Instructions Flosteron suspension for injection ampoule 1 ml No. 5
Composition
active ingredient: 1 ml of suspension (1 ampoule) contains 2 mg of betamethasone in the form of betamethasone disodium phosphate and 5 mg of betamethasone in the form of betamethasone dipropionate;
excipients: sodium hydrogen phosphate dihydrate, sodium chloride, disodium edetate, polysorbate 80, benzyl alcohol, methylparaben (E 218), propylparaben (E 216), carmellose sodium, polyethylene glycols, concentrated hydrochloric acid, water for injections.
Dosage form
Suspension for injection.
Main physicochemical properties: transparent, colorless, slightly viscous liquid containing white particles that are easily suspended and free from foreign particles.
Pharmacotherapeutic group
Corticosteroids for systemic use. Glucocorticoids. ATC code H02A B01.
Pharmacological properties
Pharmacodynamics
Betamethasone is a synthetic corticosteroid with anti-inflammatory and immunosuppressive effects. In addition, it affects energy metabolism, glucose homeostasis, and (via negative feedback) the secretion of hypothalamic-activating factor and alimentary hormone from the adenohypophysis.
Steroids with 1,2 bonds in the A ring and other substituents near C16 of the D ring, 9 alpha-fluoro derivatives, exert strong corticosteroid activity. These substituents near C16 actually reduce mineralocorticoid activity.
The action of corticosteroids is not yet fully understood. There is sufficient evidence to indicate that the main mechanism of their action is at the cellular level. There are two clearly established receptor systems in the cell cytoplasm. Through glucocorticoid receptors, corticosteroids produce anti-inflammatory and immunosuppressive effects and regulate glucose homeostasis, and through mineralocorticoid receptors, they regulate sodium and potassium metabolism and water and electrolyte balance.
Corticosteroids are fat-soluble and readily cross the cell membrane into the target cell. Binding of the hormone to the receptor causes a conformational change in the receptor, which increases its affinity for DNA. The hormone/receptor complex enters the nucleus of the cell and binds to a regulatory region of the DNA molecule known as the glucocorticoid response element (GRE). The activated receptor, bound to the GRE or specific genes, regulates the transcription of mRNA. It can increase or decrease it. The newly formed mRNA is transported to the ribosome, resulting in the production of new proteins. Depending on the target cells and cellular processes, the formation of new proteins can be increased (tyrosine transaminase in liver cells) or decreased (IL-2 in lymphocytes). Since glucocorticoid receptors are present in all tissues, they are thought to act on most cells of the body.
The anti-inflammatory and immunosuppressive effects of corticosteroids are based on molecular and biochemical actions. The molecular anti-inflammatory action is derived from the binding of corticosteroids to glucocorticoid receptors and from changes in the expression of a number of genes that regulate the formation of a number of information molecules, proteins and enzymes involved in the anti-inflammatory response. The biochemical anti-inflammatory action of corticosteroids is derived from preventing the formation and functioning of humoral inflammatory mediators: prostaglandins, thromboxanes, cytokines and leukotrienes. Betamethasone reduces the formation of leukotrienes by releasing arachidonic acid from cellular phospholipids, which is achieved by inhibiting the action of phospholipase A2. The effect on phospholipase is not direct, but through an increase in the concentration of lipocortin (macrocortin), which is an inhibitor of phospholipase A2. The inhibitory effect of betamethasone on prostaglandin and thromboxane formation is the result of its reducing effect on the formation of specific mRNA and cyclooxygenase. In addition, by increasing the concentration of lipocortin, betamethasone reduces the formation of platelet activating factors (PAF). Other biochemical anti-inflammatory effects include a reduction in the formation of tumor necrosis factors TNF and IL-1.
Corticosteroids regulate glucose homeostasis and affect sodium, potassium metabolism, electrolyte and water balance. The anti-inflammatory effect of betamethasone exceeds that of hydrocortisone by 30 times, it has no mineralocorticoid activity.
Pharmacokinetics
Betamethasone disodium phosphate is a readily soluble component that is rapidly absorbed into the tissues and provides a rapid onset of action. Betamethasone dipropionate, which has a slower absorption, provides a prolonged effect.
The combination of these components achieves a rapid and prolonged effect. Depending on the method of administration (intra-articular, periarticular, into the lesion site, intradermally, in some cases intramuscularly), a systemic or local effect is achieved.
After intra-articular administration, the maximum concentration of the betamethasone combination in blood plasma is reached within 30 minutes.
After absorption, topical corticosteroids are metabolized through pharmacokinetic pathways similar to those of systemic corticosteroids. Corticosteroids bind to blood proteins to varying degrees. They are primarily metabolized in the liver and excreted in the urine. Some topical corticosteroids and their metabolites are excreted in the bile.
Metabolites are broken down in the liver, excreted mainly by the kidneys, and only a small part is excreted in the bile.
Indication
Dermatological diseases.
Atopic dermatitis (coin-shaped eczema), neurodermatitis, contact dermatitis, severe solar dermatitis, urticaria, lichen planus, insulin lipodystrophy, alopecia areata, discoid lupus erythematosus, psoriasis, keloid scars, pemphigus vulgaris, herpetic dermatitis, cystic acne.
Rheumatic diseases.
Rheumatoid arthritis, osteoarthritis, bursitis, tendosynovitis, tendonitis, peritendinitis, ankylosing spondylitis, epicondylitis, radiculitis, coccydynia, sciatica, lumbago, torticollis, ganglion cyst, exostosis, fasciitis, acute gouty arthritis, synovial cysts, Morton's disease, cuboid inflammation, foot diseases, bursitis on the background of a hard corn, spurs, stiffness of the big toe.
Allergic conditions.
Bronchial asthma, asthmatic status, hay fever, severe allergic bronchitis, seasonal and aperiodic allergic rhinitis, angioedema, contact dermatitis, atopic dermatitis, serum sickness, hypersensitivity reactions to medications or insect bites.
Collagen diseases.
Systemic lupus erythematosus, scleroderma, dermatomyositis, periarteritis nodosa.
Oncological diseases.
Palliative therapy of leukemia and lymphoma in adults, acute leukemia in children.
Other diseases.
Adrenogenital syndrome, ulcerative colitis, Crohn's disease, sprue, pathological changes in the blood that require corticosteroid therapy, nephritis, nephrotic syndrome.
Primary and secondary adrenal insufficiency (with mandatory simultaneous administration of mineralocorticoids).
Contraindication
Hypersensitivity to betamethasone, to other components of the drug or to other glucocorticosteroids. Systemic mycoses.
Intramuscular administration is contraindicated in patients with idiopathic thrombocytopenic purpura.
Infections at the site of application. Severe myopathies (except myasthenia gravis). Lymphadenitis after BCG vaccination.
Interaction with other medicinal products and other types of interactions
Barbiturates, hydantoins, rifampicin, ephedrine: Concomitant use of phenobarbital, rifampicin, phenytoin, or ephedrine may increase the metabolism of the drug, thereby reducing its therapeutic activity.
Diuretics: combination with diuretics such as thiazides may increase the risk of glucose intolerance. Concomitant administration of Flosteron with diuretics that cause potassium loss increases the risk of hypokalemia.
Oral contraceptives: Concomitant use of oral contraceptives may prolong the half-life of corticosteroids, which increases their biological effects and the incidence of adverse effects.
Cardiac glycosides: Potassium deficiency enhances the effect of glycosides. Concomitant use of glucocorticosteroids and cardiac glycosides increases the risk of arrhythmia or digitalis intoxication (due to hypokalemia).
Saluretics, amphotericin B: additional potassium excretion. Flosteron may enhance potassium excretion caused by amphotericin B. Serum electrolytes, particularly serum potassium, should be carefully monitored in all patients receiving one of these drug combinations.
Coumarin derivatives: the anticoagulant effect is weakened. Simultaneous administration of Flosteron and indirect anticoagulants may lead to changes in blood clotting rate, which requires dose adjustment.
Nonsteroidal anti-inflammatory drugs (NSAIDs): The combined use of glucocorticosteroids with NSAIDs or ethanol and ethanol-containing drugs increases the risk of or increases the severity of gastrointestinal bleeding and ulceration.
Salicylates: Aspirin is known to be harmful to the stomach, and glucocorticoids may mask these adverse effects. The mechanism is unknown. Glucocorticosteroids may reduce plasma concentrations of salicylates when used concomitantly. Patients should be observed for salicylic acid toxicity when corticosteroid dosage is reduced or treatment is discontinued. The combination of corticosteroids with salicylates may increase the incidence and severity of gastrointestinal ulcers. There is an increased risk of gastrointestinal bleeding and ulcers, and a risk of reduced efficacy of aspirin.
Oral antidiabetic agents: lowering blood sugar levels. In diabetic patients, it is sometimes necessary to adapt the dosage of oral antidiabetic agents or insulin, taking into account the hyperglycemic potential of corticosteroids.
Growth hormones: The effect of growth hormones may be reduced or stopped. Concomitant administration of glucocorticosteroids and somatotropin may result in delayed absorption of the latter. Betamethasone doses exceeding 300-450 mcg (0.3-0.45 mg) per m2 of body surface area per day should be avoided during the use of somatotropin.
Chloroquine, hydrochloroquine, mefloquine: increased risk of myopathies and cardiomyopathies.
Isoniazid: Glucocorticoids increase the clearance of isoniazid and reduce its serum concentration.
Bupropion: Concomitant use with systemic glucocorticoids increases the risk of seizures.
Local anesthetics: When using betamethasone topically, the compatibility of added (local) anesthetics should always be checked.
CYP3A inhibitors (including cobicistat-containing products): Concomitant therapy with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic adverse reactions. Concomitant use should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid adverse reactions; in such cases, patients should be monitored for systemic corticosteroid adverse reactions.
Live bacterial or viral vaccines: If glucocorticoid treatment is given 8 weeks before or 2 weeks after active immunization, a reduction or absence of the immunization effect should be expected.
Killed and toxoid vaccines: Inadequate protection from vaccination may be possible. The immune response to vaccination with killed or toxoid vaccines may be absent or reduced during concomitant systemic glucocorticoid therapy. Systemic glucocorticoids in pharmacological doses may suppress the immune response to exposure to pathogens. This may prevent the production of sufficient antibodies (immunoglobulins). The primary immune response is mainly affected, but the secondary immune response may also be impaired.
Impact on laboratory test results.
Corticosteroids may interfere with the nitroblue tetrazolium recovery test and give false-negative results.
When a patient is undergoing treatment with corticosteroids, this should also be taken into account when interpreting biological parameters and tests (skin tests, thyroid hormone levels).
Application features
Flosteron suspension is not intended for intravenous or subcutaneous administration.
In each case, the risks must be compared with the expected therapeutic benefit, and the underlying disease must also be controlled.
Strict adherence to asepsis rules is mandatory when using the drug.
The doctor who prescribes Flosteron must take into account the possibility of systemic effects of the drug.
Any administration of the drug (soft tissue, lesion, intraarticular) can lead to systemic action, as well as pronounced local effects.
It is also necessary to consider the side effects and contraindications of systemic glucocorticoid therapy when used topically, especially at high doses, multiple applications, and when used on large joints.
The composition of the drug Flosteron includes two betamethasone esters, one of which - betamethasone sodium phosphate - is rapidly absorbed from the injection site. Therefore, it should be taken into account that this soluble component of the drug may have a systemic effect.
Symptoms of adrenal insufficiency include discomfort, muscle weakness, mental disorders, drowsiness, muscle and bone pain, peeling skin, shortness of breath, anorexia, nausea, vomiting, fever, hypoglycemia, hypotension, dehydration, and even death after abrupt discontinuation of treatment. Treatment of adrenal insufficiency consists of the use of corticosteroids, mineralocorticoids, water, sodium chloride, and glucose.
Abrupt withdrawal or reduction of the dose during continuous use (in the case of very high doses, after a short period of use) or when the need for corticosteroids increases (due to stress: infection, trauma, surgery) may increase the adrenal insufficiency. In this case, it is necessary to gradually reduce the dosage. In the case of stress, it is sometimes necessary to take corticosteroids again or increase the dosage. Reducing the dosage should be done under strict medical supervision, sometimes it is necessary to monitor the patient's condition for a period of up to 1 year after stopping long-term treatment or using increased doses.
Rare cases of anaphylactoid/anaphylactic reactions with the possibility of shock have been observed in patients receiving parenteral corticosteroids, therefore appropriate precautions should be taken before administering the medicinal product, particularly if the patient has a history of allergy to one of the components of the drug.
With prolonged corticosteroid therapy, a switch from parenteral to oral administration should be considered after assessing the potential benefits and risks.
Intramuscular injections of glucocorticosteroids must be administered deep into the muscle to prevent local tissue atrophy.
Prolonged and repeated use of glucocorticoids in highly loaded joints may exacerbate wear-and-tear changes. It is important to clearly instruct the patient not to overexert the joints after symptomatic improvement while the inflammatory processes are still ongoing.
Special groups of patients at risk
Betamethasone should only be used by diabetics for a short period of time and only under strict medical supervision, given its glucocorticoid properties (transformation of proteins into glucose).
There is an increased effect of glucocorticosteroids in patients with hypothyroidism or cirrhosis of the liver. The use of Flosteron should be avoided in patients with herpetic eye lesions (due to the possibility of corneal perforation).
Mental disorders are possible when using the drug (especially in patients with emotional instability or a tendency to psychosis).
Precautions are necessary in the following cases: nonspecific ulcerative colitis, threat of perforation, abscess or other pyogenic infections; diverticulitis; intestinal anastomoses; gastric and duodenal ulcers; renal failure; arterial hypertension; osteoporosis; myasthenia gravis; glaucoma; acute psychoses; viral and bacterial infections; growth retardation; tuberculosis; Cushing's syndrome; diabetes; heart failure; in the case of difficult-to-treat epilepsy; predisposition to thromboembolism or thrombophlebitis; during pregnancy.
Before starting glucocorticoid therapy, the patient should be thoroughly examined, in particular to exclude gastric and duodenal ulcers. For the prevention of gastrointestinal ulcers, the appointment of drugs that suppress acidity and careful observation are indicated.
During any long-term glucocorticoid therapy, regular checks of blood sugar and blood clotting, as well as X-ray examinations of the spine and ophthalmological examinations, are necessary.
In the case of long-term treatment, in addition to disease-related monitoring, monitoring of possible side effects should be carried out at appropriate intervals, depending on the dosage and the initial condition of the patient.
Such control is mandatory for concomitant therapy of the underlying disease: diabetes mellitus, tuberculosis, acute and chronic bacterial and amoebic infections, hypertension, thromboembolic processes, heart and renal failure, acute glomerulonephritis and chronic nephritis.
Glucocorticoid therapy should only be administered with all precautions, if concomitant treatment to control the underlying disease is possible (antidiabetic, tuberculostatic, antibiotics, anticoagulants, etc.).
Since complications of corticosteroid treatment depend on the dose and duration of treatment, the risk-benefit ratio must be considered for each patient when choosing the dose and duration of treatment.
Patients receiving glucocorticosteroid therapy should not be vaccinated against smallpox. Other immunizations should not be given to patients receiving corticosteroids (especially in high doses) due to the risk of neurological complications and low immune response (lack of antibody formation). Immunization is possible in cases of replacement therapy (e.g., Addison's disease).
Patients, particularly children, receiving Flosteron in doses that suppress immunity should avoid contact with patients with chickenpox and measles.
Corticosteroids may mask some signs of infectious disease or make it more difficult to detect infection. New infections may occur during use due to decreased resistance.
The drug should only be used in active tuberculosis in cases of transient or disseminated tuberculosis in combination with adequate anti-tuberculosis therapy. If corticosteroids are prescribed to patients with latent tuberculosis or those who respond to tuberculin, strict monitoring is necessary, since relapse of the disease is possible. With prolonged therapy with corticosteroids, patients should also receive chemoprophylaxis. If patients use rifampicin in a chemoprophylaxis program, the potentiating effect of corticosteroids on metabolic clearance in the liver should be monitored; corticosteroid dosage adjustment may be necessary.
Prolonged use of glucocorticosteroids may lead to the development of posterior subcapsular cataracts (especially in children), glaucoma with possible damage to the optic nerve, and may cause the development of secondary eye infections (fungal or viral). Regular ophthalmological examinations are necessary, especially for patients receiving Flosteron for more than 6 weeks.
Results from a single, multicenter, randomized, controlled trial of another corticosteroid (methylprednisolone hemisuccinate) showed an increase in early mortality (at 2 weeks) and late mortality (at 6 months) in patients with traumatic brain injury who received methylprednisolone compared with placebo. The causes of mortality in the methylprednisolone group were not determined. This trial did not include patients who had a direct indication for corticosteroids.
Moderate and high doses of corticosteroids can cause increased blood pressure, fluid and sodium retention in the tissues, and increased potassium excretion (which may manifest as edema and cardiac dysfunction). These effects are less likely with synthetic derivatives unless used in high doses. A salt-restricted diet and potassium supplements are recommended. All corticosteroids increase calcium excretion.
Acetylsalicylic acid should be taken with caution in combination with the drug for hypoprothrombinemia due to the possibility of increased bleeding.
It is also necessary to remember the possibility of developing secondary adrenal insufficiency within several months after the end of therapy.
When using glucocorticosteroids, changes in sperm motility and number are possible.
Vision impairment
Visual impairment may occur with systemic and topical corticosteroids. If symptoms such as blurred vision or other visual disturbances occur, the patient should be evaluated by an ophthalmologist to evaluate possible causes of visual impairment, which may include cataracts, glaucoma, or rare conditions such as central serous chorioretinopathy, which have been reported following the use of systemic and topical corticosteroids.
Cases of pheochromocytoma crisis, which can be fatal, have been reported following the use of systemic corticosteroids. Corticosteroids should be prescribed to patients with suspected or established pheochromocytoma only after a risk/benefit assessment.
The excipient benzyl alcohol contained in Flosteron is contraindicated in infants and children under 3 years of age. This drug should not be used in premature infants or full-term newborns.
Since corticosteroids can retard growth in children, including infants, and suppress endogenous corticosteroid production, it is important to carefully monitor the growth and development of children during long-term treatment.
Methylparaben and propylparaben usually cause delayed-type reactions, such as contact dermatitis, and rarely cause immediate reactions, such as urticaria and bronchospasm.
This medicinal product contains less than 1 mmol (23 mg) sodium/dose, i.e. essentially 'sodium-free'.
Use during pregnancy or breastfeeding
Due to the lack of controlled studies on the safety of the drug for pregnant women, breastfeeding women, and women of reproductive age, Flosteron should be prescribed after careful assessment of the benefit to the mother and the possible potential risk to the fetus/child.
Pregnancy
When prescribing corticosteroids in the prenatal period, the benefits and drawbacks of such treatment and the clinical effect should be weighed against side effects (including growth retardation and increased risk of infections).
In some cases, it is necessary to continue treatment with corticosteroids during pregnancy or even increase the dosage (for example, in the case of corticosteroid replacement therapy).
Intramuscular administration of betamethasone leads to a significant reduction in the incidence of dyspnea in the fetus if the drug is administered more than 24 hours before delivery (before the 32nd week of pregnancy).
Published data indicate that the issue of prophylactic use of corticosteroids after 32 weeks of gestation is still controversial. Therefore, when prescribing corticosteroids after 32 weeks of gestation, the physician should weigh all the benefits of such treatment against the potential risks to the woman and fetus.
Corticosteroids are not prescribed to treat hyaline membrane disease in newborns.
In the case of prophylactic treatment of hyaline membrane disease in premature infants, corticosteroids should not be administered to pregnant women with preeclampsia and eclampsia or those with placental involvement.
Children born to mothers who received high doses of corticosteroids during pregnancy should be monitored for early signs of adrenal insufficiency.
When betamethasone was administered to pregnant women before delivery, transient inhibition of fetal growth hormone and possibly pituitary hormones that regulate steroid production was observed in the infants, both in the definitive and fetal zones of the adrenal glands in the fetus. However, inhibition of fetal hydrocortisone production did not affect the pituitary-adrenal stress response after delivery.
Women who have received corticosteroids during pregnancy should be monitored during and after labor and delivery for early detection of adrenal insufficiency due to the stress of childbirth.
Studies have shown an increased risk of neonatal hypoglycemia after antenatal administration of a short course of betamethasone in women at risk of late preterm birth.
Breast-feeding
Corticosteroids cross the placental barrier and are excreted in breast milk.
If it is necessary to prescribe the drug Flosteron, the issue of stopping breastfeeding or stopping therapy should be decided, taking into account the importance of therapy for the mother (due to possible undesirable side effects in children).
Ability to influence reaction speed when driving vehicles or other mechanisms
Usually, Flosteron does not affect the patient's reaction speed when driving or working with other mechanisms, but in rare cases, muscle weakness, seizures, visual disturbances, dizziness, headache, mood changes, depression (with pronounced psychotic reactions), increased irritability may occur, therefore it is recommended to refrain from driving or working with other mechanisms during treatment with the drug.
Method of administration and doses
Flosteron is recommended to be administered intramuscularly if systemic administration of glucocorticosteroid is necessary; directly into the affected soft tissue or as intraarticular and periarticular injections for arthritis; as intradermal injections for various skin diseases; as local injections into the lesion for some foot diseases.
The dosage regimen and method of administration are determined by the doctor individually depending on the indications, severity of the disease and the patient's response to treatment.
The dose should be minimal, and the period of use should be as short as possible.
The dose should be adjusted to obtain a satisfactory clinical effect. If a satisfactory clinical effect is not achieved within a certain period of time, treatment with the drug should be discontinued by progressive dose reduction and other appropriate therapy should be instituted.
In the event of a favorable response, an appropriate dose should be determined and maintained by gradually reducing the initial dose at appropriate intervals until the lowest dose with an adequate clinical response is reached.
Flosteron suspension is not intended for intravenous or subcutaneous administration.
Systemic application.
The initial dose of the drug in most cases is 1-2 ml. The injection is repeated if necessary, depending on the patient's condition. The drug is administered deep intramuscularly into the buttock:
- in severe conditions (lupus erythematosus and asthmatic status) requiring emergency measures, the initial dose of the drug may be 2 ml;
- for various dermatological diseases, 1 ml of the drug is usually sufficient;
- in diseases of the respiratory system, the effect of the drug begins within several hours after intramuscular injection of Flosteron; 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 the drug;
- for acute and chronic bursitis, the dose for intramuscular administration is 1-2 ml of the drug. If necessary, several repeated injections are performed.
Local application.
The simultaneous use of a local anesthetic is necessary only in rare cases (the injection is almost painless). If simultaneous administration of an anesthetic is desired, a 1% or 2% solution of procaine hydrochloride or lidocaine, or similar local anesthetics, should be used, using dosage forms that do not contain parabens. Anesthetics containing methylparaben, propylparaben, phenol and other similar substances are not allowed. When using an anesthetic in combination with the drug Flosterons, first draw the required dose of the drug from the vial into the syringe, then draw the required amount of local anesthetic from the ampoule into the same syringe and shake the syringe for a short period of time.
In acute bursitis (subdeltoid, subscapular, ulnar, and anteropopliteal), injecting 1-2 ml of Flosteron into the synovial bursa can relieve pain and fully restore mobility within a few hours.
Chronic bursitis should be treated with lower doses of the drug after the acute attack of the disease has subsided.
In acute tendosynovitis, tendinitis and peritendinitis, a single injection of Flosteron alleviates the patient's condition, in chronic cases, the injection of the drug should be repeated depending on the reaction. It is necessary to avoid administering the drug directly into the tendon.
In rheumatoid arthritis and osteoarthritis, intra-articular administration of the drug in a dose of 0.5-2 ml reduces pain, tenderness, and stiffness of the joints within 2-4 hours after administration. The duration of the therapeutic effect of the drug varies significantly and can be 4 weeks or more.
In case of dermatological diseases, intradermal administration of the drug directly into the lesion is effective. Inject 0.2 ml/cm2 of Flosteron into the skin (not under the skin) using a tuberculin syringe and a needle with a diameter of approximately 0.9 mm. The total amount of the drug injected into the injection site should not exceed 1 ml.
In case of corticosteroid-sensitive foot diseases. Bursitis under the corn can be overcome by two consecutive injections of 0.25 ml each. In diseases such as hallux valgus, hallux valgus and acute gouty arthritis, relief can come very quickly.
Recommended single doses of Flosteron (with an interval of 1 week between injections): for hard corns – 0.25-0.5 ml; for spurs – 0.5 ml; for stiffness of the big toe – 0.5 ml; for varus little toe – 0.5 ml; for synovial cysts – from 0.25 to 0.5 ml; for tendosynovitis – 0.5 ml; for cuboid inflammation – 0.5 ml; for acute gouty arthritis – from 0.5 to 1 ml. It is recommended to use a tuberculin syringe with a needle with a diameter of approximately 1 mm for administration.
If a stressful situation (not related to the disease) occurs or is threatened, it may be necessary to increase the dose of the drug.
Discontinuation of the drug after long-term therapy should be carried out by gradually reducing the dose. The patient's condition should be monitored for at least a year after the end of long-term therapy or after using the drug in high doses.
Children
There is insufficient clinical data on the use of the drug in children, therefore it is undesirable to use it in patients of this age category (possible growth retardation and development of secondary adrenal insufficiency).
Since corticosteroids may retard growth in children, including infants, and suppress endogenous corticosteroid production, it is important to carefully monitor the growth and development of children during long-term treatment.
Overdose
Acute overdose of betamethasone does not create life-threatening situations. The administration of high doses of glucocorticosteroids for several days does not lead to undesirable consequences (except in cases of very high doses or in the case of use in diabetes mellitus, glaucoma, exacerbation of erosive-ulcerative lesions of the gastrointestinal tract, or in the case of use in patients who are simultaneously undergoing therapy with cardiac glycosides, indirect anticoagulants or potassium-sparing diuretics).
Treatment. Careful medical monitoring of the patient's condition is required. It is necessary to maintain optimal fluid intake and monitor the electrolyte content in blood plasma and urine (especially the balance of sodium and potassium in the body). If an imbalance of these ions is detected, appropriate therapy should be carried out.
Adverse reactions
Adverse reactions, as with other glucocorticosteroids, are dose- and duration-related. These reactions are usually reversible and can be reduced by reducing the dose.
On the part of the immune system: increased susceptibility to infections and severity of infections with suppression of clinical symptoms and signs, hypersensitivity reactions (shock-like conditions, drop in blood pressure), anaphylactic and anaphylactoid reactions.
On the part of the endocrine system: clinical symptoms of Cushing's syndrome; fetal or child growth retardation; impaired carbohydrate tolerance; manifestations of latent diabetes mellitus; complications of existing diabetes mellitus, secondary adrenocortical and pituitary insensitivity, especially during stress, for example, during trauma, surgery or illness, menstrual disorders.
