication of the results of the Scandinavian Simvastatin Survival Study (4S) ...
Simvastatin is a commonly used cholesterol lowering agent (statin) that is associated with mild, asymptomatic and self-limited ... Large controlled trial of simvastatin vs placebo; ALT levels ,2 times ULN occurred in 1.3% of patients on simvastatin vs 1.8% ... Continuation of trial [Bayes 2004] with 1104 patients continuing in extension study of simvastatin vs simvastatin/ezetimibe in ... 3 to simvastatin/ezetimibe, and one each to pravastatin, fluvastatin, and simvastatin, but most cases were mild or not clearly ...
simvastatin acid simvastatin. 8.5. 10.6. 9.5. 11.4. Gemfibrozil. 600 mg BID for 3 days. 40 mg. simvastatin acid simvastatin. ... simvastatin acid. simvastatin. 2.69. 3.10. 2.69. 2.88. Diltiazem. 120 mg BID for 14 days. 20 mg on Day 14. simvastatin. 4.6. ... simvastatin. 13.1. Posaconazole. 100 mg (oral suspension) QD for 13 days. 40 mg. simvastatin acid simvastatin. 7.3. 10.3. 9.2. ... Do not exceed simvastatin 20 mg daily (or simvastatin 40 mg daily for patients who have previously taken simvastatin 80 mg ...
Simvastatin belongs to the group of medicines called statins. It works to reduce the amount of cholesterol in the blood by ... Sitagliptin and simvastatin combination is used together with a proper diet and exercise to treat type 2 diabetes. It is also ... Adults-At first, 100 milligrams (mg) of sitagliptin and the dose of simvastatin you are already taking. It is taken once a day ... For patients who are not taking sitagliptin or simvastatin: * Adults-At first, 100 milligrams (mg) of sitagliptin and 40 mg of ...
On this page about Simvastatin (GA) you will find information relating to side effects, age restrictions, food interactions, ... Other medicines containing the same active ingredients: simvastatin *Can I take Simvastatin (GA) in sport? Find out on the ... Simvastatin is indicated in patients at high risk of CHD (with or without hypercholesterolaemia), including patients with ... Simvastatin is indicated as an adjunct to diet for treatment of hypercholesterolaemia. Prior to initiating therapy with ...
Toxicity. Simvastatin has very high chronic toxicity.. Risk. More fat-soluble statins (simvastatin, atorvastatin) may be quite ... Persistence. Simvastatin is degraded in the environment.. Bioaccumulation. Simvastatin has high potential for bioaccumulation. ... Because the OECD 308 study demonstrated a DT50 ≤ 32d for the total system, the summary phrase "Simvastatin is degraded in the ... Following an oral dose of radioactive simvastatin in humans, 13% of the radioactivity is excreted in the urine and 60% in the ...
Simvastatin reduced the generation of autophagosomes and the ultrastructural injuries to myocardium.,i, Conclusion,/i,. ... Beclin-1, LC3-II/I, P62, AMPK, and the phosphorylation of AMPK in cardiomyocytes were detected.,i, Results,/i,. Simvastatin ... To investigate the effect and mechanism of simvastatin on myocardial injury in cardiac valve surgery with CPB.,i, Methods,/i,. ... Simvastatin was administered preoperatively and postoperatively. Duration of intensive care unit stay, duration of assisted ...
On this page about Ezetimibe Simvastatin 10/10 (Pharmacor) you will find information relating to side effects, age restrictions ... Brand name: Ezetimibe Simvastatin 10/10 (Pharmacor) TM. Active ingredients: ezetimibe + simvastatin ... Other medicines containing the same active ingredients: ezetimibe + simvastatin *Can I take Ezetimibe Simvastatin 10/10 ( ... For the active ingredient ezetimibe + simvastatin. You should seek advice from your doctor or pharmacist about taking this ...
The use of simvastatin was not associated with cognitive improvements in children with neurofibromatosis type 1, contrary to ... The use of simvastatin was not associated with cognitive improvements in children with neurofibromatosis type 1, contrary to ... The negative outcome of this trial suggests that simvastatin should not be prescribed to ameliorate the cognitive deficits ... TUESDAY, July 15 (HealthDay News) -- The use of simvastatin was not associated with cognitive improvements in children with ...
BCI SIMVASTATIN, 20MG, TABLET. Common uses. This medication belongs to the statin family. Typically, it is used to decrease ...
... both in vivo and in vitro with simvastatin. Three-month-old male Wistar rats treated for 21 days with simvastatin or vehicle ... Our results show that HMGR inhibition by simvastatin induces anxiogenic-like effects in the social interaction but not in the ... both in vivo and in vitro with simvastatin. Three-month-old male Wistar rats treated for 21 days with simvastatin or vehicle ... Table 1 Effect of Simvastatin on Lipid Composition of Selected Brain Regions. Full size table. ...
Free coupons for simvastatin / ezetimibe (vytorin). Discounts up to 80% off the retail price. ... Compare Simvastatin / ezetimibe (vytorin) 10/10 mg prices from verified online pharmacies or local U.S. pharmacies. ... Simvastatin / ezetimibe Prices - (Vytorin) Compare Simvastatin / Ezetimibe (Vytorin) prices available at Canadian and ... Sign up for Simvastatin / Ezetimibe Price Alerts. PharmacyChecker provides free monthly email updates of the latest prices. ...
... die wie Simvastatin-TEVA 5 mg den Wirkstoff Simvastatin enthalten; inkl. Preisvergleich ... 5 mg Simvastatin pro Filmtablette 50 Filmtabletten k.A. Simvastatin AL 5mg Filmtabletten 5 mg Simvastatin pro Filmtablette 100 ... 5 mg Simvastatin pro Filmtablette 100 Filmtabletten k.A. Simvastatin-TEVA 5 mg 5 mg Simvastatin pro Filmtablette 30 ... 5 mg Simvastatin pro Filmtablette 50 Filmtabletten k.A. Simvastatin Sandoz 5mg Filmtabletten 5 mg Simvastatin pro Filmtablette ...
... simvastatin) 80 mg, compared to patients taking lower doses of simvastatin and possibly other drugs in the statin class. ... Simvastatin Dose Limitations. These limitations apply to ALL patients taking simvastatin.. Do not use simvastatin with these ... simvastatin) 80 mg, compared to patients taking lower doses of simvastatin and possibly other drugs in the "statin" class. ... in 6031 patients taking 80 mg of simvastatin compared to 6033 patients taking 20 mg of simvastatin. All patients in the study ...
Simvastatin is used along with a proper diet to help lower ... SIMVASTATIN 40 MG TABLET. USES: Simvastatin is used along with ... Other medications can affect the removal of simvastatin from your body, which may affect how simvastatin works. Examples ... PRECAUTIONS: Before taking simvastatin, tell your doctor or pharmacist if you are allergic to it; or if you have any other ... Simvastatin may harm an unborn baby. It is important to prevent pregnancy while taking this medication. Consult your doctor for ...
Online download statistics by month: February 2003 to November ...
... a 3-month treatment with simvastatin does not reduce circulating inflammatory markers. ... The influence of simvastatin on selected inflammatory markers in patients with chronic obstructive pulmonary disease Pol Arch ... Simvastatin is a hypolipemic drug with proven efficacy in the prevention of cardiovascular diseases. Observational studies ... Objectives: The aim of this study was to evaluate the influence of simvastatin on inflammatory markers in patients with COPD. ...
Results of a randomized trial show that simvastatin, but not pravastatin, appears to interfere with sleep quality and increase ... Simvastatin, but Not Pravastatin, May Reduce Sleep Quality. *Authors: News Author: Susan Jeffrey. CME Author: Laurie Barclay, ... which was greater with simvastatin; or to some other unknown factors. For patients reporting sleep problems with simvastatin, ... Simvastatin, but Not Pravastatin, May Reduce Sleep Quality. Authors: News Author: Susan Jeffrey CME Author: Laurie Barclay, MD ...
The generic Simvastatin comes from Canada also called Teva Simvastatin manufactured by Teva and the UK by a different ... When is the best time to take Simvastatin?. According to healthline.com, Simvastatin works better if taken in the evening. ... We also carry the generic Simvastatin in the strength of 5 mg tablets. Usage. Zocor (Simvastatin) is a prescription medication ... Simvastatin may harm an unborn baby. If you become pregnant or think you may be pregnant, inform your doctor right away. It is ...
Simvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins).... ... Pregnancy: Simvastatin should not be taken during pregnancy. It may cause harm to the unborn baby. If you become pregnant, stop ... Simvastatin belongs to the group of medications known as HMG CoA reductase inhibitors (statins). It is used in addition to ... Simvastatin works by blocking an enzyme that helps create cholesterol in the body. As a result, less cholesterol is made and ...
... simvastatin) on Dokteronline ✔️ Reliable prescription from a registered doctor. ✔️ Delivered quickly and discreetly to your ... Zocor (simvastatin). Zocor tablets contain the active ingredient simvastatin, which is a type of medicine called a statin. (NB ... Simvastatin is also available without a brand name, ie as the generic medicine.) Simvastatin works by reducing the production ... Simvastatin is also available without a brand name, ie as the generic medicine.) Simvastatin works by reducing the production ...
Resveratrol, Curcumin or Simvastatin treated animals displayed significantly increased numbers of regulatory T cells and ... Methodology/Principal Findings Here we show that after peroral administration of Resveratrol, Curcumin or Simvastatin, mice ... Conclusion/Significance Oral treatment with Resveratrol, Curcumin or Simvastatin ameliorates acute small intestinal ... Curcumin and Simvastatin have been demonstrated in various experimental models of inflammation. We investigated the potential ...
Our data show that simvastatin results in an elongated cell morphology, reduced endothelial cell contractility, enhanced cell- ... Our data suggest that simvastatin may be beneficial in preventing atherosclerosis beyond its traditional lipid lowering effects ... this investigation examined the effect of simvastatin (Zocor®), a common statin, on endothelial cell morphology, cell traction ... Our data show that simvastatin results in an elongated cell morphology, reduced endothelial cell contractility, enhanced cell- ...
Simvastatin) - Drug Info, User Reviews, Side Effects, Research, Clinical Trials ... Clinical Trials Related to Zocor (Simvastatin) Clinical Trial of Zocor (Simvastatin) and Vytorin (Ezetimibe/Simvastatin) in ... Published Studies Related to Zocor (Simvastatin) Simvastatin as an adjuvant therapy to fluoxetine in patients with moderate to ... The purpose of the study is to establish the safety of ezetimibe/simvastatin and simvastatin in adolescents with Type 1 ...
Handla Simvastatin SUN, filmdragerad tablett 10 mg, 30 tablett(er) på Apoteket.se för 72,60. Varan finns i lager för snabb ...
Handla Simvastatin Bluefish, Filmdragerad tablett 20 mg, 30 tablett(er) på Apoteket.se för 78,13. Varan finns i lager för snabb ...
Get up-to-date information on Simvastatin side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about ... Take simvastatin exactly as prescribed.. Simvastatin comes in tablet form and is given once a day at bedtime, with or without ... Simvastatin falls into category X. It has been shown that women taking simvastatin during pregnancy may have babies with ... Serious side effects have been reported with simvastatin. See the "Simvastatin Precautions" section. ...
TP1-11 MS-STAT2: a phase 3 trial of high dose simvastatin in secondary progressive multiple sclerosis ... TP1-11 MS-STAT2: a phase 3 trial of high dose simvastatin in secondary progressive multiple sclerosis ... TP1-11 MS-STAT2: a phase 3 trial of high dose simvastatin in secondary progressive multiple sclerosis ...
Twenty-six of the patients were treated with simvastatin (20 mg/day) and 19 individuals were given ezetimibe / simvastatin ... Conclusions:These results showed that both the combined ezetimibe/simvastatin treatment and the simvastatin monotherapy proved ... simvastatin treatment with simvastatin monotherapy. Material and Method:The data of 45 patients with NAFLD associated with ... simvastatin treatment and simvastatin monotherapy in patients with NAFLD and high cardiovascular risk disease. The secondary ...
... than that of simvastatin (48400) (Serajuddin et al., 1991). The high lipophilicity of simvastatin has been linked with side ... adrenal CLuptake of simvastatin (1.55 ml/min/g tissue) was larger than hepatic CLuptake, and simvastatin was distributed to ... with 20 mg of simvastatin, and the effect of rosuvastatin was significantly larger than either pravastatin or simvastatin ( ... 2B), and [14C]simvastatin (Fig. 2C). The CLuptake values (i.e., the slopes of the integration plots) are summarized in Fig.3. ...

No FAQ available that match "simvastatin"

No images available that match "simvastatin"