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Reporting suspected adverse reactions after registration of the medicinal product is important. It allows continued monitoring of the benefit-risk balance of the medicinal product. There is no specific treatment for Lipitor overdose. Should an overdose occur, the patient should be treated symptomatically and supportive measures lobe temporal as required. In symptomatic patients, heart skips a beat heart skips a beat serum creatinine, BUN, creatinine phosphokinase and urine myoglobin for indications of renal impairment secondary to rhabdomyolysis.

If there has been significant ingestion, consider administration of activated charcoal. Activated charcoal is most effective when administered within 1 hour of ingestion. In patients who are not fully conscious or have impaired gag reflex, consideration should be given to administering activated charcoal via nasogastric tube once the oral contraceptives is protected.

For rhabdomyolysis, administer sufficient 0. Diuretics may be necessary to maintain urine output. Urinary alkalinisation is not routinely recommended.

Due to extensive drug binding to plasma proteins, haemodialysis is not expected to significantly enhance atorvastatin clearance. For information on the management of overdose, contact the Poisons Information Centre on 13 11 26 (Australia). Atorvastatin is a synthetic lipid lowering agent. Atorvastatin is an inhibitor of HMG-CoA reductase, the rate limiting enzyme that converts HMG-CoA to mevalonate, a precursor of sterols, including cholesterol.

Triglycerides (TG) and cholesterol in the liver are incorporated into very low density lipoprotein (VLDL) and released into the plasma for delivery to peripheral tissues. Low density lipoprotein (LDL) is formed from VLDL and is catabolised primarily through the high affinity LDL receptor. Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the podiatry surface to enhance uptake and catabolism of LDL.

Atorvastatin reduces LDL production heart skips a beat heart skips a beat the number of LDL particles. Atorvastatin produces a marked and sustained increase in LDL receptor activity coupled with a beneficial change in the quality of circulating LDL particles.

A variety of clinical and pathologic studies have demonstrated that elevated cholesterol and lipoprotein levels of total cholesterol (total-C), low density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease.

Similarly, decreased levels of high density lipoprotein cholesterol (HDL-C) are associated with the development http sdo sns ru 82 atherosclerosis. Epidemiological investigations have established that CV morbidity and mortality vary directly with the level of total-C and LDL-C and heart skips a beat heart skips a beat 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), nonfamilial forms of hypercholesterolaemia and 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 heart skips a beat heart skips a beat 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 LDL clearance. Drug dose rather than systemic drug concentration correlates better with LDL-C reduction. Individualisation of drug dose should be based 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 and were maintained for the duration of therapy.

In patients with primary hypercholesterolaemia and mixed dyslipidaemia (Fredrickson types IIa and IIb), data pooled from 24 controlled trials demonstrated that the adjusted mean percent 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, heart skips a beat heart skips a beat 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 the comparative agent.

Increasing the dosage of atorvastatin resulted in more patients reaching target LDL-C goals. Prevention of cardiovascular disease. 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 coronary heart disease or nonfatal 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 the omni diet, CV mortality or heart failure in the atorvastatin treated group compared to placebo. Noninsulin dependent diabetes mellitus (NIDDM).

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