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Antilipemic agents

Hyperlipidemia is an excess of fatty substances called lipids, largely cholesterol and triglycerides, in the blood. It is also called hyperlipoproteinemia, because these fatty substances travel in the blood attached to proteins. A subcategory of hyperlipidemia is hypercholesterolemia, in which there is a high level of total cholesterol. Common secondary etiologies of hypercholesterolemia include diabetes mellitus, hypothyroidism, pregnancy, nephrotic syndrome, obstructive jaundice, and chronic renal failure. Hyperlipidemia, along with diabetes, hypertension (high blood pressure), a positive family history, and smoking are all major risk factors for coronary heart disease.

LIPITOR - GENERIC (generic - what is it?)
Subtance: Atorvastatin

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100 tab
USD 89.00
20 mg
100 tab
USD 129.00
ZOCOR
Substance: Simvastatin
Manufacturer: Merck & Co., INC.

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10 mg
28 tab
USD 39.00
10 mg
84 tab
USD 115.00
20 mg
28 tab
USD 59.00
20 mg
84 tab
USD 169.00

ZOCOR - GENERIC (generic - what is it?)
Substance: Simvastatin
Manufactured in India

 
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10 mg
30 caps
USD 29.00
10 mg
60 caps
USD 59.00
10 mg
90 caps
USD 74.00
20 mg
30 caps
USD 34.00
20 mg
60 caps
USD 63.00
20 mg
90 caps
USD 99.00
MEVACOR
Generic name: Lovastatin
Manufacturer: Merck & Co., INC. (Germany)


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28 tab
USD 48.00
40 mg
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USD 73.00

LESCOL
Generic name: Fluvastatin
Manufacturer: Novartis

 
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20 mg
28 tab
USD 39.00
40 mg
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USD 49.00

Treatment of Hyperlipidemia.
Evaluation of lipid fractions is essential before therapy for hyperlipidemia is initiated. Treatment may include dietary changes, weight reduction, exercise, and medications.
It is necessary to identify and treat any underlying problem, such as diabetes. If there is no contributing problem, the primary treatment for Types II, III, and IV is often dietary management - namely restricting cholesterol intake.
The most effective treatment for Type V hyperlipoproteinemia is often weight reduction and long-term maintenance of a low-fat diet. Drugs and a special diet may help, but the chance of cure is uncertain because the person with Type V risks developing pancreatitis. Increased fat intake may cause recurrent bouts of illness, possibly leading to the formation of cysts, hemorrhage, and death.

Research articles on Antilipemic agents.
J Antimicrob Chemother. 2005 Mar 10.
Lipid disorders in antiretroviral-naive patients treated with lopinavir/ritonavir-based HAART: frequency, characterization and risk factors.
Montes ML, Pulido F, Barros C, Condes E, Rubio R, Cepeda C, Dronda F, Antela A, Sanz J, Navas E, Miralles P, Berenguer J, Perez S, Zapata A, Gonzalez-Garcia JJ, Pena JM, Vazquez JJ, Arribas JR.
Internal Medicine Service, La Paz Hospital, Autonoma University School of Medicine, Madrid, Spain.

OBJECTIVES: The aim of this study was to evaluate the frequency, characteristics and risk factors of lipid changes associated with lopinavir/ritonavir treatment in antiretroviral-naive patients. METHODS: A prospective cohort of 107 antiretroviral-naive HIV-infected patients was followed for 12 months after starting lopinavir/ritonavir-based highly active antiretroviral therapy. RESULTS: At 12 months, percentages of patients with hypercholesterolaemia and hypertriglyceridaemia were 17.4% and 40%, respectively. Mean increases in total cholesterol and triglycerides were 40.7 and 73.3 mg/dL. There was a significant increase in both low-density and high-density (HDL) cholesterol, and no increase in the total cholesterol/HDL ratio (from 4.16 at baseline to 4.49 after 12 months). Baseline cholesterol > 200 mg/dL and triglycerides > 150 mg/dL were independent risk factors for dyslipidaemia, while hepatitis C coinfection appeared to be protective. CONCLUSIONS: Patients with elevated lipid values at baseline have the greatest risk of developing hypercholesterolaemia and hypertriglyceridaemia after starting lopinavir/ritonavir. Antiretroviral-naive patients coinfected with hepatitis C have a low risk of developing hyperlipidaemia after starting lopinavir/ritonavir.

Ann Intern Med. 2003 Oct 21;139(8):670-82.
Effects of statins on nonlipid serum markers associated with cardiovascular disease: a systematic review.
Balk EM, Lau J, Goudas LC, Jordan HS, Kupelnick B, Kim LU, Karas RH.
Tufts University School of Medicine and Tufts-New England Medical Center, Boston, Massachusetts 02111, USA.

BACKGROUND: Statins reduce cardiovascular events to a greater extent than can be explained by their effect on lipids. Several studies have attempted to elucidate mechanisms by which statins reduce cardiovascular risk. PURPOSE: To summarize the effects of statins on nonlipid serum markers and to correlate statins' effect on serum markers with lipid levels and cardiovascular outcomes. DATA SOURCES: MEDLINE (1980 to 2003) search limited to English-language articles. STUDY SELECTION: Studies reporting original data in at least 10 participants on the effect of statins on outcomes of interest, excluding studies of cerivastatin, drug combinations, and patients with organ transplants. DATA EXTRACTION: Study design, sample size, treatment, and outcome data extracted on the basis of preestablished criteria. When appropriate, meta-analysis was performed by using a random-effects model. DATA SYNTHESIS: All statins are effective at lowering C-reactive protein levels, and the effect is not dose-dependent. Studies do not demonstrate a correlation between statins' effects on C-reactive protein levels and on lipids or cardiovascular outcomes. Statins do not affect fibrinogen levels, and limited data suggest little effect on lipid oxidation, tissue plasminogen activator, or plasminogen activator inhibitor. Platelet aggregation data are inconclusive. CONCLUSIONS: Among nonlipid serum markers examined, only C-reactive protein levels are statistically significantly affected by statins. These findings suggest that statin-mediated anti-inflammatory effects may contribute to the ability of statins to reduce risk for cardiovascular disease. Overall, however, available data are insufficient to support recommendations for using nonlipid serum markers in decisions regarding statin therapy for individual patients.

 

Int J Artif Organs. 1995 Dec;18(12):786-93.
Four years' treatment efficacy of patients with severe hyperlipidemia. Lipid lowering drugs versus LDL-apheresis.
Schiel R, Bambauer R, Muller UA.
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.

Arzneimittelforschung. 1981;31(12):2168-9.
Lipid-lowering effect of the new drugs eniclobrate and beclobrate in patients with hyperlipidemia type II a and type II b.
Najemnik C, Lageder H, Regal H, Irsigler K.

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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