Rosuvastatin | rosuvastatin tablets coated. 20 mg 30 pcs. pack
Special Price
$28.52
Regular Price
$40.00
In stock
SKU
BID499897
Latin name
ROSUVASTATIN
ROSUVASTATIN
Latin name
ROSUVASTATIN
Pharmacological action
Pharmaceutical group:
lipid-lowering agent - HMG-CoA reductase inhibitor.
Pharmaceutical action:
Hypolipidemic drug, a selective competitive inhibitor of HMG-CoA reductase converting 3-hydroxy-3-methylglutaryl CoA to mevalonate, a cholesterol precursor.
The main target of action is the liver, where cholesterol synthesis and LDL catabolism are performed. It inhibits the activity of HMG-CoA reductase (90% of the drug circulates in the blood).
Increases the number of LDL receptors on the surface of hepatocytes, increasing the uptake and catabolism of LDL, which leads to inhibition of the synthesis of VLDL, reducing the total number of LDL and VLDL.
Lowers cholesterol-LDL cholesterol, non-HDL cholesterol, VLDL cholesterol, total cholesterol, TG, TG-VLDL, apolipoprotein B (ApoV), the ratio of LDL cholesterol / HDL cholesterol, total cholesterol / HDL cholesterol, non-HDL cholesterol / HDL cholesterol, ApoV / ApoA-I, increases the concentration of ApoA-I cholesterol. The lipid-lowering effect is directly proportional to the amount of the prescribed dose.
The therapeutic effect appears within 1 week after the start of therapy, after 2 weeks reaches 90% of the maximum, the maximum effect is usually achieved by 4 weeks and after that remains constant.
Effective in adult patients with hypercholesterolemia with or without hypertriglyceridemia (regardless of race, gender or age), incl. in patients with diabetes mellitus and familial hypercholesterolemia.
The additive effect is observed in combination with fenofibrate (in relation to lowering the concentration of TG) and nicotinic acid (in relation to lowering the concentration of HDL cholesterol).
Pharmacokinetics:
Bioavailability - 20%. Food reduces the rate of absorption. Communication with plasma proteins (mainly with albumin) - 90%. TCmax - 3-5 hours. Penetrates through the placental barrier. Accumulates in the liver. Distribution volume - 134 l.
Metabolized in the liver 10% of the administered dose. As in the case of other HMG-CoA reductase inhibitors, a specific membrane cholesterol carrier is involved in the process of hepatic uptake of the drug, which plays an important role in its hepatic elimination. It was shown that rosuvastatin is a non-core substrate for metabolism by enzymes of the cytochrome P450 system.
main isoenzyme, involved in the metabolism of rosuvastatin, is CYP2C9. Enzymes CYP2C19, CYP3A4, CYP2D6 are less involved in metabolism. The main metabolite is N-desmethyl, which has 1 / 6-1 / 2 of the activity of rosuvastatin, lactone metabolites are pharmacologically inactive. T1 / 2 - 19 hours (does not change with increasing dose). The geometric mean plasma clearance is 50 l / h.
It is excreted mainly in unchanged form (90%) with feces (including adsorbed and non-adsorbed rosuvastatin), the rest - with urine. It is not excreted by hemodialysis.
Gender and age do not have a clinically significant effect on the pharmacokinetics of rosuvastatin.
Pharmacokinetic parameters depend on race: AUC in Japanese and Chinese is 2 times higher than in Europeans and North America.
In patients with mild to moderate renal failure, the plasma concentration of rosuvastatin or N-dysmethyl does not change significantly. In patients with severe renal failure (CKU of patients with various stages of liver failure with a score of 7 or lower on the Child-Pyug scale, no increase in T1 / 2 of rosuvastatin was revealed in 2 patients with points of 8 and 9 on the Child-Pyug scale, an elongation of T1 / 2 in 2 times There is no experience with the drug in patients with more severe impaired liver function
Indications
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 methods of treatment (physical exercise, weight loss).
Family homozygous hypercholesterolemia as a supplement to diet and other cholesterol lowering therapy (LDL-apheresis) or in cases where such therapy is not suitable for the patient.
Contraindications
Hypersensitivity,
liver disease in the active phase (including a persistent increase in the activity of “liver” transaminases, as well as any increase in the activity of “liver” transaminases in blood serum by more than 3 times compared with the upper limit of normal) ,
severe renal impairment (CK pregnancy, lactation of women of reproductive age, not using adequate methods of contraception
age under 18 years (effectiveness and safety have not been established).
Caution. renal failure,
hypothyroidism, personal or family history of hereditary muscle diseases and a previous history of muscle toxicity when using other HMG-CoA reductase inhibitors or fibrates),
alcohol dependence,
over 65 years old,
history of liver disease, sepsis, arterial hypotension, srdlp interventions, injuries,
severe metabolic, endocrine or electrolyte disturbances, proteinuria, uncontrolled epilepsy,
Asians (Japanese and Chinese).
Special instructions
Before starting therapy and throughout the treatment period, a standard lipid-lowering diet should be followed. During treatment, every 2-4 weeks, a lipid profile should be monitored and, if necessary, adjusted the dose of the drug according to it.
Doses of 40 mg are contraindicated in patients with risk factors for rhabdomyolysis (moderate renal failure (CC less than 60 ml / min), hypothyroidism, a personal or family history of muscle diseases, myotoxicity while taking other HMG-CoA reductase inhibitors or fibrates, alcohol abuse conditions, accompanied by an increase in the concentration of the drug in the systemic circulation), concomitant use of fibrates, patients of the Asian race).
In patients taking a dose of 40 mg, it is recommended to monitor renal function indicators.
Determination of CPK activity should not be carried out after intense physical exertion or in the presence of other possible reasons for the increase in CPK, which may lead to an incorrect interpretation of the results. With an increase in the initial CPK 5 times higher than the upper limit of the norm, a repeated measurement should be carried out after 5-7 days. Therapy should not be started if a repeat test confirms the initial increased activity of CPK by more than 5 times compared with the upper limit of normal.
In patients with existing risk factors for rhabdomyolysis, it is necessary to consider the ratio of risk and possible benefits of therapy and to carry out clinical observation throughout the course of treatment.
Inform patient that immediate medical attention should be given to cases of sudden onset of muscle pain, muscle weakness, or cramping, especially in combination with malaise and fever. In such patients, CPK activity should be monitored. Therapy should be discontinued if the activity of CPK is increased by more than 5 times compared with the upper limit of the norm, or if muscle symptoms are pronounced and cause daily discomfort (even if the activity of CPK is 5 times lower compared to the upper limit of the norm). If symptoms disappear and CPK activity returns to normal, consideration should be given to re-prescribing the drug or other HMG-CoA reductase inhibitors in lower doses with careful monitoring of the patient. Routine monitoring of CPK activity in the absence of symptoms of rhabdomyolysis is not advisable.
An increase in the incidence of myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors in combination with fibric acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid, azole antifungal drugs, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when combined with certain HMG-CoA reductase inhibitors. Thus, the simultaneous administration of rosuvastatin and gemfibrozil is not recommended. The ratio of risk to possible benefit should be carefully weighed when the combined use of rosuvastatin and fibrates or nicotinic acid.
It is recommended that liver function tests be determined prior to initiation of therapy and 3 months after initiation of therapy. If the activity of “liver” transaminases in blood serum is 3 times higher than the upper limit of normal, the dose should be reduced or discontinued.
In most cases, proteinuria decreases or disappears during therapy and does not indicate the onset or progression of an existing kidney disease.
With a combination of hypercholesterolemia and hypothyroidism or nephrotic syndrome, therapy of the underlying diseases should be carried out before treatment with rosuvastatin.
Caution should be exercised when driving or working with increased concentration and psychomotor reaction (dizziness may occur during therapy).
Women of reproductive age should use adequate methods of contraception. Since cholesterol and substances synthesized from cholesterol are important for fetal development, the potential risk of inhibiting HMG-CoA reductase exceeds the benefit of using the drug during pregnancy. In a study on rats (use in doses of 2-50 mg / kg / day), a decrease in fetal weight, a delay in ossification of bones in the fetus, and a decrease in the survival of offspring were revealed. In case of pregnancy during therapy, the drug should be stopped immediately. Data on the allocation of rosuvastatin with milk of women are not available, therefore, breastfeeding must be stopped.
Composition
Rosuvastatin 20 mg.
Dosage and Administration
Inside, do not chew or grind the tablet, swallow whole, washed down with water, can be taken at any time of the day, regardless of food intake. The recommended initial dose is 10 mg once a day, if necessary, the dose can be increased to 20 mg after 4 weeks, increasing the dose to 40 mg is possible only under medical supervision in patients with severe homozygous familial hypercholesterolemia with a high risk of cardiovascular complications (especially in patients with familial hypercholesterolemia), in which the desired result of therapy is not achieved when taking a dose of 20 mg.
In patients with risk factors for myopathy, the initial dose should be 5 mg.
When prescribed with gemfibrazil, the dose of rosuvastatin should not exceed 10 mg / day.
With renal failure of mild or moderate severity, as well as in the elderly, dose adjustment is not required.
There is no experience with the use of the drug in patients with liver failure above 9 on the Childe-Pugh scale.
Side effects
The incidence of side effects is dose dependent: often (1-10%), less often (0.1-1%), rarely (0.01-0.1%).
From the nervous system: often - headache, dizziness, asthenic syndrome less often - anxiety, depression, insomnia, neuralgia, paresthesia.
From the gastrointestinal tract: often - constipation, nausea, abdominal pain, frequency is unknown - a reversible transient dose-dependent increase in the activity of "liver" transaminases is less common - dyspepsia (including diarrhea, flatulence, vomiting), gastritis, gastroenteritis.
From the respiratory system: often - pharyngitis less often - rhinitis, sinusitis, asthma, bronchitis, cough, shortness of breath, pneumonia.
On the part of heart rate: less often - angina pectoris, increased blood pressure, palpitations, vasodilation.
From the musculoskeletal system: often - myalgia less often - arthralgia, arthritis, muscle hypertonicity, back pain, pathological pearl of the extremity (without damage) rarely - myopathy, rhabdomyolysis (simultaneously with impaired renal function, while taking the drug in a dose of 40 mg).
From the urinary system: tubular proteinuria (in less than 1% of cases for doses of 10 and 20 mg, 3% of crying for doses of 40 mg) less often - peripheral edema (arms, legs, ankles, lower legs), pain in the lower abdomen, urinary tract infections.
Allergic reactions: less often - skin rash, itchy skin rarely - angioedema.
On the part of laboratory indicators: a transient dose-dependent increase in KFK activity (with an increase in KFK activity by more than 5 times compared with the upper limit of the norm, therapy should be temporarily suspended).
Other: less often - accidental trauma, anemia, chest pain, diabetes mellitus, ecchymosis, flu-like syndrome, periodontal abscess.
Drug interaction
Does not affect the plasma concentration of cyclosporine. Cyclosporin enhances the effect of rosuvastatin (slows its excretion, increases AUC by 7 times, Cmax - by 11 times), vitamin K antagonists (including warfarin, can lead to an increase in prothrombin time, its monitoring is recommended).
Gemfibrozil enhances the effect of rosuvastatin (increases its Cmax and AUC by 2 times).
Antacids containing Al3 + and Mg2 + lead to a decrease in the plasma concentration of rosuvastatin by about 50% (antacids should be used 2 hours after taking rosuvastatin, the clinical significance of this interaction has not been studied).
Erythromycin enhances gastrointestinal motility, which leads to a decrease in the effect of rosuvastatin (reduces its AUC by 20% and Cmax by 30%).
Enhances the effect of oral contraceptives (increases the AUC of ethinyl estradiol and norgestrel by 26% and 34%, respectively, which should be taken into account when selecting a dose of oral contraceptives). Pharmacokinetic data on the simultaneous use of rosuvastatin and hormone replacement therapy are absent, therefore, a similar effect cannot be ruled out when using this combination.
No clinically significant interaction of rosuvastatin with digoxin or fenofibrate is expected.
Gemfibrozil, other fibrates and lipid-lowering doses of nicotinic acid (high doses or equivalent 1 g / day) increase the risk of myopathy while using other HMG-CoA reductase inhibitors, possibly due to the fact that they themselves can cause myopathy when used as monotherapy.
In vivo and in vitro studies have shown that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 enzymes. In addition, rosuvastatin is a non-core substrate for these enzymes. There was no clinically significant interaction between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4) and ketoconazole (an inhibitor of CYP2A6 and CYP3A4). The combined use of rosuvastatin and itraconazole (a CYP3A4 inhibitor) increases the AUC of rosuvastatin by 28% (clinically insignificant). Thus, interactions associated with metabolism via the cytochrome P450 system are not expected.
Concomitant use with drugs that reduce the concentration of endogenous steroid hormones (including cimetidine, ketoconazole, spironolactone) increases the risk of a decrease in endogenous steroid hormones.
Deystvuyuschee substance
Rosuvastatin
Pharmacy terms
Prescription
dosage form
tablets
ROSUVASTATIN
Pharmacological action
Pharmaceutical group:
lipid-lowering agent - HMG-CoA reductase inhibitor.
Pharmaceutical action:
Hypolipidemic drug, a selective competitive inhibitor of HMG-CoA reductase converting 3-hydroxy-3-methylglutaryl CoA to mevalonate, a cholesterol precursor.
The main target of action is the liver, where cholesterol synthesis and LDL catabolism are performed. It inhibits the activity of HMG-CoA reductase (90% of the drug circulates in the blood).
Increases the number of LDL receptors on the surface of hepatocytes, increasing the uptake and catabolism of LDL, which leads to inhibition of the synthesis of VLDL, reducing the total number of LDL and VLDL.
Lowers cholesterol-LDL cholesterol, non-HDL cholesterol, VLDL cholesterol, total cholesterol, TG, TG-VLDL, apolipoprotein B (ApoV), the ratio of LDL cholesterol / HDL cholesterol, total cholesterol / HDL cholesterol, non-HDL cholesterol / HDL cholesterol, ApoV / ApoA-I, increases the concentration of ApoA-I cholesterol. The lipid-lowering effect is directly proportional to the amount of the prescribed dose.
The therapeutic effect appears within 1 week after the start of therapy, after 2 weeks reaches 90% of the maximum, the maximum effect is usually achieved by 4 weeks and after that remains constant.
Effective in adult patients with hypercholesterolemia with or without hypertriglyceridemia (regardless of race, gender or age), incl. in patients with diabetes mellitus and familial hypercholesterolemia.
The additive effect is observed in combination with fenofibrate (in relation to lowering the concentration of TG) and nicotinic acid (in relation to lowering the concentration of HDL cholesterol).
Pharmacokinetics:
Bioavailability - 20%. Food reduces the rate of absorption. Communication with plasma proteins (mainly with albumin) - 90%. TCmax - 3-5 hours. Penetrates through the placental barrier. Accumulates in the liver. Distribution volume - 134 l.
Metabolized in the liver 10% of the administered dose. As in the case of other HMG-CoA reductase inhibitors, a specific membrane cholesterol carrier is involved in the process of hepatic uptake of the drug, which plays an important role in its hepatic elimination. It was shown that rosuvastatin is a non-core substrate for metabolism by enzymes of the cytochrome P450 system.
main isoenzyme, involved in the metabolism of rosuvastatin, is CYP2C9. Enzymes CYP2C19, CYP3A4, CYP2D6 are less involved in metabolism. The main metabolite is N-desmethyl, which has 1 / 6-1 / 2 of the activity of rosuvastatin, lactone metabolites are pharmacologically inactive. T1 / 2 - 19 hours (does not change with increasing dose). The geometric mean plasma clearance is 50 l / h.
It is excreted mainly in unchanged form (90%) with feces (including adsorbed and non-adsorbed rosuvastatin), the rest - with urine. It is not excreted by hemodialysis.
Gender and age do not have a clinically significant effect on the pharmacokinetics of rosuvastatin.
Pharmacokinetic parameters depend on race: AUC in Japanese and Chinese is 2 times higher than in Europeans and North America.
In patients with mild to moderate renal failure, the plasma concentration of rosuvastatin or N-dysmethyl does not change significantly. In patients with severe renal failure (CKU of patients with various stages of liver failure with a score of 7 or lower on the Child-Pyug scale, no increase in T1 / 2 of rosuvastatin was revealed in 2 patients with points of 8 and 9 on the Child-Pyug scale, an elongation of T1 / 2 in 2 times There is no experience with the drug in patients with more severe impaired liver function
Indications
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 methods of treatment (physical exercise, weight loss).
Family homozygous hypercholesterolemia as a supplement to diet and other cholesterol lowering therapy (LDL-apheresis) or in cases where such therapy is not suitable for the patient.
Contraindications
Hypersensitivity,
liver disease in the active phase (including a persistent increase in the activity of “liver” transaminases, as well as any increase in the activity of “liver” transaminases in blood serum by more than 3 times compared with the upper limit of normal) ,
severe renal impairment (CK pregnancy, lactation of women of reproductive age, not using adequate methods of contraception
age under 18 years (effectiveness and safety have not been established).
Caution. renal failure,
hypothyroidism, personal or family history of hereditary muscle diseases and a previous history of muscle toxicity when using other HMG-CoA reductase inhibitors or fibrates),
alcohol dependence,
over 65 years old,
history of liver disease, sepsis, arterial hypotension, srdlp interventions, injuries,
severe metabolic, endocrine or electrolyte disturbances, proteinuria, uncontrolled epilepsy,
Asians (Japanese and Chinese).
Special instructions
Before starting therapy and throughout the treatment period, a standard lipid-lowering diet should be followed. During treatment, every 2-4 weeks, a lipid profile should be monitored and, if necessary, adjusted the dose of the drug according to it.
Doses of 40 mg are contraindicated in patients with risk factors for rhabdomyolysis (moderate renal failure (CC less than 60 ml / min), hypothyroidism, a personal or family history of muscle diseases, myotoxicity while taking other HMG-CoA reductase inhibitors or fibrates, alcohol abuse conditions, accompanied by an increase in the concentration of the drug in the systemic circulation), concomitant use of fibrates, patients of the Asian race).
In patients taking a dose of 40 mg, it is recommended to monitor renal function indicators.
Determination of CPK activity should not be carried out after intense physical exertion or in the presence of other possible reasons for the increase in CPK, which may lead to an incorrect interpretation of the results. With an increase in the initial CPK 5 times higher than the upper limit of the norm, a repeated measurement should be carried out after 5-7 days. Therapy should not be started if a repeat test confirms the initial increased activity of CPK by more than 5 times compared with the upper limit of normal.
In patients with existing risk factors for rhabdomyolysis, it is necessary to consider the ratio of risk and possible benefits of therapy and to carry out clinical observation throughout the course of treatment.
Inform patient that immediate medical attention should be given to cases of sudden onset of muscle pain, muscle weakness, or cramping, especially in combination with malaise and fever. In such patients, CPK activity should be monitored. Therapy should be discontinued if the activity of CPK is increased by more than 5 times compared with the upper limit of the norm, or if muscle symptoms are pronounced and cause daily discomfort (even if the activity of CPK is 5 times lower compared to the upper limit of the norm). If symptoms disappear and CPK activity returns to normal, consideration should be given to re-prescribing the drug or other HMG-CoA reductase inhibitors in lower doses with careful monitoring of the patient. Routine monitoring of CPK activity in the absence of symptoms of rhabdomyolysis is not advisable.
An increase in the incidence of myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors in combination with fibric acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid, azole antifungal drugs, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when combined with certain HMG-CoA reductase inhibitors. Thus, the simultaneous administration of rosuvastatin and gemfibrozil is not recommended. The ratio of risk to possible benefit should be carefully weighed when the combined use of rosuvastatin and fibrates or nicotinic acid.
It is recommended that liver function tests be determined prior to initiation of therapy and 3 months after initiation of therapy. If the activity of “liver” transaminases in blood serum is 3 times higher than the upper limit of normal, the dose should be reduced or discontinued.
In most cases, proteinuria decreases or disappears during therapy and does not indicate the onset or progression of an existing kidney disease.
With a combination of hypercholesterolemia and hypothyroidism or nephrotic syndrome, therapy of the underlying diseases should be carried out before treatment with rosuvastatin.
Caution should be exercised when driving or working with increased concentration and psychomotor reaction (dizziness may occur during therapy).
Women of reproductive age should use adequate methods of contraception. Since cholesterol and substances synthesized from cholesterol are important for fetal development, the potential risk of inhibiting HMG-CoA reductase exceeds the benefit of using the drug during pregnancy. In a study on rats (use in doses of 2-50 mg / kg / day), a decrease in fetal weight, a delay in ossification of bones in the fetus, and a decrease in the survival of offspring were revealed. In case of pregnancy during therapy, the drug should be stopped immediately. Data on the allocation of rosuvastatin with milk of women are not available, therefore, breastfeeding must be stopped.
Composition
Rosuvastatin 20 mg.
Dosage and Administration
Inside, do not chew or grind the tablet, swallow whole, washed down with water, can be taken at any time of the day, regardless of food intake. The recommended initial dose is 10 mg once a day, if necessary, the dose can be increased to 20 mg after 4 weeks, increasing the dose to 40 mg is possible only under medical supervision in patients with severe homozygous familial hypercholesterolemia with a high risk of cardiovascular complications (especially in patients with familial hypercholesterolemia), in which the desired result of therapy is not achieved when taking a dose of 20 mg.
In patients with risk factors for myopathy, the initial dose should be 5 mg.
When prescribed with gemfibrazil, the dose of rosuvastatin should not exceed 10 mg / day.
With renal failure of mild or moderate severity, as well as in the elderly, dose adjustment is not required.
There is no experience with the use of the drug in patients with liver failure above 9 on the Childe-Pugh scale.
Side effects
The incidence of side effects is dose dependent: often (1-10%), less often (0.1-1%), rarely (0.01-0.1%).
From the nervous system: often - headache, dizziness, asthenic syndrome less often - anxiety, depression, insomnia, neuralgia, paresthesia.
From the gastrointestinal tract: often - constipation, nausea, abdominal pain, frequency is unknown - a reversible transient dose-dependent increase in the activity of "liver" transaminases is less common - dyspepsia (including diarrhea, flatulence, vomiting), gastritis, gastroenteritis.
From the respiratory system: often - pharyngitis less often - rhinitis, sinusitis, asthma, bronchitis, cough, shortness of breath, pneumonia.
On the part of heart rate: less often - angina pectoris, increased blood pressure, palpitations, vasodilation.
From the musculoskeletal system: often - myalgia less often - arthralgia, arthritis, muscle hypertonicity, back pain, pathological pearl of the extremity (without damage) rarely - myopathy, rhabdomyolysis (simultaneously with impaired renal function, while taking the drug in a dose of 40 mg).
From the urinary system: tubular proteinuria (in less than 1% of cases for doses of 10 and 20 mg, 3% of crying for doses of 40 mg) less often - peripheral edema (arms, legs, ankles, lower legs), pain in the lower abdomen, urinary tract infections.
Allergic reactions: less often - skin rash, itchy skin rarely - angioedema.
On the part of laboratory indicators: a transient dose-dependent increase in KFK activity (with an increase in KFK activity by more than 5 times compared with the upper limit of the norm, therapy should be temporarily suspended).
Other: less often - accidental trauma, anemia, chest pain, diabetes mellitus, ecchymosis, flu-like syndrome, periodontal abscess.
Drug interaction
Does not affect the plasma concentration of cyclosporine. Cyclosporin enhances the effect of rosuvastatin (slows its excretion, increases AUC by 7 times, Cmax - by 11 times), vitamin K antagonists (including warfarin, can lead to an increase in prothrombin time, its monitoring is recommended).
Gemfibrozil enhances the effect of rosuvastatin (increases its Cmax and AUC by 2 times).
Antacids containing Al3 + and Mg2 + lead to a decrease in the plasma concentration of rosuvastatin by about 50% (antacids should be used 2 hours after taking rosuvastatin, the clinical significance of this interaction has not been studied).
Erythromycin enhances gastrointestinal motility, which leads to a decrease in the effect of rosuvastatin (reduces its AUC by 20% and Cmax by 30%).
Enhances the effect of oral contraceptives (increases the AUC of ethinyl estradiol and norgestrel by 26% and 34%, respectively, which should be taken into account when selecting a dose of oral contraceptives). Pharmacokinetic data on the simultaneous use of rosuvastatin and hormone replacement therapy are absent, therefore, a similar effect cannot be ruled out when using this combination.
No clinically significant interaction of rosuvastatin with digoxin or fenofibrate is expected.
Gemfibrozil, other fibrates and lipid-lowering doses of nicotinic acid (high doses or equivalent 1 g / day) increase the risk of myopathy while using other HMG-CoA reductase inhibitors, possibly due to the fact that they themselves can cause myopathy when used as monotherapy.
In vivo and in vitro studies have shown that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 enzymes. In addition, rosuvastatin is a non-core substrate for these enzymes. There was no clinically significant interaction between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4) and ketoconazole (an inhibitor of CYP2A6 and CYP3A4). The combined use of rosuvastatin and itraconazole (a CYP3A4 inhibitor) increases the AUC of rosuvastatin by 28% (clinically insignificant). Thus, interactions associated with metabolism via the cytochrome P450 system are not expected.
Concomitant use with drugs that reduce the concentration of endogenous steroid hormones (including cimetidine, ketoconazole, spironolactone) increases the risk of a decrease in endogenous steroid hormones.
Deystvuyuschee substance
Rosuvastatin
Pharmacy terms
Prescription
dosage form
tablets
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