Cardyl - General Information:Cardyl (Lipitor) is a member of the drug class known as statins. It is used for lowering cholesterol. Cardyl inhibits the rate-determining enzyme located in hepatic tissue that produces mevalonate, a small molecule used in the synthesis of cholesterol and other mevalonate derivatives. This lowers the amount of cholesterol produced which in turn lowers the total amount of LDL cholesterol. Cardyl is a competitive inhibitor of HMG-CoA reductase.
Pharmacology:Cardyl, a selective, competitive HMG-CoA reductase inhibitor, is used to lower cholesterol and triglycerides in patients with hypercholesterolemia and mixed dyslipidemia and in the treatment of homozygous familial hypercholesterolemia. Cardyl has a unique structure, long half-life, and hepatic selectivity, explaining its greater LDL-lowering potency compared to other HMG-CoA reductase inhibitors.
Cardyl for patients
Lipitor is a HMG-CoA Reductase Inhibitor, also known as a statin. This class of treatments for high cholesterol is fairly new, and appears to work by blocking a liver enzyme which generates cholesterol. This medication appears to be the most effective in this class of drugs at lowering unhealthy LDL (low-density lipoprotein) cholesterol levels, in some cases up to 51%. It can be virtually as effective as an angioplasty in treating stable coronary artery disease. Currently, this drug is approved for use in patients with high cholesterol (hypercholesterolemia) due to high LDL levels, hereditary elevated fat levels (dysbetalipoproteinemia), familial high cholesterol, and to increase HDL (high-density lipoprotein) levels in patients with high cholesterol and those with both high cholesterol and high triglycerides (mixed dyslipidemia). Other accepted uses include the treatment of stable coronary artery diseas, preventing coronary heart disease, preventing clogged stents (tubes) placed in coronary arteries after surgery, preventing bone loss in type two diabetics, stabilizing lipid levels that have been altered by treatment with protease inhibitors. This treatment should be considered a last resort. The best way to lower cholesterol is through a program of healthy diet and exercise, and these should be maintained during treatment with Lipitor.
The risk of myopathy during treatment with drugs of this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, niacin (nicotinic acid), erythromycin, azole antifungals.
Antacid: When atorvastatin and MaaloxÒ TC suspension were coadministered, plasma concentrations of atorvastatin decreased approximately 35%. However, LDL-C reduction was not altered.
Antipyrine: Because atorvastatin does not affect the pharmacokinetics of antipyrine, interactions with other drugs metabolized via the same cytochrome isozymes are not expected.
Colestipol: Plasma concentrations of atorvastatin decreased approximately 25% when colestipol and atorvastatin were coadministered. However, LDL-C reduction was greater when atorvastatin and colestipol were coadministered than when either drug was given alone.
Cimetidine: Atorvastatin plasma concentrations and LDL-C reduction were not altered by coadministration of cimetidine.
Digoxin: When multiple doses of atorvastatin and digoxin were coadministered, steady-state plasma digoxin concentrations increased by approximately 20%. Patients taking digoxin should be monitored appropriately.
Erythromycin: In healthy individuals, plasma concentrations of atorvastatin increased approximately 40% with coadministration of atorvastatin and erythromycin, a known inhibitor of cytochrome P450 3A4.
Oral Contraceptives: Coadministration of atorvastatin and an oral contraceptive increased AUC values for norethindrone and ethinyl estradiol by approximately 30% and 20%. These increases should be considered when selecting an oral contraceptive for a woman taking atorvastatin.
Warfarin: Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin treatment.
HMG-CoA reductase inhibitors interfere with cholesterol synthesis and theoretically might blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration or impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with drugs that may decrease the levels or activity of endogenous steroid hormones, such as ketoconazole, spironolactone, and cimetidine.
Brain hemorrhage was seen in a female dog treated for 3 months at 120 mg/kg/day. Brain hemorrhage and optic nerve vacuolation were seen in another female dog that was sacrificed in moribund condition after 11 weeks of escalating doses up to 280 mg/kg/day. The 120 mg/kg dose resulted in a systemic exposure approximately 16 times the human plasma area-under-the-curve (AUC, 0-24 hours) based on the maximum human dose of 80 mg/day. A single tonic convulsion was seen in each of 2 male dogs (one treated at 10 mg/kg/day and one at 120 mg/kg/day) in a 2-year study. No CNS lesions have been observed in mice after chronic treatment for up to 2 years at doses up to 400 mg/kg/day or in rats at doses up to 100 mg/kg/day. These doses were 6 to 11 times (mouse) and 8 to 16 times (rat) the human AUC (0-24) based on the maximum recommended human dose of 80 mg/day.
CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other members of this class. A chemically similar drug in this class produced optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in clinically normal dogs in a dose-dependent fashion at a dose that produced plasma drug levels about 30 times higher than the mean drug level in humans taking the highest recommended dose.
Active liver disease or unexplained persistent elevations of serum transaminases.
Hypersensitivity to any component of this medication.
Pregnancy and Lactation
Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause fetal harm when administered to pregnant women. Therefore, HMG-CoA reductase inhibitors are contraindicated during pregnancy and in nursing mothers. ATORVASTATIN SHOULD BE ADMINISTERED TO WOMEN OF CHILDBEARING AGE ONLY WHEN SUCH PATIENTS ARE HIGHLY UNLIKELY TO CONCEIVE AND HAVE BEEN INFORMED OF THE POTENTIAL HAZARDS. If the patient becomes pregnant while taking this drug, therapy should be discontinued and the patient apprised of the potential hazard to the fetus.
Additional information about CardylCardyl Indication: For management as an adjunct to diet to reduce elevated total-C, LDL-C, apo B, and TG levels in patients with primary hypercholesterolemia and mixed dyslipidemia.
Mechanism Of Action: Cardyl selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. As HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, this results in a decrease in mevalonate, a precursor of cholesterol, and a subsequent decrease in hepatic cholesterol levels and increase in uptake of LDL cholesterol.
Drug Interactions: Amprenavir Amprenavir can possibly increase the statin
Atazanavir Atazanavir increases the effect and toxicity of the statin
Bosentan Bosentan could decrease atorvastatin
Carbamazepine Carbamazepine decreases the effect of the statin
Clarithromycin The macrolide possibly increases the statin toxicity
Cyclosporine Possible myopathy and rhabdomyolysis
Delavirdine The NNRT inhibitor increases the effect and toxicity of the statin
Diltiazem Diltiazem increases the effect and toxicity of atorvastatin
Efavirenz The NNRT inhibitor increases the effect and toxicity of the statin
Erythromycin The macrolide possibly increases the statin toxicity
Fenofibrate Increased risk of myopathy/rhabdomyolysis
Fluconazole Increased risk of myopathy/rhabdomyolysis
Fosamprenavir Amprenavir can possibly increase the statin toxicity
Gemfibrozil Increased risk of myopathy/rhabdomyolysis
Imatinib Imatinib increases the effect and toxicity of atorvastatin
Indinavir Indinavir increases the effect and toxicity of atorvastatin
Itraconazole Increased risk of myopathy/rhabdomyolysis
Josamycin The macrolide possibly increases the statin toxicity
Ketoconazole Increased risk of myopathy/rhabdomyolysis
Nefazodone Nefazodone increases the effect and toxicity of the statin drug
Nelfinavir Nelfinavir increases the effect and toxicity of the statin
Nevirapine The NNRT inhibitor increases the effect and toxicity of the statin
Quinupristin This combination presents an increased risk of toxicity
Rifabutin The rifamycin decreases the effect of the statin drug
Rifampin The rifamycin decreases the effect of the statin drug
Ritonavir Ritonavir increases the effect and toxicity of the statin
Saquinavir Saquinavir increases the effect and toxicity of atorvastatin
Tacrolimus Tacrolimus increases the effect and toxicity of the statin
Telithromycin Telithromycin may possibly increase statin toxicity
Verapamil Verapamil increases the effect and toxicity of the statin
Bezafibrate Increased risk of myopathy/rhabdomyolysis
Colchicine Increased risk of rhadbomyolysis with this combination
Food Interactions: Avoid drastic changes in dietary habit.
Avoid taking grapefruit or grapefruit juice throughout treatment.
Grapefruit can significantly increase serum levels of this product.
Take with low fat meal.
Food may decrease maximum plasma levels and area under the curve, but this is inconsequential according to the manufacturer.
Generic Name: Atorvastatin
Synonyms: Atorvastatin calcium
Drug Category: Anticholesteremic Agents; Hydroxymethylglutaryl-CoA Reductase Inhibitors
Drug Type: Small Molecule; Approved
Other Brand Names containing Atorvastatin: Cardyl; Lipitor; Sotis; Torvast; Tozalip; Xavator; Sortis; Torvacard; Totalip; Tulip; Xarator; Atorpic; Liprimar;
Absorption: Atorvastatin is rapidly absorbed after oral administration. The absolute bioavailability of atorvastatin (parent drug) is approximately 14% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%.
Toxicity (Overdose): Symptoms of overdose include rhabdomyolysis, eye hemorrhages, and liver problems.
Protein Binding: 98%
Biotransformation: Atorvastatin is extensively metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites.
Half Life: 14 hours
Dosage Forms of Cardyl: Tablet Oral
Chemical IUPAC Name: (3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid
Chemical Formula: C33H35FN2O5
Atorvastatin on Wikipedia: http://en.wikipedia.org/wiki/Atorvastatin
Organisms Affected: Humans and other mammals
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