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Mechanism of action

MERTENIL is a hypolipidemic agent from the group of statins, an inhibitor of HMG-CoA reductase. According to the principle of competitive antagonism, the statin molecule binds to the part of the coenzyme A receptor where this enzyme is attached. Another part of the statin molecule inhibits the conversion of hydroxymethylglutarate to mevalonate, an intermediate product in the synthesis of the cholesterol molecule. Inhibition of the activity of HMG-CoA reductase leads to a series of consecutive reactions, which result in a decrease in the intracellular cholesterol content and a compensatory increase in the activity of LDL receptors and, accordingly, an acceleration of cholesterol catabolism (Xc) of LDL.

The lipid-lowering effect of statins is associated with a decrease in total Xc due to Xc-LDL. A decrease in the level of LDL is dose-dependent and is not linear, but exponential.

Statins do not affect the activity of lipoprotein and hepatic lipases, do not have a significant effect on the synthesis and catabolism of free fatty acids, therefore their effect on the TG level is secondary and indirectly through their main effects on reducing the level of Xc-LDL. A moderate decrease in the level of TG in the treatment with statins seems to be associated with the expression of the remnant (apo E) receptors on the surface of hepatocytes involved in the catabolism of LPPP, which are approximately 30% TG.

In addition to the lipid-lowering action, statins have a positive effect on endothelial dysfunction (preclinical sign of early atherosclerosis), on the vascular wall, atheroma, improve the rheological properties of blood, have antioxidant, anti-proliferative properties.

The therapeutic effect is manifested within 1 week. after the start of therapy and after 2 weeks of treatment, it is 90% of the maximum possible effect, which is usually achieved by week 4 and then remains constant.

Indications and usage

Hypercholesterolemia (type IIa, including familial heterozygous hypercholesterolemia) or mixed hypercholesterolemia (type IIb) as a supplement to the diet, when diet and other non-drug therapies (eg exercise, weight loss) are insufficient.

Familial homozygous hypercholesterolemia as an adjunct to diet and other cholesterol-lowering therapy or in cases where such therapy is not suitable for the patient.


Liver diseases in the active phase (including a persistent increase in liver transaminase activity or any increase in transaminase activity by more than 3 times as compared with VGN), pronounced renal dysfunction (CC <30 ml / min), myopathy, cyclosporine co-administration, pregnancy, lactation (breastfeeding), women of reproductive age who do not use adequate methods of contraception, children and adolescents under 18 years old (since efficacy and safety have not been established), increased sensitivity to Rosuvastatin.

Pregnancy and Breastfeeding


Dosage and administration

Is ingested. The recommended initial dose is 10 mg 1 time / If necessary, the dose may be increased to 20 mg after 4 weeks. Increasing the dose to 40 mg is possible only in patients with severe hypercholesterolemia and a high risk of cardiovascular complications (especially in patients with familial hypercholesterolemia) with insufficient effectiveness at a dose of 20 mg and subject to the supervision of a physician.

Adverse reactions

From the side of the central nervous system: often - headache, dizziness, asthenic syndrome; possible - anxiety, depression, insomnia, neuralgia, paresthesia.

From the digestive system: often - constipation, nausea, abdominal pain; possible - reversible transient dose-dependent increase in the activity of hepatic transaminases, dyspepsia (includingdiarrhea, flatulence, vomiting), gastritis, gastroenteritis.

Respiratory: often - pharyngitis; possibly rhinitis, sinusitis, bronchial asthma, bronchitis, cough, dyspnea, pneumonia.

Cardiovascular: possible - angina, increased blood pressure, palpitations, vasodilation.

Musculoskeletal system: often myalgia; arthralgia, arthritis, muscle hypertonus, back pain, pathological pearl of a limb (without injuries) are possible; rarely - myopathy, rhabdomyolysis (simultaneously with impaired renal function, while receiving the drug in a dose of 40 mg).

Urogenital: tubular proteinuria (in less than 1% of cases - for doses of 10 and 20 mg, 3% of cases - for a dose of 40 mg); possible - peripheral edema (arms, legs, ankles, legs), lower abdominal pain, urinary tract infections.

Allergic reactions: possible - skin rash, pruritus; rarely - angioedema.

From the laboratory indicators: a transient dose-dependent increase in the activity of CPK (with an increase in the activity of CPK by more than 5 times compared to VGN, therapy should be temporarily suspended).

Other: often - asthenic syndrome; possibly - accidental trauma, anemia, chest pain, diabetes, ecchymosis, flu-like syndrome, periodontal abscess.

Drug Interactions

With the simultaneous use of rosuvastatin and cyclosporine, the AUC of rosuvastatin was on average 7 times higher than that observed in healthy volunteers, while the plasma concentration of cyclosporin did not change.

Initiation of rosuvastatin therapy or an increase in the dose in patients receiving vitamin K antagonists (eg, warfarin) at the same time can lead to an increase in prothrombin time and INR, and the withdrawal of rosuvastatin or a decrease in dose can lead to a decrease in INR (monitoring of INR is recommended in such cases).

The combined use of rosuvastatin and gemfibrozil leads to a 2-fold increase in Cmax in plasma and AUC of rosuvastatin.

The simultaneous use of rosuvastatin and 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 is unknown).

The simultaneous use of rosuvastatin and Erythromycin leads to a decrease in AUC of rosuvastatin by 20% and Cmax of rosuvastatin by 30% (probably as a result of increased motility of the intestine caused by taking erythromycin).

The simultaneous use of rosuvastatin and oral contraceptives increases the AUC of ethinyl estradiol and AUC of norgestrel by 26% and 34%, respectively. Such interaction cannot be ruled out with simultaneous use of rosuvastatin and hormone replacement therapy.

Gemfibrozil, other fibrates and lipid-lowering doses of nicotinic acid (≥1 g /) increased the risk of myopathy, while being used with other HMG-CoA reductase inhibitors, probably because they can cause myopathy and when used as monotherapy.

The combined use of rosuvastatin and itraconazole (CYP3A4 inhibitor) increases the AUC of rosuvastatin by 28% (clinically insignificant).

In a dry, dark place at a temperature of no higher than 30 ° C.


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