Atorvastatin pills 10mg 30pcs

Composition

Active ingredients:

Atorvastatin 10 mg.

Auxiliary substances:

Microcrystalline cellulose – 52.52 mg;

Pre-gelatinized corn starch-52.51 mg;

Colloidal silicon dioxide – 0.38 mg;

Magnesium carbonate – 33 mg;

Magnesium stearate – 0.75 mg

Pharmacological action

Clinical and pharmacological group: Hypolipidemic drug. Pharmacotherapy group: Hypolipidemic agent – HMG-CoA reductase inhibitor Pharmacological action

Hypolipidemic agent from the statin group. According to the principle of competitive antagonism, the statin molecule binds to the part of the coenzyme A receptor where HMG-CoA reductase is attached. Another part of the statin molecule inhibits the conversion of hydroxymethylglutarate to mevalonate, an intermediate in the synthesis of the cholesterol molecule. Inhibition of HMG-CoA reductase activity leads to a series of sequential reactions, which result in a decrease in the intracellular cholesterol content and a compensatory increase in the activity of LDL receptors and, accordingly, an acceleration of LDL cholesterol (Xc) catabolism.

The hypolipidemic effect of statins is associated with a decrease in the level of total cholesterol due to LDL-C. The decrease in LDL levels is dose-dependent and is not linear, but exponential. The inhibitory effect of atorvastatin on HMG-CoA reductase is approximately 70% determined by the activity of its circulating metabolites.

Statins do not affect the activity of lipoprotein and hepatic lipases, do not significantly affect the synthesis and catabolism of free fatty acids, so their effect on TG levels is secondary and mediated through their main effects on lowering LDL-C levels. A moderate decrease in TG levels during statin treatment appears to be associated with the expression of remnant (apo E) receptors on the surface of hepatocytes involved in the catabolism of STDs, which comprise approximately 30% of TG. Compared to other statins (with the exception of rosuvastatin), atorvastatin causes a more pronounced decrease in TG levels.

In addition to the hypolipidemic effect, statins have a positive effect on endothelial dysfunction (a preclinical sign of early atherosclerosis), on the vascular wall, the state of atheroma, improve the rheological properties of blood, have antioxidant, antiproliferative properties.

Atorvastatin reduces cholesterol levels in patients with homozygous familial hypercholesterolemia, which usually does not respond to treatment with lipid-lowering agents.

Pharmacokinetics

Atorvastatin is rapidly absorbed from the gastrointestinal tract. Absolute bioavailability is low – about 12%, due to presystemic clearance in the gastrointestinal mucosa and/or due to the “first pass” through the liver, mainly at the site of action.

Atorvastatin is metabolized with the participation of the CYP3A4 isoenzyme to form a number of substances that are inhibitors of HMG-CoA reductase.

T1 / 2 from plasma is about 14 hours, although the T1 / 2 of an inhibitor of HMG-CoA reductase activity is approximately 20-30 hours, due to the participation of active metabolites.

Binding to plasma proteins is 98%.

Atorvastatin is excreted in the form of metabolites mainly in the bile.

Indications

• Primary hypercholesterolemia when diet therapy is ineffective;

• Combined hypercholesterolemia and hypertriglyceridemia;

• Heterozygous and homozygous familial hypercholesterolemia with ineffective diet therapy.

Contraindications

• of liver disease in the active stage;

• Increased activity of serum transaminases by more than 3 times of unknown origin;

• Pregnancy, lactation (breastfeeding);

• Women of reproductive age who do not use reliable contraceptives;

• Hypersensitivity to atorvastatin.

Side effects

Nervous system disorders:  > 1% – insomnia, dizziness. >

From the side of the senses:  < 1% of amblyopia, tinnitus, dryness of the conjunctiva, disturbance of accommodation, bleeding in the retina of the eye, deafness, glaucoma, parosmia, loss of taste, taste perversion.

From the cardiovascular system:  > 1% – chest pain. >

From the hematopoietic system:  < 1% – anemia, lymphadenopathy, thrombocytopenia.

Respiratory system disorders:  > 1% – bronchitis, rhinitis. >

From the digestive system:  > 1% – nausea. >

Musculoskeletal disorders:  > 1% – arthritis. >

From the genitourinary system:  > 1% – urogenital infections, peripheral edema; >

Dermatological reactions:  > 1% – alopecia, xeroderma, photosensitization, increased sweating, eczema, seborrhea, ecchymosis, petechiae.

From the endocrine system:  < 1% – gynecomastia, mastodynia.

From the side of metabolism:  < 1% – increase in body mass, aggravation of gout.

Allergic reactions:  < 1% – itching, skin rash, contact dermatitis, and rarely urticaria, angioedema, facial edema, anaphylaxis, erythema multiforme exudative (including Stevens-Johnson syndrome), toxic epidermal necrolysis (Lyell’s syndrome).

Laboratory parameters:  < 1% – hyperglycemia, hypoglycemia, increased serum CPK, albuminuria.

Interaction

When atorvastatin is co-administered with digoxin, the concentration of digoxin in the blood plasma slightly increases.

Diltiazem, verapamil, izradipine inhibit the CYP3A4 isoenzyme, which is involved in the metabolism of atorvastatin, so when used simultaneously with these calcium channel blockers, it is possible to increase the concentration of atorvastatin in blood plasma and increase the risk of developing myopathy.

Concomitant use of itraconazole significantly increases the concentration of atorvastatin in blood plasma, apparently due to inhibition of itraconazole metabolism in the liver, which occurs with the participation of the CYP3A4 isoenzyme; increased risk of myopathy.

With simultaneous use of colestipol, it is possible to reduce the concentration of atorvastatin in blood plasma, while the lipid-lowering effect is enhanced.

When used concomitantly, antacids containing magnesium hydroxide and aluminum hydroxide reduce the concentration of atorvastatin by about 35%.

Concomitant use of cyclosporine, fibrates (including gemfibrozil), antifungal drugs derived from azole, nicotinic acid increases the risk of developing myopathy.

Concomitant use of erythromycin and clarithromycin increases the plasma concentration of atorvastatin moderately, and increases the risk of developing myopathy.

Concomitant use of ethinyl estradiol, norethisterone (norethindrone) slightly increases the concentration of ethinyl estradiol, norethisterone and (norethindrone) in blood plasma.

Concomitant use of protease inhibitors increases the concentration of atorvastatin in blood plasma, since protease inhibitors are inhibitors of the CYP3A4 isoenzyme.

How to take, course of use and dosage

Treatment is carried out against the background of a standard diet for patients with hypercholesterolemia. The dose is set individually, depending on the initial cholesterol level. They are taken orally. The initial dose is usually 10 mg 1 time/day. The effect manifests itself within 2 weeks, and the maximum effect-within 4 weeks. If necessary, the dose can be gradually increased at intervals of 4 weeks or more. The maximum daily dose is 80 mg.

Form of production

Tablets covered with a film-coated white or almost white color, round, biconvex; on the cross section-the core is white or almost white.

Active ingredient

Atorvastatin

Conditions of release from pharmacies

By prescription

Dosage form

Tablets

Description

For adults as directed by your doctor

Indications

Atherosclerosis, Prevention of heart attacks and strokes