Instructions for use BICARD-LF
The effectiveness and tolerability of bisoprolol may be affected by concomitant use of other medications. This interaction may also occur if there is a short period of time between medications. The patient should inform the doctor about taking other medications, including medications purchased without a prescription.
Combinations not recommended
Calcium channel blockers such as verapamil, and to a lesser extent diltiazem:
- inhibitory effect on myocardial contractile function and AV conductivity. IV administration of verapamil can lead to severe arterial hypotension and AV blockade in patients taking beta-blockers.
Antihypertensive drugs with a central mechanism of action (clonidine, methyldopa, moxonidine, rilmenidine):
- coadministration may result in worsening heart failure. During combination therapy, abrupt discontinuation of these drugs may increase the risk of reflex hypertension.
Combinations requiring special caution
When used simultaneously with class I antiarrhythmic drugs (for example, quinidine, disopyramide, lidocaine, phenytoin, flecainide, propafenone), the inhibitory effect on AV conductivity and myocardial contractile function may be enhanced.
Calcium antagonists such as dihydropyridine (for example, nifedipine, felodipine, amlodiline) may increase the risk of arterial hypotension. The possibility of increased negative inotropic effects in patients with heart failure cannot be ruled out.
Class III antiarrhythmic drugs (for example, amiodarone) may enhance the inhibitory effect on AV conduction.
When used together with parasympathomimetics, it is possible to increase AV conduction time and increase the risk of bradycardia.
When used simultaneously with local beta-blockers (for example, those contained in eye drops for the treatment of glaucoma), the effect of bisoprolol may be enhanced.
Bisoprolol enhances the effect of insulin and oral hypoglycemic drugs. Symptoms of hypoglycemia may be masked. Such an interaction is most likely when using non-selective beta-blockers.
When using anesthetic agents while taking bisoprolol, the risk of myocardial function depression and arterial hypotension increases.
Cardiac glycosides (digitalis preparations) can reduce heart rate and increase AV conduction time.
NSAIDs may weaken the hypotensive effect of bisoprolol.
When using beta-sympathomimetics (for example, isoprenaline, dobutamine) in combination with bisoprol, the therapeutic effect of both drugs may be reduced.
When bisoprolol is combined with adrenomimetics that affect α- and β-adrenergic receptors (for example, norepinephrine, epinephrine), it is possible to enhance the vasoconstrictor effects caused by the action on α-adrenergic receptors, which leads to an increase in blood pressure. Such an interaction is more likely when using non-selective beta-blockers.
Antihypertensive drugs, as well as other drugs with a possible antihypertensive effect (for example, tricyclic antidepressants, barbiturates, phenothiazines), can enhance the hypotensive effect of bisoprolol.
Combinations to Consider
Mefloquine may increase the risk of bradycardia.
MAO inhibitors (except MAO B inhibitors) may enhance the hypotensive effect of beta-blockers. Concomitant use may also lead to the development of a hypertensive crisis.
Bicard
Name: Bicard Pharmacological action: Bicard is a highly selective β1-blocker that has a cardiotropic effect and affects hemodynamic parameters. Bisoprolol acts mainly on β1-adrenergic receptors of the heart. The drug binds to receptors and prevents their interaction with catecholamines, as a result of which the synthesis of cAMP slows down. These changes disrupt processes in membrane calcium channels and change the concentration of calcium in the cells of the conduction system, which reduces heart rate, inhibits conduction through the AV node and the bundle of Kent, and reduces automaticity in the nodes. Inhibition of conduction processes has an antiarrhythmic effect. As a result of the lack of calcium ions in cardiomyocytes, the interaction between actin and myosin is disrupted, which leads to a decrease in the force of heart contractions.
A reduced number of heart contractions and a decrease in their intensity reduce the oxygen demand of myocardial fibers and, as a result, an antianginal effect appears and myocardial perfusion increases. Bisoprolol is able to stabilize lysosomal and cellular membranes and inhibit blood platelet aggregation. The drug blocks beta1-adrenergic receptors in the JGA of the kidney, which reduces the level of renin and angiotensin II, and with the simultaneous presence of these effects with a decrease in heart rate and contraction strength, bisoprolol causes a persistent decrease in blood pressure. The drug affects the restructuring of the baroreflex effects of the aortic arch and carotid sinus, and increases the release of vasodilating substances such as PG, nitric oxide, and ANP. Bisoprolol does not affect beta 2 adrenergic receptors, which reduces the frequency and severity of its negative effects and makes it well tolerated. In large doses it can influence β1 and β2 adrenergic receptors.
The drug is well absorbed from the gastrointestinal tract. Cmax in the blood is observed after 60-180 minutes. Binds to blood albumin by 30%. Bisoprolol is able to penetrate the blood-brain barrier and the uteroplacental barrier and minimally penetrates into breast milk. The half-life is up to 12 hours, the duration of circulation and the manifestation of pharmacological effects is up to 24 hours. Bisoprolol is an amphophilic substance, therefore the drug is excreted in two equally effective ways - up to 50% is eliminated in the liver and 50% is excreted in the form of active metabolites through the kidneys, i.e. has balanced ground clearance. This allows it to be used equally successfully for liver and kidney dysfunctions without changing or adjusting the dose of the drug.
Indications for use: — Arterial hypertension; - stable and unstable angina; — secondary prevention of coronary artery disease; - heart failure; - symptomatic treatment of hyperthyroidism, migraine and for perioperative reduction of the risk of death from cardiac causes.
Directions for use: Tablets are intended for oral administration. The recommended dose is once a day, in the first half of the day, preferably in the morning. The tablets are washed down with a small amount of water and taken regardless of meals. Do not chew, do not bite. The primary therapeutic dose is 5 mg of the drug once a day. Gradually increase the dosage by 5 mg each week, sometimes the starting dose is 10 mg. Increasing the dosage may be accompanied by negative effects, which requires a return to the previous dose. The maximum therapeutic dose is 20 mg once a day.
In patients with impaired functional state of the liver and kidneys, no dose adjustment is required. In severe chronic renal failure, the dose of the drug should not exceed 10 mg per day. The course of treatment is long.
Side effects: Bisoprolol has a satisfactory safety profile. The incidence of side effects is quite low. This drug is characterized by changes in the central nervous system in the form of asthenic phenomena, dizziness, headaches, which appear at the beginning of therapy; sleep disturbances, depression, paresthesia may occur; in isolated cases, hallucinations have been observed. These changes disappear on their own 10-14 days after the start of treatment. Characteristic disorders of the visual organs are decreased tear production, conjunctivitis, and blurred vision. Adverse effects from the cardiovascular system are possible - decreased heart rate, hypotension, rhythm disturbances and blockade, heart failure with symptoms of peripheral edema, transient intermittent claudication at the beginning of treatment with the drug. Rarely, respiratory system disorders occur in the form of bronchospasms.
Dyspeptic manifestations, stool disorders, increased activity of liver transaminases are observed, and hepatitis may develop. In rare cases, arthralgia, muscle weakness, and cramps were observed. During therapy, allergic reactions may develop, which requires discontinuation of the drug. In patients with diabetes, the drug can cause hypoglycemia; in people without diabetes, in rare cases, impaired glucose tolerance and increased TG were observed. Men may experience erectile dysfunction and alopecia when using bisoprolol.
Contraindications: The drug is not used in persons with symptoms of sinoatrial, atrioventricular block of the 2nd-3rd degree, with a heart rate less than 50 beats per minute, with sick sinus syndrome, with low systolic blood pressure (less than 90 mmHg), for severe peripheral circulatory disorders. Bicard is not recommended for bronchial asthma, COPD. Not prescribed for patients with pheochromocytoma, psoriasis, or for persons on therapy with MAO inhibitors. Contraindicated for use in pregnant and lactating women.
Pregnancy: Bisoprolol is not prescribed to women during pregnancy and lactation. The drug is capable of delaying intrauterine development, depressing the respiratory center in the fetus, and after delivery, provoking severe hypoglycemic conditions in a newborn baby during the first 72 hours of life.
Interaction with other drugs: Bisoprolol interacts with antihypertensive drugs in a synergistic manner, enhancing their pharmacological activity. Severe bradycardia is observed when bisoprolol is combined with reserpine, clonidine, guanfacine, and alpha-methyldopa. The combined use of clonidine or guanfacine, or the drugs digitalis and bisoprolol causes atrioventricular block and conduction disturbances. Sympathomimetics reduce the pharmacological activity of bisoprolol.
Nifedipine and calcium channel blockers (dihydropyridine derivatives) initiate severe hypotension. Verapamil, diltiazem, and antiarrhythmic drugs cause persistent bradycardia, hypotension, cardiac arrhythmias, including heart failure and cardiac arrest while taking Bicard. Ergotamine derivatives, when combined with Bicard, potentiate the phenomena of peripheral circulatory disorders. Rifampicin reduces the half-life of bisoprolol, which has no clinical significance. Bisoprolol interferes with the effectiveness of glycemic control in diabetes mellitus. Nonsteroidal anti-inflammatory drugs reduce the hypotensive effect of Bicard.
Bisoprolol increases the half-life of muscle relaxants and anticoagulants (coumarins). Antidepressants, sedatives, hypnotics, neuroleptics, ethanol expressly depress the central nervous system when combined with Bicard. MAO inhibitors disrupt Bicard's metabolism, which increases the manifestation of its negative effects. The break between therapy with Bicard and MAO inhibitors should be at least 2 weeks. Sulfasalazine in combination with bisoprolol increases the Cmax of the latter in the blood plasma. X-ray contrast agents (iodine-containing), when administered while taking bisoprolol, can in rare cases cause severe anaphylaxis.
Overdose: When using high doses of the drug, the development of bradycardia, rhythm disturbances, arterial hypotension, bronchospasm, fainting, heart failure, and convulsive attacks is possible. To provide medical care, use: gastric lavage, taking sorbents; in case of bradycardia and hypotension, atropine 1.5-2 mg, epinephrine, dopamine are administered intravenously. In situations of developing heart failure, cardiac glycosides, glucagon, and diuretics are prescribed. For bronchospasm - inhalation of β2 adrenergic agonists.
Release form: Tablets of 5 (10) mg in blisters No. 10. 3 blisters in a cardboard package.
Storage conditions: Recommended storage temperature up to 25 degrees Celsius.
Synonyms: Bidop, Bisogamma, Corbis, Concor, Cordinorm, Coronal, Bisokard.
Composition: Active ingredient: bisoprolol fumarate. 1 tablet contains bisoprolol fumarate 5 (10) mg. Excipients: Magnesium stearate, Aerosil, Сrospovidone, Cellulose microcrystallic, Talk, Polyethylene glycerol, Titanium Dioxide, Polyvinyl alcohol, Iron(III) oxide, yellow, Quinoline Yellow E-104, Orange Yellow E-110, corn starch.
Additionally: Bicard tablets do not have a dividing strip, therefore they are indivisible. The drug is prescribed with caution for Prinzmetal angina, 1st degree atrioventricular block, in the presence of metabolic acidosis and in persons prone to alcoholism. The use of the drug against the background of diabetes mellitus causes hidden hypoglycemia, which worsens the course of the disease. There have been cases of the development of lichen planus during therapy with β-adrenergic receptor blockers and the development of a psoriasis-like rash against its background. Treatment with bisoprolol must be carried out under the strict supervision of a doctor. Bicard is not used for treatment in the pediatric age group, because There is no data on the safe use of the drug in this category of people.
If the drug is used during pregnancy, bisoprolol should be discontinued 72 hours before birth to avoid negative effects in the newborn. If this was not possible, then the child must be carefully observed in the first 3 days. The drug does not affect male fertility. At the beginning of therapy, it is possible to develop reversible reactions that change the ability to drive vehicles, so at this stage it is necessary to avoid driving and working with complex mechanisms.
Attention! The description of the drug " Bicard " on this page is a simplified and expanded version of the official instructions for use. Before purchasing or using the drug, you should consult your doctor and read the instructions approved by the manufacturer. Information about the drug is provided for informational purposes only and should not be used as a guide to self-medication. Only a doctor can decide to prescribe the drug, as well as determine the dose and methods of its use.
Bisoprolol is a selective beta1-blocker without its own sympathomimetic activity (SMA); has hypotensive, antiarrhythmic and antianginal effects. By blocking the beta1-adrenergic receptors of the heart in low doses, it reduces the formation of cAMP from ATP stimulated by catecholamines, reduces the intracellular Ca2+ current, has a negative chrono-, dromo-, bathmo- and inotropic effect (reduces the heart rate (HR), inhibits conductivity and excitability, reduces myocardial contractility). With increasing dose, it has a beta2-adrenergic blocking effect. Total peripheral vascular resistance (TPVR) at the beginning of the use of beta-blockers, in the first 24 hours, increases (as a result of a reciprocal increase in the activity of alpha-adrenergic receptors and the elimination of stimulation of beta2-adrenergic receptors), which after 1-3 days returns to the original level, and with prolonged use destination is reduced.
The hypotensive effect is associated with a decrease in minute blood volume (MBV), sympathetic stimulation of peripheral vessels, a decrease in the activity of the renin-angiotensin-aldosterone system (RAAS) (of greater importance for patients with initial hypersecretion of renin), restoration of the sensitivity of the baroreceptors of the aortic arch (there is no increase in their activity in response to a decrease in blood pressure (BP)) and effects on the central nervous system (CNS). In case of arterial hypertension, the effect occurs after 2-5 days, a stable effect occurs after 1-2 months.
The antianginal effect is due to a decrease in myocardial oxygen demand as a result of a decrease in heart rate and decreased contractility, prolongation of diastole, and improved myocardial perfusion. By increasing end-diastolic pressure in the left ventricle and increasing the stretch of ventricular muscle fibers, it can increase oxygen demand, especially in patients with chronic heart failure (CHF).
The antiarrhythmic effect is due to the elimination of arrhythmogenic factors (tachycardia, increased activity of the sympathetic nervous system, increased cAMP content, arterial hypertension), a decrease in the rate of spontaneous excitation of sinus and ectopic pacemakers and a slowdown in atrioventricular (AV) conduction (mainly in the antegrade and to a lesser extent in the retrograde directions through the AV node) and along additional paths.
Unlike non-selective beta-blockers, when prescribed in average therapeutic doses, it has a less pronounced effect on organs containing beta2-adrenergic receptors (pancreas, skeletal muscles, smooth muscles of peripheral arteries, bronchi and uterus) and on carbohydrate metabolism, does not cause Na+ retention in organism; the severity of the atherogenic effect does not differ from the effect of propranolol. When used in large doses, it has a blocking effect on both subtypes of beta-adrenergic receptors.
Composition, dosage and application
1 ml of solution contains:
Active ingredient: netakimab – 60 mg;
Excipients: sodium acetate trihydrate – 1.74 mg, trehalose dihydrate – 80 mg, poloxamer 188 – 0.5 mg, glacial acetic acid – up to pH 5.0, water for injection – up to 1.0 ml.
Indications for use
• Treatment of moderate to severe plaque psoriasis in adult patients when systemic therapy or phototherapy is indicated.
• Treatment of active ankylosing spondylitis in adult patients with insufficient response to standard therapy.
• Treatment of active psoriatic arthritis in monotherapy or in combination with methotrexate in case of insufficient response to standard therapy.
Directions for use and doses
The use of Efleira® should be under the supervision of physicians with experience in treating diseases for which Efleira® is indicated. After appropriate training, it is possible for the patient to administer the drug independently, subject to dynamic supervision by the attending physician.
Efleira® is administered in a dose of 120 mg in the form of two subcutaneous injections of 1 ml of the drug with a concentration of 60 mg/ml.
Treatment of moderate to severe plaque psoriasis in adult patients when systemic therapy or phototherapy is indicated:
The recommended dose is 120 mg in the form of two subcutaneous injections of 1 ml (60 mg) of the drug each administered once a week in weeks 0, 1 and 2, then once every 4 weeks.
Treatment of active ankylosing spondylitis with insufficient response to standard therapy:
The recommended dose is 120 mg in the form of two subcutaneous injections of 1 ml (60 mg) of the drug each. The drug is administered once a week in weeks 0, 1 and 2, then every 2 weeks.
Treatment of active psoriatic arthritis in monotherapy or in combination with methotrexate in case of insufficient response to standard therapy:
The recommended dose is 120 mg in the form of two subcutaneous injections of 1 ml (60 mg) of the drug each. The drug is administered once a week in weeks 0, 1 and 2, then every 2 weeks until week 10 inclusive. Then, from week 14, the drug is administered at a dose of 120 mg in the form of two subcutaneous injections of 1 ml (60 mg) each, once every 4 weeks.
Indication | Single dose | Induction | Maintenance therapy |
Plaque psoriasis | 120 mg | 0, 1, 2 Weeks | Once every 4 weeks, starting from week 6 |
Ankylosing spondylitis | 120 mg | 0, 1, 2 Weeks | Once every 2 weeks, starting from week 4 |
Psoriatic arthritis | 120 mg | 0, 1, 2 Weeks | Once every 2 weeks, starting from week 4 to week 10 inclusive, then once every 4 weeks from week 14 |
If the next injection is missed for any reason, the injection of Efleira® should be given as quickly as possible. The date of the next administration is calculated based on the duration of the delay in administering the drug: if no more than 3 days have passed since the missed administration, then the next injection of the drug must be performed according to the current schedule; if more than 3 days have passed since the missed administration, then a new countdown for the date of the next administration begin from the moment of the actual injection of the drug Efleira®.
Genferon supp 250 thousand IU N10 (Biocard)
GENFERON® is a combination drug, the effect of which is determined by the components included in its composition. Has local and systemic effects. The composition of the drug Genferon® includes recombinant human interferon alpha-2b, produced by a strain of the bacterium Escherichia coli, into which the human interferon alpha-2b gene was introduced using genetic engineering methods. Interferon alpha-2b has antiviral, immunomodulatory, antiproliferative and antibacterial effects. The antiviral effect is mediated by the activation of a number of intracellular enzymes that inhibit viral replication. The immunomodulatory effect is manifested, first of all, by enhancing cell-mediated reactions of the immune system, which increases the effectiveness of the immune response against viruses, intracellular parasites and cells that have undergone tumor transformation. This is achieved through the activation of CD8+ T killer cells, NK cells (natural killer cells), increased differentiation of B lymphocytes and their production of antibodies, activation of the monocyte-macrophage system and phagocytosis, as well as increased expression of molecules of the major histocompatibility complex type I, which increases the likelihood recognition of infected cells by cells of the immune system. Activation under the influence of interferon of leukocytes contained in all layers of the mucous membrane ensures their active participation in the elimination of pathological foci; in addition, due to the influence of interferon, restoration of the production of secretory immunoglobulin A is achieved. The antibacterial effect is mediated by reactions of the immune system, enhanced under the influence of interferon. Taurine helps normalize metabolic processes and tissue regeneration, has membrane-stabilizing and immunomodulatory effects. Being a strong antioxidant, taurine directly interacts with reactive oxygen species, the excessive accumulation of which contributes to the development of pathological processes. Taurine helps maintain the biological activity of interferon, enhancing the therapeutic effect of the drug. Benzocaine (anesthetic) is a local anesthetic. Reduces the permeability of the cell membrane to sodium ions, displaces calcium ions from receptors located on the inner surface of the membrane, and blocks the conduction of nerve impulses. Prevents the occurrence of pain impulses at the endings of sensory nerves and their conduction along nerve fibers. It has an exclusively local effect, without being absorbed into the systemic