Flosterone, 7 mg/ml suspension 1 ml 5 pcs

Name: Flosterone, 7 mg/ml suspension 1 ml 5 pcs
SKU: 98877
Availability: InStock

€46.54

EAN: 3838989505547 SKU: 98877 Categories: Corticosteroid hormones, Medicine, Pain and fever

Treatment of adult patients with conditions and diseases in which GCS therapy allows achieving the necessary clinical effect (it is necessary to take into account that in some diseases GCS therapy is additional and does not replace standard therapy):

– diseases of the musculoskeletal system and soft tissues, including rheumatoid arthritis, osteoarthritis, bursitis, ankylosing spondylitis, epicondylitis, coccygodynia, torticollis, ganglion cyst, fasciitis;

– allergic diseases, including bronchial asthma, hay fever (pollinosis), allergic bronchitis, seasonal or year-round rhinitis, drug allergy, serum sickness, reactions to insect bites;

– dermatological diseases, including atopic dermatitis, nummular eczema, neurodermatitis, contact dermatitis, severe photodermatitis, urticaria, lichen planus, alopecia areata, discoid lupus erythematosus, psoriasis, keloid scars, pemphigus vulgaris, cystic acne;

– systemic connective tissue diseases, including systemic lupus erythematosus, scleroderma, dermatomyositis, periarteritis nodosa;

– hemoblastoses (palliative therapy of leukemia and lymphomas in adult patients, acute leukemia in children);

– primary or secondary adrenal cortex insufficiency (with mandatory simultaneous use of mineralocorticosteroids);

– other diseases and pathological conditions requiring systemic GCS therapy (adrenogenital syndrome, regional ileitis, pathological changes in the blood when GCS therapy is required).

Composition

1 ampoule – 1 ml of injection suspension contains:

Active ingredient:

Betamethasone in the form of:

– betamethasone dipropionate 6.43 mg (which corresponds to 5 mg betamethasone),

– betamethasone sodium phosphate 2.63 mg (which corresponds to 2 mg betamethasone).

Excipients: disodium phosphate dihydrate 2.50 mg, sodium chloride 5.00 mg, disodium edetate 0.10 mg, polysorbate 80 0.50 mg, benzyl alcohol 9.00 mg, methyl parahydroxybenzoate 1.30 mg, propyl parahydroxybenzoate 0.20 mg, sodium croscarmellose 5.00 mg, macrogol (polyethylene glycol) 20.00 mg, hydrochloric acid, concentrated qs. water for injection up to 1.00 ml

Pharmacodynamics

Betamethasone is a synthetic GCS that inhibits the release of interleukin-1, interleukin-2, and gamma interferon from lymphocytes and macrophages. It has anti-inflammatory, antiallergic, desensitizing, anti-shock, antitoxic, and immunosuppressive effects. It inhibits the release of adrenocorticotropic hormone (ACTH) and beta-lipotropin by the pituitary gland, but does not reduce the concentration of beta-endorphin circulating in the blood plasma. It inhibits the secretion of thyroid-stimulating hormone (TSH) and follicle-stimulating hormone (FSH).

Increases excitability of the central nervous system (CNS), reduces the number of lymphocytes and eosinophils. Increases the number of erythrocytes (due to increased production of erythropoietins).

Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus and stimulates the synthesis of matrix ribonucleic acid (RNA), the latter induces the formation of proteins, including linocortin, mediating cellular effects. Linocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, prostaglandins (Pg), leukotrienes, which contribute to inflammation, allergy, etc.

Protein metabolism: reduces the amount of protein in blood plasma (due to globulins) with an increase in the albumin/globulin ratio, increases the synthesis of albumins in the liver and kidneys, and enhances protein catabolism in muscle tissue.

Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.

Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract (GIT), increases the activity of glucose-6-phosphatase, leading to an increase in the flow of glucose from the liver into the blood, increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases, leading to the activation of gluconeogenesis.

Water-electrolyte metabolism: retains Na+ ions and water in the body, stimulates the excretion of K+ ions (mineralocorticosteroid activity), reduces the absorption of Ca2+ from the gastrointestinal tract, “washes out” Ca2+ ions from the bones, increases the excretion of Ca2+ ions by the kidneys.

The anti-inflammatory effect is associated with the suppression of the release of inflammatory mediators by eosinophils; induction of the formation of linocortin and a decrease in the number of mast cells that produce hyaluronic acid; a decrease in capillary permeability; stabilization of cell membranes and organelle membranes (especially lysosomal).

The antiallergic effect develops as a result of suppression of the synthesis and secretion of allergy mediators, inhibition of the release of histamine and other biologically active substances, T- and B-lymphocytes, mast cells from sensitized mast cells and basophils, decreased sensitivity of effector cells to allergy mediators, inhibition of antibody formation, and changes in the body’s immune response.

In chronic obstructive pulmonary disease (COPD), the action is based mainly on inhibition of inflammatory processes, suppression of development or prevention of mucosal edema, inhibition of eosinophilic infiltration of the submucosal layer of bronchial epithelium, deposition of circulating immune complexes in the bronchial mucosa, and inhibition of erosion and desquamation of the mucosa. Increases the sensitivity of beta-adrenergic receptors of small and medium-sized bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces mucus viscosity by inhibiting or reducing its production.

Anti-shock and antitoxic effects are associated with an increase in blood pressure (BP) (due to an increase in the concentration of catecholamines circulating in the blood plasma and restoration of the sensitivity of adrenoreceptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane-protective properties, and activation of liver enzymes involved in the metabolism of endo- and xenobiotics.

The immunosuppressive effect is due to inhibition of cytokine release (interleukin-1, interleukin-2, interferon gamma) from lymphocytes and macrophages. Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous GCS. Suppresses connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.

Betamethasone sodium phosphate is a readily soluble compound that is well absorbed after parenteral administration into tissues and provides a rapid effect. Betamethasone dipropionate has a slower absorption. By combining these salts, it is possible to create a drug with both short-term (but fast) and long-term action.

Depending on the method of administration (intravenous (IV), intramuscular (IM), intraarticular, periarticular, intradermal (ID)) a general or local effect is achieved.

Contraindications

– Hypersensitivity to betamethasone or other components of the drug, or other GCS;

– systemic mycoses;

– intravenous or subcutaneous administration;

– for intra-articular administration: unstable joint, infectious arthritis;

– introduction into infected cavities and into the intervertebral space;

– epidural, intrathecal administration and administration of the drug directly into muscle tendons;

– coagulation disorders (including treatment with anticoagulants);

– simultaneous administration of immunosuppressive doses of the drug with live or attenuated vaccines;

– cerebral edema due to traumatic brain injury;

– breastfeeding period;

– children under 3 years of age (contains gasoline alcohol).

How to take, course of administration and dosage

Intramuscular, intra-articular, periarticular, intrabursal, intradermal, intratissue and intrafocal injections.

The small size of betamethasone dipropionate crystals allows the use of small-diameter needles (up to 26 gauge) for intradermal administration and administration directly into the lesion.

DO NOT INTRODUCE INTRAVENOUSLY! DO NOT INTRODUCE SUBCUTANEOUSLY!

Strict adherence to aseptic rules is mandatory when using the drug Flosteron®.

The dosage regimen and route of administration are determined individually, depending on the indications, severity of the disease and the patient’s response.

For systemic therapy, the initial dose of Flosteron® in most cases is 1-2 ml. The administration is repeated as needed, depending on the patient’s condition.

Intramuscular administration of GCS should be performed deep into the muscle, choosing large muscles and avoiding penetration into other tissues (to prevent atrophic changes).

The drug is administered intramuscularly:

– in severe conditions requiring emergency measures. The initial dose is 2 ml;

– for various dermatological diseases, as a rule, it is sufficient to administer 1 ml of the Flosteron® suspension;

– in respiratory diseases, the onset of action of the drug occurs within a few hours after intramuscular administration of the drug. In bronchial asthma, hay fever, allergic bronchitis and allergic rhinitis, a significant improvement in the condition is achieved after the administration of 1-2 ml of Flosteron®;

– for acute and chronic bursitis. The initial dose for intramuscular administration is 1-2 ml of suspension. If necessary, several repeated injections are administered.

If a satisfactory clinical response does not occur within a certain period of time, Flosteron® should be discontinued and other therapy should be prescribed.

When administered locally, simultaneous use of a local anesthetic is necessary only in rare cases. If desired, 1% or 2% solutions of procaine hydrochloride or lidocaine that do not contain methylparaben, propylparaben, phenol or other similar substances are used. In this case, mixing is performed in a syringe, first drawing the required dose of the Flosteron® suspension from the vial into the syringe. Then the required amount of local anesthetic is drawn from the ampoule into the same syringe and shaken for a short period of time.

In acute bursitis (subdeltoid, subscapular, elbow and prepatellar), the introduction of 1-2 ml of suspension into the synovial sac relieves pain and restores joint mobility within a few hours. After stopping the exacerbation of chronic bursitis, smaller doses of the drug are used.

In acute tendosynovitis, tendinitis and peritendinitis, one injection of Flosteron® improves the patient’s condition; in chronic cases, the injection is repeated depending on the patient’s response. Direct injection of the drug into the tendon should be avoided.

Intra-articular administration of Flosteron® at a dose of 0.5-2 ml relieves pain, limitation of joint mobility in rheumatoid arthritis and osteoarthrosis within 2-4 hours after administration. The duration of the therapeutic effect varies significantly and can be 4 weeks or more.

The recommended doses of Flosteron® for administration into large joints are 1 to 2 ml, into medium joints – 0.5-1 ml, into small joints – 0.25-0.5 ml.

In some dermatological diseases, intravenous administration of Flosteron® directly into the lesion is effective, the dose is 0.2 ml/cm. The lesion is evenly injected using a tuberculin syringe and a needle with a diameter of about 0.9 mm. The total amount of the drug injected into all areas should not exceed 1 ml within 1 week. For administration into the lesion, it is recommended to use a tuberculin syringe with a 25-gauge needle.

Recommended single doses of Flosteron® (with an interval between injections of 1 week) for bursitis: for calluses – 0.25-0.5 ml (as a rule, 2 injections are effective), for spurs – 0.5 ml, for limited mobility of the big toe – 0.5 ml, for synovial cysts – 0.25-0.5 ml, for tendosynovitis – 0.5 ml, for acute gouty arthritis – 0.5-1.0 ml. A tuberculin syringe with a 25-gauge needle is suitable for most injections.

After achieving the therapeutic effect, the maintenance dose is selected by gradually reducing the dose of betamethasone administered at appropriate intervals. The dose of Flosteron® is reduced until the minimum effective dose is reached.

If a stressful situation (not related to the disease) occurs or is threatened, it may be necessary to increase the dose of Flosteron®. The drug is discontinued after long-term therapy by gradually reducing the dose.

The patient’s condition should be monitored for at least one year after the end of long-term therapy or use in high doses.

Special instructions

The dosage regimen and route of administration are determined individually depending on the indications, severity of the disease and the patient’s response.

The dose should be as low as possible and the period of use as short as possible. The initial dose is selected until the desired therapeutic effect is achieved. If after a sufficient period of time the therapeutic effect is not observed, the drug is discontinued by gradually reducing the dose of Flosteron® and another appropriate treatment method is selected.

If a stressful situation (not related to the disease) occurs or is threatened, it may be necessary to increase the dose of Flosteron®.

Discontinuation of the drug after long-term therapy is carried out by gradually reducing the dose.

The patient’s condition should be monitored for at least one year after the end of long-term therapy or use in high doses.

The introduction of the drug into soft tissues, into the lesion and into the joint can, with a pronounced local effect, simultaneously lead to a systemic effect.

Given the likelihood of developing anaphylactoid reactions with parenteral administration of GCS, the necessary precautions should be taken before administering the drug, especially if the patient has a history of allergic reactions to drugs.

The drug Flosteron® contains two active substances – betamethasone derivatives, one of which – betamethasone sodium phosphate – quickly penetrates into the systemic bloodstream. When using the drug Flosteron®, the possible systemic effect of the rapidly soluble fraction of the drug should be taken into account.

Against the background of the use of the drug Flosteron®, mental disorders are possible (especially in patients with emotional instability or a tendency to psychosis).

The effect of GCS is enhanced in patients with liver cirrhosis or hypothyroidism.

When using Flosteron® in patients with diabetes mellitus, correction of hypoglycemic therapy may be required.

Patients receiving GCS should not be vaccinated against smallpox. Other immunizations should not be performed in patients receiving GCS therapy (especially in high doses) due to the possibility of developing neurological complications and a low immune response (lack of antibody formation). Flosteron® should not be administered 8 weeks before and 2 weeks after vaccination with killed or inactivated viral and antibacterial vaccines. However, immunization is possible during replacement therapy (e.g., in primary adrenal cortex insufficiency).

Patients using Flosteron® in immunosuppressant doses should be warned of the need to avoid contact with people with chickenpox and measles (especially important when using the drug in children).

When using Flosteron®, it should be taken into account that GCS can mask the signs of an infectious disease and reduce the body’s resistance to infections. The use of Flosteron® in active tuberculosis is possible only in cases of fulminant or disseminated tuberculosis in combination with adequate anti-tuberculosis therapy. When using Flosteron® in patients with latent tuberculosis or with a positive reaction to tuberculin, the issue of prophylactic anti-tuberculosis therapy should be addressed. When using rifampicin prophylactically, the acceleration of hepatic clearance of betamethasone should be taken into account (dose adjustment may be required).

If there is fluid in the joint cavity, a septic process should be excluded. A noticeable increase in pain, swelling, an increase in the temperature of the surrounding tissues and further limitation of joint mobility indicate infectious arthritis. If the diagnosis is confirmed, antibacterial therapy should be prescribed.

Repeated injections into the joint in osteoarthritis may increase the risk of joint destruction. The introduction of GCS into the tendon tissue gradually leads to tendon rupture. After successful intra-articular therapy, the patient should avoid overloading the joint.

Long-term use of GCS may lead to posterior subcapsular cataract (especially in children), glaucoma with possible damage to the optic nerve and may contribute to the development of secondary eye infection (fungal or viral). Periodic ophthalmological examination is necessary, especially in patients using Flosteron® for more than 6 months.

In case of increased blood pressure, fluid retention and hypernatremia and increased excretion of potassium ions from the body (less likely than with other GCS), patients are recommended a diet with limited table salt and additionally prescribed potassium-containing drugs. All GCS increase the excretion of calcium ions.

When using Flosteron® simultaneously with cardiac glycosides or drugs that affect the electrolyte composition of blood plasma, monitoring of water and electrolyte balance is required.

Acetylsalicylic acid should be used with caution simultaneously with the drug Flosteron® in case of hypoprothrombinemia.

The development of secondary adrenal insufficiency due to too rapid discontinuation of GCS therapy is possible within several months after the end of therapy. If a stressful situation occurs or is threatened during this period, therapy with Flosteron® should be resumed and a mineralocorticosteroid drug should be prescribed simultaneously (due to possible disruption of mineralocorticosteroid secretion). Gradual discontinuation of GCS therapy helps reduce the risk of secondary adrenal insufficiency.

Suppression of the reaction during skin testing may occur with the use of GCS. GCS should be used with caution in patients with hypothyroidism or myasthenia gravis.

Particular caution should be exercised when considering the use of systemic corticosteroids in patients with active herpetic ocular disease (herpes simplex keratitis).

Cases of Kaposi’s sarcoma have been reported in patients receiving GCS; discontinuation of this therapy may result in remission of the disease.

Symptoms of peritoneal irritation or pain relief from perforation of the stomach or intestine may be minimal or absent in patients receiving GCS.

The immunosuppressive effect of GCS may lead to activation of latent infections or exacerbation of intercurrent infections, including infections caused by microorganisms: Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia or Ameba.

Particular caution should be exercised when administering corticosteroids to patients with confirmed or suspected Strongyloides infection. In such patients, corticosteroid-induced immunosuppression may result in Strongyloides hyperinfection and dissemination of infection by larval migration, often accompanied by severe enterocolitis and gram-negative septicemia, possibly fatal.

Because corticosteroids may aggravate latent amebiasis, all patients with unexplained diarrhea or those arriving from tropical climates should be evaluated for amebiasis before initiating corticosteroid therapy.

If a stressful situation (not related to the disease) occurs or is threatened, it may be necessary to increase the dose of Flosteron®; the drugs of choice as an addition should be hydrocortisone and cortisone preparations.

During long-term therapy with GCS, it is advisable to consider the possibility of switching from parenteral GCS to oral GCS, taking into account the assessment of the benefit/risk ratio.

Application in pediatrics

Children undergoing therapy with Flosteron® (especially long-term) should be closely monitored for possible growth retardation and development of adrenal cortex insufficiency.

Fertility

When using GCS, changes in sperm motility and number are possible.

Additional information