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SIMVASTATIN
(brand name: Zocor)
Pharmacological category:
antihyperlipidemic, HMG-CoA reductase inhibitor
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Reviews |
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J Cereb Blood Flow Metab. 2005 Feb
16.
Protective effects of statins involving both
eNOS and tPA in focal cerebral ischemia.
Asahi M, Huang Z, Thomas S, Yoshimura SI, Sumii T, Mori
T, Qiu J, Amin-Hanjani S, Huang PL, Liao JK, Lo EH, Moskowitz MA.
1Neuroprotection Research Laboratory, Departments of Neurology and Radiology,
Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts,
USA.
Previous studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)
reductase inhibitors (statins) protect the brain against ischemic injury
by upregulating endothelial nitric oxide synthase (eNOS). Here, we tested
the hypothesis that statins provide additional beneficial effects by also
upregulating endogenous tissue plasminogen activator (tPA) and enhancing
clot lysis in a mouse model of embolic focal ischemia. Heterologous blood
clots (0.2 mm) were injected into the distal internal carotid artery to
occlude blood flow in the middle cerebral artery territory after long-term
(14 days) simvastatin, atorvastatin or vehicle treatment. Ischemic lesion
volume, neurologic deficits, as well as residual blood clots were measured
at 22 h. Reverse transcription-polymerase chain reaction assessed mRNA levels
of eNOS, tPA, and the endogenous plasminogen activator inhibitor PAI-1.
Ischemic lesion volumes and neurologic deficits were significantly reduced
in wild-type mice by both simvastatin and atorvastatin. Statins increased
eNOS and tPA mRNA levels but did not change mRNA levels of PAI-1. In eNOS
knockout mice, atorvastatin reduced the volume of ischemic tissue and improved
neurologic outcomes after arterial occlusion by blood clot emboli. In contrast,
statins did not have protective effects in tPA knockout mice after embolic
focal ischemia, but only in a filament model where focal ischemia was achieved
via mechanical occlusion. These results suggest that statins protect against
stroke by multiple mechanisms involving both eNOS and tPA. The involvement
of each pathway may be revealed depending on the choice of experimental
stroke model.Journal of Cerebral Blood Flow & Metabolism advance online
publication, 16 February 2005; doi:10.1038/sj.jcbfm.9600070. |
Clin Rheumatol. 2005 Mar 2.
Effects of simvastatin on bone mineral density
and remodeling parameters in postmenopausal osteopenic subjects: 1-year
follow-up study.
Tikiz C, Tikiz H, Taneli F, Gumuser G, Tuzun C.
Department of Physical Medicine and Rehabilitation, Faculty of Medicine,
University of Celal Bayar, Manisa, Turkey.
Observational studies suggest that statin use may be associated with lower
incidence of fracture. However, there are conflicting data for their effects
on bone remodeling parameters and bone mineral density (BMD). In the present
study, we aimed to investigate the effects of simvastatin on bone metabolism
and BMD in subjects with hypercholesterolemia (>240 mg/dl). For this
purpose, 32 postmenopausal osteopenic subjects who were given simvastatin
treatment (20 mg/day) and not on osteoporosis treatment were included in
the study. During the 1-year follow-up period, the total cholesterol level
decreased from 262.1+/-30.9 to 202.2+/-30.1 mg/dl (p<0.0001). At a period
as early as the 3rd month, levels of the anabolic markers, e.g., bone-specific
alkaline phosphatase (BSAP) and osteocalcin (OCL), were found to be significantly
increased (from 120.8+/-56.6 to 149.5+/-57.6 IU/l, p=0.008, and from 20.8+/-12.6
to 34.7+/-18.4 mug/l, p=0.015, respectively) while no significant change
was observed in the resorptive marker of serum N-telopeptide of type I collagen
(CTX). At the 6th and 12th month, BSAP and OCL were both found to be decreased
below the pretreatment values. While a significant reduction was found in
BSAP levels (from 120.8+/-56.6 to 55.9+/-18.8 IU/l, p<0.001), no significant
change was observed in CTX levels after the 6-month treatment period. Parathyroid
hormone showed a gradual profound increase during the follow-up period (from
62.7+/-41.5 to 108.4+/-51.7 pg/ml, p<0.001). No significant change was
found in BMD levels at the spine, femoral neck, Ward's triangle, and trochanter
at the end of the 1-year follow-up period. In conclusion, simvastatin treatment
showed a short-lasting anabolic effect on bone metabolism. However, this
effect was lost by prolongation of therapy. The decrease in both anabolic
and resorptive markers at the 6th and 12th month suggests that simvastatin
affects bone metabolism mostly in favor of inhibition of the bone turnover
in a long-term observation period although this inhibitory effect was not
reflected in BMD. |
| Am J Cardiol 2001
Aug 16;88(4 Suppl):10F-5F.
Are we aggressive enough in lowering cholesterol?
Waters DD.
Cardiology Division, Department of Medicine, San Francisco General
Hospital, San Francisco, California 94110, USA.
To date, 5 major randomized, placebo-controlled statin trials--the Scandinavian
Simvastatin Survival Study, West of Scotland Coronary Prevention Study,
Cholesterol and Recurrent Events trial, Long-term Intervention with Pravastatin
in Ischaemic Disease, and Air Force/Texas Coronary Atherosclerosis Prevention
Study--have convincingly shown that total mortality and major coronary
events can be significantly reduced by lowering levels of low-density
lipoprotein cholesterol (LDL-C) with statin therapy. These results were
achieved in a broad range of patients including those with and without
a history of coronary artery disease and with elevated or average LDL-C
levels. The results also support the large body of epidemiologic evidence
demonstrating that the lower the cholesterol level, the lower the cardiovascular
risk. Evidence now substantially supports the urgency of physicians to
aggressively target the lowering of LDL-C levels for the primary and secondary
prevention of coronary disease. |
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Drug information |
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| GENERIC NAME: simvastatin
BRAND NAME: Zocor
DRUG CLASS AND MECHANISM: Simvastatin is a cholesterol-
lowering medicine. It inhibits the production of cholesterol by the liver.
It lowers overall blood cholesterol as well as blood LDL cholesterol levels.
LDL cholesterol is believed to be the "bad" cholesterol that
is primarily responsible for the development of coronary artery disease.
Lowering LDL cholesterol levels retards progression and may even reverse
coronary artery disease.
PREPARATIONS: tablets: 5 mg,10 mg, 20 mg, 40 mg
STORAGE: Tablets should be stored at room temperature
in a tightly closed container.
PRESCRIBED FOR: High blood cholesterol is first treated
with exercise, weight loss, and a diet low in cholesterol and saturated
fats. When these measures fail, cholesterol-lowering medications such
as simvastatin can be added. The National Cholesterol Education Program
(NCEP) has published treatment guidelines for use of these medications.
These treatment guidelines take into account the level of LDL cholesterol
as well as the presence of other risk factors such as diabetes, hypertension,
cigarette smoking, low HDL cholesterol level, and family history of early
coronary heart disease. The effectiveness of the medication in lowering
cholesterol is dose related. Blood cholesterol determinations are performed
in regular intervals during treatment so that dosage adjustments can be
made.
DOSING: May be taken on an empty or full stomach.
DRUG INTERACTIONS: Simvastatin is generally well- tolerated.
The medication should be used with caution in patients with alcohol or
other liver diseases. Persistently abnormal liver tests during treatment
are rare, but may lead to a discontinuation of the medication. Rare cases
of muscle inflammation (myositis) and breakdown have been reported with
simvastatin. Muscle breakdown causes the release of muscle protein (myoglobin)
into the blood and kidney tubules, resulting in acute kidney failure.
The risk of muscle breakdown is increased when simvastatin is given together
with other medications such as cyclosporine (Sandimmune), gemfibrozil
(Lopid), erythromycin and nicotinic acid. Simvastatin may interact with
cholestyramine (Questran), warfarin (Coumadin), and cimetidine (Tagamet)
to alter the blood levels of these medicines. When Coumadin is given together
with simvastatin, blood clotting times require monitoring to avoid excessive
blood thinning and bleeding. Simvastatin should not be used in children.
Simvastatin is not habit forming.
PREGNANCY: Simvastatin should not be used by pregnant
women.
NURSING MOTHERS: Simvastatin should not be used by nursing
mothers because of potential adverse side effects to the nursing infant.
SIDE EFFECTS: Simvastatin is generally well-tolerated
and side effects are rare. Minor side effects include constipation, diarrhea,
fatigue, gas, heartburn, and headache. Major side effects include abdominal
pain or cramps, blurred vision, dizziness, easy bruising or bleeding,
itching, muscle pain or cramps, rash, and yellowing of the skin or eyes.
Caution! Before starting
to take this medicine, it is vital that you should consult your doctor!
Do not use it on your own initiative, without medical advice.
Also, you should read carefully important health information about this
drug given here:
www.nlm.nih.gov
my.webmd.com |
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Order now ! |
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ZOCOR
Substance: Simvastatin
Manufacturer: Merck & Co., INC.
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Dosage |
Packing |
Price |
Pay now |
10 mg |
28 tab |
USD 39.00 |
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10 mg |
84 tab |
USD 115.00 |
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20 mg |
28 tab |
USD 59.00 |
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20 mg |
84 tab |
USD 169.00 |
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Dosage |
Packing |
Price |
Pay now |
10 mg |
30 caps |
USD 29.00 |
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10 mg |
60 caps |
USD 59.00 |
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10 mg |
90 caps |
USD 74.00 |
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20 mg |
30 caps |
USD 34.00 |
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20 mg |
60 caps |
USD 63.00 |
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20 mg |
90 caps |
USD 99.00 |
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