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Atorvastatin decreases the concentration of cholesterol and lipoproteins in the blood plasma by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of “liver” LDL receptors on the cell surface, what is anadrol  which leads to increased trapping and Ac-LDL catabolism.

Atorvastatin reduces the formation of LDL-C and the number of LDL particles, causes a marked and sustained increase in the activity of LDL-receptors in combination with favorable qualitative changes in LDL particles, and reduces LDL-C in patients with homozygous hereditary familial hypercholesterolemia, resistant to treatment by other hypolipidemic means.

Atorvastatin in doses ranging from 10 mg to 80 mg lowers total cholesterol by 30% – 46%, of LDL-C – 41% – 61%, apolipoprotein-B – by 34% – 50% and TG – 14% – 33% . Results similar therapy in patients with heterozygous familial hypercholesterolemia, non-family forms of hypercholesterolemia, and mixed hyperlipidemia, including patients with non-insulin dependent diabetes mellitus. In patients with isolated hypertriglyceridemia, atorvastatin reduces total cholesterol, LDL-C, LDL-VLDL, apo B, and TG, and increases HDL-cholesterol levels. Patients with disbetalipoproteinemiey atorvastatin reduces cholesterol intermediate density lipoproteins.

In patients with hyperlipoproteinemia type IIa and IIb by Frederickson average value Xc increasing HDL content in the treatment of atorvastatin (10-80 mg) when compared to baseline of 5.1% – 8.7% and is independent of dose. There is a significant dose-dependent reduction of the ratio: total cholesterol / LDL-HDL and LDL-C / LDL-HDL cholesterol by 29% -44% and 37% -55%, respectively. Liprimar® at a dose of 80 mg significantly reduced the risk of ischemic events and mortality by 16% after 16 weeks of treatment, and the risk of re-hospitalization for angina, accompanied by signs of myocardial ischemia by 26%. In patients with different initial concentrations of LDL-C Lipitor causes a decrease in ischemic complications and risk of death (in patients with myocardial infarction without Q-wave MI and unstable angina, as well as men and women, and in patients younger than 65 years of age and older). Reduction in blood plasma of LDL-C is better correlated with the dose of the drug than its concentration in plasma.Dose picked based on the therapeutic effect (see. “Dosage and Administration” section).

The therapeutic effect is achieved within 2 weeks after initiation of therapy, reaching a peak at 4 weeks and maintained throughout the treatment period.

Prevention of cardiovascular events

In the Anglo-Scandinavian study of cardiovascular disease (lipid-lowering branch (ASCOT-LLA) atorvastatin effect on fatal and non-fatal outcomes of coronary heart disease (CHD) found that the effect of atorvastatin therapy at a dose of 10 mg significantly exceede.

A study of reverse development of coronary atherosclerosis with intensive lipid-lowering therapy (REVERSAL), atorvastatin 80 mg in patients with coronary heart disease found that the mean reduction in total atheroma volume (the primary criterion of effectiveness) from the beginning of the study was 0.4%.

Recurrent stroke
in the program of intensive cholesterol lowering (SPARCL) it was found that atorvastatin 80 mg per day reduced the risk of recurrent fatal or nonfatal stroke in patients with stroke or transient ischemic attack (TIA) without prior CVD by 15% compared with placebo. At the same time significantly reduced the risk of major cardiovascular events and revascularization procedures. Reducing the risk of cardiovascular disorders during therapy with atorvastatin was observed in all groups except the one, which included patients with primary or recurrent hemorrhagic stroke (7 in the atorvastatin group vs. 2 in the placebo group).

Hemorrhagic stroke
in patients receiving therapy with atorvastatin 80 mg dose, the incidence of hemorrhagic or ischemic stroke (265 v. 311) or IHD (123 vs. 204) was less than the control group.

Secondary prevention of cardiovascular complications
in the treatment of the New Case Study (TNT) compared the effect of atorvastatin at a dose of 80 mg / day and 10 mg / day on the risk of cardiovascular complications in patients with clinically confirmed coronary artery disease.

Atorvastatin is rapidly absorbed after oral administration: the time to reach its maximum concentration (TSmah) in plasma reaches a maximum within 1-2 hours. Women atorvastatin maximum concentration (Cmax) is 20% higher and the area under “concentration-time” curve (AUC) – 10% lower than in men. The degree of absorption and plasma concentration increase proportionally with dose. The absolute bioavailability – about 14% and the systemic bioavailability of inhibitory activity against HMG-CoA reductase inhibitors – about 30%. The low systemic bioavailability due to first pass metabolism in the mucosa of the gastrointestinal tract and / or “first pass” through the liver. Food somewhat reduces the rate and extent of absorption of the drug (25% and 9%, respectively, as evidenced by the results of determination of Cmax and AUC, but LDL-C reduction is similar to that when receiving atorvastatin empty stomach. Despite the fact that after administration of atorvastatin in the evening while its concentration in blood plasma below (Cmax and AUC, approximately 30%) than after reception in the morning, the reduction of LDL-C level is independent of the time of day that take medication.

The mean volume of distribution of atorvastatin is approximately 381 liters. Communication with plasma proteins is not less than 98%. The ratio of the erythrocyte / plasma is about 0.25, ie Atorvastatin does not penetrate into erythrocytes.

Atorvastatin is largely metabolized with formation of ortho- and para-hydroxylated derivatives, and various products in the oxidation. In vitro and ortho paragidroksilirovannye metabolites have an inhibitory effect on HMG-CoA reductase, comparable to that of atorvastatin. Approximately 70% reduction in the activity of HMG-CoA reductase is due to actions of active circulating metabolites. Results of in vitro studies give reason to assume that the isoenzyme cytochrome CYP3A4 liver plays an important role in the metabolism of atorvastatin. In favor of this fact indicates increased concentration of drug in the plasma while taking erythromycin, which is an inhibitor of that isoenzyme. In vitro studies have also shown that atorvastatin is a weak inhibitor isoenzyme cytochrome CYP3A4. Atorvastatin has no clinically significant what is anadrol impact on the concentration of terfenadine in the blood plasma, which is metabolized primarily by cytochrome CYP3A4 isoenzyme, therefore a significant effect on the pharmacokinetics of other substrates isoenzyme cytochrome CYP3A4 is unlikely (cm. “The interaction with other drugs” section).

of atorvastatin and its metabolites are excreted mainly in the bile after hepatic and / or extrahepatic metabolism (atorvastatin expressed does not undergo enterohepatic recirculation). The half-life (T1 / 2) of the drug is about 14 hours, during which the drug inhibitory effect against HMG-CoA reductase inhibitor of approximately 70% determined by the activity of circulating metabolites and persists for about 20-30 hours due to their presence. After ingestion found in the urine of less than 2% of the dose of the drug.

Special patient groups

Elderly patients
concentrations of atorvastatin in the blood of patients 65 years and above plasma (Cmax approximately 40%, AUC by about 30%) than in young adult patients. No differences in efficacy and safety, and achieving the objectives of lipid-lowering therapy in elderly patients compared with the general population have been identified.

Research pharmacokinetics of the drug have not been conducted in children.

Kidney failure
Renal impairment does not affect the concentration of atorvastatin in plasma or its effects on lipid metabolism, thereby changing the dose in patients with impaired renal function is not required (see., “Dosage and Administration” section). Atorvastatin is not displayed during hemodialysis due to intense binding to plasma proteins.

Insufficient function of the liver
concentration of the drug is significantly increased (Cmax approximately 16-fold, AUC about 11-fold) in patients with alcoholic cirrhosis (stage B according to Child-Pugh classification) (see. “Contraindications”).

Primary hypercholesterolaemia (heterozygous familial and non-family hypercholesterolemia (type IIa by Frederickson)
combined (mixed) hyperlipidemia (IIa and IIb types for Frederickson)
Disbetalipoproteinemiya (III type for Frederickson) (as an adjunct to diet);
Family endogenous hypertriglyceridemia (IV type according to Frederickson), resistant to diet,
homozygous familial hypercholesterolemia, the lack of effectiveness of diet therapy and other nёfarmakologicheskih treatments;
Primary prevention of cardiovascular complications in patients without clinical evidence of coronary heart disease but with multiple factors in its risk – age over 55 years, nicotine addiction, hypertension, diabetes, low levels of LDL-HDL cholesterol in the blood plasma, genetic predisposition, including on the background of dyslipidemia,
secondary prevention of cardiovascular events in patients with coronary artery disease to reduce total mortality, myocardial infarction, stroke, rehospitalization for angina and the need for revascularization.

: Hypersensitivity to any component of the formulation. Active liver disease or increased activity of “liver” transaminases of unknown origin in the blood plasma to more than 3 times the upper limit of normal.

Age 18 years (insufficient clinical data on the efficacy and safety of the drug in this age group).

The caution
in patients who abuse alcohol; in patients with a history of liver disease.

Pregnancy and lactation
Lipitor ® is contraindicated during pregnancy.
Women of childbearing age during treatment should use adequate contraception methods. Lipitor ® can be administered to women of childbearing age only when the probability of pregnancy are very low, and the patient is informed about the possible risk of treatment to the fetus. Lipitor ® is contraindicated during lactation. It is not known whether atorvastatin is excreted in breast milk. If necessary, the appointment during lactation, breast-feeding should be stopped to avoid the risk of adverse events in infants.

Dosing and Administration

Inside. Take any time of the day regardless of the meal. Before starting treatment with Liprimarom® should try to achieve control hypercholesterolemia with diet, exercise and weight loss in obese patients, as well as treatment of the underlying disease. In appointing the drug to the patient should be advised to standard hypocholesterolemic diet, which he must adhere to throughout the treatment period.

Dose ranging from 10 mg to 80 mg 1 time per day and titrated based on the initial content of LDL-C, and the goal of therapy effect of the individual to treatment.

The maximum daily dose for single dose is 80 mg. At the beginning of the treatment and / or during increasing doses of the drug Lipitor ® needed every 2-4 weeks to control the level of lipids in blood plasma and adjust the dose.

Primary hypercholesterolaemia and combined (mixed) hyperlipidaemia
The majority of patients – 10 mg 1 time per day; therapeutic effect is apparent within 2 weeks, and usually reaches maximum within 4 weeks. Long-term treatment effect persists.

Homozygous familial hypercholesterolaemia
In most cases, prescribe 80 mg 1 time a day (reduction of LDL-C in the range 18-45%).

Insufficiency of liver function
In case of insufficiency of liver function the dose of Lipitor ® should be reduced, with constant monitoring of “liver” transaminases activity: aspartate aminotransferase (ACT) and alanine aminotransferase (ALT).

Lack of renal function
Impaired renal function did not affect the concentration of atorvastatin in plasma or the degree of reduction of LDL-C level during therapy with Lipitor ® , so the correction dose is not required.

Elderly patients
differences in the effectiveness, safety or therapeutic effect of the drug Lipitor in older patients compared with the general population is not detected and dose adjustment is required what is anadrol (see. “Pharmacokinetics” section). online anabolic steroids pharmacy

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