Crestor pills 40 mg 28 pcs
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Active ingredients
Rosuvastatin
Release form
Pills
Composition
Rosuvastatin (in the form of rosuvastatin calcium) 40 mg adjuvants: lactose monohydrate - 164.72 mg, microcrystalline cellulose - 54.92 mg, calcium phosphate - 20 mg, crospovidone - 15 mg, magnesium stearate - 3.76 mg. Film composition: lactose monohydrate - 3.6 mg, hypromellose - 2.52 mg, triacetin (glycerol triacetate) - 0.72 mg, titanium dioxide - 2.11 mg, iron dye red oxide - 0.05 mg.
Pharmacological effect
Lipid-lowering drug, a selective competitive inhibitor of HMG-CoA reductase. Crestor reduces elevated concentrations of LDL cholesterol (LDL-C), total cholesterol, triglycerides (TG), increases the concentration of high-density cholesterol-lipoprotein (LDL-C), and also lowers the concentration apolipoprotein B (ApoV), cholesterol-non-LPVP, cholesterol-VLDL, TG-VLDL and increases the concentration of apolipoprotein AI (ApoA-I) (see Tables 1 and 2), reduces the ratio of cholesterol-LDL / cholesterol-HDL, total cholesterol / cholesterol - LPVP and XC-non-LPVP / XC-HDL and ApoV / ApoA-1 ratio. Therapeutic effect azvivaetsya within one week after the beginning of therapy with Crestor, after 2 weeks of treatment up to 90% of the maximum possible effect. The maximum therapeutic effect is usually achieved by the 4th week of therapy and is maintained with regular use of the drug. Crestor is effective in adult patients with hypercholesterolemia with or without hypertriglyceridemia; regardless of race, gender or age, incl. in patients with diabetes and familial hypercholesterolemia. In 80% of patients with hypercholesterolemia IIa and IIb type according to Fredrikson (the average initial concentration of LDL-C LDL is about 4.8 mmol / l) while receiving the drug at a dose of 10 mg, the concentration of LDL-C cholesterol reaches less than 3 mmol / l. In patients with heterozygous familial hypercholesterolemia, receiving Crestor at a dose of 20-80 mg, showed a positive dynamics of lipid profile (study with 435 patients). After titration to a daily dose of 40 mg (12 weeks of therapy), a decrease in the concentration of LDL-C by 53% is noted. In 33% of patients, the concentration of cholesterol-LDL is less than 3 mmol / l. In patients with homozygous familial hypercholesterolemia who take Crestor at a dose of 20 mg and 40 mg, the average decrease in the concentration of cholesterol-LDL is 22%. In patients with hypertriglyceridemia with an initial concentration of TG from 273 to 817 mg / dl, treated with Crestor at a dose of 5 mg to 40 mg once a day for 6 weeks, the plasma TG concentration significantly decreased (seetable 2). The additive effect is observed in combination with fenofibrate in relation to the concentration of triglycerides and with nicotinic acid in lipid-lowering doses in relation to the concentration of HDL-C (see also Special Instructions section). In the METEOR study of 984 patients aged 45-70 years with a low risk of developing coronary heart disease (10-year risk on the Framingham scale less than 10%), an average concentration of cholesterol-LDL 4.0 mmol / l (154.5 mg / dl) and subclinical atherosclerosis (as measured by the thickness of the intima-media complex of the carotid arteries - TCIM) the effect of rosów was studied a statin on the thickness of the intima-media complex. Patients received rosuvastatin at a dose of 40 mg / day or placebo for 2 years. Rosuvastatin therapy significantly slowed the rate of progression of maximal TCIM for 12 carotid artery segments compared with placebo with a difference of -0.0145 mm / year [95% confidence interval from -0.0196 to -0.0093; shorter than 0.001]. Compared to baseline values in the rosuvastatin group, there was a decrease in the maximum TKIM value by 0.0014 mm / year (0.12% / year (unreliable difference)) compared with an increase in this indicator by 0.0131 mm / year (1.12% / year (less than 0.001) ) in the placebo group. To date, no direct relationship has been shown between a decrease in TCIM and a decrease in the risk of cardiovascular events. The METEOR study was conducted in patients with a low risk of coronary artery disease for whom the dose of Crestor 40 mg is not recommended. A dose of 40 mg should be administered to patients with severe hypercholesterolemia and a high risk of cardiovascular diseases. The results of the JUPITER study (Substantiation of the use of statins for primary prevention: a interventional study evaluating rosuvastatin) in 17802 patients showed that rosuvastatin significantly reduced the risk of cardiovascular complications (252 in the placebo group compared with 142 in the rosuvastatin group) (p <0.001) with a 44% decrease in relative risk. The effectiveness of therapy was noted after 6 first months of use of the drug. A statistically significant reduction of 48% of the combined criterion was noted, including death from cardiovascular causes, stroke and myocardial infarction (risk ratio 0.52, 95% confidence interval 0.40–0.68, less than 0.001), a 54% decrease in the occurrence of fatal or nonfatal myocardial infarction (risk ratio: 0.46, 95%, confidence interval 0.30–0.70) and 48% for fatal or nonfatal stroke.Total mortality decreased by 20% in the group of rosuvastatin (risk ratio: 0.80, 95%, confidence interval 0.67–0.97, p = 0.02). The safety profile of patients taking rosuvastatin at a dose of 20 mg was generally similar to the safety profile in the placebo group.
Pharmacokinetics
Absorption and distribution of Cmax of rosuvastatin in the blood plasma is achieved approximately 5 hours after ingestion. Absolute bioavailability is approximately 20%. Rozuvastatin is metabolized primarily by the liver, which is the main site of cholesterol synthesis and XC-LDL metabolism. Vd rosuvastatin is approximately 134 liters. Approximately 90% of rosuvastatin binds to plasma proteins, mainly albumin. Metabolism Limited metabolism (about 10%). Rosuvastatin is a non-core substrate for metabolism by cytochrome P450 enzymes. The main isoenzyme involved in rosuvastatin metabolism is the isoenzyme CYP2C9. CYP2C19, CYP3A4, and CYP2D6 isoenzymes are less involved in metabolism. The main identified metabolites of rosuvastatin are N-desmethylrozuvastatin and lactone metabolites. N-desmethylrosuvastatin is approximately 50% less active than rosuvastatin, lactone metabolites are pharmacologically inactive. More than 90% of the pharmacological activity of inhibiting circulating HMG-CoA reductase is provided by rosuvastatin, the rest is provided by its metabolites. Excretion About 90% of the dose of rosuvastatin is excreted unchanged through the intestine (including absorbed and unabsorbed rosuvastatin). The rest is excreted by the kidneys. Plasma T1 / 2 is approximately 19 hours. T1 / 2 does not change with increasing dose of the drug. The geometric mean plasma clearance is approximately 50 l / h (coefficient of variation 21.7%). As with other inhibitors of HMG-CoA reductase, membrane cholesterol transporter is involved in the process of hepatic uptake of rosuvastatin, which plays an important role in the hepatic elimination of rosuvastatin. Linearity The systemic exposure of rosuvastatin increases in proportion to the dose. Pharmacokinetic parameters do not change when taken daily. Pharmacokinetics in special clinical situations. Age and gender do not have a clinically significant effect on rosuvastatin pharmacokinetics. Ethnic groups.Pharmacokinetic studies have shown an approximately twofold increase in the median AUC and Cmax of rosuvastatin in patients of Asian ethnicity (Japanese, Chinese, Filipinos, Vietnamese and Koreans) compared with Europeans; Indian patients showed an increase in the median AUC and Cmax by a factor of 1.3. Pharmacokinetic analysis revealed no clinically significant differences in pharmacokinetics among Europeans and representatives of the Negroid race. Renal failure. In patients with mild and moderate renal insufficiency, the plasma concentration of rosuvastatin or N-desmethylrozuvastatin does not change significantly. In patients with severe renal insufficiency (CC less than 30 ml / min), plasma plasma concentration of rosuvastatin is 3 times higher, and N-desmethylrozuvastatin concentration is 9 times higher than in healthy volunteers. The concentration of rosuvastatin in the blood plasma of patients on hemodialysis was about 50% higher than in healthy volunteers. Hepatic insufficiency. In patients with various stages of liver failure, there was no increase in Rosuvastatin T1 / 2 in patients with a score of 7 or less on the Child-Pugh scale. Two patients with 8 and 9 points on the Child-Pugh scale showed an increase in T1 / 2, at least 2 times. Experience with rosuvastatin in patients with more than 9 points on the Child-Pugh scale is absent. Genetic polymorphism. HMG-CoA reductase inhibitors, incl. Crestor, bind to the transport proteins OATP1B1 (a polypeptide transporting organic anions that is involved in the capture of statins by hepatocytes) and BCRP (efflux transporter). In carriers of the SLCO1B1 (OATP1B1) c.521CC and ABCG2 (BCRP) c.421AA genotypes, there was an increase in exposure (AUC) to rosuvastatin by 1.6 and 2.4 times, respectively, compared to the carriers of SLCO1B1 c.521TT and ABCG2 c.421SS genotypes.
Indications
- Fredrikson's primary 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 (for example; exercise, weight loss) are insufficient; - family homozygote; hypercholesterolemia as an adjunct to diet and other lipid-lowering therapy (for example, LDL-apheresis), or in caseswhen such therapy is not effective enough - hypertriglyceridemia (type IV according to Fredrikson) as a supplement to the diet; to slow down the progression of atherosclerosis as a supplement to the diet in patients who have been shown therapy to reduce the concentration of total cholesterol and LDL-C; cardiovascular complications (stroke, heart attack, arterial revascularization) in adult patients without clinical signs of coronary heart disease, but with an increased risk of its development (age over 50 years for men and over 60 years for the same increased concentration of C-reactive protein (≥ 2 mg / l) in the presence of at least one of the additional risk factors such as arterial hypertension, low concentration of HDL-C, smoking, family history of early onset of CHD).
Contraindications
For pills 10 mg and 20 mg: - hypersensitivity to rosuvastatin or any of the components of the drug; - liver disease in the active phase, including a persistent increase in serum transaminase activity and any increase in serum transaminase activity (more than 3 times as compared with VGN ); - pronounced renal dysfunction (CC less than 30 ml / min); - myopathy; - simultaneous use of cyclosporine; - in women: pregnancy, lactation, lack of adequate contraceptive methods; - patients susceptible to the development of myotoxic complications; - lactose intolerance, lactase deficiency or glucose-galactose malabsorption (the drug contains lactose). For 40 mg pills: - hypersensitivity to rosuvastatin or any of the components of the drug; - simultaneous use of cyclosporine; - in women: pregnancy, lactation, lack of adequate methods of contraception; - liver disease in the active phase, including a persistent increase in serum transaminase activity and any increase in serum transaminase activity (more than 3 times as compared to B GN); - patients with risk factors for the development of myopathy / rhabdomyolysis, namely: moderate renal insufficiency (CC less than 60 ml / min), hypothyroidism, personal or family history of muscular diseases, myotoxicity while taking other HMG-CoA reductase inhibitors or a history of fibrates; - excessive alcohol consumption; - conditionswhich can lead to an increase in plasma concentration of rosuvastatin; simultaneous administration of fibrates; patients of the Asian race; lactose intolerance, lactase deficiency or glucose-galactose malabsorption (the preparation contains lactose). With caution For pills of 10 mg and 20 mg: the risk of myopathy / rhabdomyolysis - renal failure, hypothyroidism, personal or family history of hereditary muscular diseases and a previous history of muscular toxicity using other HMG-CoA reductase inhibitors or f brethren; excessive drinking; age over 65; conditions in which there is an increase in the plasma concentration of rosuvastatin; race (Asian race); co-administration with fibrates (see Pharmacokinetics; history of liver disease; sepsis; arterial hypotension; extensive surgical interventions, injuries; severe metabolic, endocrine or electrolyte disturbances; uncontrollable convulsive seizures. For 40 mg pills: low severity renal insufficiency (KK) more than 60 ml / min); over 65 years of age; history of liver disease; sepsis; hypotension; extensive surgical interventions, injuries, severe metabolic, endocrine or elec krolitnye violations; uncontrolled convulsive seizures.Application in pediatric practiceEfficiency and safety of the drug in children under 18. Not 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 not recommended use Crestor in children under 18. Patients with liver failure. There is no data or experience of using the drug in patients with a score above 9 on the Child-Pugh scale. .
Precautionary measures
Application for violations of liver functionWith caution, you should prescribe the drug for violations of the liver.It is not necessary to change the dose in case of renal dysfunction. The concentration of amplodipine in the blood plasma does not depend on the degree of reduction of renal function. Use in children It is contraindicated in children and adolescents under the age of 18. Application in elderly patients With caution in elderly patients.
Use during pregnancy and lactation
Crestor is contraindicated in pregnancy and lactation (breastfeeding). Women of reproductive age should use adequate methods of contraception. Because cholesterol and other products of cholesterol biosynthesis are important for the development of the fetus, the potential risk of inhibiting HMG-CoA reductase exceeds the benefits of using the drug in pregnant women. In the event of pregnancy in the course of therapy, the drug should be discontinued immediately. There are no data on the release of rosuvastatin in breast milk. therefore, during the breastfeeding period, the drug should be stopped.
Dosage and administration
Inside, do not chew or crush the pill, swallow whole, washed down with water. The drug can be prescribed at any time of the day, regardless of the meal. Before starting treatment with Crestor, the patient should begin to follow the standard cholesterol-lowering diet and continue to follow it during treatment. The dose of the drug should be selected individually depending on the goals of therapy and the therapeutic response to treatment, taking into account the current recommendations on target lipid concentrations. The recommended initial dose for patients starting the drug or for patients transferred from taking other HMG-CoA reductase inhibitors , should be 5 or 10 mg of the drug Crestor 1 time / day. When choosing the initial dose, one should be guided by the individual concentration of cholesterol and take into account the possible risk of cardiovascular complications, as well as the potential risk of side effects. If necessary, the dose can be increased to more after 4 weeks (see Pharmacodynamics section). Due to the possible development of side effects when taken at a dose of 40 mg, compared with lower doses of the drug (see section Side Effects), increase doses up to 40 mg, after an additional dose above the recommended initial dose within 4 weeks of therapy, can be performed only in patients with severe hypercholesterolemia and with a high risk of cardiovascular complications (especially in patients with familial hypercholesteritis erinemia), in which the desired result of treatment was not achieved when taking a dose of 20 mg, and which will be under the supervision of a specialist (see section Special Instructions).Particularly careful monitoring of patients receiving the drug at a dose of 40 mg is recommended. Prescribing the drug at a dose of 40 mg is not recommended for patients who have not previously visited a doctor. After 2-4 weeks of therapy and / or with an increase in the dose of Crestor, monitoring of lipid metabolism indices is necessary (dose adjustment is required if necessary). Elderly patients do not need dose adjustment. In patients with mild or moderate severity, dose adjustment is not required. In patients with severe renal failure (CC less than 30 ml / min), the use of the drug Crestor is contraindicated. The use of the drug in a dose of 40 mg is contraindicated in patients with moderately impaired renal function (CC 30-60 ml / min) (see the section Specific Instructions and Pharmacodynamics). For patients with moderately impaired renal function, an initial dose of 5 mg is recommended. Patients with liver failure: Crestor is contraindicated in patients with liver disease in the active phase (see Contraindications). Ethnic groups. When studying the pharmacokinetic parameters of rosuvastatin in patients belonging to different ethnic groups, an increase in the systemic concentration of rosuvastatin among Japanese and Chinese was observed (see the section on Specific Instructions). This fact should be taken into account when administering Crestor to these groups of patients. When prescribing doses of 10 and 20 mg, the recommended initial dose for patients of the Mongoloid race is 5 mg. The purpose of the drug in a dose of 40 mg is contraindicated for patients of the Mongoloid race (see the section Contraindications). Genetic polymorphism. In carriers of the SLCO1B1 genotypes (OATP1B1) C.521CC and ABCG2 (BCRP) p.421AA, there was an increase in exposure (AUC) to rosuvastatin compared to carriers of the SLCO1B1 genotypes p.521TT and ABCG2 p.421CC. For patients carrying genotypes p.521CC or p.421AA, the recommended maximum dose of Crestor is 20 mg 1 time / day (see Pharmacokinetics, Special Instructions and Interaction with other drugs). Patients predisposed to myopathy. The prescription of the drug in a dose of 40 mg is contraindicated in patients with factors that may indicate a predisposition to the development of myopathy (see section Contraindications). When prescribing doses of 10 and 20 mg, the recommended initial dose for this group of patients is 5 mg (see section Contraindications). Concomitant therapy. Rosuvastatin binds to various transport proteins (in particular, OATP1B1 and BCRP).Combined use of the drug Crestor with drugs (such as cyclosporine, some HIV protease inhibitors, including a combination of ritonavir with atazanavir, lopinavir and / or tipranavir), increases the concentration of rosuvastatin in the plasma due to interaction with transport proteins, may increase the risk of myopathy (including rhabdomyolysis ) (see sections Special instructions and Interaction with other drugs). You should read the instructions for use of these drugs before their appointment in conjunction with the drug Crestor. In such cases, you should evaluate the possibility of prescribing alternative therapy or temporary cessation of taking the drug Crestor. If the use of the above preparations is necessary, the ratio of the benefits and risks of concomitant therapy with Crestor should be evaluated and the possibility of reducing its dose should be considered (see the Interaction with other drugs section).
Side effects
Side effects observed when taking the drug Crestor, usually expressed slightly and pass on their own. As with the use of other inhibitors of HMG-CoA reductase, the frequency of side effects is mostly dose-dependent. The frequency of adverse reactions: often (more than 1/100, less than 1/10); infrequently (more than 1/1000, less than 1/100); rarely (more than 1/10 000, less than 1/1000); very rare (less than 1/10 000), unspecified frequency (cannot be calculated according to the available data). From the immune system: rarely - hypersensitivity reactions, including angioedema. From the endocrine system: often - type 2 diabetes. Со CNS sides: often - headache, dizziness. From the digestive system: often - constipation, nausea, abdominal pain; rarely - pancreatitis. From the side of the skin: infrequently - pruritus, rash, urticaria. From the side of the musculoskeletal system: often - myalgia; rarely - myopathy (including myositis), rhabdomyolysis. Others: often - asthenic syndrome. From the urinary system: proteinuria can be detected in patients who received Crestor. Changes in the amount of protein in the urine (from the absence or trace amounts to ++ or more) are observed in less than 1% of patients receiving 10-20 mg of the drug, and in approximately 3% of patients receiving 40 mg of the drug.A slight change in the amount of protein in the urine was noted when taking a dose of 20 mg. In most cases, proteinuria decreases or disappears during therapy and does not mean the onset or the progression of an existing kidney disease. From the musculoskeletal system: when using the Crestor drug in all doses, especially when taken in doses exceeding 20 mg, the following effects were reported on the musculoskeletal system: myalgia, myopathy (including myositis); in rare cases, rhabdomyolysis with or without acute renal failure. A dependent increase in CPK activity is observed in an insignificant number of patients taking rosuvastatin. In most cases, it was minor, asymptomatic and temporary. In the case of increased activity of CPK (more than 5 times compared to VGN), therapy should be suspended. Liver: when rosuvastatin is used, a dose-dependent increase in the activity of hepatic transaminases is observed in an insignificant number of patients. In most cases, it is insignificant, asymptomatic, and temporary. Laboratory indicators: the following changes in laboratory parameters were also observed when using Crestor: an increase in the concentration of glucose, bilirubin, GGT, alkaline phosphorus, thyroid function disorders.
Overdose
When several daily doses are taken simultaneously, the pharmacokinetic parameters of rosuvastatin do not change. There is no specific treatment for an overdose of rosuvastatin. In case of overdose, it is recommended to carry out symptomatic treatment and measures aimed at maintaining the functions of vital organs and systems. The control of liver function and the level of CPK is necessary. It is unlikely that hemodialysis will be effective.
Interaction with other drugs
Effect of the use of other drugs on rosuvastatin Transport protein inhibitors: Rosuvastatin binds to certain transport proteins, in particular, OATP1B1 and BCRP. The concomitant use of drugs that are inhibitors of these transport proteins may be accompanied by an increase in plasma concentration of rosuvastatin and an increased risk of myopathy (seetable 3 and sections Dosage regimen and special instructions). Cyclosporin: with simultaneous use of rosuvastatin and cyclosporin, AUC of rosuvastatin was on average 7 times higher than the value observed in healthy volunteers (see table 3). It does not affect the plasma concentration of cyclosporine. Crestor is contraindicated in patients taking cyclosporine (see section Contraindications). HIV protease inhibitors: although the exact mechanism of interaction is unknown, co-administration of HIV protease inhibitors can lead to a significant increase in rovuvastatin exposure (see table 3). A pharmacokinetic study on the simultaneous use of 20 mg of rosuvastatin with a combination preparation containing two HIV protease inhibitors (400 mg of lopinavir / 100 mg of ritonavir) in healthy volunteers resulted in an approximately twofold and fivefold increase in AUC0-24 and Cmax of rosuvastatin, respectively. Therefore, concomitant use of rosuvastatin and HIV protease inhibitors is not recommended (see sections Dosage regimen, Specific instructions, table 3). Gemfibrozil and other lipid-lowering drugs: combined use of rosuvastatin and gemfibrozil causes a 2-fold increase in Cmax of rosuvastatin in blood plasma and AUC of rosuvastatin ( see section Special instructions). Based on data on specific interactions, pharmacokinetically significant interactions with fenofibrates are not expected, pharmacodynamic interactions are possible. Gemfibrozil, fenofibrate, other fibrates and lipid-lowering doses of nicotinic acid increased the risk of myopathy with simultaneous use with HMG-CoA reductase inhibitors, possibly due to that they can cause myopathy when used in monotherapy (see section Special Instructions). While taking the drug with gemfibrozil, fibrates, nicotinic acid in lipid-lowering doses (more than 1 g / day), an initial dose of 5 mg is recommended for patients, 40 mg is contraindicated when taken together with fibrates (see sections Contraindications, Dosage regimen, Special indications). Ezetimibe: simultaneous use of the drug Crestor at a dose of 10 mg and ezetimibe at a dose of 10 mg was accompanied by an increase in AUC of rosuvastatin in patients with hypercholesterolemia (see Table 3).An increase in the risk of side effects due to the pharmacodynamic interaction between Crestor and ezetimibm cannot be ruled out. Antacids: the simultaneous use of rosuvastatin and suspensions of antacids containing magnesium and aluminum 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. Erythromycin: the simultaneous use of rosuvastatin and erythromycin leads to a decrease in AUC of rosuvastatin by 20% and Cmax of rosuvastatin by 30%. Such an interaction may occur as a result of increased intestinal motility caused by taking erythromycin. Cytochrome P450 isoenzymes: the results of in vivo and in vitro studies have shown that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a weak substrate for these isoenzymes. Therefore, the interaction of rosuvastatin with other drugs at the metabolic level with the participation of cytochrome P450 isoenzymes is not expected. There was no clinically significant interaction of rosuvastatin with fluconazole (an inhibitor of CYP2C9 and CYP3A4 isoenzymes) and ketoconazole (an inhibitor of CYP2A6 and CYP3A4 isoenzymes). Fusidic acid: studies on the interaction of rosuvastatin and fusidic acid have not been conducted. As with other statins, post-marketing reports of cases of rhabdomyolysis with rosuvastatin and fusidic acid were received. It is necessary to closely monitor patients. If necessary, it is possible to temporarily stop taking rosuvastatin. Interaction with drugs, which requires dose adjustment of rosuvastatin (see table 3) The dose of Crestor should be adjusted if necessary to be used together with drugs that increase exposure to rosuvastatin. You should read the instructions for use of these drugs before their appointment in conjunction with the drug Crestor. If exposure is expected to increase by 2 times or more, the initial dose of Crestor should be 5 mg 1 time / day.The maximum daily dose of Crestor should also be adjusted so that the expected exposure to rosuvastatin does not exceed that for a dose of 40 mg taken without the simultaneous prescription of drugs interacting with rosuvastatin. For example, the maximum daily dose of Crestor with simultaneous use with gemfibrozil is 20 mg (1.9 times increase in exposure), with ritonavir / atazanavir - 10 mg (3.1 times increase). Antagonists of vitamin K: start of rosuvastatin therapy or increase the dose of the drug patients receiving concurrent vitamin K antagonists (for example, warfarin) can lead to an increase in the International Normalized Relationship (MHO). Canceling rosuvastatin or lowering the dose may result in a decrease in MPE. In such cases, MHO control is recommended. Oral contraceptives / hormone replacement therapy: the simultaneous use of rosuvastatin and oral contraceptives increases the AUC of ethinyl estradiol and AUC norgestrel by 26% and 34%, respectively. Such an increase in plasma concentration should be considered when selecting the dose of plasma concentration should be taken into account when selecting the dose of oral contraceptives. Pharmacokinetic data on the simultaneous use of the drug Crestor and hormone replacement therapy are not available, therefore, a similar effect cannot be excluded when using this combination. However, this combination was widely used during clinical trials and was well tolerated by patients. Other medicines: the clinically significant interaction of rosuvastatin with digoxin is not expected.
special instructions
Effect on the kidneys of patients receiving high doses of Crestor (mainly 40 mg), tubular proteinuria was observed, which, in most cases, was transient. Such proteinuria did not indicate acute kidney disease or progression of kidney disease. Patients taking the drug in a dose of 40 mg are recommended to monitor renal function during treatment. From the musculoskeletal system When using the drug Crestor in all doses, especially in doses of more than 20 mg, the following effects on the musculoskeletal system were reported: myalgia ,myopathy, in rare cases - rhabdomyolysis. Determination of KFC activity The activity of CPK should not be performed after intense physical exertion or if there are other possible causes for an increase in the activity of CPK, which can lead to incorrect interpretation of the results. If the initial activity of CPK is significantly increased (5 times higher than VGN), then in 5-7 days it is necessary to re-measure. You should not start therapy if the repeated test confirms the initial activity of CPK (more than 5 times higher than VGN). Before initiating therapyWhen prescribing the drug Crestor, as well as the appointment of other inhibitors of HMG-CoA reductase, you should be careful risk factors for myopathy / rhabdomyolysis (see the section with caution), it is necessary to consider