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    Mevacor Lovastatin is a cholesterol lowering agent isolated from a strain of Aspergillus terreus. After oral ingestion, lovastatin, which is an inactive lactone, is hydrolyzed to the corresponding hydroxyacid form. This is a principal metabolite and an inhibitor of 3hydroxy-3methylglutaryl-coenzyme A HMGCoA reductase. This enzyme catalyzes the conversion of HMGCoA to mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol. Lovastatin is 1S-1R,3,7,82S,4S, 8a-1,2,3,7, 8,8ahexahydro-3,7dimethyl-8-2tetrahydro-4-hydroxy-6-oxo-2H-pyran-2ylethyl-1-naphthalenyl 2-methylbutanoate. The empirical formula of lovastatin is C24H36O5and its molecular weight is 404.55. Its structural formula is: Lovastatin is a white, nonhygroscopic crystalline powder that is insoluble in water and sparingly soluble in ethanol, methanol, and acetonitrile. Tablets Mevacor are supplied as 20 mg and 40 mg tablets for oral administration. In addition to

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    The involvement of low-density lipoprotein cholesterol LDLC in atherogenesis has been well-documented in clinical and pathological studies, as well as in many animal experiments. Epidemiological and clinical studies have established that high LDLC and low high-density lipoprotein cholesterol HDLC are both associated with coronary heart disease. However, the risk of developing coronary heart disease is continuous and graded over the range of cholesterol levels and many coronary events do occur in patients with total cholesterol totalC and LDLC in the lower end of this range. Mevacor has been shown to reduce elevated LDLC concentrations. LDL is formed from very low-density lipoprotein VLDL and is catabolized predominantly by the high affinity LDL receptor. The mechanism of the LDL-lowering effect of Mevacor may involve both reduction of VLDLC concentration, and induction of the LDL receptor, leading to reduced production andor increased catabolism of LDLC. Apolipoprot

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    Therapy with Mevacor should be a component of multiple risk factor intervention in those individuals with dyslipidemia at risk for atherosclerotic vascular disease. Mevacor should be used in addition to a diet restricted in saturated fat and cholesterol as part of a treatment strategy to lower totalC and LDLC to target levels when the response to diet and other nonpharmacological measures alone has been inadequate to reduce risk.

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    Lovastatin, like other inhibitors of HMGCoA reductase, occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase CK above ten times the upper limit of normal ULN. Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and rare fatalities have occurred. The risk of myopathy is increased by high levels of HMGCoA reductase inhibitory activity in plasma. The risk of myopathyrhabdomyolysis

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    Persistent increases to more than 3 times the upper limit of normal in serum transaminases occurred in 1.9 of adult patients who received lovastatin for at least one year in early clinical trials see ADVERSE REACTIONS. When the drug was interrupted or discontinued in these patients, the transaminase levels usually fell slowly to pretreatment levels. The increases usually appeared 3 to 12 months after the start of therapy with lovastatin, and were not associated with jaundice or other cli

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    Lovastatin may elevate creatine phosphokinase and transaminase levels see WARNINGS and ADVERSE REACTIONS. This should be considered in the differential diagnosis of chest pain in a patient on therapy with lovastatin.

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