Lipodemin 20 mg tablets №30
|Amount in a package||30|
|The main medicament||Lipodemin|
Lipodemin (LIPODEMIN) instructions for use
active ingredient: atorvastatin; 1 tablet contains atorvastatin calcium 10,36 mg or 20,72 mg, which corresponds to 10 mg or 20 mg of atorvastatin;
auxiliary substances: mannitol, microcrystalline cellulose, crospovidone, sodium carbonate anhydrous, povidone, methionine, magnesium stearate
Sheath: film coating mixture Opadry White 03F28446 (hypromellose, titanium dioxide (E 171), macrogol), talc.
Drugs that lower the level of cholesterol and triglycerides in the blood serum. Inhibitors of HMG-CoA reductase.ATX Code C10A A05.
As a supplement to the diet for the treatment of patients with elevated total cholesterol, LDL cholesterol, apolipoprotein B, triglycerides, in order to increase high density cholesterol lipoproteins in patients with primary hypercholesterolemia (heterozygous familial and non-hereditary hypercholesterolemia), combined hyperlipidemia (Fredrickson type IIa and IIb), elevated serum triglyceride levels (Fredrickson type IV) and patients with disbetalipoproteinemia (Fredrickson type iii) in cases where the diet is not about espechivaet proper effect.
To reduce the level of total cholesterol and LDL cholesterol in patients with homozygous familial hypercholesterolemia, when the diet and other non-drug products do not provide the proper effect.
Patients without clinical cardiovascular disease, with or without dyslipidemia, but with several risk factors for cardiovascular disease, such as smoking, hypertension, diabetes mellitus, low HDL cholesterol, or having a family history of cardiovascular disease at a young age, in order to reduce the risk:
- lethal manifestations of coronary heart disease and non-lethal myocardial infarction
- occurrence of a stroke;
- risk of angina pectoris and the need for performing myocardial revascularization procedures.
Patients with clinical symptoms of coronary disease atorvastatin is indicated to reduce the risk:
- non-lethal myocardial infarction;
- lethal and non-lethal stroke;
- revascularization procedures;
- hospitalization for congestive heart failure;
- angina pectoris.
Children (10-17 years)
Atorvastatin is prescribed as an adjuvant to the diet to reduce the level of total cholesterol, LDL-C and apolipoprotein B in boys and girls in the postmenarchical period, aged 10 to 17, with heterozygous familial hypercholesterolemia, even if the diet is adequate
- the level of LDL-C remains ≥ 190 mg / dl (1.90 g / l);
- the level of LDL-C remains ≥ 160 mg / dl (1.6 g / l);
- in a family history there is information about cardiovascular disease at a young age;
- In patients with children, there are two or more other risk factors for cardiovascular disease (smoking, hypertension, diabetes, low HDL-C, or having a family history of cardiovascular disease at a young age).
Atorvastatin is contraindicated in patients with hypersensitivity to active components of the liver or unstated persistent transaminase activity, which is three times the norm.
Dosing and Administration
Before starting therapy with atorvastatin, you should determine the level of hypercholesterolemia against the background of the appropriate diet, prescribe physical exercises and measures to reduce body weight in obese patients, and treat other diseases. During treatment with lipodemine, patients should follow a standard anti-cholesterol diet. The drug is prescribed in a dose of 10-80 mg once a day, at any time of the day, regardless of food intake. Starting and maintenance doses can be individualized according to the baseline level of LDL-C, the objectives of therapy and its effectiveness. In 2-4 weeks after the start of treatment and / or dose adjustment, Lipodemin should determine the lipidogram and adjust the dose accordingly.
Primary hypercholesterolemia and combined (mixed) hyperlipidemia. In most cases, it is enough to prescribe 10 mg once a day. The result of treatment becomes noticeable after 2 weeks, the maximum effect is observed after 4 weeks.Positive changes are sustained by prolonged use.
Homozygous familial hypercholesterolemia. In most cases, in patients with homozygous familial hypercholesterolemia, the result is achieved due to the use of 80 mg of atorvastatin 1 time per day, which reduces the level of LDL cholesterol by more than 15% (18-45%).
Heterozygous familial hypercholesterolemia in pediatric practice (patients aged 10 to 17 years). It is recommended to prescribe Lipodemin in an initial dose of 10 mg once a day daily. The maximum recommended dose is 20 mg once daily on a daily basis (doses exceeding 20 mg have not been studied in this age group). The dose can be individualized in accordance with the objectives of therapy, dose adjustment can be done at intervals of 4 weeks or more.
Patients with renal insufficiency. Kidney disease does not affect the concentration of atorvastatin or a decrease in LDL cholesterol in the plasma. Therefore, there is no need for dose adjustment.
Elderly patients. Differences in safety, efficacy, or achievement of the goal of treating hypercholesterolemia in elderly patients and patients of other age groups do not.
Most often (≥ 1%), the side effect of atorvastatin was
- Mental disorders: insomnia;
- Nervous system: headache, dizziness;
- The digestive tract: nausea, diarrhea, abdominal pain, indigestion, constipation, flatulence;
- Musculoskeletal system and connective tissue: myalgia;
- Common manifestations: asthenia.
In addition to those noted in clinical trials, such side effects of atorvastatin
- Metabolism and digestion: hypoglycemia, hyperglycemia, anorexia;
- Nervous system: peripheral neuropathy, paresthesia;
- Alimentary tract: pancreatitis, vomiting;
- Hepatobiliary system: hepatitis, cholestatic jaundice;
- Skin and subcutaneous tissue: alopecia, itching, rash, urticaria;
- Musculoskeletal system and connective tissue: myopathy, myositis, muscle cramps;
- Reproductive system: impotence.
Not all of the above manifestations had a close causal relationship with the use of atorvastatin.
Pediatric patients (10-17 years). In patients receiving atorvastatin, there were side effects, similar manifestations in patients in the placebo group. The most common adverse event that was observed in both groups, not counting the causal relationship, was infection.
During post-marketing research, these side effects
- blood and lymphatic system: thrombocytopenia;
- immune system: allergic reactions (including anaphylaxis);
- injuries, poisoning: tendon ruptures;
- Metabolism: weight gain;
- nervous system: hypoesthesia, amnesia, dizziness, dysgeusia;
- hearing organs ringing in the ears;
- skin and subcutaneous tissue: Stevens-Johnson syndrome, toxic epidermal necrolysis, erythema multiforme, bullous rash, urticaria;
- musculoskeletal system and connective tissue: rhabdomyolysis, arthralgia, back pain;
- common manifestations: pain in the chest, peripheral edema, malaise, fatigue.
There is no specific treatment for overdose of atorvastatin. In case of an overdose, symptomatic and supportive therapy is performed. Since atorvastatin binds to plasma proteins, hemodialysis does not significantly reduce the concentration of the drug in the plasma.
Use during pregnancy and lactation
Atorvastatin is contraindicated during pregnancy. Women of reproductive age should comply with the appropriate contraceptives. Atorvastatin can be prescribed to women of childbearing age only when they categorically reject this contraindication and are well aware of the possible risk to the fetus.
Lipodemin is contraindicated in the period of breastfeeding. It is not known whether atorvastatin is excreted in breast milk. Since there is a potential risk for infants receiving breast milk, when breast treatment with Lipodemin should stop breastfeeding.
The drug is used in children aged 10 years. Experience with children under the age of 10 years is not available.
Influence on the liver. As with the use of other hypolipoproteinemic drugs of the same class, a moderate increase in the activity of serum transaminases (three times higher than the upper level of the norm (BPH)) is possible in the treatment with atorvastatin. The liver function was monitored at the pre- and post-marketing stages of the study of the use of atorvastatin in doses of 10, 20, 40 and 80 mg. A persistent increase in transaminase activity (three times greater than BPH in 2 or more cases) was observed in 0.7% of patients who received atorvastatin during these studies. The limits of these deviations were 0.2, 0.2, 0.6 and 2.3% with 10, 20, 40 and 80 mg respectively. An increase in the activity of transaminases was not accompanied by jaundice or other clinical manifestations. If the dose of atorvastatin was reduced, interrupted or discontinued, the level of transaminases normalized. Most patients continued treatment with lower doses of atorvastatin without negative consequences.
The liver function should be determined before the start of treatment and periodically monitored during the course of treatment. Patients who have manifestations of liver dysfunction should determine its indicators. Patients in whom an increase in transaminase activity is observed should be monitored prior to the normalization of the indices. In the case of more than threefold increase in ALT or ACAT activity, the dose of Lipodemin should be reduced or discontinued beyond normal. Lipodemin can cause an increase in the activity of transaminases.
Lipodemin should be administered with caution to patients who abuse alcohol and / or liver disease in a history.Diseases of the liver in the active phase or increased activity of transaminases for unknown reasons is a contraindication for the appointment of Lipodemin.
Influence on skeletal muscles. During treatment with atorvastatin, patients may experience myopathy. Myopathy should be understood as muscle pain or muscle weakness, combined with an increase in the level of CK (CK) 10 times the BPH. The probability of this condition should be assumed in patients with diffuse myalgia, tenderness or weakness of the muscles and / or a significant increase in the level of CK. Patients should be warned about the possible occurrence of muscle pain and muscle weakness, sometimes with weakness or fever. In the event of an increase in the level of CKK or a confirmed or probable diagnosis of myopathy, treatment with Lipodemin should be discontinued. The risk of myopathy during treatment with drugs of this group increases with simultaneous use of cyclosporine, fibrin acid derivatives, erythromycin, niacin or azole antifungal agents. Most of these drugs suppress the metabolism of cytochrome 450 ZA4 and / or the distribution of the drug in the body. Atorvastatin is metabolized, first of all, with the help of the liver enzyme CYP ZA4. Doctors who prescribe atorvastatin in combination with fibrin acid derivatives, erythromycin, immunosuppressants or azole antifungal agents or lipoprotein modifying doses of niacin should weigh possible positive results and adverse effects and monitor patients to identify such manifestations as muscle pain and muscle weakness , especially in the first months of treatment and after increasing the dose of one of these drugs. In this regard, this reduction in the starting and maintenance dose of atorvastatin should be considered when it is used simultaneously with the above drugs.
For this, a periodic determination of CK is recommended, but it should be remembered that this test is not sufficient for the timely diagnosis of severe myopathy. Atorvastatin may cause an increase in CK.
In the treatment with atorvastatin, as with the use of similar drugs in this group, occasional cases of rhabdomyolysis in combination with secondary renal failure caused by myoglobinuria were observed. Therapy with atorvastatin should be interrupted or discontinued if the patient's condition is severe and it is suspected that these changes are caused by myopathy, or if there are risk factors for secondary renal failure in rhabdomyolysis (such as severe acute infection, arterial hypotension, severe surgery, trauma, severe endocrine , metabolic or electrolyte disorders and uncontrolled convulsions).
Therapy with atorvastatin 80 mg in patients without cardiovascular disease, 6 months or less before the start of treatment, had a stroke or TIA (transient ischemic attack), increases the incidence of hemorrhagic strokes. In patients who had a hemorrhagic stroke at the beginning of therapy, the risk of repeated hemorrhagic stroke increased.Atorvastatin at a dose of 80 mg reduces the total number of strokes and reduces the incidence of cardiovascular diseases.
The ability to influence the reaction rate when driving vehicles or other mechanisms
Interaction with other drugs and other interactions
The risk of myopathy during treatment with HMG-CoA reductase inhibitors increases with simultaneous use of cyclosporine, fibrolic acid derivatives, a lipid-modifying dose of niacin, erythromycin, and antifungal agents of the azole group.
Inhibitors of cytochrome 450 OA4 Atorvastatin is metabolized by cytochrome 450 CA4. The concomitant use of atorvastatin with cytochrome 450 ZA4 inhibitors can cause an increase in the concentration of atorvastatin. The strength of the interaction and the potentiation of the effect depends on the variability of the action on cytochrome P 450 ZA4.
Inhibitors of the vector. Atorvastatin and its metabolites are the substances of the OATP1B1 transporter. Inhibitors of OATP1B1 (eg, cyclosporine) may increase the bioavailability of atorvastatin. Simultaneous use of atorvastatin 10 mg and cyclosporine 5.2 mg / kg / day leads to an increase in 7.7 times the exposure of atorvastatin.
Erythromycin / clarithromycin. Simultaneous use of atorvastatin and erythromycin (500 mg 4 times a day) or clarithromycin (500 mg twice daily), which inhibit cytochrome 450 APA, was accompanied by an increase in the level of atorvastatin in plasma (see Section "Peculiarities of use." Effect on skeletal muscles).
Inhibitors of proteases. Simultaneous use of atorvastatin and protease inhibitors, which suppress the action of cytochrome 450 APA, is accompanied by an increase in the concentration of atorvastatin in plasma.
Diltiazema hydrochloride. Simultaneous use of atorvastatin 40 mg with diltiazem 240 mg causes an increase in plasma concentrations of the first.
Cimetidine. There were no significant effects of interaction between these drugs and atorvastatin.
Itraconazole. Simultaneous use of atorvastatin (20-40 mg) and itraconazole (200 mg) was accompanied by an increase in AUC (area under the concentration-time curve) of the first.
Grapefruit juice contains substances that are inhibitors of cytochrome 450 ZA4 and can increase the concentration of atorvastatin, especially when consuming grapefruit juice more than 1.2 liters per day.
Stimulators of cytochrome 450. Simultaneous use of atorvastatin and stimulants P 450 ZA4 (rifampicin, efavirenz) can cause different levels of decrease in the concentration of atorvastatin in plasma. Rifampicin, due to the double mechanism of action (inducer of cytochrome 450 ZA4 and inhibitor of the transporter enzyme OATP1B1 in the liver), is recommended to be used simultaneously with atorvastatin, since the delayed use of atorvastanin after rifampicin therapy was accompanied by a significant decrease in the concentration of atorvastatin in the blood plasma.
Antacids. The simultaneous use of atorvastatin and a suspension of oral antacids containing aluminum and magnesium hydroxides reduces the concentration of atorvastatin in the plasma by about 35%, but this did not affect the decrease in LDL-C.
Antipyrine. Since atorvastatin does not alter the pharmacokinetics of the antipyrin, interaction with other drugs that are metabolized by the same cytochrome (such as terfenadine, tolbutamide, triazolam, oral contraceptives) is unlikely.
Holestipol. The concentration of atorvastatin in plasma is reduced by 25% with simultaneous application of colestipol.However hypolipidemic effect is more pronounced while the use of atorvastatin and colestipol than with one of these drugs.
Digoxin.Prolonged use of digoxin and simultaneous use of 10 mg of atorvastatin digoxin level in the plasma was not changed. However, digoxin concentrations increased by approximately 20% while the use of 80 mg of atorvastatin per day. It is necessary to properly monitor the status of patients receiving digoxin.
Azithromycin. Simultaneous use of atorvastatin (10 mg daily) and azithromycin (500 mg daily) did not alter the concentration of atorvastatin in plasma.
Oral contraceptives. The simultaneous use of oral contraceptives containing norethindrone and ethinyl estradiol increase AUC of the two drugs at approximately 30 and 20%. This effect should be considered when choosing a contraceptive for women who used atorvastatin.
Warfarin. No significant effects of the interaction between these drugs and atorvastatin. Amlodipine. During medicaments interaction experiments simultaneous use with atorvastatin 80 mg 10 mg amlodipine in healthy volunteers was accompanied by an increase in exposure of atorvastatin, although it did not have a clinically meaningful effect.
Other concomitant therapy. During the study, atorvastatin was used in conjunction with antihypertensive drugs and estrogenzaminnimy drugs without significant interaction effects. Interactions with other drugs have not been studied.
Atorvastatin is a selective, competitive inhibitor reductase 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) - an enzyme that regulates the rate of conversion of HMG-CoA to mevalonate - precursor sterols (including cholesterol Ch.). In patients with homozygous and heterozygous familial hypercholesterolemia (WG), non-hereditary form of hypercholesterolemia and mixed dyslipidemia, atorvastatin reduces the concentration of total cholesterol, LDL-cholesterol (LDL-C) and apolipoprotein B (a B on). Atorvastatin also reduces the concentration of LDL-VLDL (X-VLDL) and triglycerides (TG) and increases the number of multiple high density lipoprotein-cholesterol (HDL-C).
Atorvastatin reduces cholesterol and lipoproteins in the plasma due to inhibition of HMG-CoA reductase and cholesterol synthesis in the liver and increase the number of hepatic LDL receptors on the cell surface, which causes increased LDL catabolism and capture.
Atorvastatin reduces the synthesis of LDL and the amount of LDL particles. It causes a marked and persistent increase in LDL receptor activity, combined with favorable changes in the quality of LDL particles circulating. Atorvastatin reduces LDL cholesterol in patients with homozygous familial hypercholesterolemia, for whom conventional therapy is lipid-lowering drugs are often ineffective.
In humans, the pharmacological activity manifests as atorvastatin, and some of its metabolites. The primary site of action of atorvastatin is the liver that plays a central role in cholesterol synthesis and clearance of LDL. Lowering LDL-C level is well correlated with the dose of the drug and its concentration in the body. The individual dosage formulation based on therapeutic response.
When studying the effect of atorvastatin dose (10-80 mg) reduced serum total cholesterol (30-46%), LDL-C (41-61%), while the D (34-50%) and TG (14-33%). Such a result is stable patients with heterozygous familial hypercholesterolemia, non-hereditary form of hypercholesterolemia and hyperlipidemia mixed form, including patients with insulin-dependent diabetes mellitus.
For patients with isolated hypertriglyceridemia atorvastatin reduces total cholesterol (TC), LDL-C, X-VLDL, apolipoprotein B, triglycerides, cholesterol, low density lipoprotein cholesterol, and increases HDL-C. Patients with disbetalipoproteinemiey atorvastatin reduces the average density lipoprotein-cholesterol level (X-LSSCH).
In patients with hyperlipoproteinemia type Fredriksonovsky IIa and II B average percentage increase HDL-C in the application of 10-80 mg was 5,1-8,7% independently on the dose. Furthermore, there was a significant dose-dependent decrease cholesterol ratios / HDL-cholesterol and LDL-C / HDL-C.
Effect of atorvastatin 80 mg per day for 16 weeks, the occurrence of ischemia and total mortality in patients with unstable angina or myocardial infarction without tooth
Q was significant reduction in the risk of myocardial ischemia and mortality, reduced risk cases regospitalizatsii for angina and confirmed myocardial ischemia. Atorvastatin reduced the risk of death and ischemia inversely proportional to the concentration of LDL-C. Atorvastatin reduced the risk of ischemia and death in patients with myocardial infarction without Q-wave MI and unstable angina equally in men and women age, both before and 65 years.
Prevention of cardiovascular complications.
Atorvastatin significantly reduced the incidence of fatal cardiovascular diseases and non-fatal myocardial infarction, the overall incidence of cardiovascular diseases, lethal and non-lethal stroke frequency, decreased need for revascularization.
In the application of atorvastatin total mortality and mortality from cardiovascular disease decreased slightly, but there were favorable trends. The therapeutic effect was independent of sex, age or initial LDL cholesterol level.
Heterozygous familial hypercholesterolemia in pediatric practice.
The boys and girls postmenarhialny period (10-17 years) with heterozygous familial hypercholesterolaemia or severe hypercholesterolemia, atorvastatin 10-20 mg once daily significantly reduced total cholesterol, LDL-C, triglycerides, and apolipoprotein B in plasma. In this case, there was no significant effect on growth and sexual maturation in boys or on menstrual cycle length in girls. Safety and efficacy of doses above 20 mg in children has not been studied. Effect of long-term effectiveness of atorvastatin therapy in childhood to reduce morbidity and mortality is not set in adulthood.
Patients with no cardiovascular disease at 6 or less months prior to treatment had a stroke or TIA (transient ischemic attacks), atorvastatin 80 mg reduced the risk of fatal and nonfatal stroke by 15%, significantly reduced the incidence of cardiovascular diseases the risk of major coronary events, revascularization procedures.
Atorvastatin in the same dosage reduced the incidence of ischemic strokes, and increased incidence of hemorrhagic strokes. Atorvastatin has no effect on mortality from hemorrhagic strokes. It has been demonstrated to reduce the risk of cardiovascular events with atorvastatin 80 mg for each group of patients, except for patients who have had a hemorrhagic stroke or hemorrhagic stroke, repeated at the beginning of therapy. Atorvastatin 80 mg reduces the amount of stroke and coronary events.
Secondary prevention of cardiovascular events
In the treatment with atorvastatin 80 mg per day significantly reduces the incidence of major coronary events, with a relative risk reduction of 22%.
There was no significant difference in the groups studied on total mortality. The proportion of patients who death occurred due to cardiovascular disease, including coronary artery disease and fatal myocardial infarction was significantly lower in the group of patients treated with atorvastatin 80 mg compared to those who took it in a dose of 10 mg. The percentage of patients in the 80 mg atorvastatin application, which cause no death associated with cardiovascular diseases, quantitatively greater than the corresponding percentage in the group of patients treated at a dose of 10 mg.
Metabolism. Suction. Atorvastatin is rapidly absorbed after oral administration; plasma concentration reaches a maximum in 1-2 hours. Suction and plasma concentration increased proportionally with dose. Atorvastatin tablets bioavailability is 95-99% compared to the solution. Atorvastatin bioavailability is about 12% and the systemic availability of inhibitory activity against HMG-CoA reductase inhibitors - about 30%. Low systemic bioavailability linked to presystemic clearance in the mucosa of the gastrointestinal tract and / or biotransformation in the first pass through the liver. Although the proportion and degree of absorption of the drug are reduced when administered with food by approximately 25% and 9%, respectively, estimating on C max and AUC, lowering LDL-C level is not depended on taking atorvastatin together with food or not.In applying his evening atorvastatin plasma concentration lower (approximately 30% for C max and AUC), than in the morning administration. However, the reduction in LDL-C is not dependent on the time of dosing.
Distribution.The mean volume of distribution of atorvastatin is approximately 381 l. More than 98% of the drug is bound to plasma proteins. The ratio of the erythrocyte / plasma is about 0.25, which indicates a weak penetration of the drug into erythrocytes.
Metabolism. Atorvastatin is metabolized to ortho- and paragidroksilirovannyh derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase due to ortho- and paragidroksilirovannyh metabolites almost equal steps atorvastatin. The inhibitory effect of the drug against HMG-CoA reductase is realized approximately by the activity of circulating metabolites by 70%. Studies in vitro have shown the importance of the cytochrome P 450 ZA4 for metabolism of atorvastatin, which may manifest itself in increasing concentrations of atorvastatin in human plasma by co-use with erythromycin, which is an inhibitor of said enzyme. In in vitro studies have also found that atorvastatin is a weak inhibitor of cytochrome ZA4 450. Simultaneous use of atorvastatin and terfenadine - compoundis mainly metabolized by cytochrome 450 ZA4 not give a significant effect of increasing terfenadine plasma concentrations. So, it is unlikely that atorvastatin will significantly alter the pharmacokinetics of other substrates of cytochrome 450 ZA4. Animals ortogidroksilni metabolites undergo further glucuronidation.
Isolation. Atorvastatin and its metabolites are excreted mainly in the bile as a result of hepatic and / or extrahepatic metabolism. However, the drug does not undergo significant enterohepatic recirculation. The half-life of atorvastatin in man is approximately 14 hours, but the half-life of the inhibitory activity against HMG-CoA reductase due to circulating active metabolites ranges from 20 hours to 30 hours. Less than 2% of the dose after oral administration of atorvastatin excreted in the urine.
Elderly patients. The level of concentration of atorvastatin in plasma of healthy elderly people (over 65 years) is higher (approximately 40% for C max and 30% - for AUC), than in the young.
No difference effectiveness of atorvastatin treatment of elderly patients and patients in other age groups.
Children. Pediatric pharmacokinetics study was carried out.
Paul. Level in the plasma concentration of atorvastatin in females is different from the concentration level in the plasma in men (about 20% higher for C max and 10% lower for AUC). However, no clinically significant difference in the effect of the impact on lipids in men and women.
Renal insufficiency. kidney disease does not affect the level of drug concentration in plasma or effect of atorvastatin on lipids. Therefore there is no need to change the dose in patients with renal insufficiency.
Hemodialysis. Studies conducted, not covered patients with end-stage renal disease probably hemodialysis does not significantly alter clearance of atorvastatin, as the drug almost completely bound to plasma proteins.
Liver failure . Level atorvastatin plasma concentration increases markedly (C max of about 16 times, and AUC - 11-fold) in patients with alcoholic liver cirrhosis (Child-Pugh B).
Carcinogenesis, Mutagenesis, harmful effects on fertility. In animal studies atorvastatin showed no carcinogenic effect.
Basic physical and chemical properties
For dosing 10 mg tablets white elliptical shape with biconvex surface coated with embossing "10" and "A" on the other hand.
For dosing 20 mg tablets white elliptical shape with biconvex surfaces coated with "20" embossed "A" on the other hand.
Stored in original package at a temperature not higher than 25 ° S.Hranit the reach of children.
10 tablets in a blister, 3 blisters in a pack.