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Pitavastatin: evidence for its place in treatment of hypercholesterolemia.

Alagona P - Core Evid (2010)

Bottom Line: Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are the most potent pharmacologic agents for lowering total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C).Considering the numbers of patients who need LDL-C-lowering therapy and questions of individual tolerance and therapeutic response, having a variety of agents to choose from is beneficial for patient care.This paper presents background information on statin treatment and reviews data regarding a new agent, pitavastatin, which has recently been approved for clinical use.

View Article: PubMed Central - PubMed

Affiliation: Penn State Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania, USA.

ABSTRACT
Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are the most potent pharmacologic agents for lowering total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). They have become an accepted standard of care in the treatment of patients with known atherosclerotic cardiovascular disease (secondary prevention) and also those at increased risk of cardiovascular events. There are currently six statin drugs commercially available in the US. Although they are chemically similar and have the same primary mechanisms of action in lowering TC and LDL-C, there are differences in their efficacy or potency, metabolism, drug-drug interactions, and individual tolerability. Considering the numbers of patients who need LDL-C-lowering therapy and questions of individual tolerance and therapeutic response, having a variety of agents to choose from is beneficial for patient care. This paper presents background information on statin treatment and reviews data regarding a new agent, pitavastatin, which has recently been approved for clinical use.

No MeSH data available.


Related in: MedlinePlus

HMG-CoA reductase inhibitors (statins) reduce TC and LDL-C via a number of mechanisms: Decreased hepatic synthesis of cholesterol, decreased hepatic intracellular cholesterol pool stimulating upregulation of LDL receptor activity, reduced VLDL secretion from hepatocytes leading to decreased remnant lipoproteins and increased tissue uptake of apoB particles from the circulation.
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f3-ce-5-091: HMG-CoA reductase inhibitors (statins) reduce TC and LDL-C via a number of mechanisms: Decreased hepatic synthesis of cholesterol, decreased hepatic intracellular cholesterol pool stimulating upregulation of LDL receptor activity, reduced VLDL secretion from hepatocytes leading to decreased remnant lipoproteins and increased tissue uptake of apoB particles from the circulation.

Mentions: The synthesis of sterols, including cholesterol, begins with acetyl CoA. However, the rate-limiting enzymatic reaction is two steps further down the chain with the conversion of HMG-CoA to mevalonate by HMG-CoA reductase. Statins inhibit this reaction and the production of mevalonate, thereby reducing cholesterol synthesis (Figure 2). The number and type of chemical bonds a statin can establish with HMG-CoA reductase determines its potency and therefore determines its effects on cholesterol production.2 Decreased production of cholesterol decreases the hepatic intracellular pool and subsequently provokes increased transcription of LDL receptors on the surface of hepatocytes. These receptors bind with apoproteins B (apoB) and E (apoE) on the surface of very low-density lipoprotein (VLDL) and its remnant particles, including LDL, intermediate density lipoprotein (IDL), and lipoprotein (a) [Lp(a)],3 resulting in increased uptake and decreased plasma levels of these particles. This is the major mechanism leading to significant reduction of not only LDL-C but all apoB particles (Figure 3). Statins also decrease VLDL and apoB production in the liver.4 Powerful reduction of plasma TC and apoB lipoproteins does not appear to lead to any known harmful structural (cellular, tissue) or metabolic perturbations in adults. A variety of nonstatin treatments resulting in TC-lowering, including ileal bypass5 and use of the bile acid sequestrant, cholestyramine, have also led to decreased cardiovascular events.6


Pitavastatin: evidence for its place in treatment of hypercholesterolemia.

Alagona P - Core Evid (2010)

HMG-CoA reductase inhibitors (statins) reduce TC and LDL-C via a number of mechanisms: Decreased hepatic synthesis of cholesterol, decreased hepatic intracellular cholesterol pool stimulating upregulation of LDL receptor activity, reduced VLDL secretion from hepatocytes leading to decreased remnant lipoproteins and increased tissue uptake of apoB particles from the circulation.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3065553&req=5

f3-ce-5-091: HMG-CoA reductase inhibitors (statins) reduce TC and LDL-C via a number of mechanisms: Decreased hepatic synthesis of cholesterol, decreased hepatic intracellular cholesterol pool stimulating upregulation of LDL receptor activity, reduced VLDL secretion from hepatocytes leading to decreased remnant lipoproteins and increased tissue uptake of apoB particles from the circulation.
Mentions: The synthesis of sterols, including cholesterol, begins with acetyl CoA. However, the rate-limiting enzymatic reaction is two steps further down the chain with the conversion of HMG-CoA to mevalonate by HMG-CoA reductase. Statins inhibit this reaction and the production of mevalonate, thereby reducing cholesterol synthesis (Figure 2). The number and type of chemical bonds a statin can establish with HMG-CoA reductase determines its potency and therefore determines its effects on cholesterol production.2 Decreased production of cholesterol decreases the hepatic intracellular pool and subsequently provokes increased transcription of LDL receptors on the surface of hepatocytes. These receptors bind with apoproteins B (apoB) and E (apoE) on the surface of very low-density lipoprotein (VLDL) and its remnant particles, including LDL, intermediate density lipoprotein (IDL), and lipoprotein (a) [Lp(a)],3 resulting in increased uptake and decreased plasma levels of these particles. This is the major mechanism leading to significant reduction of not only LDL-C but all apoB particles (Figure 3). Statins also decrease VLDL and apoB production in the liver.4 Powerful reduction of plasma TC and apoB lipoproteins does not appear to lead to any known harmful structural (cellular, tissue) or metabolic perturbations in adults. A variety of nonstatin treatments resulting in TC-lowering, including ileal bypass5 and use of the bile acid sequestrant, cholestyramine, have also led to decreased cardiovascular events.6

Bottom Line: Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are the most potent pharmacologic agents for lowering total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C).Considering the numbers of patients who need LDL-C-lowering therapy and questions of individual tolerance and therapeutic response, having a variety of agents to choose from is beneficial for patient care.This paper presents background information on statin treatment and reviews data regarding a new agent, pitavastatin, which has recently been approved for clinical use.

View Article: PubMed Central - PubMed

Affiliation: Penn State Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania, USA.

ABSTRACT
Statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, are the most potent pharmacologic agents for lowering total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). They have become an accepted standard of care in the treatment of patients with known atherosclerotic cardiovascular disease (secondary prevention) and also those at increased risk of cardiovascular events. There are currently six statin drugs commercially available in the US. Although they are chemically similar and have the same primary mechanisms of action in lowering TC and LDL-C, there are differences in their efficacy or potency, metabolism, drug-drug interactions, and individual tolerability. Considering the numbers of patients who need LDL-C-lowering therapy and questions of individual tolerance and therapeutic response, having a variety of agents to choose from is beneficial for patient care. This paper presents background information on statin treatment and reviews data regarding a new agent, pitavastatin, which has recently been approved for clinical use.

No MeSH data available.


Related in: MedlinePlus