Egilok tablets 25 mg bottle No. 60

Instructions for Egilok tablets 25 mg bottle No. 60

Composition

active ingredient: metoprolol;

1 tablet contains metoprolol tartrate 25 mg or 50 mg or 100 mg;

Excipients: magnesium stearate, povidone, colloidal anhydrous silicon dioxide, sodium starch glycolate (type A), microcrystalline cellulose.

Dosage form

Pills.

Main physicochemical properties:

25 mg: white or almost white, round biconvex tablets with a cross-shaped score line and a double bevel ("double snap") on one side and engraved with a stylized letter "E" and the number 435 on the other side, odorless or almost odorless;

50 mg: white or almost white, round biconvex tablets with a score on one side and engraved with the stylized letter “E” and the number 434 on the other side, odorless or almost odorless;

100 mg: white or almost white, round biconvex tablets, with a bevel, a score on one side and engraved with a stylized letter "E" and the number 432 on the other side, odorless or almost odorless.

The score line on the tablet is intended only to facilitate breaking and swallowing, not to divide the medication into equal doses.

Pharmacotherapeutic group

Selective β-adrenergic blockers.

ATX code C07A B02.

Pharmacological properties

Pharmacodynamics.

Metoprolol is a cardioselective β1-adrenoceptor blocker. It does not have a membrane-stabilizing effect and does not have intrinsic sympathomimetic activity.

It inhibits the cardiac effects of increased sympathetic activity, significantly reducing heart rate, cardiac contractility, cardiac output, and blood pressure.

In hypertension, metoprolol reduces blood pressure in patients both in the standing and supine positions. The long-lasting antihypertensive effect of the drug

associated with a gradual decrease in total peripheral vascular resistance.

In patients with arterial hypertension, long-term use of the drug leads to a statistically significant decrease in left ventricular mass and improvement in left ventricular diastolic function.

In men with mild to moderate hypertension, metoprolol reduces mortality from cardiovascular disease (primarily the incidence of sudden death, fatal myocardial infarction, and stroke).

By reducing systemic blood pressure, heart rate, and cardiac contractility, metoprolol reduces myocardial oxygen demand. By reducing heart rate and thus prolonging diastole, metoprolol improves

perfusion and oxygenation of myocardial areas with impaired blood supply.

In addition, the drug reduces the frequency, duration, and severity of angina attacks, as well as asymptomatic ischemia, and increases exercise tolerance.

In myocardial infarction, metoprolol reduces the risk of sudden death. This effect is primarily associated with the prevention of ventricular fibrillation. The reduction in mortality is observed regardless of whether metoprolol was prescribed at an early or late stage of the disease, as well as in cases of increased risk and in patients with diabetes mellitus.

When metoprolol is prescribed after a myocardial infarction, the drug reduces the possibility of a second heart attack.

In congestive heart failure due to dilated cardiomyopathy, metoprolol, initially administered at a low dose (2 × 5 mg per day) and then gradually increased, improved cardiac function, quality of life, and physical performance of patients; it reduced the number of rehospitalizations for heart failure and the need for heart transplantation.

In supraventricular tachycardia, atrial fibrillation and ventricular extrasystole, metoprolol reduces the ventricular rate and the number of extraventricular beats.

In therapeutic doses, the peripheral vasoconstrictor and bronchoconstrictor effect of metoprolol is less pronounced than that of non-selective β-blockers.

Compared with nonselective β-blockers, metoprolol has much less effect on insulin production and carbohydrate metabolism. It only slightly alters the cardiovascular response to hypoglycemia or prolongs the duration of a hypoglycemic attack.

In short-term clinical studies, metoprolol induced a slight increase in triglycerides and a slight decrease in serum free fatty acids. In some cases, a slight decrease in HDL-C (high-density lipoprotein cholesterol) was also observed, but this was less than with non-selective β-blockers. However, in a long-term clinical study, a significant decrease in total serum cholesterol was demonstrated after several years of treatment with metoprolol.

Pharmacokinetics.

Metoprolol is rapidly and almost completely absorbed from the gastrointestinal tract. The pharmacokinetic parameters of metoprolol are linear in the therapeutic dose range.

Concomitant food intake may increase the bioavailability of metoprolol by 30–40%.

Plasma protein binding is low, about 5-10%.

Metoprolol is widely distributed in tissues and has a high apparent volume of distribution (5.6 l/kg).

Metoprolol is metabolized in the liver by cytochrome P450 enzymes. The metabolites do not contribute to the clinical effect.

The half-life (t1/2) is 3.5 hours on average (it varies within 1-9 hours).

Total clearance is approximately 1 l/min.

More than 95% of the dose taken can be detected in the urine, 5% is excreted unchanged. In some cases, the latter value can increase to 30%.

In elderly patients, the pharmacokinetic parameters of metoprolol do not change significantly.

Renal insufficiency does not affect the systemic bioavailability and elimination of metoprolol. However, in such cases, the excretion of metabolites is reduced. Significant accumulation of metabolites has been observed in severely ill patients with renal insufficiency (glomerular filtration rate - 5 ml / min). However, the accumulation of metabolites does not increase the degree of β-blockade.

Hepatic insufficiency has little effect on the pharmacokinetic parameters of metoprolol. However, in severe cirrhosis of the liver and after portocaval anastomosis surgery, the bioavailability of metoprolol may increase and the total clearance may decrease. In patients after portocaval anastomosis surgery, the total clearance decreased to approximately 0.3 l/min and the area under the concentration-time curve increased approximately 6-fold compared to healthy subjects.

Indication

Arterial hypertension.

Angina pectoris (including post-infarction).

Arrhythmia (including supraventricular tachycardia).

Prevention of cardiac death and recurrent infarction after the acute phase of myocardial infarction.

As part of complex therapy for thyrotoxicosis.

Prevention of migraine attacks.

Contraindication

Hypersensitivity to any component of the drug or to other β-blockers;

atrioventricular block (AV block) II and III degrees, sinoatrial block;

sick sinus syndrome;

decompensated heart failure (pulmonary edema, hypoperfusion syndrome or arterial hypotension); long-term or intermittent isotropic therapy with β-receptor agonists;

severe bradycardia (heart rate (HR) ≤ 45 per minute);

cardiogenic shock;

severe peripheral circulatory disorders with pain or trophic changes;

arterial hypotension (systolic blood pressure < 100 mm Hg);

metabolic acidosis;

untreated pheochromocytoma;

prolonged or intermittent inotropic therapy with β-receptor agonists;

concomitant therapy with monoamine oxidase-A inhibitors;

severe bronchial asthma, severe form of chronic obstructive bronchopulmonary diseases;

The use of metoprolol is contraindicated in patients receiving intravenous calcium antagonists such as verapamil and diltiazem or other antiarrhythmic drugs (such as disopyramide).

Metoprolol should not be prescribed to patients with suspected acute myocardial infarction with a heart rate less than 45 beats/min, a P–Q interval > 0.24 s, or a systolic blood pressure < 100 mm Hg.

Note: In patients with decompensated heart failure who tolerate other medications well, the use of metoprolol is possible with individual dose titration.

Interaction with other medicinal products and other types of interactions

Metoprolol is a substrate of the CYP 2D6 enzyme. The concentration of metoprolol in the blood plasma may be affected by drugs that inhibit CYP 2D6, for example: quinidine, terbinafine, paroxetine, fluoxetine, sertraline, celecoxib, propafenone and diphenhydramine. At the beginning of treatment with these drugs, it may be necessary to reduce the dose of the drug Egilok®.

Barbituric acid derivatives: barbiturates (particularly pentobarbital) stimulate the metabolism of metoprolol by enzyme induction.

The simultaneous administration of Egilok® with the following medicines should be avoided:

Patients should be closely monitored if they are taking ganglioblockers, other β-blockers (e.g. eye drops) or monoamine oxidase inhibitors (MAOIs) concomitantly with Egilok®.

Propafenone: Concomitant administration with propafenone should be avoided. In 4 patients treated with metoprolol, plasma concentrations of metoprolol were reported to increase 2-5-fold after administration of propafenone, and 2 patients experienced side effects typical of metoprolol. The interaction was confirmed in 8 healthy volunteers. This interaction may be due to the fact that propafenone, like quinidine, inhibits the metabolism of metoprolol via cytochrome P450 2D6. The outcome of this combination is unpredictable, as propafenone also has β-blocking properties.

Concomitant use of Egilok® with the following drugs may require dose adjustment:

In patients who are taking calcium antagonists of the verapamil type or diltiazem and/or drugs for the treatment of arrhythmias simultaneously with Egilok®, negative inotropic and chronotropic effects are possible. Patients taking β-blockers should not be given intravenous verapamil due to the risk of cardiac arrest. β-blockers may enhance the negative inotropic and chronotropic effects of drugs for the treatment of arrhythmias (quinidine analogues or amiodarone).

Amiodarone: Clinical case reports suggest that patients taking amiodarone may develop severe sinus bradycardia when co-administered with metoprolol. Amiodarone has an extremely long half-life (approximately 50 days) meaning that interactions may occur long after discontinuation of this drug.

Class I antiarrhythmics: Class I antiarrhythmics and beta-blockers have additive negative inotropic effects that may lead to serious hemodynamic side effects in patients with impaired left ventricular function. This combination should also be avoided in patients with sick sinus syndrome and atrioventricular conduction disorders. This interaction is best described with disopyramide.

Nonsteroidal anti-inflammatory/antirheumatic drugs (NSAIDs): NSAIDs have been shown to antagonize the antihypertensive effects of beta-blockers. Indomethacin has been studied primarily. This interaction is unlikely to occur with sulindac. A negative interaction study has been conducted with diclofenac.

In patients treated with β-blockers, inhalation anesthetics enhance the cardiodepressive effect. Inducers or inhibitors of metabolism may affect the plasma concentration of metoprolol.

Metoprolol plasma concentrations are decreased by rifampicin or may be increased by cimetidine, phenytoin, alcohol, hydralazine, and serotonin reuptake inhibitors (paroxetine, fluoxetine, and sertraline).

With concomitant treatment with indomethacin or other drugs that inhibit prostaglandin synthetase, the antihypertensive effect of β-blockers may be reduced.

Cardioselective β-blockers have a much smaller effect on blood pressure when patients are given adrenaline than nonselective β-blockers.

Diltiazem: Diltiazem and β-blockers have additive inhibitory effects on AV conduction and sinus node function. Marked bradycardia may occur.

Epinephrine: Severe hypertension and bradycardia have been reported (approximately 10 reports) following administration of epinephrine (adrenaline) to patients receiving non-selective beta-blockers (including pindolol and propranolol). It is also suggested that epinephrine, which is found in local anesthetics, may precipitate these reactions when administered intravascularly. The risk is likely to be lower with cardioselective beta-blockers.

Phenylpropanolamine: Phenylpropanolamine (norephedrine) in a single dose of 50 mg may cause a pathological increase in diastolic blood pressure in healthy volunteers. Propranolol generally counteracts the increase in blood pressure caused by phenylpropanolamine. β-blockers may provoke paradoxical hypertensive reactions in patients receiving high doses of phenylpropanolamine. Two cases of hypertensive crisis have been described during treatment with phenylpropanolamine alone.

In patients receiving β-blockers, it may be necessary to re-adjust the dose of oral antidiabetic agents. When β-blockers are taken concomitantly with insulin or oral antidiabetic agents, their effect may be enhanced or prolonged. In this case, the symptoms of hypoglycemia (especially tachycardia and tremor) may be masked or disappear. In such cases, regular monitoring of blood glucose levels is necessary.

Concomitant administration with barbiturates should be avoided, as barbiturates (studied on pentobarbital) stimulate the metabolism of metoprolol by enzyme induction.

The plasma concentration of metoprolol may be affected by drugs that inhibit CYP 2D6, such as: quinidine, terbinafine, paroxetine, fluoxetine, sertraline, celecoxib, propafenone and diphenhydramine. At the beginning of treatment with these drugs, it may be necessary to reduce the dose of metoprolol.

Digitalis glycosides: Concomitant use of digitalis glycosides and β-receptor blockers may increase atrioventricular conduction time and cause bradycardia.

Diphenhydramine: Diphenhydramine reduces (by 2.5-fold) the clearance of metoprolol to α-hydroxymetoprolol via the CYP 2D6 system in subjects who are rapid hydroxylators. The effects of metoprolol are enhanced. It is possible that diphenhydramine may inhibit the metabolism of other CYP 2D6 substrates.

Rifampicin: Rifampicin may stimulate the metabolism of metoprolol, leading to a decrease in its plasma levels.

Caution should be exercised when combined with nitrates due to the risk of arterial hypotension and/or bradycardia.

Patients receiving sympathetic ganglion blockers concomitantly with metoprolol should be closely monitored.

Metoprolol should be prescribed with caution to patients taking β2-receptor and β1-receptor stimulants, as well as dihydropyridines.

Caution should be exercised when metoprolol is used concomitantly with ergotamine.

Caution should be exercised when combining metoprolol with other drugs with antihypertensive effects.

Application features

When taking metoprolol tartrate, as with other β-blockers, it is necessary to monitor heart rate (HR) and blood pressure (BP) (initially daily, then once a month).

Patients taking β-blockers should not be given intravenous verapamil-type calcium antagonists.

As a rule, in the treatment of asthma patients, β2-agonists (in tablets or aerosols) are prescribed concomitantly. In cases where these patients start taking the drug, an increase in the dose of β2-agonists may be required. The risk of the drug affecting β2 receptors is lower than in the case of the use of conventional non-selective β1-blockers in tablets.

Particularly careful medical supervision is necessary in the treatment of patients with diabetes mellitus (blood glucose control), patients with unstable blood sugar levels, when using a strict fasting diet. During treatment with metoprolol, there is a minimal risk of affecting sugar metabolism or masked hypoglycemia compared to treatment with non-selective β-blockers.

Metoprolol may mask some clinical manifestations of thyrotoxicosis (e.g. tachycardia). Abrupt withdrawal of the drug in patients with thyrotoxicosis is contraindicated due to possible exacerbation of symptoms.

Patients undergoing treatment for heart failure should be treated for this disease before starting metoprolol and during this treatment.

Very rarely, pre-existing AV conduction disorders may progress to more severe AV block. Patients with first-degree AV block should be treated with this drug with great caution.

Abrupt withdrawal of beta-blockers is dangerous, especially for high-risk patients, and may worsen chronic heart failure, as well as increase the risk of myocardial infarction and sudden death. Therefore, discontinuation of Egilok® for any reason should be done gradually, if possible, over a period of at least 2 weeks, with the dose of the drug being halved at each stage to a final dose of 25 mg. The last dose should be taken for at least 4 days before complete withdrawal of the drug. In case of recurrence of symptoms, it is recommended to slow down the dose reduction.

Metoprolol should be used with caution in patients with myasthenia gravis.

Metoprolol may exacerbate pre-existing bradycardia. In the event of bradycardia (heart rate less than 50-55 beats/min) during treatment with metoprolol, the dose should be reduced and/or the drug should be gradually discontinued.

Due to its hypotensive effect, the drug may increase the symptoms of peripheral circulatory disorders, such as intermittent claudication.

If the drug is used in patients with pheochromocytoma, an α-sympatholytic drug should be used in parallel.

Before general anesthesia, the anesthesiologist should be informed that the patient is taking Egilok®. In the event of surgery, the anesthesiologist should be informed that the patient is taking metoprolol. It is not recommended to discontinue treatment with β-blockers in patients undergoing surgery. If metoprolol is considered necessary, it should be discontinued, if possible, at least 48 hours before general anesthesia. Urgent use of high doses of metoprolol in patients undergoing non-cardiac surgery should be avoided, as it has been associated with bradycardia, hypotension, and stroke, including fatal outcomes in patients with cardiovascular risk factors.

However, for some patients, beta-blockers may be desirable as premedication. In such cases, an anesthetic with a low negative inotropic effect should be chosen to minimize the risk of myocardial depression.

Treatment with the drug should be discontinued gradually, reducing the dose to 25 mg over 10 days. Treatment should not be discontinued abruptly due to the possibility of developing withdrawal syndrome (increased angina attacks, increased blood pressure).

There is insufficient experience with the use of metoprolol in patients with heart failure and the following concomitant factors: unstable heart failure (NYHA IV (according to the New York Heart Association classification system)); acute myocardial infarction or unstable angina within the previous 28 days; impaired renal and hepatic function; patient age over 80 years and under 40 years; hemodynamically significant valvular disease; hypertrophic obstructive cardiomyopathy; during or within 4 months after cardiac surgery. Treatment of such patients should be carried out by physicians with special skills and experience.

If treatment must be discontinued and whenever possible, it should be discontinued over a period of 10-14 days with a daily dose reduction of 25 mg per day for the last 6 days. During this period, special attention should be paid to patients with coronary artery disease. The risk of cardiac arrest, including sudden death, may be increased when β-blocker treatment is discontinued.

In patients with Prinzmetal's angina, the frequency and severity of angina attacks may increase due to α-receptor-mediated coronary vasoconstriction. Therefore, nonselective β-blockers should not be prescribed to such patients, and selective β1-blockers should be used with caution.

In patients receiving β-blockers, adrenaline may increase blood pressure and cause (reflex) bradycardia; this reaction is less likely with selective β-blockers.

Since metoprolol must be discontinued before surgery, discontinuation should be carried out no later than 48 hours before surgery, except in special cases, such as thyrotoxicosis or pheochromocytoma.

However, in some cases, preoperative administration of β-blockers may be beneficial because they can reduce the arrhythmogenic effects and reduce coronary blood flow during surgical stress, which favors sympathetic tone. If a patient is given a β-blocker for these reasons, an anesthetic with a weak negative isotropic effect should be chosen to reduce the risk of myocardial depression.

Very rarely, existing moderate atrioventricular conduction disorders may worsen, sometimes with the development of atrioventricular block.

Anaphylactic shock is severe in patients treated with β-blockers.

Patients with a history of severe allergic reactions should be treated with metoprolol with caution. Special attention should also be paid to patients with allergic reactions who are undergoing treatment with vaccines (desensitization therapy). The effect of the administration of usual doses of adrenaline may be absent.

Patients who wear contact lenses should be aware that the drug may reduce tear secretion.

Treatment with metoprolol should be prescribed to patients with psoriasis or a history of depressive disorders only after careful consideration of the benefit-risk ratio.

The bioavailability of metoprolol may be increased in liver cirrhosis.

Special attention should be paid to patients with severe renal impairment, with serious acute conditions accompanied by metabolic acidosis, and patients receiving combination treatment with digitalis drugs.

Use during pregnancy or breastfeeding

Egilok®, like other medicines, should not be used during pregnancy or breastfeeding unless clearly necessary. Like other β-blockers, metoprolol may cause side effects, such as bradycardia and hypoglycemia, in the fetus and newborn or in the breastfed infant.

As a rule, β-blockers suppress placental blood flow, which can cause fetal growth retardation. Metoprolol can cause bradycardia, hypotension, hypoglycemia, and respiratory depression in the newborn, so its use should be discontinued 48-72 hours before the expected onset of labor. If this is not possible, the infant should be closely monitored for 48-72 hours after birth.

On the other hand, the amount of metoprolol that the infant receives in breast milk to achieve a potential β-blockade effect is insignificant if the mother's metoprolol dose is within the normal therapeutic range. Breastfed infants should be closely monitored for potential β-blockade effects.

Ability to influence reaction speed when driving vehicles or other mechanisms

The use of metoprolol may affect activities that require high speed of mental and physical reactions, quick decision-making (e.g., driving vehicles, operating machinery and mechanisms, working at heights), therefore, during the treatment period, you should refrain from driving vehicles, operating machinery and mechanisms, and working at heights.

Method of administration and doses

Egilok® is intended for daily use, preferably in the morning. The tablets should be taken regardless of meals. The tablet should be taken without chewing, with sufficient amount of drinking water.

The dose should be adjusted individually, gradually increasing it to avoid excessive bradycardia. During the dose adjustment period, the heart rate should be monitored to prevent bradycardia. The maximum daily dose is 400 mg.

Arterial hypertension

The recommended dose is 100 mg (once in the morning or in two doses - morning and evening). If the therapeutic effect is not achieved with this dosage, the daily dose can be increased to 200 mg (once in the morning or in two doses - morning and evening) or the drug can be combined with other antihypertensive drugs.

Angina pectoris

The recommended dose of the drug is 50-100 mg 2-3 times a day. If necessary, the drug can be combined with other drugs for the treatment of angina pectoris.

Arrhythmia

The recommended dose is 50 mg 2-3 times a day. If necessary, the daily dose can be increased to 300 mg, divided into 2-3 doses.

In case of myocardial infarction (it is advisable to start treatment within the first 12 hours after the onset of chest pain)

The recommended dose is 50 mg every 6 hours for 48 hours, the recommended maintenance daily dose is 200 mg, divided into two doses. The course of treatment is at least 3 months.

Hyperthyroidism (thyrotoxicosis)

The recommended dose is 50 mg 4 times a day. When the therapeutic effect is achieved, the dose should be gradually reduced.

Prevention of migraine attacks

The recommended daily dose is 100-200 mg per day, in 2 divided doses.

Patients with renal impairment

There is no need to adjust the dose.

Patients with hepatic impairment

Dose adjustment (reduction of the metoprolol dose) is usually necessary for patients with limited liver function (e.g., patients with cirrhosis).

Elderly patients

There is no need to adjust the dose.

Arterial hypertension: for mild to moderate hypertension, the initial dose is 25 mg.

Children.

The use of the drug in children is contraindicated.

Overdose

Toxicity. In an adult, a dose of 7.5 g caused fatal intoxication. Ingestion of 100 mg of the drug by a 5-year-old child was not accompanied by symptoms of intoxication after gastric lavage. Moderate intoxication was caused by a dose of 450 mg in a 12-year-old child and a dose of 1.4 g in an adult, serious intoxication in an adult was caused by a dose of 2.5 g, and 7.5 g - very serious intoxication.

Symptoms. The most severe are cardiovascular symptoms, but in some cases, especially in children and young people, central nervous system (CNS) symptoms and respiratory depression may predominate. Arterial hypotension, sinus bradycardia, AV block I-III degree, prolongation of the QT interval (exceptional case), heart failure, cardiogenic shock, asystole, nausea, vomiting, bronchospasm, cyanosis, hypoglycemia, loss of consciousness, coma, in some cases - hypokalemia. Respiratory depression, respiratory arrest.

Others: fatigue, confusion, fine tremor, convulsions, sweating, paresthesias, bronchospasm, nausea, vomiting, possible esophageal spasm, hypoglycemia (especially in children) or hyperglycemia, hyperkalemia. Effects on the kidneys. Transient myasthenic syndrome. The first signs of overdose may occur 20 minutes to 2 hours after taking an excessive dose.

Concomitant use of alcohol, antihypertensive drugs, quinidine, or barbiturates may worsen the patient's condition.

Treatment: Intensive care and close monitoring of the patient (circulatory and respiratory parameters, renal function, blood glucose, serum electrolytes) are necessary. If the drug has been ingested recently, further absorption can be reduced by gastric lavage, induction of vomiting, and administration of activated charcoal.

NB! Atropine (0.25-0.5 mg intravenously in adults, 10-20 μg/kg body weight in children) should be administered before gastric lavage (due to the risk of vagal stimulation). Incubation and use of artificial respiration may be necessary; adequate volume replacement; glucose infusion; ECG; repeated intravenous administration of atropine 1-2 mg (mainly for vagal symptoms). In case of myocardial depression: infusion of dobutamine or dopamine and calcium gluconate 9 mg/ml, 10-20 ml.

Glucagon 50–150 mcg/kg body weight intravenously over 1 minute can be given, as can amrinone. In some cases, the addition of adrenaline (epinephrine) has been effective.

Sodium infusion (chloride or bicarbonate) in case of QRS prolongation and arrhythmia. A pacemaker may be used. In case of circulatory arrest, resuscitation measures may be required for several hours. In case of bronchospasm, terbutaline (injection or inhalation) is prescribed. Symptomatic therapy.

Side effects

Metoprolol is well tolerated by patients, and the side effects that occur are usually minor and transient.

The table below lists the adverse reactions to metoprolol grouped by MedDRA system organ class:

Table

*The incidence of adverse effects such as skin reactions or eye irritation is low, and symptoms usually disappear after discontinuation of therapy.

Expiration date

3 years.

Storage conditions

Store at a temperature not exceeding 25 ºС in a place inaccessible to children.

Incompatibility

Unknown.

Packaging

60 tablets (25 mg and 50 mg); 60 or 30 tablets (100 mg) in a glass bottle in a cardboard box.

Vacation category

According to the recipe.

Producer

EGIS Pharmaceuticals PLC, Hungary.

Location of the manufacturer and its business address

1165, Budapest, Bokenyfoldi ut. 118-120, Hungary/1165 Budapest, Bokenyfoldi ut. 118-120, Hungary.

9900, Kormend, Matyas kiraly ut. 65, Hungary/ 9900, Kormend, Matyas kiraly ut. 65, Hungary