Atotin-EZ (Atorvastatin 10mg + Ezetimibe 10mg) – 10 Strips
Composition: Atorvastatin 10mg + Ezetimibe 10mg
Ezetimibe and atorvastatin combination is used together with a proper diet to treat high cholesterol and triglyceride (fats) levels in the blood. This medicine may help prevent medical problems (eg, heart attack, stroke) caused by clogged blood vessels. It is also used to treat a condition called homozygous familial hypercholesterolemia (HoFH).
Ezetimibe is a cholesterol absorption inhibitor and atorvastatin is an HMG-CoA reductase inhibitor, or statin. These medicines will reduce the absorption of cholesterol from foods and the production of cholesterol in your body.
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.
Atotin-EZ 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)
Atotin-EZ 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.
Limitations Of Use
No incremental benefit of Atotin-EZ on cardiovascular morbidity and mortality over and above that demonstrated for atorvastatin has been established. Atotin-EZ has not been studied in Fredrickson type I, III, IV, and V dyslipidemias.
Along with its needed effects, a medicine may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.
Check with your doctor immediately if any of the following side effects occur:
- Abdominal or stomach pain
- difficult breathing
- difficulty with moving
- irregular heartbeat
- muscle, joint, or bone pain
- muscle stiffness
- muscle weakness
- nausea or vomiting
- numbness or tingling in the hands, feet, or lips
- weakness or heaviness of the legs
- feeling of warmth
- pain or tenderness around the eyes and cheekbones
- redness of the face, neck, arms, and occasionally, upper chest
- stuffy or runny nose
- sudden sweating
- tightness in the chest
Mechanism of Action
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 [see Clinical Studies].
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.
Clinical studies have demonstrated that elevated levels of total-C, LDL-C and Apo B, the major protein constituent of LDL, promote human atherosclerosis. In addition, decreased levels of HDL-C are associated with the development of atherosclerosis. Epidemiologic studies have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C and inversely with the level of HDL-C. Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including very-lowdensity lipoproteins (VLDL), intermediate-density lipoproteins (IDL), and remnants, can also promote atherosclerosis. The independent effect of raising HDL-C or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.
Atorvastatin as well as some of its metabolites are pharmacologically active in humans. The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance. Drug dosage, rather than systemic drug concentration, correlates better with LDL-C reduction. Individualization of drug dosage should be based on therapeutic response.
- Keep out of the reach of children.
- Do not keep outdated medicine or medicine no longer needed.
- Ask your healthcare professional how you should dispose of any medicine you do not use.
- Store the medicine in a closed container at room temperature, away from heat, moisture, and direct light. Keep from freezing.
- Keep your medicine in the blister pack until you are ready to use it. After opening the blister pack, store it in a dry place and protect from moisture and light. Once a tablet is removed, slide the blister card back into its folded card.