Atorvastatin + Ezetimibe

Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted
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Therapy with lipid-altering agents should be only one component of multiple risk factor intervention in individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Drug therapy is indicated as an adjunct to diet when the response to a diet restricted in saturated fat and cholesterol and other nonpharmacologic measures alone has been inadequate.
Primary Hyperlipidemia
: Anzitor EZ tablet is indicated for the reduction of elevated total cholesterol (total-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and non-high-density lipoprotein cholesterol (non-HDL-C), and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary (heterozygous familial and non-familial) hyperlipidemia or mixed hyperlipidemia.
Homozygous Familial Hypercholesterolemia (HoFH)
: Anzitor EZ tablet is indicated for the reduction of elevated total-C and LDL-C in patients with homozygous familial hypercholesterolemia, as an adjunct to other lipid lowering treatments (e.g., LDL apheresis) or if such treatments are unavailable.

Dosage & Administration

The dosage range is 10/10 mg to 80/20 mg daily. The recommended starting dose is 10/10 mg or 20/10 mg daily. This can be administered as a single dose at any time of the day, with or without food. The recommended starting dose for patients who require a larger reduction in LDL-C (greater than 55%) is 40/10 mg daily. After initiation and/or upon titration of this medicine, lipid levels should be analyzed within 2 or more weeks and dosage adjusted accordingly.
Patients with Homozygous Familial Hypercholesterolemia
: The dosage in patients with homozygous familial hypercholesterolemia is 40/10 mg or 80/10 mg daily. This should be used as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) in these patients or if such treatments are unavailable.
Patients with Hepatic Impairment
: This is contraindicated in patients with active liver disease or unexplained persistent elevations in hepatic transaminase levels.
Patients with Renal Impairment
: A history of renal impairment may be a risk factor for statin-associated myopathy. These patients need closer monitoring for skeletal muscle effects. In patients with renal impairment, no dosage adjustment is necessary.

Common side effects are rhabdomyolysis, myopathy, liver enzyme abnormalities, myalgia, abdominal pain, increased hepatic enzymes.

Atorvastatin:
In animal models, 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 cell surface to enhance uptake and catabolism of LDL; atorvastatin also reduces LDL production and the number of LDL particles.
Ezetimibe
: Ezetimibe reduces blood cholesterol by inhibiting the absorption of cholesterol by the small intestine. The molecular target of ezetimibe has been shown to be the sterol transporter, Niemann-Pick C1-Like 1 (NPC1L1), which is involved in the intestinal uptake of cholesterol and phytosterols. In a 2-week clinical study in 18 hypercholesterolemic patients, ezetimibe inhibited intestinal cholesterol absorption by 54%, compared with placebo. Ezetimibe had no clinically meaningful effect on the plasma concentrations of the fat-soluble vitamins A, D, and E and did not impair adrenocortical steroid hormone production. Ezetimibe does not inhibit cholesterol synthesis in the liver or increase bile acid excretion. Ezetimibe localizes at the brush border of the small intestine and inhibits the absorption of cholesterol, leading to a decrease in the delivery of intestinal cholesterol to the liver. This causes a reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood; this distinct mechanism is complementary to that of statins.