Rosucard pills 10mg, 60pcs

Composition

Each 10 mg film coated tablet contains:

Active ingredient:

rosuvastatin-10,000 mg (in the form of rosuvastatin calcium-10,400 mg);

excipients:

core:

lactose monohydrate-60,000 mg, microcrystalline cellulose-45,400 mg, croscarmellose sodium-1,200 mg, colloidal silicon dioxide-0.600 mg, magnesium stearate-2,400 mg;

film coating:

hypromellose 2910/5 – 2,500 mg, macrogol 6000-0.400 mg, titanium dioxide-0.325 mg, talc-0.475 mg, iron oxide red dye-0.013 mg

Pharmacological action

Hypolipidemic drug from the statin group. Selective competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, an enzyme that converts HMG-CoA to mevalonate, a cholesterol precursor.

Increases the number of LDL receptors on the surface of hepatocytes, which leads to increased uptake and catabolism of LDL, inhibition of VLDL synthesis, reducing the total concentration of LDL and VLDL. Reduces the concentration of LDL-C, high-density lipoprotein cholesterol (HDL-C), VLDL-C, total cholesterol, TG, VLDL-C, apolipoprotein B (apoB), reduces the ratio of LDL-C/HDL-C, total Cholesterol/HDL-C, Non-HDL-C/HDL-C, apoB/apolipoprotein A-1 (ApoA-1), increases the concentration of HDL-C and ApoA-1.

The hypolipidemic effect is directly proportional to the prescribed dose. The therapeutic effect appears within 1 week after the start of therapy, after 2 weeks it reaches 90% of the maximum, by 4 weeks it reaches its maximum and then remains constant.

Clinical efficacy

It is effective in adult patients with hypercholesterolemia with or without hypertriglyceridemia (regardless of race, gender, or age), including those with diabetes mellitus and familial hypercholesterolemia. In 80% of patients with hypercholesterolemia type IIa and IIb (according to the Fredrickson classification) with an average initial LDL-C concentration of about 4.8 mmol/l against the background of taking the drug at a dose of 10 mg, the LDL-C concentration reaches values of less than 3 mmol/l.

In patients with heterozygous familial hypercholesterolemia receiving rosuvastatin at a dose of 20-80 mg/day, there is a positive dynamics of lipid profile indicators.

An additive effect is observed in combination with fenofibrate in relation to the concentration of TG and with nicotinic acid in lipid-lowering doses (more than 1 g / day)in relation to reducing the concentration of HDL-C.

Indications

• Primary hypercholesterolemia (Fredrickson type IIa), including heterozygous hereditary hypercholesterolemia or mixed (combined) hypercholesterolemia (Fredrickson type IIB), as an adjunct to diet and other non-drug measures (exercise and weight loss) if diet therapy and non-drug measures are ineffective;
• Homozygous form of hereditary hypercholesterolemia and when diet therapy and other lipid-lowering treatments are not effective enough (for example, LDL apheresis), or if such treatments are not suitable for the patient.
• Hypertriglyceridemia (Fredrickson type IV) as a dietary supplement.
• To slow the progression of atherosclerosis as an adjunct to diet in patients who are indicated for therapy to reduce the concentration of total cholesterol and LDL-C.
• 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 over 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 HDL-C concentration, smoking, family history of early

Contraindications

• Hypersensitivity to rosuvastatin or other components of the drug;
• Liver diseases in the active phase or a steady increase in the serum activity of “hepatic” transaminases (more than 3 times compared to the upper limit of normal) of unknown origin, liver failure (severity from 7 to 9 points on the Child-Pugh scale);
• An increase in the concentration of creatinine phosphokinase (CPK) in the blood by more than 5 times compared to the upper limit of normal (ULN);
• Hereditary diseases, such as lactose intolerance, lactase deficiency, or glucose-galactose malabsorption (due to the presence of lactose in the composition).
• Severe renal impairment (creatinine clearance less than 30 ml / min);
• Myopathy;
• Patients predisposed to the development of myotoxic complications;
• Simultaneous use of cyclosporine;
• Co-use with HIV protease inhibitors;
• Women of reproductive age who do not use adequate methods of contraception;
• Pregnancy and lactation;
• Age up to 18 years (efficacy and safety have not been established).

Side effects

• The frequency of adverse reactions was determined according to the following gradation (classification of the World Health Organization):

• very often-more than 1/10,
• often-from more than 1/100 to less than 1/10,
• infrequently – from more than 1/1000 to less than 1/100,
• rarely-from more than 1/10000 to less than 1/1000,
• very rarely – from less than 1/10000, including individual messages.
• an unspecified frequency.
• From the central nervous system: often – headache, dizziness, asthenic syndrome; very rarely-peripheral neuropathy, memory loss.
• From the digestive system: often – nausea, constipation, abdominal pain; infrequently-vomiting; rarely-pancreatitis; very rarely-hepatitis, jaundice; unspecified frequency-diarrhea.
• Respiratory system disorders: infrequently-cough, dyspnoea.
• From the endocrine system: often – type 2 diabetes mellitus.
• From the musculoskeletal system: often -myalgia; very rarely-arthralgia; rarely-myopathy (including myositis), rhabdomyolysis.
• Allergic reactions: infrequently-pruritus, urticaria, rash; rarely-angioedema.
• Skin and subcutaneous tissue: unspecified frequency-Stevens-Johnson syndrome, peripheral edema.
• From the urinary system: often-proteinuria (with a frequency of more than 3% in patients receiving a dose of 40 mg), which decreases during therapy and is not associated with the occurrence of kidney disease, urinary tract infection; very rarely – hematuria.
• Laboratory parameters: infrequently-a transient dose-dependent increase in the activity of serum creatine phosphokinase (CPK), with an increase of more than 5 times compared to the upper limit of normal, therapy should be temporarily suspended; rarely – a transient increase in the activity of aspartate aminotransferase and alanine aminotransferase.
• As with other HMG-CoA reductase inhibitors, the frequency of occurrence is dose-dependent, and side effects are usually mild and resolve on their own.
• When using ROSUCARD®, changes in the following laboratory parameters were noted: increased glucose concentration, bilirubin, alkaline phosphatase activity, gamma-glutamyltransferase.
• The following side effects have been reported with other statins: depression, insomnia, decreased potency. Isolated cases of interstitial lung disease have been reported with prolonged use of rosuvastatin.

Interaction

Concomitant use of rosuvastatin and cyclosporine does not affect the plasma concentration of cyclosporine, but the effect of rosuvastatin is enhanced (its excretion slows down, AUC increases by 7 times, Cmax – by 11 times).

Erythromycin enhances intestinal motility, which leads to a decrease in the effect of rosuvastatin (AUC decreases by 20% and Cmax by 30%).

In patients receiving vitamin K antagonists (for example, warfarin), monitoring of the international normalized ratio (INR) is recommended, since starting therapy with rosuvastatin or increasing the dose of the drug may lead to an increase in INR, and discontinuing rosuvastatin or reducing its dose may lead to a decrease in it. Gemfibrozil enhances the effect of rosuvastatin (increases Cmax and AUC by 2 times). Simultaneous use of rosuvastatin and antacids containing aluminum and magnesium hydroxide leads to a decrease in the plasma concentration of rosuvastatin by about 50%. This effect is less pronounced if antacids are applied 2 hours after taking rosuvastatin.

Concomitant use of rosuvastatin and oral contraceptives increases the AUC of ethinyl estradiol and AUC of norgestrel by 26% and 34%, respectively, which should be taken into account when selecting the dose of oral contraceptives. Pharmacokinetic data on the simultaneous use of rosuvastatin and hormone replacement therapy are not available, therefore, a similar effect cannot be excluded when using this combination.

The results of studies showed that rosuvastatin is neither an inhibitor nor an inducer of the action of cytochrome P450 isoenzymes. Rosuvastatin is a non-core substrate for these isoenzymes. There were no clinically significant interactions with drugs such as fluconazole, ketoconazole, and itraconazole that are metabolized to the cytochrome P450 system. There was no clinically significant interaction of rosuvastatin with digoxin or fenofibrate, Gemfibrozil, other fibrates, and hypolipidemic doses of nicotinic acid (at least 1 g/day) increased the risk of myopathy when co-administered with other HMG-CoA reductase inhibitors.Possibly due to the fact that they can cause myopathy and when used as monotherapy.

Co-use of rosuvastatin and ezetimibe did not result in changes in the AUC or Cmax of either drug. The use of HIV protease inhibitors (human immunodeficiency virus) with rosuvastatin can significantly enhance the effect of rosuvastatin. A pharmacokinetic study of co-use of 20 mg rosuvastatin and a combination of two HIV protease inhibitors (400 mg lopinavir / 100 mg ritonavir) in healthy volunteers resulted in approximately two – and five-fold increases in AUC(0-24) and Cmax, respectively. Therefore, co-use of rosuvastatin with HIV protease inhibitors is not recommended in patients infected with HIV.

How to take, course of use and dosage

Inside, without chewing or grinding, swallow whole, washed down with water, at any time of the day, regardless of food intake. Before starting therapy with ROSUCARD®, the patient should begin to follow a 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 current generally accepted recommendations for target lipid levels. If you need to take the drug at a dose of 5 mg, you should divide the 10 mg tablet into two parts according to the risk.

The recommended starting dose of ROSUCARD® for patients starting to take the drug, or for patients transferred from taking other HMG-CoA reductase inhibitors, is 5 or 10 mg 1 time per day. When choosing the initial dose, the patient’s cholesterol level should be guided and the risk of developing cardiovascular complications should be taken into account, as well as the potential risk of side effects should be evaluated. If necessary, the dose of the drug can be increased after 4 weeks.

Due to the possible development of side effects when taking a dose of 40 mg compared to lower doses of the drug (see the section “Side effects”) final titration to a maximum dose of 40 mg should only be performed in patients with severe hypercholesterolemia and a high risk of cardiovascular complications (especially in patients with hereditary hypercholesterolemia), who did not reach the target cholesterol level at a dose of 20 mg, and who will be under medical supervision.

Patients with hepatic insufficiencyIn patients with hepatic insufficiency with values on the Child-Pugh scale below 7 points, dose adjustment of ROSUCARD® is not required.

Patients with renal insufficiencyNo dose adjustment is required in patients with mild renal insufficiency. The recommended starting dose of ROSUKARD® is 5 mg per day.

In patients with severe renal insufficiency (creatinine clearance less than 30 ml/min), the use of ROSUCARD® is contraindicated. In patients with moderate renal insufficiency (creatinine clearance 30-60 ml/min), the use of ROSUKARD® at a dose of 40 mg per day is contraindicated (see the section “Contraindications”).

Special populations. Elderly patientsNo dose adjustment is required in patients over 65 years of age.

Patients with a predisposition to myopathyThe use of ROSUKARD® at a dose of 40 mg per day is contraindicated in patients with a predisposition to myopathy (see the section “Contraindications”). When prescribing doses of 10 mg and 20 mg per day, the recommended initial dose of ROSUCARD® for this group of patients is 5 mg per day.

Ethnic groupsWhen studying the pharmacokinetic parameters of rosuvastatin, an increase in the systemic concentration of the drug was noted in representatives of the Mongolian race (see the section “Pharmacokinetics”). This fact should be taken into account when prescribing ROSUCARD® to patients of the Mongolian race. When prescribing doses of 10 and 20 mg, the recommended initial dose of ROSUCARD®for this group of patients is 5 mg per day. The use of ROSUKARD® at a dose of 40 mg per day in representatives of the Mongoloid race is contraindicated (see the section “Contraindications”).

When prescribing ROSUCARD® with gemfibrozil, the dose should not exceed 10 mg per day.

Overdose

With simultaneous use of several daily doses, the pharmacokinetic parameters of rosuvastatin do not change.

Treatment: there is no specific treatment, but symptomatic therapy is performed to maintain the functions of vital organs and systems. Monitoring of liver function and CKD activity is necessary. Hemodialysis is ineffective.

Special instructions

During treatment, especially during the period of dose adjustment of ROSUCARD®, the lipid profile should be monitored every 2-4 weeks and the dose of the drug should be changed if necessary.

It is recommended to determine liver function indicators before the start of therapy and 3 months after the start of therapy. ROSUCARD® should be discontinued or the dose of the drug should be reduced if the level of activity of “hepatic” transaminases in the blood serum is 3 times higher than the upper limit of normal. When using the drug ROZUKARD® at a dose of 40 mg, it is recommended to monitor the indicators of renal function. In patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome, treatment of the underlying diseases should be performed before starting treatment with ROSUCARD®.

In patients with existing risk factors for rhabdomyolysis, it is necessary to consider the ratio of expected benefit and potential risk and conduct clinical monitoring throughout the course of treatment.

The patient should be informed of the need to immediately inform the doctor about cases of unexpected muscle pain, muscle weakness or spasms, especially in combination with malaise and fever. In such patients, the level of CPK should be determined. Therapy should be discontinued if CKD activity is significantly increased (more than 5 times the upper limit of normal) or if muscle symptoms are severe and cause daily discomfort. If symptoms disappear and CK levels return to normal, consideration should be given to re-prescribing ROSUCARD® or other HMG-CoA reductase inhibitors in smaller doses, with careful monitoring of the patient.

Determination of CKD activity should not be performed after intense physical exertion or in the presence of other possible causes of increased CKD activity, which may lead to misinterpretation of the results obtained. If the initial CPK level is significantly increased, a second measurement should be performed after 5-7 days – do not start therapy if the repeated test confirms the initial CPK activity (5 times higher than normal).

Routine monitoring of CPK activity in the absence of symptoms is not advisable. An increased incidence of myositis and myopathy has been reported in patients treated with other HMG-CoA reductase inhibitors in combination with fibrinic acid derivatives (including gemfibrozil), cyclosporine, nicotinic acid, azole antifungal drugs, protease inhibitors, and macrolide antibiotics. The ratio of expected benefit and potential risk should be carefully weighed when ROSUCARD® is co-administered with fibrates or nicotinic acid (at least 1 g / day), and concomitant use of gemfibrozil a is not recommended.

In most cases, proteinuria decreases or disappears during therapy and does not mean the occurrence of acute or exacerbation of existing kidney disease. Evaluation of renal function should be carried out during routine examination of patients receiving a dose of 40 mg

. 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 HMG-CoA reductase inhibition exceeds the benefit of using the drug during pregnancy. If pregnancy occurs during therapy, the drug should be discontinued immediately. There are no data on the excretion of rosuvastatin in women’s milk, so breast-feeding should be discontinued.

Co-use of rosuvastatin and HIV protease inhibitors is not recommended.

Isolated cases of interstitial lung disease have been reported with prolonged use of rosuvastatin. If interstitial lung disease is suspected, ROSUCARD®therapy should be discontinued.

When studying the pharmacokinetic parameters of rosuvastatin, an increase in the systemic concentration of the drug was noted in representatives of the Mongolian race (see the section “Pharmacokinetics”). This fact should be taken into account when prescribing ROSUCARD® to patients of the Mongolian race.

Influence on the ability to drive vehicles and work with mechanisms. Caution should be exercised when driving vehicles and engaging in activities that require increased concentration and speed of psychomotor reactions (dizziness may occur during therapy).

Form of production

oblong, biconvex tablets with a risk, covered with a film-coated light pink color

Storage conditions

 In a dark place, at a temperature not exceeding 25 °C.

Shelf life

2 years

Active ingredient

Rosuvastatin

Conditions of release from pharmacies

By prescription

Dosage form

Tablets