Crestor pills 10 mg 126 pcs
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Description
Crestor pills - a lipid-lowering drug, selective competitive inhibitor of HMG-CoA reductase. Crestor reduces elevated concentrations of LDL cholesterol, total cholesterol, triglycerides, increases the concentration of high-density cholesterol-lipoproteins, and also reduces the concentration of apolipoprotein B and increases the concentration of apolipoprotein AI.
Active ingredients
Rosuvastatin
Release form
Pills
Composition
Rosuvastatin (in the form of rosuvastatin calcium) 10 mg. Adjuvants: lactose monohydrate - 89.5 mg, microcrystalline cellulose - 29.82 mg, calcium phosphate - 10.9 mg, crospovidone - 7.5 mg, magnesium stearate - 1.88 mg. Film coating composition: lactose monohydrate - 1.8 mg, hypromellose - 1.26 mg, triacetin (glycerol triacetate) - 0.36 mg, titanium dioxide - 1.06 mg, iron dye red oxide - 0.02 mg.
Indications
- Fredrikson's primary hypercholesterolemia (type IIa, including familial heterozygous hypercholesterolemia) or mixed hypercholesterolemia (type IIb) as a supplement to the diet, when diet and other non-pharmacological treatment methods (for example, exercise, weight loss) are insufficient, - familial homozygote. hypercholesterolemia as an adjunct to diet and other lipid-lowering therapy (for example, LDL-apheresis), or in cases when such therapy is not effective enough, hypertriglyceridemia (such as p IV according to Fredrikson) as a supplement to the diet, to slow the progression of atherosclerosis as a supplement to the diet in patients who have been shown therapy to reduce the concentration of total cholesterol and LDL-C, is the primary prevention of major cardiovascular complications (stroke, heart attack, arterial revascularization) in adult patients without clinical signs of coronary artery disease, 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) if present, ak at least one additional risk factors such as hypertension, low concentrations of HDL-C, smoking, family history of early onset coronary artery disease).
Precautionary measures
Patients who received high doses of Crestor (mostly 40 mg) had tubular proteinuria, which, in most cases, was transient. Such proteinuria did not indicate acute kidney disease or progression of kidney disease.In patients taking the drug in a dose of 40 mg, it is recommended to monitor indicators of renal function during treatment. When using the drug Crestor in all doses, especially in doses over 20 mg, the following effects on the musculoskeletal system were reported: myalgia, myopathy, in rare cases - rhabdomyolysis. Determination of the level of CPK should not be carried out after intense physical exertion or if there are other possible reasons for increasing the activity of CPK, which can lead to incorrect interpretation of the results. If the initial level of CPK is significantly increased (5 times higher than VGN), after 5-7 days it is necessary to re-measure. You should not begin therapy if the repeated test confirms the initial activity of CPK (more than 5 times higher than VGN). When prescribing the drug Crestor, as well as the appointment of other HMG-CoA reductase inhibitors, caution should be exercised in patients with existing factors risk of myopathy / rhabdomyolysis, it is necessary to consider the ratio of risk and possible benefits of therapy and to conduct clinical observation. It is necessary to inform the patient about the need for an immediate report to the doctor about cases of unexpected appearance of muscle pain, muscle weakness or cramps, especially when combined with malaise and fever. In such patients, the activity of CPK should be determined. Therapy should be discontinued if the activity of CPK is significantly increased (more than 5 times compared to VGN) or if the symptoms of the muscles are pronounced and cause daily discomfort (even if the activity of KFK is 5 times less than VGN). symptoms disappear, and CPK activity returns to normal, consideration should be given to reappointment of Crestor or other HMG-CoA reductase inhibitors in smaller doses with careful observation of the patient. Routine control of CPK activity in the absence of symptoms tree-like. Very rare cases of immune-mediated necrotizing myopathy with clinical manifestations in the form of persistent weakness of the proximal muscles and an increase in the level of CPK in the serum during treatment or when discontinuation of statins, incl. Rosuvastatin. Additional studies of the muscular system and nervous system, serological studies, and therapy with immunosuppressive agents may be required. There are no signs of an increase in the effect on skeletal muscles when taking Crestor and concomitant therapy.However, an increase in the incidence of myositis and myopathy was reported in patients taking other HMG-CoA reductase inhibitors in combination with fibrin acid derivatives, including gemfibrozil, cyclosporine, nicotinic acid, azole antifungal agents, protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when used together with some HMG-CoA reductase inhibitors. Thus, the simultaneous use of the drug Crestor and gemfibrozil is not recommended. It is necessary to carefully weigh the balance of risk and possible benefit when using the Crestor and fibrates or lipid-lowering doses of nicotinic acid together. Reception of a drug Crestor in a dose of 40 mg together with fibrates is contraindicated. 2-4 weeks after the start of treatment and / or with an increase in the dose of Crestor, monitoring of lipid metabolism indices is necessary (dose adjustment is required if necessary). It is recommended to determine liver function indices before starting therapy and 3 months after starting therapy. Reception of the drug Crestor should be stopped or reduced dose of the drug, if the activity of transaminases in the blood serum: 3 times higher than VGN.U patients with hypercholesterolemia due to hypothyroidism or nephrotic syndrome, the treatment of major diseases should be carried out before the start of treatment with Crestor. HIV protease inhibitors. The drug should not be used in patients with lactase deficiency, galactose intolerance and glucose-galactose malabsorption. Menen some statins especially for a long time it has been reported rare cases of interstitial lung disease. Manifestations of the disease can be shortness of breath, unproductive cough and worsening, general well-being (weakness, weight loss and fever). If interstitial lung disease is suspected, statin therapy should be discontinued. In patients with a glucose concentration of 5.6 to 6.9 mmol / l, Crestor therapy was associated with an increased risk of developing type 2 diabetes.
Use during pregnancy and lactation
Crestor is contraindicated in pregnancy and lactation (breastfeeding). Women of reproductive age should use adequate methods of contraception. Because cholesterol and other products of cholesterol biosynthesis are important for the development of the fetus, the potential risk of inhibiting HMG-CoA reductase exceeds the benefits of using the drug in pregnant women. In the event of pregnancy in the course of therapy, the drug should be discontinued immediately. There are no data on the release of rosuvastatin in breast milk. therefore, during the breastfeeding period, the drug should be stopped.
Dosage and administration
Inside, do not chew or crush the pill, swallow whole, washed down with water. The drug can be prescribed at any time of the day, regardless of the meal. Before starting treatment with Crestor, the patient should begin to follow the standard cholesterol-lowering diet and continue to follow it during treatment. The dose of the drug should be selected individually depending on the goals of therapy and the therapeutic response to treatment, taking into account the current recommendations on target lipid concentrations. The recommended initial dose for patients starting the drug or for patients transferred from taking other HMG-CoA reductase inhibitors , should be 5 or 10 mg of the drug Crestor 1 time / day. When choosing the initial dose, one should be guided by the individual concentration of cholesterol and take into account the possible risk of cardiovascular complications, as well as the potential risk of side effects. If necessary, the dose can be increased to more after 4 weeks. Due to the possible development of side effects when taking a dose of 40 mg, compared with lower doses of the drug, increasing the dose to 40 mg, after an additional dose of higher than the recommended initial dose within 4 weeks of therapy, can be performed only in patients with severe hypercholesterolemia and with a high risk of cardiovascular complications (especially in patients with familial hypercholesterolemia) who have not achieved the desired result erapii when receiving doses of 20 mg, and which will be under the supervision of a specialist.Particularly careful monitoring of patients receiving the drug at a dose of 40 mg is recommended. Prescribing the drug at a dose of 40 mg is not recommended for patients who have not previously visited a doctor. After 2-4 weeks of therapy and / or with an increase in the dose of Crestor, control of lipid metabolism indices is necessary (dose adjustment is required if necessary). Patients of advanced age do not need dose adjustment.
Side effects
Side effects observed when taking the drug Crestor, usually expressed slightly and pass on their own. As with the use of other inhibitors of HMG-CoA reductase, the frequency of side effects is mostly dose-dependent. The frequency of adverse reactions: often (> 1/100, <1/10), rarely (> 1/1000, < 1/100), rarely (> 1/10 000, <1/1000), very rarely (<1/10 000), including individual messages. From the immune system: rarely - hypersensitivity reactions, including angioedema. From the side endocrine system: often - type 2 diabetes. For the central nervous system: often - headache, dizziness. For the digestive system: ca one hundred - constipation, nausea, abdominal pain, rarely - pancreatitis. On the skin side: infrequently - pruritus, rash, urticaria. On the musculoskeletal system: often - myalgia, rarely - myopathy (including myositis), rhabdomyolysis. side of the urinary system: in patients treated with Crestor, proteinuria can be detected. Changes in the amount of protein in the urine (from the absence or trace amounts to ++ or more) are observed in less than 1% of patients receiving the drug in a dose of 10-20 mg, and in about 3% of patients receiving the drug in a dose of 40 mg. A slight change in the amount of protein in the urine was noted when taking a dose of 20 mg. In most cases, proteinuria diminishes or disappears during therapy and does not mean the onset or acute progression of existing kidney disease. From the musculoskeletal system: when using the Crestor drug in all doses, especially at doses over 20 mg, myalgia, myopathy (including myositis) in rare cases, rhabdomyolysis with or without acute renal failure. A dependent increase in the level of CPK is observed in an insignificant number of patients taking rosuvastatin. In most cases, it was minor, asymptomatic and temporary. In the case of increased activity of CPK (more than 5 times compared to VGN), therapy should be suspended. Liver: a dose-dependent increase in the activity of hepatic transaminases in an insignificant number of patients.In most cases, it is insignificant, asymptomatic and temporary. Laboratory indicators: an increase in the concentration of glucose, bilirubin, GGT activity, ALP, thyroid gland dysfunction. Others: often - asthenic syndrome.
Overdose
When several daily doses are taken simultaneously, the pharmacokinetic parameters of rosuvastatin do not change. There is no specific treatment for an overdose of rosuvastatin. In case of overdose, it is recommended to carry out symptomatic treatment and measures aimed at maintaining the functions of vital organs and systems. The control of liver function and the level of CPK is necessary. It is unlikely that hemodialysis will be effective.
Interaction with other drugs
Cyclosporine: with simultaneous use of rosuvastatin and cyclosporine, the AUC of rosuvastatin was on average 7 times higher than that observed in healthy volunteers. The combined use leads to an increase in the concentration of rosuvastatin in the plasma, blood 11 times. It does not affect the plasma concentration of cyclosporine. Indirect anticoagulants: starting therapy with rosuvastatin or increasing the dose of the drug in patients who receive both indirect anticoagulants (for example, warfarin), can lead to an increase in prothrombin time (MHO). Canceling rosuvastatin or lowering the dose may result in a decrease in MPE. In such cases, it is recommended to control MHO.Hemfibrozil and other lipid-lowering drugs: the combined use of rosuvastatin and gemfibrozil results in a 2-fold increase in Cmax of rosuvastatin in plasma and AUC of rosuvastatin. Based on data on specific interactions, pharmacokinetically significant interactions with fenofibrates are not expected, pharmacodynamic interactions are possible. Gemfibrozil, fenofibrate, other fibrates and lipid-lowering doses of nicotinic acid increased the risk of myopathy with simultaneous use with HMG-CoA reductase inhibitors, possibly due to that they can cause myopathy and when used as monotherapy. While taking the drug with gsmfibrozil, fibrates, nicotinic acid in a dose of more than 1 g / day, patients are recommended an initial dose of 5 mg. Ezetimibe: the simultaneous use of Crestor and ezetimibe was not accompanied by changes in the AUC and Cmax of both drugs. HIV protease inhibitors: despite that the exact interaction mechanism is unknown,co-administration of HIV protease inhibitors can lead to a significant increase in the exposure of rosuvastatin. A pharmacokinetic study on the simultaneous use of 20 mg of rosuvastatin with a combination preparation containing two HIV protease inhibitors (400 mg of lopinavir / 100 mg of ritonavir) in healthy volunteers resulted in an approximately twice and fivefold increase in AUC0 -24 and Cmax of rosuvastatin, respectively. Therefore, concomitant use of rosuvastatin and HIV protease inhibitors in the treatment of patients with HIV infection is not recommended. Antacids: the simultaneous use of rosuvastatin and suspensions of antacids containing aluminum and magnesium hydroxide, reduces the plasma concentration of rosuvastatin by about 50%. This effect is less pronounced if antacids are applied 2 hours after taking rosuvastatin. The clinical significance of this interaction has not been studied. Erythromycin: simultaneous use of rosuvastatin and erythromycin leads to a decrease in AUC0-24 of rosuvastatin by 20% and Cmax of rosuvastatin by 30%. Such an interaction may occur as a result of increased intestinal motility caused by taking erythromycin. Oral contraceptives / hormone replacement therapy: the simultaneous use of rosuvastatin and oral contraceptives increases the AUC of ethinyl estradiol and AUC norgestrel by 26% and 34%, respectively. Such an increase in plasma concentration should be considered when selecting the dose of plasma concentration should be taken into account when selecting the dose of oral contraceptives. Pharmacokinetic data on the simultaneous use of the drug Crestor and hormone replacement therapy are not available, therefore, a similar effect cannot be excluded when using this combination. However, this combination was widely used during clinical trials and was well tolerated by patients. Other medicines: no clinically significant interaction of rosuvastatin with digoxin is expected. The cytochrome P450 isoenzymes: the results of in vivo and in vitro studies showed that rosuvastatin is neither an inhibitor nor inducer isoenzymes of cytochrome P450. In addition, rosuvastatin is a weak substrate for these enzymes.There was no clinically significant interaction between rosuvastatin and fluconazole (an inhibitor of CYP2C9 and CYP3A4 isoenzymes) and ketoconazole (an inhibitor of CYP2A6 and CYP3A4 isoenzymes). The combined use of rosuvastatin and itraconazole (an inhibitor of the isoenzyme CYP3A4) increases the AUC of rosuvastatin by 28% (clinically insignificant). Thus, interactions associated with the metabolism of cytochrome P450 are not expected.