Rosuvastatin-Vertex, 20 mg 90 pcs

Rosuvastatin is a selective competitive inhibitor of HMG-CoA reductase – an enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A into mevalonic acid, cholesterol precursor.

The main target of rosuvastatin action is the liver, where the synthesis of cholesterol (Chs) and catabolism of low-density lipoprotein cholesterol (LDL-C) are performed. Rosuvastatin increases the number of X-LDL receptors on the surface of liver cells, increasing capture and catabolism of X-LDL, which in turn leads to inhibition of synthesis of very low-density lipoprotein cholesterol (VLDL), thereby reducing the total amount of X-LDL and X-LDL.

Rosuvastatin reduces elevated concentrations of Chs-LDL, total cholesterol, triglycerides (TG), increases the concentration of high-density lipoprotein cholesterol (HDL-C), and reduces the concentration of apolipoprotein B (ApoB), high-density lipoprotein cholesterol (Xs-NLDL), Xs-LDL, TG and increases the concentration of apolipoprotein A I (ApoA-I), reduces the ratio of Xs-LDL/Hs-LDL, total cholesterol/Hs-LDL and Xs-NLDL/Hs-LDL and the apoB/apoA-I ratio.

The therapeutic effect develops within one week after the start of therapy with rosuvastatin, after 2 weeks of treatment it reaches 90% of the maximum possible effect. The maximum therapeutic effect is usually achieved by the 4th week of therapy and is maintained with regular use of the drug.

Rosuvastatin is effective in adult patients with hypercholesterolemia, with or without hypertriglyceridemia, including patients with diabetes and familial hypercholesterolemia. Additive effect is observed in combination with fenofibrate (for TG concentration) and with nicotinic acid in lipid-lowering doses (for HDL-C concentration), but the possibility of such combinations should be assessed by the attending physician taking into account possible risks

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Special Instructions

In patients receiving high doses of rosuvastatin (particularly 40 mg/day), tubular proteinuria has been observed, which was detected with test strips and in most cases was intermittent or transient.

Such proteinuria is not indicative of acute disease or progression of concomitant renal disease. The incidence of serious renal function abnormalities noted in a post-marketing study of rosuvastatin is higher at the 40 mg/day dose.

In patients taking the drug at a dose of 30 or 40 mg/day, it is recommended to monitor renal function parameters during treatment (at least once every 3 months). Effect on the musculoskeletal system.

When using rosuvastatin at all doses, but especially at doses exceeding 20 mg/day, the following effects on the musculoskeletal system have been reported: myalgia, myopathy, in rare cases rhabdomyolysis.

Very rare cases of rhabdomyolysis have been reported with concomitant use of HMG-CoA reductase inhibitors and ezetimibe. Such combination should be used with caution because pharmacodynamic interaction cannot be excluded. As in the case of other HMG-CoA reductase inhibitors, the incidence of rhabdomyolysis during post-marketing use of rosuvastatin is higher when using 40 mg/day dose. Determination of CPK activity.

CPK activity should not be determined after vigorous physical activity and in the presence of other possible causes of increase in its activity; it may lead to misinterpretation of the obtained results. If the baseline CPK activity is significantly exceeded (5 times the ULN), the analysis should be repeated in 5-7 days.

The therapy should not be started if the results of the repeated test confirm the initial high activity of CPK (more than 5 times the ULN). Before therapy Depending on the daily dose in patients with existing risk factors for myopathy/rhabdomyolysis, rosuvastatin is either contraindicated or should be administered with caution (see “Contraindications”, “Limitations of Use”).

Such factors include: renal dysfunction; hypothyroidism; muscle diseases in the anamnesis (includingincluding familial); myotoxic phenomena when taking other HMG-CoA reductase inhibitors or fibrates in the history; excessive use of alcohol; age over 65 years; conditions in which plasma concentrations of rosuvastatin may increase; concomitant use of fibrates.

In such patients it is necessary to assess the risk and possible benefit of therapy. Clinical monitoring is also recommended. If baseline CPK activity is more than 5-fold higher than ICH, rosuvastatin therapy should not be started.

During therapy with rosuvastatin the patient should be informed to seek immediate medical attention in case of sudden onset of muscle pain, muscle weakness or cramps, especially in combination with malaise and fever. In such patients, CPK activity should be determined. The therapy should be stopped if CPK activity is significantly increased (more than 5 times of IGN) or muscle symptoms are severe and cause daily discomfort (even if CPK activity is not more than 5 times of IGN).

If symptoms disappear and CPK activity returns to normal, resumption of rosuvastatin or other HMG-CoA reductase inhibitors at lower doses with close medical supervision should be considered. Monitoring of CPK activity in the absence of symptoms is unnecessary.

There have been very rare cases of immune-mediated necrotizing myopathy with clinical manifestations as persistent proximal muscle weakness and increased serum CPK activity during therapy or upon discontinuation of HMG-CoA reductase inhibitors, including rosuvastatin.

Additional muscular and nervous system studies, serological studies and therapy with immunosuppressive agents may be required. No evidence of increased skeletal muscle effects with rosuvastatin and concomitant therapy has been noted.

However an increase in myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors in combination with fibric acid derivatives (e.g. gemfibrozil), cyclosporine, nicotinic acid at lipid-lowering doses (over 1 g/day), antifungal agents – azole derivatives, HIV protease inhibitors and macrolide antibiotics.

Simultaneous use with some HMG-CoA reductase inhibitors increases the risk of myopathy. Thus, concomitant use of rosuvastatin and gemfibrozil is not recommended. The benefits of further changes in plasma lipid concentrations when combining this drug with fibrates or nicotinic acid in lipid-lowering doses should be carefully weighed against the possible risk.

Rosuvastatin at a dose of 30 mg/day is contraindicated for combination therapy with fibrates. Due to the increased risk of rhabdomyolysis, rosuvastatin should not be used in patients with acute conditions that may lead to myopathy or conditions predisposing to the development of renal failure (such as sepsis, arterial hypotension, extensive surgery, trauma, severe metabolic, endocrine and electrolyte disorders or uncontrolled seizures).

Liver. Depending on the daily dose, rosuvastatin is contraindicated or should be used with caution in patients with excessive alcohol consumption and/or with a history of liver disease (see “Contraindications”, “Limitations on use”).

It is recommended to determine liver function tests before the therapy start and 3 months after the start of therapy. Rosuvastatin should be discontinued or the dose of this agent should be reduced if hepatic serum transaminase activity exceeds 3 times VHF.

In patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome before treatment with rosuvastatin therapy of underlying diseases should be conducted. Ethnic peculiarities. During pharmacokinetic studies, increased plasma concentrations of rosuvastatin have been observed in mongoloid race compared to Caucasoid race. Interstitial lung disease.

Single cases of interstitial lung disease have been reported with some HMG-CoA reductase inhibitors, especially for long periods of time. Manifestations of the disease may include shortness of breath, non-productive cough and deterioration of general well-being (weakness, weight loss and fever).

If interstitial lung disease is suspected, therapy with HMG-CoA reductase inhibitors should be discontinued. Diabetes mellitus type 2. In patients with glucose concentrations between 5.6 and 6.9 mmol/L, therapy with rosuvastatin has been associated with an increased risk of developing type 2 diabetes mellitus. Influence on the ability to drive a car or perform work requiring increased speed of physical and mental reactions.

Studies to study the effect of rosuvastatin on the ability to drive vehicles and work with mechanisms have not been conducted. Nevertheless, taking into account the possibility of dizziness and other side effects, caution should be exercised when driving vehicles and operating other mechanisms that require high concentration and rapid psychomotor reactions.

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