Rosuvastatin is effective in adults with hypercholesterolaemia, with and without hypertriglyceridaemia, regardless of race, gender or age, including patients with diabetes mellitus and familial hypercholesterolemia.
80% of patients with hypercholesterolemia IIa and what is testosterone propionate classification Fredrickson at application rosuvastatin concentration reaches the values
in patients with heterozygous familial hypercholesterolemia treated with rosuvastatin in dosages from 20 to 80 mg scheme for accelerated titration dose, there was a positive dynamics of the lipid profile. After titration to a daily dose of 40 mg per day (12 weeks) concentration decreased by 53%. In 33% of patients had achieved a reduction in the concentration .
In patients with homozygous familial hypercholesterolemia treated with rosuvastatin at doses of 20 and 40 mg, the mean reduction.
The additive effect was observed in combination with fenofibrate against the concentration of TG and nicotinic acid (more than 1 g per day) in relation to the concentration .
in patients with lower risk for coronary heart disease and subclinical atherosclerosis, which is estimated by the thickness of the complex “intima-media” carotid artery, rosuvastatin 40 mg / day significantly slowed the rate of progression IMT for maximum of 12 segments of the carotid artery compared to placebo at a rate – 0.0145 mm / year .
The dose of 40 mg should be used only in patients with severe hypercholesterolaemia and high risk for cardiovascular disease. The maximum concentration of rosuvastatin plasma levels achieved approximately 5 hours after oral administration. The absolute bioavailability of ≈ 20%. The distribution of Rosuvastatin is metabolized mainly by the liver, which is the main site of cholesterol synthesis . The volume of distribution of rosuvastatin is approximately 134 liters. Approximately 90% of rosuvastatin is bound to plasma proteins, mainly to albumin. Metabolism Biotransformation exposed to a limited number of what is testosterone propionate (approximately 10%). The metabolism of rosuvastatin marginally associated with cytochrome isozymes system.
The main identified metabolites of rosuvastatin are what is testosterone propionate and lactone metabolites. N-desmetilrozuvastatin approximately 50% less active than rosuvastatin lactone metabolites are pharmacologically inactive. Over 90% of the pharmacological activity for the inhibition of the circulating HMG-CoA reductase inhibitor rosuvastatin is provided, and the rest – its metabolites. Excretion Approximately 90% of the accepted dose of rosuvastatin is excreted unchanged through the intestines (including unabsorbed and absorbed rosuvastatin), and the rest excreted by the kidneys. In unaltered by the kidneys is displayed for about 5% of the administered dose. The of 19 hours, does not change with increasing dose. The geometric mean plasma clearance of approximately 50 l / h (coefficient of variation 21.7%). As in the case , a process of “hepatic” capture involved rosuvastatin membrane transporter of cholesterol through the membrane. This vector plays an important role in the removal of rosuvastatin is the liver. The linearity Systemic exposure of rosuvastatin increases in proportion to dose. superdrol for sale