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Simvastatin is a cholesterol-lowering drug. Your doctor
may prescribe Simvastatin in addition to a cholesterol-lowering
diet if your blood cholesterol level is too high,
and if you have been unable to lower it by diet alone.
In people with high cholesterol and heart disease,
Simvastatin reduces the risk of heart attack, stroke
and "mini-stroke" (transient ischemic attack)
and can stave off the need for bypass surgery or angioplasty
to clear clogged arteries.
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Lovastatin is used to reduce the amounts of LDL (bad)
cholesterol and total cholesterol in your blood. These
actions are important in the prevention of heart disease
and hardening of the arteries, which can lead to heart
attacks, stroke, and peripheral vascular disease.
Lovastatin blocks the production of cholesterol (a
type of fat) in the body.
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Lescol is a competitive inhibitor of HMG-CoA reductase,
which is responsible for the conversion of 3-hydroxy-3-methylglutaryl-coenzyme
A (HMG-CoA) to mevalonate, a precursor of sterols,
including cholesterol. The inhibition of cholesterol
biosynthesis reduces the cholesterol in hepatic cells,
which stimulates the synthesis of LDL receptors and
thereby increases the uptake of LDL particles. The
end result of these biochemical processes is a reduction
of the plasma cholesterol concentration. (From FDA
Label).
Twelve placebo-controlled studies
were conducted involving subjects with Type IIa or
IIb hyperlipoproteinemia. Lescol was administered
daily to 1621 subjects for at least 6 weeks. After
24 weeks, treatment resulted in average LDL-C reductions
of 22% for the 20mg dose, 25% for the 40mg dose and
36% for the 80mg dose. Treatment with Lescol reduced
Apo B and triglycerides while increasing HDL-C.
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Department of Internal Medicine
II, University of Jena Medical School, Germany.
A total of 47 patients suffering
from heterozygous hyperlipidemia were treated with
LDL-apheresis (24 patients, aged 49.5 +/- 11.5 years),
diet and/or lipid-lowering drugs or with diet and
lipid-lowering drugs only (23 patients, aged 48.0
+/- 11.9 years). After treatment periods of 44.4 +/-
14.3 (apheresis group) and 33.5 +/- 15.9 (drug group)
months, respectively, the ensuing results revealed
significant differences (p < 0.0001): total cholesterol
decreased from 10.4 to 5.5 vs 9.9 to 8.7 mmol/l, LDL
from 7.4 to 3.9 vs 6.6 to 5.2 mmol/l, triglycerides
from 5.8 to 3.7 vs 4.8 to 4.1 mmol/l and the LDL/HDL-ratio
decreased from 7.1 to 3.4 vs 6.7 to 5.8. In the apheresis
group one patient died from myocardial infarction
vs one non-fatal myocardial infarction and the manifestation
of coronary heart disease in three cases in the drug
group. There were no severe side-effects in either
group. All patients in the apheresis group experienced
an increased clinical performance. On the other hand
physological well-being of these patients was lower
than that of the drug group (scores 42.3 +/- 8.9 vs
50.2 +/- 9.9, p < 0.002). The present trial suggests
that a continuing reduction in serum lipid concentrations
may lower in a dose dependent manner the risk of development
and progression of coronary heart disease. With respect
to clinical and laboratory results, LDL-apheresis
seems safe and appears to be the most effective therapy.
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First clinical results are presented
for two newly developed drugs. Both are diphenylmethane
derivatives named ethyl-(+/-)-2-([alpha-(p-chlorophenyl)-p-tolyl]-oxy)-2-methylbutyrate
(beclobrate, B) and (+/-)-2-(4-[(4-chlorophenyl)methyl]phenoxy)-2-methyl-butanacid-3-pyridinylmethylester
(eniclobrate, E). These drugs were given in a doubleblind
crossover trial with placebo periods before, in between
and afterwards to 6 patients with type IIb and 13
patients with type IIa hyperlipidemia. Beclobrate
was given in a dosage of 100 mg twice daily and eniclobrate
in a dosage of 130 mg twice daily. Besides effectively
reducing LDL-cholesterol in type IIa there was a remarkable
increase in HDL-cholesterol in both types of hyperlipidemia
especially for beclobrate.
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