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Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly pfizer zlt 100 the level of total-C and LDL-C and inversely with the level of HDL-C.

Atorvastatin reduces total-C, LDL-C, and apo B in both normal volunteers and in patients with homozygous and heterozygous familial hypercholesterolaemia (FH), non-familial forms of hypercholesterolaemia, Idarucizumab for Injection (Praxbind)- FDA mixed dyslipidaemia.

Atorvastatin also reduces very low density lipoprotein cholesterol (VLDL-C) and TG and produces variable increases in HDL-C and apolipoprotein A-1. Atorvastatin reduces total-C, LDL-C, VLDL-C, apo B and TG, and increases HDL-C in patients with isolated hypertriglyceridaemia.

Atorvastatin reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinaemia. In animal models, atorvastatin limits the development of lipid-enriched atherosclerotic lesions and promotes the regression of pre-established atheroma.

Atorvastatin and its metabolites are responsible for pharmacological activity in humans. The liver is its primary site of action and the principal site of cholesterol synthesis and Pfizer zlt 100 clearance. Drug dose rather than systemic drug concentration correlates better with LDL-C reduction.

Individualisation of drug dose should be retin a tretinoin on therapeutic response (see Section 4.

In a multicentre, placebo-controlled, double-blind dose-response study in patients with hypercholesterolaemia, atorvastatin was given as a single daily dose over 6 weeks. A therapeutic response was seen within 2 weeks, and maximum response achieved within 4 weeks. In three further trials, 1,148 patients with either heterozygous familial hypercholesterolaemia, nonfamilial forms of hypercholesterolaemia, or mixed dyslipidaemia were treated with atorvastatin for one year.

The results were consistent with those of the dose response study pfizer zlt 100 were maintained for the duration of pfizer zlt 100. In patients with primary hypercholesterolaemia and mixed dyslipidaemia (Fredrickson Types IIa and IIb), data pooled from 24 controlled trials demonstrated that the adjusted mean escitolapramini increases from baseline in HDL-C for atorvastatin (10-80 mg) were 5.

Clinical studies demonstrate that the starting dose of 10 mg atorvastatin is more effective than simvastatin 10 mg and pravastatin 20 mg in reducing LDL-C, total-C, triglycerides and apo B. In several multicentre, double-blind studies in patients with hypercholesterolaemia, atorvastatin was compared to other HMG-CoA reductase inhibitors.

After randomisation, patients were treated with atorvastatin 10 mg per day or the recommended starting dose of pfizer zlt 100 comparative agent. Increasing the dosage of atorvastatin resulted in more patients reaching target LDL-C goals. Prevention of cardiovascular pfizer zlt 100. Patients with a history of previous myocardial infarction or angina were excluded.

In this randomised, double blind, placebo-controlled study, patients were treated with antihypertensive therapy (goal BP The primary endpoint examined in ASCOT was the rate of fatal pfizer zlt 100 heart disease or non-fatal myocardial infarction over 3. These coronary events occurred in 1. Although this difference was statistically significant for the whole trial population, this difference was not statistically significant in specified subgroups such as diabetes, patients with left ventricular hypertrophy (LVH), previous vascular disease, or metabolic syndrome.

There was no statistically significant reduction in the rate of total mortality, Pfizer zlt 100 mortality or heart failure in the atorvastatin-treated group compared to placebo.

Non insulin dependent diabetes mellitus (NIDDM). A 26-week randomised, double-blind, comparator study in NIDDM subjects showed that atorvastatin is effective in dyslipidaemic patients with NIDDM.

Atorvastatin has also been shown to reduce LDL-C in patients with homozygous familial hypercholesterolaemia (FH), a population that has not usually responded to other lipid-lowering medication.

In an uncontrolled compassionate-use study, 29 patients aged 6 to 37 years with homozygous FH received maximum daily doses of 20 pfizer zlt 100 to 80 mg of atorvastatin.

Experience in paediatric patients has been limited to patients with homozygous FH. A constant proportion of atorvastatin is absorbed intact. However, LDL-C reduction is the same regardless of the time of day of drug administration (see Section 4. The mean volume of distribution of atorvastatin is about 400 litres. Based pfizer zlt 100 observations in rats, atorvastatin is likely to be secreted in human milk (see Section 4. In humans, atorvastatin is extensively metabolised to ortho- and para-hydroxylated derivatives.

In vitro inhibition of HMG-CoA reductase by ortho- and para-hydroxylated metabolites is equivalent to that of atorvastatin. In vitro studies suggest munchausen by proxy importance of atorvastatin metabolism by CYP 3A4, consistent with increased plasma concentrations of atorvastatin in humans following co-administration with erythromycin, a known inhibitor of this isozyme (see Section 4.

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Comments:

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