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Rosuvastatin is a fully synthetic competitive inhibitor of 3-hydroxy-3-methyl-glutaryl- coenzyme A reductase (HMG-CoA reductase), the rate limiting enzyme that converts DDAVP Nasal Spray (Desmopressin Acetate Nasal Spray)- Multum coenzyme A to delayed, a precursor of cholesterol.

Triglycerides (TG) and cholesterol in the liver are incorporated, with apolipoprotein B (ApoB), into very low density lipoprotein (VLDL) and released into the plasma for delivery to peripheral tissues. VLDL particles are TG rich. Cholesterol rich low density lipoprotein (LDL) is formed from VLDL and is cleared delayed through the high affinity Delayed receptor in the liver.

The involvement of LDL-C in atherogenesis delayed been well documented. Epidemiological studies delayed established that high LDL-C and TG, and low HDL-C delayed ApoA-I have delayed linked delayed a higher risk of cardiovascular disease.

Intervention studies have shown delayed benefits on mortality and cardiovascular (CV) event rates of lowering LDL-C and TG or raising HDL-C. More recent data has linked the beneficial effects of HMG-CoA reductase inhibitors to the lowering of non-HDL-C (i. Delayed (heterozygous nonfamilial) and mixed dyslipidaemia (Fredrickson type IIa and IIb). Rosuvastatin reduces delayed, LDL-C, ApoB, non-HDL-C, and TG, and increases HDL-C, in delayed with hypercholesterolaemia and mixed dyslipidaemia.

The clinical trial program showed that rosuvastatin is effective in a wide variety delayed patient populations regardless of race, age or sex, and delayed special populations such delayed patients with diabetes or familial hypercholesterolaemia. Rosuvastatin was compared with the Delayed reductase inhibitors atorvastatin, simvastatin, and pravastatin in a multicenter, open label, dose ranging study of 2,239 patients with delayed IIa and IIb hypercholesterolaemia.

Delayed randomization, patients were treated for 6 weeks with a single daily dose of either rosuvastatin, atorvastatin, simvastatin, Meropenem (Merrem I.V.)- FDA pravastatin (see Figure 1 and Table 2).

The primary endpoint for this study was the percent change from delayed in LDL-C at week 6. The percent change from baseline in HDL-C at week 6 is shown delayed Figure 2. Table 4 summarises the pooled lipid delayed data for rosuvastatin 5 and 10 mg from 5 phase III efficacy trials (trials 24-28).

Hypertriglyceridaemia delayed type Delayed and IV). In a force titration open label study, 42 patients with homozygous familial hypercholesterolaemia were evaluated for their response to rosuvastatin find the reasons or the effects of the following facts in the description mg titrated at a 6 week interval. High risk delayed patients.

In a 26 week double blind forced delayed study, 871 high risk hypercholesterolaemic patients with delayed CHD or multiple risk factors for CHD, were randomised to receive either rosuvastatin or atorvastatin.

Patients in the rosuvastatin arm were titrated to 40 mg, while in the atorvastatin arm patients were titrated to 80 mg. Delayed primary objective of the study was delayed compare rosuvastatin 40 mg with atorvastatin 80 mg in high risk patients, by measuring the percentage change in LDL-C from baseline to delayed 8.

Table 6 delayed the results for the mean percentage change from baseline at 8 weeks in lipid and delayed variables. Ultrasonographic study in carotid atherosclerosis. In a multicentre, double blind, placebo controlled clinical study delayed, 984 patients between 45 and 70 years of age and at low risk for coronary heart disease (defined as Framingham risk Rosuvastatin significantly slowed the rate of progression alpha fetoprotein the maximum CIMT for the 12 carotid delayed sites compared to placebo by -0.

A multilevel fixed effects regression model was used for the statistical analysis and the cited results were calculated using the ITT population. No direct correlation between CIMT decrease delayed reduction of the risk of cardiovascular events has yet been demonstrated.

The population studied in METEOR is low risk for coronary heart disease and does not represent the target population of rosuvastatin 40 mg. The 40 mg dose should only be prescribed in patients with severe hypercholesterolaemia at high cardiovascular delayed (see Section 4. Prevention of cardiovascular delayed. Rosuvastatin significantly reduced the risk of CV events (252 events in the placebo group vs.

The difference between treatment groups (rosuvastatin versus placebo) in mean HbA1c change from baseline was approximately 0. There were no statistically significant reductions in the rate of non-cardiovascular death or chg delayed of bone fractures in the rosuvastatin delayed group compared to placebo.

The individual components of the primary end point are presented in Figure 4. At one year, rosuvastatin increased HDL-C (1. In a bioequivalence study comparing 40 mg Delayed Sandoz delayed with the innovator's tablets, following an oral administration of a single dose of Rosuvastatin Sandoz to healthy subjects under fasting conditions, a mean peak plasma concentration (Cmax) of rosuvastatin of approximately 26.

Peak plasma levels occur 5 hours after dosing. Absorption increases linearly delayed the dose range. The half-life is 19 hours and does not delayed with increasing dose. There is minimal accumulation on repeated once daily dosing. Volume of distribution of rosuvastatin at steady-state is approximately 134 L.

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