Rosucard pills 10 mg 90 pcs
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Active ingredients
Rosuvastatin
Release form
Pills
Composition
Active ingredient: Rosuvastatin (Rosuvastatin) Active ingredient concentration (mg): 10
Pharmacological effect
Lipid-lowering drug from the group of statins. selective competitive inhibitor of gmg-coa-reductase - an enzyme that converts gmg-coa into mevalonate, a precursor of cholesterol (xc). increases the number of LPP receptors on the surface of hepatocytes, which leads to increased seizure and catabolism of LPNP, inhibition of the synthesis of hepatocytes, reducing the total concentration of LPNP and lonp. reduces concentrations of xc-lpnp, high density cholesterol-nonlipoproteins (xc-nelpvp), xs-lonp, total xs, tg, tg-lnnp, apolipoprotein b (apov), reduces the ratios xc-lpnp / xs-lpvp, total xs / xs - LPVP, HS-NELVP / HS-LPVP, Apo / Apolipoprotein A-1 (Apoa-1), increases the concentration of XC-LPVP and Apoa-1. Hypolipidemic action is directly proportional to the size of the dose administered. therapeutic effect appears within 1 week after the start of therapy, after 2 weeks it reaches 90% of the maximum, reaches week 4 and remains constant after this. table 1. dose-dependent effect in patients with primary hypercholesterolemia (type iia and iib according to Fredrickson classification) (average corrected percentage change from baseline) dose number of patients xc-lpnp total xc xc-lvvplazebo 13 -7 -5 -3 310 mg 17 -52 -36 1420 mg 17 -55 -40 840 mg 18 -63 -46 10 dose amount patients tg xc-nelpvp apo in apo a-i placebo 13 -3 -7 -3 010 mg 17 -10 -48 -42 420 mg 17 -23 -51 -46 540 mg 18 -28 -60 -54 0 table 2. dose-dependent effect in patients with hypertriglyceridemia (type iib and iv according to Fredrickson classification ) (average percentage change compared with baseline) dose number of patients tg xc-lpnp total hplicebo 26 1 5 110 mg 23 -37 -45 -4020 mg 27 -37 -31 -3440 mg 25 -43 -43 -40 dose of patients xc-lpvp xs-nelpvp xs-lonp tg-lonpplazebo 26 -3 2 2 610 mg 23 8 -49 -48 -3920 mg 27 22 -43 -49 -4040 mg 25 17 -51 -56 -48clinical efficacy in adult patients with hypercholesterolemia with or without hypertriglyceridemia, not dependent on race, gender or age, incl. in patients with diabetes and familial hypercholesterolemia. in 80% of patients with hypercholesterolemia type IIa and iib (according to Fredrickson classification) with an average initial concentration of xc-lpnp of about 4.8 mmol / l while taking the drug in a dose of 10 mg, the concentration of xc-lpnp reaches values less than 3 mmol / l. Heterozygous familial hypercholesterolemia, receiving rosuvastatin at a dose of 20-80 mg / day, showed a positive dynamics of lipid profile.after titration to a daily dose of 40 mg (12 weeks of therapy), a decrease in the concentration of xs-lpnp by 53% was noted. 33% of patients achieved a concentration of HS-lpnp less than 3 mmol / l. in patients with homozygous familial hypercholesterolemia receiving rosuvastatin at a dose of 20 mg and 40 mg, the average decrease in the concentration of hs-lpnp was 22%. from 273 mg / dL to 817 mg / dL, treated with rosuvastatin in doses from 5 mg to 40 mg 1 time / day for 6 weeks, plasma concentration of Tg significantly decreased (see table 2). the additive effect is observed in combination with fenofibrate in relation to the concentration of tg and nicotino oh acid in lipid-lowering doses (more than 1 g / day) against concentration xc-lpvp.v meteor study rosuvastatin treatment significantly slowed the rate of progression of the maximum thickness of the intima-media complex (IMT) of the carotid artery segment 12 compared with placebo. compared with baseline values in the rosuvastatin group, a decrease in the maximum value by 0.0014 mm / year was observed compared with an increase in this indicator by 0.0131 mm / year in the placebo group. So far, no direct relationship has been demonstrated between a decrease in cardiovascular events and a decrease in the risk of cardiovascular events. The results of the jupiter study showed that rosuvastatin significantly reduced the risk of cardiovascular complications with a relative risk reduction of 44%. efficacy of therapy was noted after the first 6 months of use of the drug. There was a statistically significant reduction of 48% of the combined criterion, including death from cardiovascular causes, stroke and myocardial infarction, a 54% reduction in the occurrence of fatal or nonfatal myocardial infarction and a 48% decrease in fatal or nonfatal stroke. total mortality decreased by 20% in the rosuvastatin group. the safety profile of patients taking rozuvastatin at a dose of 20 mg was, in general, similar to the safety profile in the placebo group.
Pharmacokinetics
After taking the drug inside Cmax of rosuvastatin in the blood plasma is reached in approximately 5 hours. The absolute bioavailability is approximately 20%. Distribution Binding to plasma proteins (mainly albumin) is approximately 90%.Vd - 134 l. Rozuvastatin is predominantly absorbed by the liver, which is the main site for the synthesis of Xc and Xc-LDL metabolism. It penetrates the placental barrier. Metabolism Biotransformation in the liver to a small extent (about 10%), being a non-core substrate for isoenzymes of the P450 cytochrome system. involved in the metabolism of rosuvastatin is the isoenzyme CYP2C9. CYP2C19, CYP3A4 and CYP2D6 isoenzymes are less involved in metabolism. The main metabolites of rosuvastatin are N-dismethyl and lactone metabolites. N-dismethyl is about 50% less active than rosuvastatin; lactone metabolites are pharmacologically inactive. More than 90% of the pharmacological activity on the inhibition of circulating HMG-CoA reductase is provided by rosuvastatin, the rest is provided by its metabolites. As in the case of other HMG-CoA reductase inhibitors, a specific membrane carrier, a polypeptide transporting an organic anion, is involved in the hepatic capture process ) 1B1, which plays an important role in its hepatic elimination. Excretion of T1 / 2 is approximately 19 hours, does not change with increasing dose of the drug. The average value of plasma clearance is approximately 50 l / h (coefficient of variation 21.7%). About 90% of the dose of rosuvastatin is excreted unchanged through the intestines, the rest - by the kidneys. Linearity The systemic exposure of rosuvastatin increases proportionally to the dose. Pharmacokinetic parameters do not change when taken daily. Pharmacokinetics in special clinical cases of patients with mild and moderately marked renal insufficiency plasma concentration of rosuvastatin -dismethyl does not change significantly. In patients with severe renal insufficiency (CC less than 30 ml / min), plasma concentration of rosuvastatin is 3 times higher, and N-dismethyl is 9 times higher than in healthy volunteers. The concentration of rosuvastatin in blood plasma in patients on hemodialysis is approximately 50% higher than in healthy volunteers. In patients with impaired liver function of 7 points and below on the Child-Pugh scale, no increase in T1 / 2 of rosuvastatin was detected; in patients with impaired liver function 8 and 9 on the Child-Pugh scale, T1 / 2 lengthening was observed in 2 times. Experience with the use of the drug in patients with more pronounced abnormal liver function is absent. Sex and age do not have a clinically significant effect on the pharmacokinetics of rosuvastatin. The pharmacokinetic parameters of rosuvastatin depend on race.The AUC of the representatives of the Mongoloid race (Japanese, Chinese, Filipinos, Vietnamese and Koreans) is 2 times higher than that of the Caucasians. Indians have an average AUC and Cmax value increased by 1.3 times. Genetic polymorphism HMG-CoA reductase inhibitors, incl. Rosuvastatin binds to OATP1B1 transport proteins (a polypeptide of organic anion transport that is involved in the capture of statins by hepatocytes) and BCRP (an efflux transporter). The carriers of the SLCO1B1 genotypes (OATP1B1) p.521CC and ABCG2 (BCRP) p.421AA showed an increase in exposure (AUC) to rosuvastatin 1.6 and 2.4 times, respectively, compared with the carriers of the SLCO1B1 genotypes p.521TT and ABCG2 p.421SS.
Indications
Primary hypercholesterolemia (type IIa according to Fredrickson), including heterozygous hereditary hypercholesterolemia or mixed (combined) hypercholesterolemia (type II according to Fredrickson), as a supplement to diet and other non-drug measures (exercise and weight loss) while not using a healthy diet. Homozygous form of hereditary hypercholesterolemia and with insufficient effectiveness of diet therapy and other types of treatment aimed at reducing the level of lipids (for example, LDL apheresis), or if such treatments are not suitable for the patient. Hypertriglyceridemia (type IV according to Fredrikson) as a supplement to the diet. To slow the progression of atherosclerosis as a supplement to the diet in patients who have been shown therapy to reduce total cholesterol and Cholesterol - LDL. Prevention of major cardiovascular complications (stroke, heart attack, arterial revascularization) in adult patients without clinical signs of coronary heart disease (CHD), but with an increased risk of its development (age rshe 50 years for men and over 60 years for women, 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, familial history of early onset CHD).
Contraindications
Hypersensitivity to rosuvastatin or other components of the drug, liver disease in the active phase or a steady increase in serum activity of liver transaminases (more than 3 times compared with the upper limit of normal) of unclear genesis,liver failure (severity from 7 to 9 points on the Child-Pugh scale); Increasing the concentration of creatinine phosphokinase (CPK) in the blood by more than 5 times compared with the upper limit of normal (VGN); Hereditary diseases such as lactose intolerance, lactase deficiency or glucose-galactose malabsorption (due to the presence in the composition of lactose); Severe kidney function (CC less than 30 ml / min); Myopathy; Patients predisposed to the development of myotoxic complications; Simultaneous administration of cyclosporine; Combined use with and HIV protease inhibitors; Women of reproductive age who do not use adequate methods of contraception; Pregnancy and lactation period; Age up to 18 years (efficacy and safety have not been established).
Precautionary measures
The drug should be stored out of the reach of children, in its original packaging, at a temperature not exceeding 25 ° C.
Use during pregnancy and lactation
Rosucardum is contraindicated during pregnancy and lactation (breastfeeding). Use of the drug Rossardo in women of reproductive age is possible only if reliable contraceptive methods are used and if the patient is informed of the possible risk of treatment for the fetus. Since cholesterol and substances synthesized from cholesterol are important for development fetus, the potential risk of inhibition of HMG-CoA reductase exceeds the benefits of the use of the drug during pregnancy. If pregnancy is diagnosed during drug therapy, Rosacard should be immediately discontinued, and the patient should be warned of the potential risk to the fetus. If you need to use the drug during lactation, taking into account the possibility of undesirable effects in infants, you should decide whether to stop breastfeeding.
Dosage and administration
Inside, without chewing and chopping, swallow whole, washed down with water, at any time of the day, regardless of the meal. Before starting therapy with Rosukard, the patient must begin to follow the standard lipid-lowering diet and continue to follow it during treatment. The dose of the drug should be selected individually depending on the indications and therapeutic response, taking into account the current generally accepted recommendations for target lipid levels.If you need to take the drug in a dose of 5 mg, a 10 mg tablet should be divided into two parts according to the risk. The recommended starting dose of Rosucard for patients starting the drug or for patients transferred from other HMG-CoA reductase inhibitors is 5 or 10 mg once a day. When choosing the initial dose, one should be guided by the patient’s cholesterol content and take into account the risk of cardiovascular complications, and the potential risk of side effects should be assessed. If necessary, the dose may be increased after 4 weeks. Due to the possible development of side effects when taking a dose of 40 mg compared with lower doses of the drug, final titration to the maximum dose of 40 mg should be carried out only in patients with severe hypercholesterolemia and high risk cardiovascular complications (especially in patients with hereditary hypercholesterolemia) in whom the target cholesterol level was not reached when taking a dose of 20 mg and who will be under medical Patients with hepatic impairment: Patients with hepatic impairment with Child-Pugh scores below 7 dozens of dose-adjusting dosage requirements are not required. Patients with renal insufficiency: Patients with renal insufficiency of mild dose adjustment are not required. The initial dose of rosacardium is recommended - 5 mg per day. In patients with severe renal insufficiency (QC less than 30 ml / min), use of roscard is contraindicated. In patients with moderate renal insufficiency (QC 30 - 60 ml / min) use of roscard is 40 mg per day is contraindicated. Specific populations. Elderly patientsDuring patients over 65 years of age, dose adjustment is not required. Patients with a predisposition to myopathy: The use of Rosucard at a dose of 40 mg per day is contraindicated in patients with a predisposition to myopathy. When prescribing doses of 10 mg and 20 mg per day, the recommended initial dose of rocardia for this group of patients is 5 mg per day. Ethnic groups An increase in the systemic concentration of the drug in representatives of the Mongoloid race was observed when studying the pharmacokinetic parameters of rosuvastatin. This fact should be taken into account in the appointment of Rosukard to patients of the Mongoloid race.When prescribing doses of 10 and 20 mg, the recommended initial dose of roscard for this group of patients is 5 mg per day. The use of roscard in a dose of 40 mg per day is not recommended for representatives of the Mongoloid race. When prescribing rosucard with gemfibrozil, the dose should not exceed 10 mg per day.
Side effects
From the side of blood and lymphatic system: rarely - thrombocytopenia. From the nervous system: often - headache, dizziness; very rarely - peripheral neuropathy, memory loss or loss; frequency is unknown - sleep disturbances, including insomnia and nightmares. Psychiatric disorders: frequency is unknown - depression. On the part of the digestive system: often - nausea, constipation, abdominal pain; infrequently - vomiting; rarely - pancreatitis; frequency is unknown - diarrhea. From the side of the liver and biliary tract: rarely - transient increase in the activity of AST and ALT; very rarely - hepatitis, jaundice. On the respiratory system: frequency unknown - cough, dyspnea. On the immune system: rarely - hypersensitivity reactions, including angioedema. On the musculoskeletal and connective tissues: often myalgia; rarely, myopathy (including myositis), rhabdomyolysis (in patients treated with doses of> 20 mg / day); very rarely - arthralgia, tendinopathy, possibly with tendon rupture; frequency is unknown - immune-mediated necrotizing myopathy. From the sides of the skin and subcutaneous tissues: infrequently - pruritus, urticaria, skin rash; frequency unknown - Stevens-Johnson syndrome. From the kidneys and urinary tract: often - proteinuria (with a frequency of more than 3% in patients receiving a dose of 40 mg), decreasing in the course of therapy and not associated with the occurrence of kidney disease, urinary tract infection; hematuria is very rare. From the genital organs and the mammary gland: gynecomastia is very rare. Effect on laboratory and instrumental studies: infrequently, a transient dose-dependent increase in the activity of serum CK, with an increase of more than 5 times compared to VGN, therapy should be temporary suspended, increasing the concentration of glycated hemoglobin in the blood plasma. Other: often - asthenia; frequency unknown - peripheral edema.
Overdose
When several daily doses are taken simultaneously, the pharmacokinetic parameters of rosuvastatin do not change. Treatment: there is no specific treatment, symptomatic therapy is carried out to maintain the functions of vital organs and systems. Monitoring of liver function and CPK activity is necessary. Hemodialysis is ineffective.
Interaction with other drugs
Effect 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 transport proteins may be accompanied by an increase in plasma plasma concentration of rosuvastatin and an increased risk of myopathy (see Table 3). Cyclosporine: while rosuvastatin and cyclosporine were used at the same time, rosuvastatin was, on average, 7 times higher than noted in healthy volunteers. It does not affect the plasma concentration of cyclosporine. Rosuvastatin is contraindicated in patients taking cyclosporine. HIV protease inhibitors: although the exact mechanism of interaction is unknown, the combined use of HIV protease inhibitors can lead to a significant increase in the exposure of rosuvastatin (see table 3). A pharmacokinetic study on the simultaneous use of rozuvastatin at a dose of 20 mg and a combined 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 AUC (0-24) and Cmax of rosuvastatin, respectively. Therefore, concomitant use of the drug Rozukard and HIV protease inhibitors is not recommended (see table 3). Gemfibrozil and other lipid-lowering agents: the combined use of rosuvastatin and gemfibrozil leads to a 2-fold increase in Cmax and AUC of rosuvastatin. Based on data on specific interactions, pharmacokinetically significant interactions with fenofibrate are not expected; pharmacodynamic interactions are possible. Gemfibrozil, fenofibrate, other fibrates and nicotinic acid in lipid-lowering doses (more than 1 g / day) increase the risk of myopathy while being used with HMG-CoA reductase inhibitors, possibly due to the fact that they can cause myopathy and when used in as monotherapy.At the same time taking the drug with gemfibrozil, fibrates, nicotinic acid in lipid-lowering doses, an initial dose of Rosucard 5 mg is recommended for patients, 40 mg is contraindicated when taken together with fibrates. Fusidic acid: there were no specific studies on the drug interaction of fusidic acid and rosuvastatin. , but there were separate reports of cases of rhabdomyolysis. Ezetimibe: simultaneous use of the drug Rozukard in a dose of 10 mg and ezetimibe in a dose of 10 mg increase in AUC axis of rosuvastatin in patients with hypercholesterolemia (see. Table 3). An increase in the risk of side effects due to the pharmacodynamic interaction between rosardard and ezetimib cannot be ruled out. Erythromycin: the simultaneous use of rosuvastatin and erythromycin reduces the AUC (0-t) 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. Antacids: the simultaneous use of rosuvastatin and suspensions of antacids containing aluminum or 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. Cytochrome P450 system enzymes: 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 enzymes. 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 between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4 isoenzymes) and ketoconazole (an inhibitor of isoenzymes CYP2A6 and CYP3A4). combined with drugs that increase the exposure of rosuvastatin.If exposure is expected to increase by 2 times or more, the initial dose of the drug Rosucard should be 5 mg 1 time / day. You should also adjust the maximum daily dose of the drug Rozukard so that the expected exposure of rosuvastatin does not exceed that for a dose of 40 mg, taken without the simultaneous prescription of drugs that interact with rosuvastatin. For example, the maximum daily dose of rosuvastatin with simultaneous use with gemfibrozil is 20 mg (1.9 times increase in exposure), with ritonavir / atazanavir - 10 mg (3.1 times increase in exposure). Table 3. The effect of concomitant therapy on the exposure of rosuvastatin (AUC, data are listed in descending order) - results of published clinical studiesCompetitive therapy regimen Rosuvastatin regimen Changes Rosuvastatin AUC change 75-200 mg 2 times / day, 6 months 10 mg 1 time / day, 10 days Increase 7.1 timesAtazanivi p 300 mg / ritonavir 100 mg 1 time / day, 8 days 10 mg once Increase by 3.1 times Semepremir 150 mg 1 time / day, 7 days 10 mg once Increase 2.8 times Lopinavir 400 mg / ritonavir 100 mg 2 times / day, 17 days 20 mg 1 time / day, 7 days 2.1 times increaseKlopidogrel 300 mg (loading dose), then 75 mg in 24 hours 20 mg once 2 times increase Gemfibrozil 600 mg 2 times / day, 7 days 80 mg once Increases 1.9 times Eltrombopag 75 mg 1 time / day, 10 days 10 mg once Increase by 1.6 times Darunavir 600 mg / ritonavir 100 mg 2 times / day, 7 days 10 mg 1 time / day, 7 days Increase by 1.5 times Typr Navir 500 mg / ritonavir 200 mg 2 times / day, 11 days 10 mg once Increase 1.4 times Dronedarone 400 mg 2 times / day No data Increase 1.4 times Itraconazole 200 mg 1 time / day, 5 days 10 mg or 80 mg once Increase in 1.4 times Ezetimibe 10 mg 1 time / day, 14 days 10 mg 1 time / day, 14 days Increase 1.2 times Fosamprenavir 700 mg / ritonavir 100 mg 2 times / day, 8 days 10 mg once No change Aleglitazar 0.3 mg, 7 days 40 mg, 7 days No change Silymarin 140 mg 3 times / day, 5 days 10 mg one time No change phenofibrate 67 mg 3 times / day, 7 days 10 mg, 7 days No change Rifampin 450 mg 1 p s / day, 7 days 20 mg once No changes Ketoconazole 200 mg 2 times / day, 7 days 80 mg once No changes Fluconazole 200 mg 1 time / day, 11 days 80 mg once No changes Erythromycin 500 mg 4 times / day, 7 days 80 mg one-time Reduction of 28% Baikalin 50 mg 3 times / day, 14 days 20 mg one-time Reduction of 47% Effect of the use of rosuvastatin on other drugs Vitamin K antagonists: initiation of rosuvastatin therapy or increasing the dose of rosuvastatin in patients receiving vitamin K antagonists (for example, warfarin or other coumarin antico gulyanty) may lead to an increase in INR.Canceling or lowering the dose of rosardard may cause a decrease in INR. In such cases, an INR 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 taken into account when selecting the dose of oral contraceptives. There are no pharmacokinetic data on the simultaneous use of rosuvastatin and hormone replacement therapy. We cannot exclude a similar effect with the simultaneous use of rosuvastatin and hormone replacement therapy. 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 kidneys In patients who received high doses of rosuvastatin (mostly 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. In patients taking the drug in a dose of 40 mg, it is recommended to monitor indicators of renal function during treatment. Effect on the musculoskeletal system When using rosuvastatin in all doses, and especially in doses over 20 mg, the following effects on the musculoskeletal system were reported: myalgia, myopathy, in rare cases rhabdomyolysis. Determination of KFC activity, the activity of KFC should not be performed after intense physical exertion or if there are other possible reasons for the increase in KFK activity, which can t lead to misinterpretation 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. Therapy should not be started if the repeated test confirms the initial activity of CPK (more than 5 times higher than VGN). Before initiating therapyWhen using the drug Rosukard, as well as using other HMG-CoA reductase inhibitors, in patients with existing risk factors for myopathy / rhabdomyolysis should be cautious.The ratio of risk and benefit should be assessed and, if necessary, therapy should be followed up with clinical observation of the patient during treatment. During therapy, the patient should be informed about the need to immediately report to the doctor about cases of sudden onset of muscle pain, muscle weakness or spasms, especially in combination with malaise and fever. In such patients, the activity of CPK should be determined. Therapy should be discontinued if the activity of CPK is significantly increased (more than 5 times higher than VGN) or if the symptoms of the muscles are pronounced and cause daily discomfort (even if the activity of CPK is less than 5 times increased compared to VGN). If the symptoms disappear and the activity of CPK returns to normal, consideration should be given to reappointment of Rosucard or other HMG-CoA reductase inhibitors in smaller doses with careful monitoring of the patient. Routine control of CPK activity in the absence of symptoms is inappropriate. Very rare cases of immune-mediated necrotizing myopathy with clinical manifestations in the form of persistent weakness of the proximal muscles and an increase in the activity of CPK in the blood serum during treatment or at the discontinuation of statins, including rozuvastatin, have been observed. Additional studies of the muscular and nervous systems, serological studies, and therapy with immunosuppressive drugs may be required. There are no signs of increased effects on skeletal muscles when taking rosuvastatin and concomitant therapy. However, an increase in the incidence of myositis and myopathy was reported in patients taking other HMG-CoA reductase inhibitors in combination with fibrin acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid in hypolipidemic doses (more than 1 g / day), azole antifungal agents, inhibitors HIV proteases and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when used together with some HMG-CoA reductase inhibitors. Thus, the simultaneous use of the drug Rosukard and gemfibrozil is not recommended. The ratio of risk and potential benefit should be carefully weighed in with the combined use of Rosucard and fibrates or lipid-lowering doses of nicotinic acid. The drug is contraindicated in a dose of 40 mg Rosucardin together with fibrates.2-4 weeks after the start of treatment and / or with an increase in the dose of Rozukard, monitoring of lipid metabolism indices is necessary (dose adjustment is required if necessary). Liver It is recommended to determine liver function indices before starting therapy and 3 months after starting therapy. Taking the drug Rozukard should be stopped or the dose should be reduced if the activity of hepatic transaminases in plasma is 3 times higher than VGN.Patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome should be treated before starting treatment with Roscard. HIV protease inhibitors Rosucard with HIV protease inhibitors. Interstitial lung disease When using some statins, especially for long periods strap, reported isolated cases of interstitial lung disease. Manifestations of the disease can be shortness of breath, unproductive cough and worsening of general well-being (weakness, weight loss and fever). If an interstitial lung disease is suspected, it is necessary to discontinue therapy with rosukard. Type 2 diabetes mellitus. Statin class drugs can cause an increase in blood glucose concentration. In some patients with a high risk of developing diabetes mellitus, such changes may lead to its manifestation, which is an indication for prescribing hypoglycemic therapy. However, reducing the risk of vascular diseases while taking statins exceeds the risk of developing diabetes, therefore this factor should not serve as a basis for discontinuation of treatment with statins. Patients at risk (blood glucose concentration on an empty stomach is 5.6-6.9 mmol / l, BMI> 30 kg / m2, hypertriglyceridemia, history of arterial hypertension) should be monitored and regular monitoring of biochemical parameters should be performed. Lactose: The drug Rosukard should not be used in patients with lactase deficiency, galactose intolerance, and glucose-galactose malabsorption. Ethnic groupsIn pharmacokinetic studies, an increase in systemic concentration was observed among Chinese and Japanese patients. and rosuvastatin compared with ratesobtained among patients of the Caucasian race. Effect on the ability to drive motor vehicles and control mechanisms. Care should be taken when driving and occupations that require high concentration of attention and speed of psychomotor reactions.