Crestor 5 mg pills №98

Latin name

CRESTOR

Release form

Coated Tablets

Composition

1 tab. contains Rosuvastatin (in the form of Calcium salt) 5 mg

Packaging

98 pcs.

pharmachologic effect

Selective competitive inhibitor of HMG-CoA reductase - an enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A into mevalonate, a precursor of cholesterol (Xc).
Rosuvastatin increases the number of liver LDL receptors on the cell surface, increasing the uptake and catabolism of LDL, which, in turn, leads to inhibition of the synthesis of VLDL, thereby reducing the total number of LDL and VLDL.
Crestor reduces the high content of Xc-LDL, total Xc, triglycerides (TG), increases the content of Xc-HDL, as well as reduces the content of apolipoprotein B (ApoB), Xc-non-LPVP, Xc-VLDL, TG-VLP and increases the level of apolipoprotein A-1 (ApoA-1), reduces the ratio of Xc-LDL / Xc-HDL, total Xc / Xc-HDL and Xc-non-LPVP / Xc-HDL and the ratio ApoV / ApoA-1.
The therapeutic effect is manifested within 1 week. after the start of therapy and after 2 weeks of treatment, it is 90% of the maximum possible effect, which is usually achieved by week 4 and then remains constant.
Crestor is effective in adult patients with hypercholesterolemia with or without hypertriglyceridemia (regardless of race, gender or age), including in patients with diabetes and familial hypercholesterolemia.
In 80% of patients with hypercholesterolemia IIa and Type IIb (the mean baseline level of Xc-LDL is about 4.8 mmol / l) while receiving the drug at a dose of 10 mg, the level of Xc-LDL reaches <3 mmol / l.
Patients with heterozygous familial hypercholesterolemia with the use of Crestor at a dose of 20-80 mg show positive dynamics of the lipid profile (study with 435 patients). After titration to a daily dose of 40 mg (12 weeks of therapy), a decrease in the level of LDL-C is noted by 53%. 33% of patients achieved a level of Xc-LDL <3 mmol / l.
In patients with homozygous familial hypercholesterolemia with the use of Crestor at a dose of 20 mg and 40 mg, the average decrease in the level of LDL-C LDL is 22%.
The additive effect is observed in combination with fenofibrate in relation to the content of TG and with nicotinic acid in relation to the content of Xc-HDL.
Studies on the effect of rosuvastatin on reducing the number of complications caused by lipid disorders (such as IHD) have not yet been completed.

Indications

- hypercholesterolemia (type IIa, including familial heterozygous hypercholesterolemia) or mixed hypercholesterolemia (type IIb) as a supplement to the diet when diet and other non-drug therapies (eg exercise, weight loss) are insufficient;
- familial homozygous hypercholesterolemia as an adjunct to diet and other cholesterol-lowering therapy, or in cases where such therapy is not suitable for the patient.

Contraindications

- liver diseases in the active phase (including a persistent increase in the activity of hepatic transaminases or any increase in the activity of transaminases by more than 3 times as compared with VGN);
- pronounced impaired renal function (CC <30 ml / min);
- myopathy;
- simultaneous administration of cyclosporine;
- pregnancy;
- lactation (breastfeeding);
- children's and teenage age up to 18 years (since efficiency and safety are not established);
- hypersensitivity to the drug.
Crestor is not prescribed to women of reproductive age who do not use adequate methods of contraception.

Use during pregnancy and lactation

Crestor is contraindicated during pregnancy and lactation. If pregnancy occurs during therapy, the drug should be discontinued immediately.
Women of reproductive age should use adequate methods of contraception. Since Xc and its biosynthesis products are important for the development of the fetus, the potential risk of inhibition of HMG-CoA reductase exceeds the benefits of the drug.
Clinical data on the allocation of rosuvastatin with breast milk are not available, so if necessary, the use of Crestor during lactation, breastfeeding should be discontinued.
ATexperimental studies Rosuvastatin was found to be excreted in rat milk.

Dosage and administration

The drug can be taken at any time of the day, regardless of the meal.The pills are swallowed whole, without chewing or crushing, drinking water.
The recommended initial dose is 10 mg 1 time / day. In most cases, the therapeutic effect is achieved when taking the drug in a dose of 10 mg. If necessary, the dose can be increased to 20 mg after 4 weeks. Increasing the dose to 40 mg is possible only in patients with severe hypercholesterolemia and high risk of cardiovascular complications (especially in patients with familial hypercholesterolemia) in cases where the desired result is not achieved when taking the drug at a dose of 20 mg and when the treatment will be carried out under medical supervision.
Elderly do not require dose adjustment.
In patients with mild to moderate renal insufficiency, dose adjustment is not required.
Crestor is contraindicated in patients with severe renal failure.
Experience with the use of the drug in patients with liver failure with a score above 9 on the Childe-Pugh scale is absent.
Crestor is contraindicated in patients with liver disease in the active phase.
Efficacy and safety in children has not been established. The experience of using the drug in pediatric practice is limited to a small number of children (8 years and older) with familial homozygous hypercholesterolemia. Currently, it is not recommended to use Crestor in children.

Side effects

The incidence of side effects is estimated as follows: often occurring (> 1% <10%), rarely occurring (> 0.01% <0.1%).
From the side of the central nervous system: often - headache, dizziness.
Gastrointestinal: often - constipation, nausea, abdominal pain. With the use of Crestor, there is a dose-dependent increase in the activity of hepatic transaminases in a small number of patients. In most cases, it is insignificant, asymptomatic and temporary.
Musculoskeletal system: often myalgia; rarely - myopathy. Rare cases of rhabdomyolysis that were occasionally associated with impaired renal function were observed in patients who received Crestor at a dose of 80 mg. In all cases, there was an improvement when cessation of therapy. A dose-dependent increase in the level of CPK is observed in an insignificant number of patients taking Crestor. In most cases, it was minor, asymptomatic and temporary. In the case of increasing the level of CPK (more than 5 times compared to VGN) therapy should be temporarily suspended.
Urogenital: in patients receiving Crestor, proteinuria, mainly tubular, may be detected. Changes in the amount of protein in the urine (from the absence or trace amounts to pronounced proteinuria) are observed in <1% of patients when using the drug at a dose of 10–20 mg / day and approximately 3% of patients at a dose of 40 mg / day. A slight change in the amount of protein in the urine was noted when taking a dose of 20 mg. In most cases, proteinuria diminishes or disappears during therapy and does not mean the onset or the progression of an existing kidney disease.
Other: often - asthenic syndrome.
The side effects observed when taking Crestor are usually mild and do not go away on their own. As with the use of other inhibitors of HMG-CoA reductase, the frequency of their occurrence is dose-dependent.

special instructions

Crestor is used with caution in the presence of risk factors for the development of rhabdomyolysis (including kidney failure, hypothyroidism, personal or family history of hereditary muscular diseases and a previous history of muscle toxicity when using other HMG-CoA reductase inhibitors or fibrates) in chronic alcoholism, in patients over the age 70 years old, with a history of liver diseases, sepsis, hypotension, with extensive surgical interventions, injuries, severe metabolic endocrine or electrolyte disturbances, with uncontrolled epilepsy.
Before starting treatment with Crestor, the patient should begin to follow a standard lipid-lowering diet and continue to follow it throughout the entire treatment period. The dose of the drug is selected individually, depending on the goals of therapy and the response to treatment, taking into account the generally accepted recommendations.
When using Crestor at a dose of 40 mg, it is recommended to monitor indicators of renal function.
In patients with existing risk factors for rhabdomyolysis, it is necessary to consider the ratio of the risk and possible benefits of therapy and conduct clinical observation.
The patient should be informed of the need to immediately report to the doctor about cases of sudden onset of muscle pain, muscle weakness or spasms, especially in combination with indisposition and fever. In such patients, the level of CPK should be determined. Therapy should be discontinued if the level of CPK is significantly increased (more than 5 times compared to VGN) or if the muscle symptoms are pronounced and cause daily discomfort (even if the level of KFK is 5 times less than VGN). If the symptoms disappear and the CK level returns to normal, consideration should be given to reappointment of Crestor or other HMG-CoA reductase inhibitors in smaller doses with careful monitoring of the patient.
Determination of CPK should not be carried out after intense physical exertion or in the presence of other possible reasons for increasing CPK, which may lead to a misinterpretation of the obtained results. If the initial level of CPK is significantly increased (5 times higher than VGN), after 5-7 days it is necessary to re-measure. It is not necessary to begin therapy if the repeated test confirms the initial level of CPK (5 times higher than VGN).
Routine monitoring of CPK in the absence of symptoms is not appropriate.
There are no signs of an increase in toxic effects on skeletal muscle in the application of Crestor as part of combination therapy. An increase in the incidence of myositis and myopathy has been reported in patientswho took other HMG-CoA reductase inhibitors in combination with fibrin acid derivatives (including gemfibrozil), cyclosporin, nicotinic acid, azole antifungal drugs, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy in combination with some inhibitors of HMG-CoA reductase. Thus, the simultaneous appointment of Crestor and gemfibrozil is not recommended. The balance of risk and potential benefit should be carefully weighed when using Crestor and fibrates or niacin together.
It is recommended to carry out the determination of indicators of liver function before the start of therapy and 3 months after the start of therapy. Reception of Crestor should be stopped or reduced dose of the drug, if the level of transaminase activity in the serum is 3 times higher than VGN. In patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome, the treatment of major diseases should be carried out before starting treatment with Crestor.
Influence on ability to drive motor transport and control mechanisms
When engaging in potentially hazardous activities, patients should be aware that dizziness may occur during therapy.

Drug interaction

With the simultaneous use of rosuvastatin and cyclosporine, the AUC of rosuvastatin was on average 7 times higher than that observed in healthy volunteers, while the plasma concentration of cyclosporin did not change.
Initiation of rosuvastatin therapy or an increase in the dose of a drug in patients receiving vitamin K antagonists (for example, warfarin) at the same time can lead to an increase in the prothrombin time of the International Normalized Relationship (INR), and withdrawal of rosuvastatin or a decrease in the dose of the drug can lead to a decrease in INR (in such cases monitoring of INR is recommended).
The combined use of rosuvastatin and gemfibrozil leads to an increase of 2 times C_max in blood plasma and rosuvastatin AUC.
The simultaneous use of rosuvastatin and antacids containing aluminum and Magnesium hydroxide, reduces the plasma concentration of rosuvastatin by about 50%. This effect is less pronounced if antacids are applied 2 hours after taking rosuvastatin. The clinical significance of this interaction has not been studied.
The simultaneous use of rosuvastatin and Erythromycin reduces the AUC of rosuvastatin by 20% and C_max rosuvastatin by 30% (probably as a result of increased intestinal motility caused by taking erythromycin).
The simultaneous use of rosuvastatin and oral contraceptives increases the AUC of ethinyl estradiol and AUC of norgestrel by 26% and 34%, respectively. Such an increase in plasma concentration should be taken into account when selecting the dose of oral contraceptives during the application of Crestor (such a combination was widely used during clinical trials and was well tolerated by patients).Pharmacokinetic data on the simultaneous use of Crestor and hormone replacement therapy are absent, therefore, a similar effect cannot be excluded when using this combination.
No clinically significant interaction of rosuvastatin with Digoxin or fenofibrate is expected. Gemfibrozil, other fibrates and hypolipidemic doses of nicotinic acid (> = 1 g / day) increased the risk of myopathy, while being used with other HMG-CoA reductase inhibitors. perhaps due to the fact that they can cause myopathy and when used as monotherapy.
The results of in vivo and in vitro studies have shown that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P isoenzymes₄₅₀. In addition, rosuvastatin is a weak substrate for these enzymes. There was no clinically significant interaction between rosuvastatin and Fluconazole (a CYP2C9 and CYP3A4 inhibitor) and Ketoconazole (a CYP2A6 inhibitor CYP3A4). The combined use of rosuvastatin and itraconazole (CYP3A4 inhibitor) increases the AUC of rosuvastatin by 28% (clinically insignificant). Thus, interactions associated with the cytochrome P system are not expected.₄₅₀.

Overdose

With simultaneous administration of several daily doses, the pharmacokinetic parameters of rosuvastatin do not change.
Treatment: there is no specific antidote. If necessary, conduct symptomatic therapy, control of liver function and the level of CPK is necessary.It is unlikely that hemodialysis will be effective.

Storage conditions

The drug should be stored out of reach of children at a temperature not exceeding 30 ° C.