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Hypolipidemic Agents

Hypolipidemic Agents



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Published by: api-3725624 on Oct 17, 2008
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Hypolipidemic agent
Hypolipidemic agents, or antihyperlipidemic agents, are a diverse group of pharmaceuticals that
are used in the treatment of hyperlipidemias. They are called lipid-lowering drugs (LLD) or agents.
Classes of hypolipidemic drugs

There are several classes of hypolipidemic drugs. They may differ in both their impact on the cholesterol profile and adverse effects. For example, some may lower the "bad cholesterol" low density lipoprotein (LDL) more so than others, while others may preferentially increase high density lipoprotein (HDL), "the good cholesterol". Clinically, the choice of an agent will depend on the patient's cholesterol profile, cardiovascular risk, and the liver and kidney functions of the patient, evaluated against the balancing of risks and benefits of the medications

are particularly well-suited for lowering LDL, the cholesterol with the strongest links to cardiovascular

are indicated for hypertriglyceridemia. Fibrates typically lower triglycerides by 20% to 50%. Level of
the good cholesterol HDL is also increased. Fibrates may decrease LDL, though generally to a lesser
degree than statins. Similar to statins, there is a risk of severe muscle damage (myopathy &
rhabdomyolysis) with fibrates.

like fibrates, is also well-suited for lowering triglycerides by 20-50%. It may also lower LDL by 5-25%
and increase HDL by 15-35%. Niacin may cause hyperglycemia, and may also cause liver damage.
Bile acid sequestrants (resins)

are particularly effective for lowering LDL-C by sequestering the cholesterol-containing bile acids
released into the gut and preventing their reabsorption from the gut. It decreases LDL by 15-30% and
raises HDL by 3-5%. It has little effect on triglycerides but can cause a slight increase. Bile acid
sequestrants may cause gastrointestinal problems, and may also reduce the absorption of other drugs and
vitamins from the gut.

\u2022Omega-3 fatty acids
Lipid modifying agents

Atorvastatin \u2022 Cerivastatin \u2022 Fluvastatin \u2022 Lovastatin \u2022
Mevastatin \u2022 Pitavastatin \u2022 Pravastatin \u2022 Rosuvastatin \u2022


Clofibrate \u2022 Bezafibrate \u2022 Aluminium clofibrate \u2022
Gemfibrozil \u2022 Fenofibrate \u2022 Simfibrate \u2022 Ronifibrate \u2022
Ciprofibrate \u2022 Etofibrate \u2022 Clofibride

Bile acid sequestrants
Colestyramine \u2022 Colestipol \u2022 Colextran \u2022 Colesevelam
Niacin and derivatives
Niceritrol \u2022 Niacin \u2022 Nicofuranose \u2022 Aluminium
nicotinate \u2022 Nicotinyl alcohol \u2022 Acipimox

Dextrothyroxine \u2022 Probucol \u2022 Tiadenol \u2022 Benfluorex \u2022
Meglutol \u2022 Omega-3-triglycerides \u2022 Magnesium pyridoxal 5-
phosphate glutamate \u2022 Policosanol \u2022 Ezetimibe


Thestatins (or HMG-CoA reductase inhibitors) form a class of hypolipidemic agents, used as
pharmaceutical agents to lower cholesterol levels in people with or at risk for cardiovascular disease.
They lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which is the rate-limiting
enzyme of the mevalonate pathway of cholesterol synthesis. Inhibition of this enzyme in the liver
stimulates LDL receptors, resulting in an increased clearance of low-density lipoprotein (LDL) from the
bloodstream and a decrease in blood cholesterol levels. The first results can be seen after one week of
use and the effect is maximal after four to six weeks.

Adverse effects
Some patients on statin therapy report myalgias, muscle cramps, or far less-frequent gastrointestinal or
other symptoms
Drug interactions

Combining any statin with a fibrate, another category of lipid-lowering drugs, increases the risks for
rhabdomyolysis to almost 6.0 per 10,000 person-years.]Most physicians have now abandoned routine
monitoring of liver enzymes and creatine kinase, although they still consider this prudent in those on
high-dose statins or in those on statin/fibrate combinations, and mandatory in the case of muscle cramps
or of deterioration in renal function.

Consumption of grapefruit or grapefruit juice inhibits the metabolism of statins\u2014furanocoumarins in grapefruit juice inhibit the cytochrome P450 enzyme CYP3A4, which is involved in the metabolism of most statins (however it is a major inhibitor of only atorvastatin, lovastatin and simvastatin) and some other medications. This increases the levels of the statin, increasing the risk of dose-related adverse

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