Liprimar pills 10mg №100

Active ingredient and dosage form

Coated Tablets:
1 pill contains Atorvastatin (in the form of a Calcium salt) 10, 20, or 40 mg;
Excipients: calcium carbonate, microcrystalline cellulose, lactose monohydrate, sodium carboxymethylcellulose, polysorbate 80, hydroxypropylcellulose, Magnesium stearate, Opadry White YS-1-7040, simethicone emulsion, powdered wax;
14 or 30 tables. packaged.

Mechanism of action

Liprimar is a lipid-lowering drug. Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase, a key enzyme that converts 3-hydroxy-3-methylglutaryl-CoA into mevalonic acid, the precursor of steroids, including cholesterol.
In patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemia, Liprimar lowers total cholesterol (Xc), low-density lipoprotein cholesterol (Xc-LDL) and apolipoprotein B, and I and Iolipoprotein B, and I also have apolipoprotein B, and I, I also have an apolipoprotein B, and I, I, too, I a group who is also a group of people who haven’t been in the control room for the same place, I, and I, I, too, I’ll I like you to have this order code for this procedure. and triglycerides, causes an unstable increase in high-density lipoprotein cholesterol (Xc-HDL).
In the liver, triglycerides and cholesterol are included in very low density lipoproteins (VLDL), enter the plasma and are transported to peripheral tissues. Low-density lipoproteins (LDL) are formed from VLDL, which are catabolized by interaction with high-affinity LDL receptors.
Like LDL, cholesterol-rich and triglyceride-rich lipoproteins (VLDL, intermediate density lipoproteins, and chylomicron residues) can also contribute to the progression of atherosclerosis. Increased plasma triglycerides are often combined with a decrease in HD-C HDL and the appearance of small LDL particles, as well as other non-lipid metabolic risk factors for CHD. In this regard, the independent role of hypertriglyceridemia, as an independent risk factor for CHD, has not been convincingly proven. The independent effect of increasing HDL or reducing triglycerides on the risk of coronary or cardiovascular complications and death from these causes is also not established.
Liprimar reduces plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and increasing the number of “liver” LDL receptors on the cell surface, which leads to increased capture and catabolism of Xc-LDL.
Atorvastatin reduces the formation of Xc-LDL and the number of LDL particles. Causes a pronounced and persistent increase in the activity of LDL receptors, in combination with favorable qualitative changes in LDL particles. Reduces the level of LDL-LDL in patients with homozygous hereditary hypercholesterolemia resistant to treatment with other lipid-lowering drugs.
Atorvastatin at a dose of 10-80 mg reduces the level of total cholesterol by 30-46%, Xc-LDL - by 41-61%, apolipoprotein B - by 34-50% and triglycerides - by 14-33%. The results of treatment are similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia, including in patients with insulin-dependent diabetes mellitus.
In patients with isolated hypertriglyceridemia, atorvastatin reduces total cholesterol, LDL-C, LDL-C, LDL-C, apolipoprotein B, triglycerides, and HD-NLPVP and increases the level of LDL-C. In patients with dysbetalipoproteinemia, lowers lipoprotein cholesterol intermediate density.
In patients with type IIa and IIb hyperlipoproteinemia, according to Fredrickson's classification, the mean value of increased HD-C HDL-C levels during treatment with atorvastatin (10-80 mg), compared with baseline, is 5.1-8.7% and does not depend on the dose. There is a significant dose-dependent decrease in the ratio: total cholesterol / Xc-HDL and Xc-LDL / Xc-HDL by 29-44% and 37-55%, respectively.
Atorvastatin in a dose of 80 mg reliably reduces the risk of ischemic complications and death by 16% after a 16-week course, and the risk of repeated hospitalization for angina, accompanied by signs of myocardial ischemia, by 26%. In patients with different baseline levels of XC-LDL, atorvastatin causes a comparable reduction in the risk of ischemic complications and death (in patients with myocardial infarction without Q wave and unstable angina, men and women, patients younger than 65 years of age).
Liprimar (10 mg / day) significantly reduces the incidence of the following complications: coronary artery disease (fatal + non-fatal heart attack) - by 36%, cardiovascular diseases and revascularization procedures - by 20%, coronary heart disease - by 29%, stroke (including with fatal outcome) - by 26%.
Significant reduction in overall mortality and mortality from cardiovascular complications was not found with Liprimar, but there was a tendency to decrease mortality.

Indications and usage

- in conjunction with a diet to reduce elevated total cholesterol, LDL-C, apolipoprotein B and triglyceride levels, and raising Xc HDL-C in patients with primary hypercholesterolemia (heterozygous familial and non-familial hypercholesterolemia) and mixed hyperlipidaemia (type IIa and IIb Fredrickson classification) in which diet therapy does not give an adequate effect;
- in combination with a diet for the treatment of patients with elevated serum levels of triglycerides (type IV according to Fredrickson classification) and patients with dysbetalipoproteinemia (type III according to Fredrickson classification), in whom diet therapy does not give an adequate effect;
- to reduce the levels of total cholesterol and LDL-LDL in patients with homozygous familial hypercholesterolemia with insufficient effectiveness of diet therapy and other non-pharmacological treatment methods;
- to reduce the risk of death of coronary heart disease and the risk of myocardial infarction, angina pectoris, stroke and to reduce the need for revascularization procedures in patients with cardiovascular diseases and / or dyslipidemia, and if these diseases are not identified,but there are at least three risk factors for the development of CHD, such as over 55 years of age, smoking, arterial hypertension, low plasma concentrations of HD-C HDL, cases of early development of CHD in relatives.

Dosage and administration

Before starting treatment with Liprimar, you should try to control hypercholesterolemia through diet, exercise and weight loss in obese patients, as well as treatment of the underlying disease.
When prescribing the drug, the patient should be advised to recommend a standard lipid-lowering diet, which he must follow during treatment.
The drug can be taken at any time of the day, regardless of the meal. The dose of the drug (from 10 to 80 mg 1 time / day) is selected based on the initial levels of LDL-C, the goal of therapy and the individual effect. At the beginning of treatment and / or during a dose increase of Liprimar, it is necessary to monitor plasma lipid levels every 2-4 weeks and adjust the dose accordingly.
With primary hypercholesterolemia and combined (mixed) hyperlipidemia in most patients, the desired effect can be achieved with the use of Liprimar at a dose of 10 mg 1 time / day. The therapeutic effect occurs within 2 weeks and usually reaches a maximum within 4 weeks. With long-term treatment, the effect is preserved.
For patients with homozygous familial hypercholesterolemia, the drug is prescribed at a dose of 80 mg 1 time / day (in most cases, therapy led to a decrease in LDL-C levels by 18-45%.
Impaired renal function does not affect the level of atorvastatin in plasma or the degree of decrease in the content of Xc-LDL when using Liprimar, therefore, changing the dose of the drug is not required.
When using the drug in elderly patients, there were no differences in safety, efficacy, or achievement of lipid-lowering therapy goals compared to the general population.

From the side of the central nervous system and peripheral nervous system: insomnia, malaise, dizziness, amnesia, headache, asthenic syndrome, paresthesia, peripheral neuropathy, hypoesthesia.
From the digestive system: vomiting, anorexia, abdominal pain, dyspepsia , nausea, loss of appetite, flatulence, constipation, diarrhea, hepatitis, pancreatitis, cholestatic jaundice.
From the musculoskeletal system: back pain, muscle cramps, myositis, myopathy, arthralgia, rhabdomyolysis.
Allergic reactions: urticaria, pruritus, skin rash, Anaphylactic reactions , bullous rash, polymorphic exudative erythema, toxic epidermal necrolysis (Lyell's syndrome), malignant exudative erythema (Stevens-Johnson syndrome).
Metabolism: hypoglycemia, hyperglycemia, increased serum CK.
From the hemopoietic system: thrombocytopenia.
Other: impotence, peripheral edema, weight gain, chest pain, secondary renal failure, fever, alopecia, tinnitus.

- active liver disease or increased serum transaminase activity (more than 3 times compared with the upper limit of the norm) of unclear genesis;
- women of reproductive age who do not use adequate methods of contraception;
- pregnancy;
- lactation (breastfeeding);
- hypersensitivity to the drug;
- in children and adolescents under the age of 18, the effectiveness and safety of Liprimar has not been established.

With caution should be used in patients who abuse alcohol and / or have a liver disease (in history).

As with the use of other lipid-lowering drugs of the same class, after treatment with Liprimar, a moderate (more than 3 times compared with the upper limit of the norm) increase in the serum activity of hepatic transaminases was noted. A persistent increase in the serum level of hepatic transaminases (more than 3 times compared with the upper limit of the norm) was observed in 0.7% of patients who received Liprimar in clinical studies. The frequency of such changes with the use of the drug in doses of 10, 20, 40 and 80 mg was 0.2%, 0.2%, 0.6% and 2.3%, respectively. Increased liver transaminase activity is usually not accompanied by jaundice or other clinical manifestations. With a decrease in the dose of Liprimar, the temporary or complete withdrawal of the drug, the activity of hepatic transaminases returned to the original level. Most patients continued taking atorvastatin in a reduced dose without any consequences.
Before the start, after 6 weeks and 12 weeks after starting the drug or after increasing the dose, as well as during the entire course of treatment, it is necessary to monitor indicators of liver function. Liver function should also be investigated when clinical signs of liver damage appear. In case of an increase in the level of hepatic transaminases, their activity should be monitored until it is normalized. If the increase in AST or ALT activity is more than 3 times higher than the upper limit of normal, a dose reduction or drug withdrawal is recommended.
Myalgia was observed in patients receiving Liprimar. The diagnosis of myopathy (pain and weakness in the muscles in combination with an increase in the activity of CPK more than 10 times compared with the upper limit of the norm) should be assumed in patients with common myalgias, muscle soreness or weakness and / or a pronounced increase in the activity of CPK. Therapy with Liprimar should be stopped in case of a pronounced increase in the activity of CPK or in the presence of confirmed or suspected myopathy. The risk of myopathy in the treatment of other drugs of this class increased with the simultaneous use of cyclosporine, fibrates, Erythromycin , nicotinic acid or azole antifungal drugs. Many of these drugs inhibit the metabolism mediated by the CYP3A4 isoenzyme of the cytochrome P450 system and / or the transport of drugs. Atorvastatin is biotransformed by CYP3A4. When prescribing Liprimar in combination with fibrates, erythromycin, immunosuppressants, azole antifungal drugs or nicotinic acid in lipid-lowering doses, the expected benefit and risk of treatment should be carefully weighed and regularly monitored by patients to identify pain or weakness in muscles, especially during the first months of treatment and periods of increasing the dose of any drug. In such situations, periodic determination of CPK activity can be recommended, although such monitoring does not prevent the development of severe myopathy.
Atorvastatin may cause an increase in CPK activity. When using Liprimar, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure caused by myoglobinuria are described. Liprimar therapy should be temporarily stopped or completely canceled if there are signs of possible myopathy or a risk factor for the development of renal failure in the presence of rhabdomyolysis (for example, severe acute infection, hypotension, serious surgery, trauma, metabolic, endocrine and electrolyte disturbances and uncontrolled seizures).
Patients should be warned that they should immediately consult a doctor if they develop unexplained pains or weakness in the muscles, especially if they are accompanied by indisposition or fever.

Store at a temperature not exceeding 25 ° C, out of the reach of children.
Shelf life - 3 years.