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    3. Rosuvastatin IC 5mg 30 tablets — Made in Ukraine — Free Delivery

    Rosuvastatin IC 5mg 30 tablets — Made in Ukraine — Free Delivery


    Brand: InterChem
    Product Code: Rosuvastatin IC
    Availability: In Stock
    $19.57
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    Pharmacological properties

    Pharmacodynamics
    Mechanism of action. Rosuvastatin is a selective and competitive inhibitor of HMC-CoA reductase, an enzyme that determines the rate of reaction and converts 3-hydroxy-3-methylglutaryl-coenzyme A into mevalonate, a precursor of CS. The main site of action of rosuvastatin is the liver, a target organ for lowering cholesterol levels.
    Rosuvastatin increases the number of LDL receptors on the surface of liver cells, enhancing the uptake and catabolism of LDL, and inhibits hepatic VLDL synthesis, thus reducing the total amount of VLDL and LDL particles.
    Pharmacodynamic effects. Rosuvastatin reduces elevated levels of LDL cholesterol, total cholesterol and triglycerides, and increases HDL cholesterol levels. It also lowers levels of apolipoprotein B (ApoB), non-HDL cholesterol, VLDL cholesterol, VLDL TG, and increases apolipoprotein A-I (ApoA-I) levels. Rosuvastatin reduces the ratio of LDL cholesterol / HDL cholesterol, total cholesterol / HDL cholesterol, non-HDL cholesterol / HDL cholesterol and ApoV / ApoA-I.
    The therapeutic effect is achieved within 1 week after the start of the preparation, 90% of the maximum effect - after 2 weeks. The maximum effect is usually achieved after 4 weeks and continues further.
    Clinical efficacy and safety. Rosuvastatin is effective in the treatment of adults with hypercholesterolemia - with or without hypertriglyceridemia - regardless of race, gender, or age, as well as in special populations such as patients with diabetes mellitus or familial hypercholesterolemia. It was reported that approximately 80% of patients with hypercholesterolemia of type IIa and IIb (average initial level of LDL-C of about 4.8 mmol / L), who took rosuvastatin at a dose of 10 mg, managed to achieve the normative target levels of LDL-C set by the European Society of Atherosclerosis ( EAS; 1998) (3 mmol / L).
    In patients with heterozygous familial hypercholesterolemia, who took rosuvastatin in doses of 20–80 mg according to the enhanced dose titration scheme, there was a favorable effect of the preparation on lipid parameters and the achievement of target levels at all doses. After titration to a daily dose of 40 mg (12 weeks of treatment), LDL cholesterol decreased by 53%. In 33% of patients, the normative levels of LDL cholesterol according to EAS (3 mmol / l) were achieved.
    The results of a study of the response to the use of rosuvastatin in doses of 20–40 mg under an enhanced dose titration scheme have been reported in patients with homozygous familial hypercholesterolemia. In the general population, the level of LDL cholesterol decreased by an average of 22%.
    When using rosuvastatin in combination with fenofibrate, an additive effect was observed in reducing the level of triglycerides. With the combined use of rosuvastatin and niacin (nicotinic acid), an additive effect was noted to increase the level of HDL cholesterol (see SPECIAL INSTRUCTIONS).
    In patients aged 45–70 years with a low risk of coronary artery disease (defined as the risk on the Framingham scale of 10% over 10 years), a mean LDL cholesterol 4.0 mmol / L (154.5 mg / dL), but with subclinical atherosclerosis (determined by the increase in the thickness of the carotid intima-media complex - TCIMSA), who used rosuvastatin at a dose of 40 mg 1 time per day for 2 years, there was a significant slowdown in the progression of the maximum TCIMSA at 12 points of the carotid artery compared with placebo. A direct correlation between a decrease in TCIMSA and a decrease in the risk of disorders from the cardiovascular system has not been demonstrated. Patients with a low risk of coronary heart disease who are not members of the target population of 40 mg rosuvastatin were recruited to this study. A dose of 40 mg should be prescribed only to patients with severe hypercholesterolemia and a high risk of cardiovascular disorders (see APPLICATION).
    It was reported that the use of rosuvastatin as a means of primary prevention of significant atherosclerotic cardiovascular diseases at a dose of 20 mg 1 time per day for 2 years in men (≥50 years) and women (≥60 years) led to a decrease in the concentration of LDL cholesterol by almost half compared with a placebo.
    Children. It was reported that patients aged 10-17 years (at II-V stages of development according to Tanner, girls whose menstruation began less than 1 year ago) with heterozygous familial hypercholesterolemia, who received rosuvastatin at a dose of 5, 10 or 20 mg / day, followed by a 40-week period of open titration of the dose of rosuvastatin, the level of LDL cholesterol decreased by 38.3%; 44.6% and 50.0%, respectively, in the groups receiving rosuvastatin at a dose of 5; 10 and 20 mg versus 0.7% in the placebo group. At the end of the 40-week period of open dose titration to achieve the target level (the maximum dose was 20 mg 1 time per day), 40.5% of patients managed to achieve the target LDL-C level of 2.8 mmol / L. After 52 weeks of study treatment, there was no effect on height, weight, body mass index (BMI), or puberty (see SPECIAL INSTRUCTIONS). The experience of use in children is limited, the long-term effects of rosuvastatin (1 year) on puberty are unknown.
    Pharmacokinetics
    Suction. Cmax of rosuvastatin in blood plasma is achieved 5 hours after oral administration. The absolute bioavailability is about 20%.
    Distribution. Rosuvastatin is largely taken up by the liver, which is the main site of cholesterol synthesis and LDL cholesterol clearance. The volume of distribution of rosuvastatin is about 134 liters. About 90% of rosuvastatin binds to blood plasma proteins, mainly albumin.
    Metabolism. Rosuvastatin undergoes limited metabolism (about 10%). In vitro metabolic studies using human hepatocytes indicate that rosuvastatin is a non-core substrate for metabolism mediated by cytochrome P450 enzymes. The main isoenzyme involved is CYP 2C9, with 2C19, 3A4 and 2D6 playing a slightly lesser role. The major metabolites identified are the N-desmethyl and lactone metabolites. The N-desmethyl metabolite is approximately 50% less active than rosuvastatin, the lactone metabolite is considered clinically inactive. Rosuvastatin accounts for more than 90% of the activity of a circulating inhibitor of HMG-CoA reductase.
    Excretion. About 90% of the dose of rosuvastatin is excreted unchanged in the feces (together with the absorbed and non-absorbed active substance), the rest is excreted in the urine. Approximately 5% is excreted unchanged in the urine. T½ from blood plasma is about 19 hours and does not increase with increasing dose. The geometric mean of the clearance of rosuvastatin from blood plasma is about 50 l / h (coefficient of variation - 21.7%). As with the use of other HMG-CoA reductase inhibitors, the hepatic uptake of rosuvastatin occurs with the participation of the membrane transporter OATP-C, which plays an important role in the hepatic elimination of rosuvastatin.
    Linearity. The systemic exposure of rosuvastatin increases in proportion to the dose. With repeated daily use, the pharmacokinetic parameters do not change.
    Special patient groups
    Age and gender. There was no clinically significant effect of age or gender on the pharmacokinetics of rosuvastatin in adults. The pharmacokinetics of rosuvastatin in children with heterozygous familial hypercholesterolemia was similar to that in adult volunteers.
    Race. Pharmacokinetic studies have shown that in patients of the Mongoloid race (Japanese, Chinese, Filipinos, Vietnamese and Koreans), the median values ​​of AUC and Cmax are approximately twice as high as in representatives of the Caucasian race; in Indians, the median values ​​of AUC and Cmax were increased by about 1.3 times. Analysis of population pharmacokinetics did not reveal clinically significant differences between patients of the European and Negroid races.
    Impaired renal function. In a study involving patients with varying degrees of renal impairment, no changes in plasma concentrations of rosuvastatin or N-desmethyl metabolite were observed in individuals with mild or moderate impairment. In patients with severely impaired renal function (creatinine clearance 30 ml / min), plasma concentrations of rosuvastatin are 3 times higher, and the levels of N-desmethyl metabolite are 9 times higher than in healthy volunteers. The equilibrium plasma concentrations of rosuvastatin in hemodialysis patients were approximately 50% higher than in healthy volunteers.
    Liver dysfunction. In a study of patients with varying degrees of liver dysfunction, there were no signs of increased exposure to rosuvastatin in patients whose condition was assessed at 7 or less on the Child-Pugh scale. However, in two patients with scores of 8 and 9 on the Child-Pugh scale, systemic exposure was at least twice as high as in patients with lower scores. There is no experience of using rosuvastatin in patients whose condition is estimated at more than 9 points on the Child-Pugh scale.
    Genetic polymorphism. The distribution of HMG-CoA reductase inhibitors, including rosuvastatin, occurs with the participation of transport proteins OATP1B1 and BCRP. Patients with genetic polymorphisms SLCO1B1 (OATP1B1) and / or ABCG2 (BCRP) are at risk of increased exposure to rosuvastatin. Individual polymorphism SLCO1B1 c. 521CC and ABCG2 c. 421AA is associated with increased exposure (AUC) of rosuvastatin compared to genotypes SLCO1B1 c. 521TT or ABCG2 c. 421CC. Special genotyping in clinical practice is not provided, but patients with such polymorphism are recommended to use a lower dose of rosuvastatin.
    Children. Pharmacokinetic parameters in children with heterozygous familial hypercholesterolemia at the age of 10–17 years have not been fully determined. A small study of the pharmacokinetics of rosuvastatin (in the form of tablets) with the participation of pediatric patients showed that the exposure of the preparation in children is similar to that in adult patients. The results also indicate that significant dose-proportional deviations are not expected.

    Indications

    Treatment of hypercholesterolemia. adults and children over the age of 10 years with primary hypercholesterolemia (type iia, including heterozygous familial hypercholesterolemia) or mixed dyslipidemia (type iib) as an adjunct to diet, when adhering to a diet and using other non-medication (e.g. exercise, weight loss body) is insufficient.
    With homozygous familial hypercholesterolemia, as an adjunct to diet and other lipid-lowering treatments (eg LDL apheresis) or when such treatment is inappropriate.
    Prevention of cardiovascular disorders. Prevention of significant cardiovascular disorders in patients who are estimated to be at high risk of a first case of cardiovascular disorder (see PHARMACOLOGICAL PROPERTIES), in addition to correcting other risk factors.

    Application

    Before starting treatment, the patient should be prescribed a standard cholesterol-lowering diet, which he should adhere to during treatment. the dose should be selected individually depending on the goal of therapy and the patient's response to treatment, guided by the recommendations of the current generally accepted guidelines.
    Rosuvastatin IC can be taken at any time of the day, with or without food.
    Treatment of hypercholesterolemia. The recommended starting dose is 5 or 10 mg orally once a day for both patients who have not previously used statins and those who have been transferred to rosuvastatin from taking another HMG-CoA reductase inhibitor. When choosing an initial dose, one should take into account the levels of cholesterol in each individual patient and the risk of cardiovascular disorders in the future, as well as the likelihood of developing adverse reactions. If necessary, the dose can be increased to the next level after 4 weeks (see PHARMACOLOGICAL PROPERTIES). Considering that, against the background of the use of the preparation at a dose of 40 mg, adverse reactions occur more often than at lower doses (see SIDE EFFECTS), it is worth finally titrating the dose to 40 mg only in patients with severe hypercholesterolemia and a high risk of cardiovascular disorders (in in particular patients with familial hypercholesterolemia), in whom the goal of treatment was not achieved with a dose of 20 mg and who will be under regular supervision (see SPECIAL INSTRUCTIONS). At the beginning of taking the preparation at a dose of 40 mg, medical supervision is recommended.
    Prevention of cardiovascular disorders. In the study, reducing the risk of disorders of the cardiovascular system, rosuvastatin was used at a dose of 20 mg / day (see PHARMACOLOGICAL PROPERTIES).
    Children. The use of the preparation in children should be carried out only by a specialist.
    Children aged 10–17 years (boys at developmental stage II and above according to Tanner and girls who started menstruating at least a year ago). The initial daily dose for children with heterozygous familial hypercholesterolemia is 5 mg / day. The preparation is taken orally, usually in doses of 5–20 mg once a day. The dose should be increased in accordance with the child's individual response to treatment and the tolerability of the preparation, following the recommendations for the treatment of children (see SPECIAL INSTRUCTIONS). Before starting rosuvastatin therapy, children should be prescribed a standard cholesterol-lowering diet, which patients should adhere to during treatment. The safety and efficacy of rosuvastatin at doses above 20 mg in this population have not been studied.
    40 mg tablets are not prescribed for children.
    Children under the age of 10. The experience of treating children under the age of 10 years is limited by the use of rosuvastatin in a small number of patients (aged 8–10 years) with homozygous familial hypercholesterolemia. Thus, the preparation is not recommended for use in children under 10 years of age.
    Elderly patients. The recommended starting dose for patients aged 70 years is 5 mg (see SPECIAL INSTRUCTIONS). No other dose adjustment is required due to age.
    Patients with renal impairment. No dose adjustment is required in patients with mild to moderate renal impairment. The recommended starting dose for patients with moderate renal impairment (creatinine clearance 60 ml / min) is 5 mg. The 40 mg dose is contraindicated in patients with moderate renal impairment. The use of rosuvastatin in patients with severe renal impairment is contraindicated in any dose (see CONTRAINDICATIONS and PHARMACOLOGICAL PROPERTIES).
    Patients with impaired liver function. In patients with hepatic impairment, which were rated at 7 or less points on the Child-Pugh scale, there was no increase in systemic exposure to rosuvastatin. However, in patients with impairments of 8 and 9 points on the Child-Pugh scale, systemic exposure increased (see PHARMACOLOGICAL PROPERTIES). In such patients, it is advisable to assess renal function (see SPECIAL INSTRUCTIONS). There is no experience of using rosuvastatin in patients who scored more than 9 points on the Child-Pugh scale. Rosuvastatin is contraindicated in patients with active liver disease (see CONTRAINDICATIONS).
    Race. In patients of the Mongoloid race, an increased systemic exposure of rosuvastatin was revealed (see CONTRAINDICATIONS, SPECIAL INDICATIONS and PHARMACOLOGICAL PROPERTIES). The recommended starting dose for patients of Asian descent is 5 mg; a dose of 40 mg is contraindicated in such patients.
    Genetic polymorphism. Certain types of genetic polymorphisms can lead to increased exposure to rosuvastatin (see PHARMACOLOGICAL PROPERTIES). A lower dose of rosuvastatin is recommended for patients with a known presence of these types of polymorphism.
    Patients with a tendency to develop myopathy. The recommended starting dose for patients with risk factors for myopathy is 5 mg (see SPECIAL INSTRUCTIONS). The 40 mg dose is contraindicated in some of these patients (see CONTRAINDICATIONS).
    Simultaneous use. Rosuvastatin is a substrate for various transport proteins (eg OATP1B1 and BCRP). The risk of myopathy (including rhabdomyolysis) increases with the concomitant use of rosuvastatin with certain preparations, which can increase the plasma concentration of rosuvastatin due to interactions with these transport proteins (for example, cyclosporine and certain protease inhibitors, including combinations of ritonavir with atazanavir, lopinavir and / or tipranavir; see SPECIAL INSTRUCTIONS and INTERACTIONS). If possible, you should consider the use of alternative preparations and, if necessary, temporarily interrupt therapy with rosuvastatin. If the concomitant use of these medicines with rosuvastatin cannot be avoided, the benefits and risks of concomitant use should be carefully weighed and the dose of rosuvastatin adjusted accordingly (see INTERACTIONS).
    Children. The preparation is not prescribed for children under 10 years of age (see CONTRAINDICATIONS, APPLICATION).

    Contraindications

    Hypersensitivity to rosuvastatin or any other component of the preparation. liver disease in the active phase, including a sustained increase in plasma transaminases of unknown etiology and any increase in transaminases in blood plasma, 3 times higher than the upper limit of normal (UHN). severe renal dysfunction (creatinine clearance 30 ml / min). myopathy. simultaneous use of cyclosporine. the period of pregnancy or lactation. the preparation is contraindicated in women of reproductive age who do not use proper contraception and in children under 10 years of age. the 40 mg dose is contraindicated in patients with a tendency to myopathy / rhabdomyolysis. the factors of such risk include:
    • moderate renal impairment (creatinine clearance 60 ml / min);
    • hypothyroidism;
    • a personal or family history of hereditary muscle diseases;
    • a history of myotoxicity against the background of the use of other inhibitors of HMG-CoA reductase or fibrates;
    • alcohol abuse;
    • situations that can lead to an increase in the concentration of rosuvastatin in the blood plasma;
    • belonging to the Mongoloid race;
    • simultaneous use of fibrates (see SPECIAL INSTRUCTIONS, INTERACTIONS and PHARMACOLOGICAL PROPERTIES).

    Side effects

    In terms of frequency, adverse reactions are distributed as follows: often (≥1 / 100 and 1/10), infrequently (≥1 / 1000 and 1/100), rarely (≥1 / 10,000 and 1/1000), very rarely (1 / 10,000), unknown (cannot be estimated from the available data).
    From the nervous system: often - headache, dizziness; very rarely - polyneuropathy, memory loss; frequency unknown - peripheral neuropathy, sleep disorders (including insomnia and nightmares).
    From the side of the psyche: the frequency is unknown - depression.
    From the digestive system: often - constipation, nausea, abdominal pain; rarely - pancreatitis; frequency unknown - diarrhea.
    On the part of the hepatobiliary system: rarely - an increase in the level of hepatic transaminases; very rarely - jaundice, hepatitis.
    From the endocrine system: often - diabetes mellitus (the frequency depends on the presence or absence of risk factors (fasting glucose level ≥5.6 mmol / L, BMI 30 kg / m2, high TG, AH levels in history)).
    Respiratory system: frequency unknown - cough, shortness of breath.
    From the side of the blood: rarely - thrombocytopenia.
    From the immune system: rarely - hypersensitivity reactions, including angioedema.
    On the part of the skin and subcutaneous tissue: infrequently - itching, rash, urticaria; frequency unknown - Stevens-Johnson syndrome.
    From the musculoskeletal system: often - myalgia; rarely - myopathy (including myositis), rhabdomyolysis; very rarely - arthralgia; frequency unknown - tendon disorders, sometimes complicated by ruptures, immune-mediated necrotizing myopathy.
    From the urinary system: very rarely - hematuria.
    Reproductive system disorders: very rarely - gynecomastia.
    General disorders: often - asthenia; frequency unknown - edema.
    As with other HMG-CoA reductase inhibitors, the frequency of adverse reactions is often dose-dependent.
    Effects on the kidneys. Proteinuria, detected as a result of analysis by test strips, mainly of tubular origin, was observed in patients taking rosuvastatin. Changes in urine protein content from 0 or traces to ++ or more were observed in 1% of patients at some time points when using the preparation at doses of 10 and 20 mg and in about 3% at a dose of 40 mg. A slight increase in the frequency of changes in the protein content in urine from 0 or traces to a value of + was revealed when using rosuvastatin at a dose of 20 mg. In most cases, proteinuria diminished or disappeared spontaneously with continued therapy. According to clinical studies and post-marketing observations, to date, no causal relationship has been identified between proteinuria and acute or progressive kidney disease.
    When using rosuvastatin, there have been cases of hematuria; according to clinical studies, their frequency is insignificant.
    Effect on the musculoskeletal system. Skeletal muscle lesions such as myalgia, myopathy (including myositis), and occasionally rhabdomyolysis with or without ARF have been reported with any dose of rosuvastatin, especially 20 mg.
    In patients taking rosuvastatin, a dose-dependent increase in CPK levels was observed; in most cases, the phenomenon was mild, asymptomatic and temporary. If CPK levels are elevated (5 × VGN), treatment should be discontinued (see SPECIAL INSTRUCTIONS).
    Effects on the liver. As with the use of other inhibitors of HMG-CoA reductase, in a small number of patients taking rosuvastatin, there was a dose-dependent increase in the level of transaminases; in most cases, the phenomenon was mild, asymptomatic and temporary.
    With the use of some statins, there have been side effects such as sexual dysfunction, isolated cases of interstitial lung disease, especially with prolonged use (see SPECIAL INSTRUCTIONS).
    Occasionally, in the post-registration period of the use of rosuvastatin, cognitive impairments (for example, memory impairment, forgetfulness, amnesia, confusion) have been reported that are associated with the use of statins. Such cognitive problems have been reported for all statins. The reported events are usually mild and resolve after statin withdrawal, and at different times before symptom onset (1 day to several years) and symptom resolution (median 3 weeks).
    During the post-registration use of rosuvastatin, such an undesirable reaction as lethal and non-lethal liver failure was identified. Since this reaction was reported spontaneously from a population of indeterminate number, it is impossible to reliably estimate its frequency or establish the presence of a causal relationship with the use of rosuvastatin.
    The frequency of reports of rhabdomyolysis, serious disorders of the kidneys and liver (mainly an increase in the activity of hepatic transaminases) is higher when using rosuvastatin at a dose of 40 mg.
    With the use of rosuvastatin, an increase in the level of glycosylated hemoglobin (HbA1c) was also noted.
    Children. An increase in CPK 10 × VGN and muscle symptoms after exercise or increased physical activity were observed more often in a 52-week clinical study with the participation of children compared with adults (see SPECIAL INSTRUCTIONS). However, the safety profile of rosuvastatin in children was similar to that in adults.

    Special instructions

    Effects on the kidneys. Proteinuria, revealed as a result of analysis by test strips and mainly of tubular origin, was observed in patients treated with high doses of rosuvastatin, in particular 40 mg, and in most cases was temporary or intermittent. proteinuria was not a precursor to acute or progressive kidney disease (see side effects). the frequency of reports of serious renal events in post-marketing studies of the use of rosuvastatin is higher with a dose of 40 mg. in patients taking the preparation at a dose of 40 mg, kidney function should be checked regularly.
    Effect on the musculoskeletal system. Musculoskeletal disorders, such as myalgia, myopathy, and rarely rhabdomyolysis, have been identified in patients taking any dose of rosuvastatin, especially 20 mg. Isolated cases of rhabdomyolysis have been reported with the use of ezetimibe in combination with HMG-CoA reductase inhibitors. The possibility of pharmacodynamic interactions cannot be ruled out (see INTERACTIONS), and therefore this combination should be used with caution.
    As with the use of other HMG-CoA reductase inhibitors, the frequency of reports of cases of rhabdomyolysis associated with the use of rosuvastatin in the post-marketing period is higher with a dose of 40 mg.
    CPK level. The CPK level should not be measured after significant physical exertion or in the presence of possible alternative reasons for an increase in CPK, which may complicate the interpretation of the results. If the baseline CPK levels are significantly increased (5 times higher than the ULN), a second analysis must be done within 5-7 days to confirm the results. If the results of repeated analysis confirm that the initial CPK value is more than 5 times higher than the ULN, the use of the preparation should not be started.
    Before starting treatment. Rosuvastatin, like other HMG-CoA reductase inhibitors, should be used with caution in patients with a tendency to myopathy / rhabdomyolysis. Factors of this risk include:
    • impaired renal function;
    • hypothyroidism;
    • a personal or family history of hereditary muscle diseases;
    • a history of myotoxicity against the background of the use of other inhibitors of HMG-CoA reductase or fibrates;
    • alcohol abuse;
    • age 70;
    • situations that can lead to an increase in blood plasma levels of rosuvastatin (see APPLICATION, INTERACTIONS and PHARMACOLOGICAL PROPERTIES);
    • concomitant use of fibrates.
    • In these patients, the risk associated with treatment should be weighed against the expected benefit; clinical monitoring is also recommended. If the baseline CPK levels are significantly increased (5 × ULN), treatment should not be started.
    During the treatment period. Patients should immediately report muscle pain, weakness, or seizures of unknown etiology to their doctor, especially if accompanied by malaise or fever. In such patients, it is necessary to measure the levels of CPK. The preparation should be discontinued if the CPK level is significantly elevated (5 × ULN) or if muscle symptoms are severe and cause daily discomfort (even if the CPK levels are ≤5 × ULN). In case of disappearance of symptoms and normalization of CPK levels, therapy with rosuvastatin or an alternative inhibitor of HMG-CoA reductase in a minimal dose and under close supervision can be restored. There is no need to regularly check CPK levels in asymptomatic patients. Very rarely, cases of immune-mediated necrotizing myopathy (IONM) have been reported during or after treatment with statins, including rosuvastatin. Clinical manifestations of IONM are persistent weakness of the proximal muscles and an increase in the level of CPK in the blood plasma, which persists even after discontinuation of statins. In this case, additional neuromuscular and serological studies, treatment with immunosuppressive preparations may be required.
    In patients taking rosuvastatin and concomitant preparations, there was no evidence of an increased effect on the musculoskeletal system. However, an increase in the incidence of myositis and myopathy was observed in patients taking other HMG-CoA reductase inhibitors together with fibric acid derivatives, including gemfibrozil, cyclosporine, niacin, azole antifungals, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when used concomitantly with some HMG-CoA reductase inhibitors. Therefore, it is not recommended to use rosuvastatin in combination with gemfibrozil. The benefits of further changes in lipid levels when using rosuvastatin in combination with fibrates or niacin should be carefully weighed against the potential risks associated with the use of such combinations. A dose of 40 mg is contraindicated with the simultaneous use of fibrates (see INTERACTIONS and SIDE EFFECTS).
    It is not recommended to use rosuvastatin in combination with fusidic acid. Cases of rhabdomyolysis (including fatalities) have been reported in patients receiving this combination (see INTERACTIONS).
    Rosuvastatin should not be used in patients with acute, serious conditions indicating myopathy or the possibility of developing renal failure as a result of rhabdomyolysis (such as sepsis, arterial hypotension, major surgery, trauma, severe metabolic, endocrine and electrolytic disturbances, or uncontrolled seizures).
    Effects on the liver. Like other HMG-CoA reductase inhibitors, rosuvastatin should be used with caution in patients with alcohol abuse and / or a history of liver disease.
    It is recommended to check the biochemical parameters of liver function before starting treatment and 3 months after it. The use of rosuvastatin should be discontinued or the dose reduced if the level of transaminases in the blood plasma is more than 3 times higher than the ULN. The frequency of reports of serious liver events (mainly an increase in the level of liver transaminases) in the post-marketing period is higher with a dose of 40 mg.
    In patients with secondary hypercholesterolemia due to hypothyroidism or nephrotic syndrome, the underlying disease should be treated first before starting rosuvastatin therapy.
    In the post-marketing period of the use of rosuvastatin, fatal or non-fatal cases of liver failure have been reported rarely in patients taking statins, including rosuvastatin. If, during treatment with rosuvastatin, serious liver damage with clinical symptoms and / or hyperbilirubinemia or jaundice develops, the use of rosuvastatin should be discontinued immediately. If no other causes are identified, treatment with rosuvastatin should not be resumed.
    Race. There is an increase in exposure in patients of the Mongoloid race compared to the representatives of the Caucasian race. For such patients, a dose adjustment of rosuvastatin is necessary (see APPLICATION, CONTRAINDICATIONS, PHARMACOLOGICAL PROPERTIES).
    Protease inhibitors. Increased systemic exposure of rosuvastatin was observed in individuals taking rosuvastatin in combination with various protease inhibitors in combination with ritonavir. It should be assessed both the benefits of lowering lipid levels with rosuvastatin in patients with HIV who receive protease inhibitors, and the possibility of increasing the concentration of rosuvastatin in blood plasma at the beginning of therapy and with an increase in the dose of rosuvastatin in patients of this group. Concomitant use of rosuvastatin with protease inhibitors is not recommended if the dose of rosuvastatin is not adjusted (see APPLICATION and INTERACTIONS).
    Lactose intolerance. Patients with rare hereditary problems of galactose intolerance, Lapp lactase deficiency or glucose-galactose malabsorption should not use this preparation.
    Interstitial lung disease. With the use of some statins, especially with long-term treatment, exceptional cases of interstitial lung disease have been reported (see SIDE EFFECTS). Manifestations of this disease include shortness of breath, unproductive cough, and general deterioration (fatigue, weight loss, and fever). If interstitial lung disease is suspected, statins should be discontinued.
    Diabetes. There is some evidence that statins increase blood glucose levels and in some patients who are at high risk of developing diabetes in the future, they can cause hyperglycemia at a level that requires proper diabetes treatment. This threat, however, outweighs the reduction in the risk of vascular disorders with statins, and therefore should not be a reason for discontinuing statin therapy. For patients at risk (fasting glucose 5.6–6.9 mmol / L, BMI 30 kg / m2, elevated TG, AH levels), both clinical and biochemical control should be established.
    It was found that rosuvastatin, which is used as monotherapy, does not cause a decrease in the base concentration of cortisol in the blood plasma and does not affect the adrenal reserve. Caution is needed with the simultaneous use of rosuvastatin and other preparations that can reduce the level or activity of endogenous steroid hormones, such as ketoconazole, spironolactone and cimetidine.
    Children. Estimation of linear growth, body weight, BMI and secondary characteristics of puberty according to Tanner at the age of 10–17 years, who took rosuvastatin, is limited to a period of 1 year. It was reported that after 52 weeks of study treatment, no effect on height, body weight, BMI or puberty was found (see PHARMACOLOGICAL PROPERTIES). In children who took rosuvastatin for 52 weeks, an increase in the CPK level 10 × VGN and muscle symptoms after exercise or increased physical activity were observed more often compared with those in adults (see SIDE EFFECTS).
    Application during pregnancy or lactation. Rosuvastatin is contraindicated during pregnancy or lactation. Women of reproductive age should use appropriate contraception.
    Since cholesterol and other products of cholesterol biosynthesis play a significant role in the development of the fetus, the potential risk from inhibition of HMG-CoA reductase outweighs the benefits of using the preparation during pregnancy. There are limited data from animal studies on reproductive toxicity. If the patient becomes pregnant while using this preparation, treatment should be stopped immediately.
    Since another preparation of this class passes into breast milk and given that HMG-CoA reductase inhibitors can cause serious adverse reactions in infants, women who require rosuvastatin treatment should be advised to refrain from breastfeeding. Rosuvastatin passes into the breast milk of animals. There is no data on the penetration of rosuvastatin into breast milk in humans (see CONTRAINDICATIONS).
    The ability to influence the reaction rate when driving vehicles or other mechanisms. The study of the effect of rosuvastatin on the ability to drive a car and work with mechanisms has not been conducted. However, given the pharmacodynamic properties of rosuvastatin, it is unlikely that the preparation will interfere with this ability. When driving or working with other mechanisms, you should take into account the possible dizziness during the treatment period.

    Interactions

    Effect of concomitant medications on rosuvastatin
    Transport protein inhibitors. Rosuvastatin is a substrate for several transport proteins, including the hepatic uptake transporter OATP1B1 and the efflux transporter BCRP. The simultaneous use of rosuvastatin with preparations that inhibit these transport proteins can lead to an increase in the concentration of rosuvastatin in the blood plasma and an increased risk of myopathy (see APPLICATION, SPECIFIC DIRECTIONS, INTERACTIONS, table below).
    Cyclosporine. During the period of combined use of rosuvastatin and cyclosporin, the AUC values ​​of rosuvastatin were, on average, about 7 times higher than those observed in healthy volunteers (see table). Rosuvastatin is contraindicated in patients receiving cyclosporine concomitantly (see CONTRAINDICATIONS). Concomitant use affected the plasma concentration of cyclosporine.
    Protease inhibitors. Although the exact mechanism of interaction is unknown, the simultaneous use of protease inhibitors can significantly increase the exposure of rosuvastatin (see table). For example, in a pharmacokinetic study, the simultaneous use of 10 mg rosuvastatin and a combination preparation containing two protease inhibitors (300 mg atazanavir / 100 mg ritonavir) in healthy volunteers was accompanied by an increase in the AUC and Cmax of rosuvastatin by about 3 and 7 times, respectively. In a pharmacological study, the simultaneous use of rosuvastatin and a combined preparation containing two protease inhibitors (400 mg lopinavir / 100 mg ritonavir) in healthy volunteers was associated with an increase in AUC (0-24) and Cmax of rosuvastatin by about 2 and 5 times, respectively. The interaction between rosuvastatin and other protease inhibitors has not been studied. The simultaneous use of rosuvastatin and some combinations of protease inhibitors is possible after a careful assessment of the dose adjustment of rosuvastatin, taking into account the expected increase in the exposure of rosuvastatin (see APPLICATION, SPECIFIC DIRECTIONS, INTERACTIONS, table below).
    Gemfibrozil and other lipid-lowering agents. The simultaneous use of rosuvastatin and gemfibrozil led to a 2-fold increase in the AUC and Cmax of rosuvastatin (see SPECIAL INSTRUCTIONS).
    Based on the data of special studies, a pharmacokinetically significant interaction with fenofibrate is not expected, however, a pharmacodynamic interaction is possible. Gemfibrozil, fenofibrate, other fibrates and hypolipidemic doses of niacin (≥1 g / day) increase the risk of myopathy when used concomitantly with HMG-CoA reductase inhibitors, probably due to the fact that they can cause the development of myopathy when used alone. A dose of 40 mg is contraindicated with the simultaneous use of fibrates (see CONTRAINDICATIONS and SPECIAL INSTRUCTIONS). Such patients should also begin therapy with a dose of 5 mg.
    Ezetimibe. The simultaneous use of rosuvastatin at a dose of 10 mg and ezetimibe at a dose of 10 mg in patients with hypercholesterolemia led to an increase in the AUC of rosuvastatin by 1.2 times (see table). A pharmacodynamic interaction between rosuvastatin and ezetimibe, which can lead to undesirable effects, cannot be ruled out (see SPECIAL INSTRUCTIONS).
    Antacids. The simultaneous use of rosuvastatin with a suspension of antacids containing aluminum or magnesium hydroxide reduced the concentration of rosuvastatin in blood plasma by about 50%. This effect was less pronounced in the case of the use of antacids 2 hours after the use of rosuvastatin. The clinical significance of this interaction has not been studied.
    Erythromycin. The simultaneous use of rosuvastatin and erythromycin reduced the AUC of rosuvastatin by 20%, and Cmax by 30%. This interaction can be caused by increased intestinal peristalsis due to the action of erythromycin.
    Cytochrome P450 enzymes. The results of in vitro and in vivo studies indicate that rosuvastatin is not inhibited and does not induce cytochrome P450 isoenzymes. In addition, rosuvastatin is a non-core substrate for these isoenzymes. Thus, preparation interactions from 450-mediated metabolism are not expected. There were no clinically significant interactions between rosuvastatin and fluconazole (an inhibitor of CYP 2C9 and CYP 3A4) or ketoconazole (an inhibitor of CYP 2A6 and CYP 3A4).
    Interactions requiring dose adjustment of rosuvastatin. If necessary, the use of rosuvastatin with other preparations that can increase the exposure of rosuvastatin, the dose of the latter should be adjusted. If the exposure of rosuvastatin is expected to increase by about 2 or more times, the use of rosuvastatin should be started with a dose of 5 mg once a day. The maximum daily dose of rosuvastatin should be adjusted so that its expected exposure does not exceed the exposure observed when taking a dose of 40 mg / day without the use of preparations interacting with the preparation; for example, when used with gemfibrozil, the dose of rosuvastatin will be 20 mg (increase in exposure by 1.9 times), when used with a combination of ritonavir / atazanavir - 10 mg (increase by 3.1 times), with simultaneous use with cyclosporine - 5 mg (increase 7.1 times).
    Effect of concomitant medications on rosuvastatin exposure (AUC; in descending order of magnitude)
    Dosage regimen of the preparation that interactsDosing regimen of rosuvastatinRosuvastatin AUC changes *
    Cyclosporin from 75 mg 2 times a day to 200 mg 2 times a day, 6 months10 mg once a day, 10 days↑ 7.1 times
    Atazanavir 300 mg / ritonavir 100 mg once daily, 8 days10 mg, single dose↑ 3.1 times
    Simeprivir 150 mg once a day, 7 days10 mg, single dose↑ 2.8 times
    Lopinavir 400 mg / ritonavir 100 mg 2 times a day, 17 days20 mg once a day, 7 days↑ 2.1 times
    Clopidogrel 300 mg single loading dose followed by 75 mg over 24 hours20 mg, single dose↑ 2.0 times
    Gemfibrozil 600 mg 2 times a day, 7 days80 mg, single dose↑ 1.9 times
    Eltrombopag 75 mg once a day, 5 days10 mg, single dose↑ 1.6 times
    Darunavir 600 mg / ritonavir 100 mg 2 times a day, 7 days10 mg once a day, 7 days↑ 1.5 times
    Tipranavir 500 mg / ritonavir 200 mg 2 times a day, 11 days10 mg, single dose↑ 1.4 times
    Dronedarone 400 mg 2 times a dayUnknown↑ 1.4 times
    Itraconazole 200 mg once a day, 5 days10 mg, single dose↑ 1.4 times **
    Ezetimibe 10 mg once a day, 14 days10 mg once a day, 14 days↑ 1.2 times **
    Fozamprenavir 700 mg / ritonavir 100 mg 2 times a day, 8 days10 mg, single dose↔
    Aleglitazar 0.3 mg, 7 days40 mg, 7 days↔
    Silymarin 140 mg 3 times a day, 5 days10 mg, single dose↔
    Fenofibrate 67 mg 3 time

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