Dexamethasone solution for injection 4mg/ml 2ml ampoules, 10pcs

Composition

Per 1 ml:

Active ingredient:

dexamethasone sodium phosphate (in terms of dexamethasone phosphate) -4.0 mg.

Auxiliary substances:  glycerol (glycerin distilled PC-94) – 22,5 mg, sodium hydrogen phosphate, dodecahydrate (sodium disodium phosphate 12-water) of -0.8 mg; disodium edetate dihydrate [(disodium salt of Ethylenediamine-N, N, N’, N’ – tetraoxane acid 2-water (Trilon B)],0.1 mg; water for injection – up to 1 ml.

Pharmacological properties

Pharmacotherapeutic group: glucocorticosteroid ATX: N 02 AB 02 Pharmacological properties

Pharmacodynamics

Dexamethasone is a synthetic hormone of the adrenal cortex, a glucocorticosteroid( GCS), and a methylated derivative of fluoroprednisolone. It has anti-inflammatory, anti-allergic, desensitizing, anti-shock, antitoxic and immunosuppressive effects.

It interacts with specific cytoplasmic GCS receptors to form a complex that penetrates the cell nucleus and stimulates the synthesis of matrix ribonucleic acid, the latter induces the formation of proteins, including lipocortin, that mediate cellular effects. Lipokortin inhibits the phospholipase A-2, inhibits the release of arachidonic acid synthesis and inhibits endoperekisey, prostaglandins, leukotrienes that promote inflammation, allergies, etc.

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

Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation occurs 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, which leads to an increase in glucose intake from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases, which leads to the activation of gluconeogenesis.

Water-electrolyte metabolism: detains sodium and water in the body, stimulates the excretion of potassium (mineralocorticoid activity), reduces the absorption of calcium from the gastrointestinal tract, “washes” calcium from the bones, increases the excretion of calcium by the kidneys.

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

The anti-allergic effect develops as a result of suppressing the synthesis and secretion of allergy mediators, inhibiting the release of histamine and other biologically active substances from sensitized mast cells and basophils, reducing the number of circulating basophils, suppressing the development of lymphoid and connective tissue, reducing the number of T and B lymphocytes, mast cells, reducing the sensitivity of effector cells to allergy mediators, inhibiting antibody formation, and changing the body’s immune response.

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

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

The immunosuppressive effect is caused by inhibition of the release of cytokines (interleukin-1 and interleukin-2, interferon gamma) from lymphocytes and macrophages.

Dexamethasone has 30 times more pronounced effects than endogenous cortisol. Therefore, it is a more potent inhibitor of the secretion of corticotropin-releasing hormone and adrenocorticotropic hormone (ACTH). In pharmacological doses, it inhibits the hypothalamic-pituitary-adrenal system, contributes to the development of secondary adrenal insufficiency. Inhibits the synthesis and release of ACTH by the pituitary gland and, secondarily, the synthesis of endogenous corticosteroids. Inhibits the secretion of thyroid-stimulating hormone and follicle-stimulating hormone. It suppresses the release of beta-lipotropin, but does not reduce the content of circulating beta-endorphin.

It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.

Increases the excitability of the central nervous system. Reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (by stimulating the production of erythropoietins).

The peculiarity of the action is a significant inhibition of pituitary function and almost complete absence of mineralocorticoid activity.

Pharmacokinetics of adsorption The maximum concentration of dexamethasone in blood plasma is reached as early as 5 minutes after intravenous use and 1 hour after intramuscular use.

Distribution due to plasma proteins (mainly albumins) – 77%. Penetrates through the blood-brain and placental barriers. The plasma half-life (T 1/2) is 190 min.

Metabolismmetabolized in the liver. A small amount of dexamethasone is metabolized in the kidneys and other organs.

Elimination About 65% of the dose is excreted by the kidneys within 24 hours.

Time of development of the clinical effectin case of intravenous application, the effect develops quickly; with intramuscular application, the clinical effect develops in 8 hours. The effect is prolonged: from 17 to 28 days after intramuscular application and from 3 days to 3 weeks after topical application. When applied topically to the joints or soft tissues (in the affected areas), absorption is slower than when applied intramuscularly.

Indications

Replacement therapy for adrenal insufficiency (in combination with sodium chloride and / or mineralocorticosteroids): acute insufficiency of the adrenal cortex (Addison’s disease, bilateral adrenalectomy); relative insufficiency of the adrenal cortex that develops after discontinuation of corticosteroid treatment; primary or secondary insufficiency of the adrenal cortex.

Symptomatic and pathogenetic therapy of other diseases requiring the introduction of fast-acting corticosteroids, as well as in cases where oral use of the drug is impossible:

– endocrine diseases (congenital hyperplasia of the adrenal cortex, subacute thyroiditis);- shock (burn, traumatic, surgical, toxic) – if vasoconstrictors, plasma-substituting drugs and other symptomatic therapy are ineffective;- cerebral edema (only after confirmation of symptoms of increased intracranial pressure by the results of magnetic resonance or computed tomography), caused by a brain tumor during traumatic brain injury, neurosurgical intervention, brain hemorrhage, encephalitis, meningitis, radiation damage; – asthmatic status; severe bronchospasm (exacerbation of bronchial asthma);- severe allergic reactions, anaphylactic shock; – rheumatic diseases; – systemic connective tissue diseases; – acute severe dermatoses;- malignant diseases (palliative treatment of leukemia and lymphoma in adult patients; acute leukemia in children; hypercalcemia in patients with malignant tumors, if oral treatment is not possible);- blood diseases (acute hemolytic anemia, agranulocytosis, idiopathic thrombocytopenic purpura in adults);- in ophthalmic practice (subconjunctival, retrobulbar or parabulbar use): keratitis, keratoconjunctivitis without epithelial damage, iritis, iridocyclitis, blepharitis, blepharoconjunctivitis, scleritis, episcleritis, inflammatory process after eye injuries and surgical interventions, sympathetic ophthalmia, immunosuppressive treatment after corneal transplantation; – local application (in the area of pathological formation): keloids, discoid lupus erythematosus, ring-shaped granuloma; – poisoning with cauterizing fluids (reduction of inflammatory phenomena and prevention of cicatricial constrictions).

Use during pregnancy and lactation

Dexamethasone passes through the placenta and can reach high concentrations in the fetus. During pregnancy (especially in the first trimester) or in women planning pregnancy, Dexamethasone is indicated if the expected therapeutic effect of the drug exceeds the risk of negative effects on the mother or fetus. Corticosteroids should be prescribed during pregnancy only for absolute indications, With prolonged therapy during pregnancy, the possibility of impaired fetal growth is not excluded. If used at the end of pregnancy, there is a risk of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in the newborn.

A small amount of dexamethasone passes into breast milk.

If it is necessary to carry out treatment with the drug during breastfeeding, breast-feeding should be discontinued, since this may lead to a delay in the growth of the child and a decrease in the secretion of its endogenous corticosteroids.

Contraindications

For short-term use for “vital” indications, the only contraindication is hypersensitivity to any of the components of the drug. Breast-feeding period, systemic mycoses. Concomitant use of live or attenuated vaccines with immunosuppressive doses of Dexamethasone.

With caution

Systemic parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently transmitted, including recent contact with the patient) – herpes simplex, herpes zoster (viremic phase), chickenpox, measles; amoebiasis, strongyloidosis (established or suspected); active or latent tuberculosis. Use in severe infectious diseases is permissible only against the background of specific antimicrobial therapy.

Vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination. Immunodeficiency conditions (including AIDS or HIV infection).

Diseases of the gastrointestinal tract: peptic ulcer of the stomach and duodenum 12, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with the threat of perforation or abscess formation, diverticulitis.

Liver failure.

Hypoalbuminemia and conditions predisposing to its occurrence.

Diseases of the cardiovascular system, including recent myocardial infarction, decompensated chronic heart failure, arterial hypertension, hyperlipidemia.

Endocrine diseases – diabetes mellitus (including impaired carbohydrate tolerance), thyrotoxicosis, hypothyroidism, Itsenko-Cushing’s disease, and grade III-IV obesity.

Severe chronic renal failure, nephrourolithiasis.

Systemic osteoporosis, myasthenia gravis, polio (except for the form of bulbar encephalitis), epilepsy, “steroid” myopathy.

Acute psychosis, severe affective disorders (including in the anamnesis, especially “steroid” psychosis).

Open-and closed-angle glaucoma, herpes of the eyes (risk of corneal perforation).

Pregnancy.

Elderly patients – due to a high risk of developing osteoporosis and arterial hypertension.

In children during the growth period, dexamethasone should be used only for absolute indications and under the careful supervision of the attending physician.

Side effects

The frequency of development and severity of side effects depend on the duration of use, the amount of dose used and the possibility of observing the circadian rhythm of use.

Endocrine system disorders: reduced glucose tolerance, “steroid” diabetes mellitus or latent diabetes mellitus, adrenal suppression, Itsenko-Cushing syndrome (moon-shaped face, pituitary-type obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis, “steroid” striae), delayed sexual development in children.

Disorders of the blood and lymphatic system: moderate leukocytosis, lymphopenia, eosinopenia, polycythemia.

Disorders of the gastrointestinal tract: nausea, vomiting, pancreatitis, “steroid” ulcers of the stomach and duodenum, erosive esophagitis, bleeding and perforation of the stomach or intestines, increased or decreased appetite, flatulence, hiccups, abdominal pain, stomach discomfort. In rare cases-increased activity of “hepatic” transaminases and alkaline phosphatase.

Disorders of the heart and blood vessels: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or aggravation of the course of chronic heart failure; changes in the electrocardiogram characteristic of hypokalemia; increased blood pressure, hypercoagulation, thrombosis; with intravenous use: “hot flashes” to the face, vasculitis, increased capillary fragility. In patients with acute and subacute myocardial infarction-the spread of the focus of necrosis, slowing the formation of scar tissue, which can lead to rupture of the heart muscle.

Mental disorders: nervousness or restlessness, insomnia, emotional lability, delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, suicidal tendencies.

Nervous system disorders: increased intracranial pressure, dizziness, headache, vertigo, pseudotumor cerebellum, convulsions.

Visual disturbances: sudden loss of vision (with parenteral use in the head, neck, nasal concha, and scalp areas, crystals of the drug may be deposited in the vessels of the eye), posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, a tendency to develop secondary bacterial, fungal, or viral eye infections, trophic changes in the cornea, exophthalmos, chemosis, ptosis, mydriasis, corneal perforation, central serous chorioretinopathy.

Metabolic and nutritional disorders: hypercholesterolemia, increased calcium excretion, hypocalcemia, weight gain, negative nitrogen balance (increased protein breakdown), increased sweating, epidural lipomatosis.

Due to mineralocorticoid activity-fluid and sodium retention (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).

Musculoskeletal and connective tissue disorders: slowing of growth and ossification processes in children (premature closure of epiphyseal growth zones), osteoporosis (very rarely – pathological bone fractures, aseptic necrosis of the head of the humerus and femur), rupture of muscle tendons, “steroid” myopathy, decreased muscle mass (atrophy).

Kidney and urinary tract disorders: leukocyturia.

Skin and subcutaneous tissue disorders: delayed wound healing, petechiae, ecchymosis, skin thinning, hyper-or hypopigmentation, “steroid” acne, “steroid” striae, tendency to develop pyoderma and candidiasis, rosacea-like perioral dermatitis, suppression of reactions during skin tests, telangiectasia, hypertrichosis.

Immune system disorders: generalized (skin rash, itchy skin, anaphylactic shock), local allergic reactions.

Infectious and parasitic diseases: the development or exacerbation of infections (the appearance of this side effect is promoted by jointly used immunosuppressants and vaccination).

General disorders and disorders at the injection site: withdrawal syndrome, local with parenteral use: burning, numbness, pain, paresthesia and infection at the injection site, rarely-necrosis of surrounding tissues, scarring at the injection site; atrophy of the skin and subcutaneous tissue with intravenous use (especially dangerous introduction to the deltoid muscle).

Interaction

Dexamethasone is pharmacologically incompatible with other medicinal products (it can form insoluble compounds). It is recommended to be administered separately from other drugs (IV bolus, or through another dropper, as a second solution). When dexamethasone solution is mixed with heparin, a precipitate is formed.

Dexamethasone-increases the toxicity of cardiac glycosides (due to the resulting hypokalemia, the risk of arrhythmias increases).

Accelerates the elimination of acetylsalicylic acid, reduces the content of its metabolites in the blood (when dexamethasone is discontinued, the concentration of salicylates in the blood increases and the risk of side effects increases).

Concomitant use with live antiviral vaccines and other types of immunizations increases the risk of virus activation and infection.

Increases the metabolism of isoniazid, mexiletine (especially in “fast acetylators”), which leads to a decrease in their concentrations in blood plasma.

Increases the risk of developing hepatotoxic effects of paracetamol (induction of liver enzymes and formation of a toxic metabolite of paracetamol).

Increases (with long-term therapy) the content of folic acid.

Dexamethasone-induced hypokalemia may increase the severity and duration of muscle block with muscle relaxants.

In high doses, it reduces the effect of somatropin.

Dexamethasone reduces the effect of hypoglycemic drugs; increases the anticoagulant effect of coumarin derivatives.

Weakens the effect of vitamin D on the absorption of calcium in the intestinal lumen. Ergocalciferol and parathyroid hormone inhibit the development of dexamethasone-induced osteopathy.

Reduces the concentration of praziquantel in the blood.

Cyclosporine (inhibits metabolism) and ketoconazole (reduces clearance) increase toxicity.

Thiazide diuretics, carbonic anhydrase inhibitors, other corticosteroids and amphotericin B increase the risk of hypokalemia, Na-containing drugs-edema and increased blood pressure.

Nonsteroidal anti-inflammatory drugs (NSAIDs) and ethanol increase the risk of gastrointestinal mucosal ulceration and bleeding; in combination with NSAIDs for the treatment of arthritis, a reduction in the dose of corticosteroids is possible due to the summation of the therapeutic effect.

Indomethacin, by displacing dexamethasone from the albumin bond, increases the risk of side effects.

Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis. The therapeutic effect of dexamethasone decreases under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin, etc. inducers of microsomal liver enzymes (increased metabolic rate). Mitotan and other adrenal cortical inhibitors may require an increased dose of dexamethasone.

Dexamethasone clearance increases with the use of thyroid hormone preparations.

Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders caused by the Epstein-Barr virus.

Estrogens (including oral estrogen-containing contraceptives) reduce the clearance of dexamethasone, prolong the half-life and their therapeutic and toxic effects.

The appearance of hirsutism and acne is promoted by the simultaneous use of other steroid hormonal drugs-androgens, estrogens, anabolics, oral contraceptives.

Tricyclic antidepressants may increase the severity of depression caused by dexamethasone (not indicated for the treatment of these side effects).

The risk of developing cataracts increases when used against the background of other corticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine. Concomitant use with m-holinoblokatorami (including antihistamines, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.

When used concomitantly with fluoroquinolones, the risk of tendopathy (mainly Achilles tendon) increases in elderly patients and in patients with tendon diseases.

Antimalarials (chloroquine, hydroxychloroquine, mefloquine) in combination with dexamethasone may increase the risk of developing myopathy, cardiomyopathy.

Angiotensin-converting enzyme inhibitors, when administered concomitantly with dexamethasone, may alter the composition of peripheral blood.

How to take, course of use and dosage

The dosage regimen is individual and depends on the indications, the patient’s condition and his response to therapy. The drug is administered intravenously (iv) slowly in a jet or drip (in acute and urgent conditions); intramuscularly (iv); local (in a pathological formation) and subconjunctival, retrobulbar or parabulbar use is also possible.

An isotonic sodium chloride solution or 5% dextrose solution should be used to prepare the solution for intravenous infusion.

The drug is administered intravenously and intramuscularly at a dose of 0.5-24 mg / day in 2 divided doses (equivalent to 1/3 – 1/2 oral dose) in the shortest possible course at the minimum effective dose, treatment is discontinued gradually. If high doses are used for more than a few days, the dose of the drug should be gradually reduced over the next few days or longer. Long-term treatment should be carried out at a dose not exceeding 0.5 mg / day. Intramuscularly, no more than 2 ml of the solution is administered in the same place.

In case of emergency, it is used in higher doses: the initial dose is 4-20 mg, which is repeated until the desired effect is achieved, the total daily dose rarely exceeds 80 mg. After the therapeutic effect is achieved, dexamethasone is administered 2-4 mg if necessary, followed by gradual discontinuation of the drug. To maintain a long-term effect, the drug is administered every 3-4 hours or as a long-term drip infusion. After acute conditions are relieved, the patient is transferred to oral dexamethasone.

In case of shock, strictly intravenous bolus is administered at a dose of 2-6 mg / kg. If necessary, repeated doses are administered every 2-6 hours or as a long-term intravenous infusion at a dose of 3 mg / kg / day. Treatment with dexamethasone should be carried out as part of a complex shock therapy. The use of pharmacological doses is permissible only in life-threatening conditions, and, as a rule, this time does not exceed 48 – 72 hours.

With cerebral edema, an initial dose of 10 mg is administered intravenously, then 4 mg every 6 hours until symptoms stop (usually within 12-24 hours). After 2-4 days, the dose is reduced and the drug is gradually discontinued for 5-7 days.

Patients with malignant neoplasms may require maintenance treatment-2 mg iv or iv 2-3 times a day.

In acute cerebral edema, short-term intensive therapy is carried out: for adults, the loading dose is 50 mg IV, then 8 mg every 2 hours is administered on day 1-3,4 mg every 2 hours on day 4,4 mg every 4 hours on day 5-8, then the daily dose is reduced by 4 mg/day until it is completely canceled. In children with a body weight of more than 35 kg, the loading dose is 25 mg IV, then 4 mg every 2 hours is administered on day 1-3,4 mg every 4 hours on day 4,4 mg every 6 hours on day 5-8, then the daily dose is reduced by 2 mg/day until it is completely canceled. In children with a body weight of less than 35 kg, the loading dose is 20 mg IV, then 4 mg every 3 hours is administered on day 1-3,4 mg every 6 hours on day 4,2 mg every 6 hours on day 5-8, then the daily dose is reduced by 1 mg/day until it is completely canceled. In acute self-limiting allergic reactions or exacerbation of chronic allergic diseases, parenteral and oral use of dexamethasone is combined: day 1-iv 4-8 mg, day 2-3-inside 1 mg 2 times a day, day 4-5-inside 0.5 mg 2 times a day, day 6-7-inside 0.5 mg once. On the 8th day, the effectiveness of therapy is evaluated.

Doses of the drug for children (i / m): the dose of the drug during replacement therapy (for adrenal cortex insufficiency) is 0.0233 mg/kg of body weight or 0.67 mg/m2 of body surface area, divided into 3 doses, every 3rd day or 0.00776-0.01165 mg/kg of body weight or 0.233-0.335 mg/m2 of body surface area daily. For other indications, the recommended dose is 0.02776 to 0.16665 mg / kg of body weight or 0.833-5 mg/m2 of body surface area every 12-24 hours.

Overdose

Symptoms: increased blood pressure, peripheral edema, peptic ulcer, hyperglycemia, impaired consciousness. Treatment: symptomatic, no specific antidote.

Description

Transparent colorless or yellowish liquid.

Special instructions

During treatment with dexamethasone (especially long-term), it is necessary to monitor the optometrist, monitor blood pressure and the state of water and electrolyte balance, as well as the picture of peripheral blood and blood glucose levels.

In order to reduce side effects, it is necessary to increase the intake of K+ in the body (diet, potassium preparations). Food should be rich in protein, vitamins, with a limited content of fats, carbohydrates and table salt.

The effect of the drug is enhanced in patients with cirrhosis of the liver. It should be taken into account that dexamethasone clearance decreases in patients with hypothyroidism, and increases in patients with thyrotoxicosis.

The drug may increase existing emotional instability or psychotic disorders. If a history of psychosis is indicated, dexamethasone in high doses is prescribed under strict medical supervision.

It should be used with caution in acute and subacute myocardial infarction – it is possible to spread the focus of necrosis, slow the formation of scar tissue and rupture of the heart muscle.

The patient should be carefully monitored for one year after the end of long-term dexamethasone therapy due to the possible development of relative insufficiency of the adrenal cortex in stressful situations.

Long-term use of high doses of the drug requires a gradual reduction in the dose in order to prevent the development of acute adrenal insufficiency.

When using dexamethasone, there is a risk of developing severe anaphylactic reactions, bradycardia.

Against the background of drug therapy, the risk of activation of strongyloidosis increases.

The dose of dexamethasone should be temporarily increased in stressful situations during therapy (surgery, trauma). A temporary increase in the dose of the drug in stressful situations is necessary both before and after stress.

Against the background of dexamethasone treatment, it is necessary to use specific antibacterial therapy in the treatment of latent tuberculosis, lymphadenitis after BCG vaccination, polio, acute and chronic bacterial and parasitic infections, and specific therapy in patients with peptic ulcer of the stomach and intestines, osteoporosis.

During therapy with the drug, careful monitoring of the condition of patients with chronic heart failure, uncontrolled arterial hypertension, corneal injuries and ulcerative lesions, glaucoma is necessary.

Myasthenia gravis may worsen.

With sudden withdrawal of the drug, especially in the case of previous use of high doses, it is possible to develop acute adrenal insufficiency; “withdrawal” syndrome (not caused by adrenal insufficiency): decreased appetite, nausea, vomiting; lethargy, headache, generalized musculoskeletal pain, asthenia; as well as exacerbation of the disease for which dexamethasone was prescribed.

In patients with diabetes mellitus, blood glucose concentrations should be monitored and, if necessary, the dose of hypoglycemic drugs should be adjusted.

Dexamethasone may increase susceptibility or mask the symptoms of infectious diseases. Chickenpox, measles, and other infections can be more severe and even fatal in unimmunized individuals. Immunosuppression is more likely to develop with prolonged use, but it can also occur with short-term treatment with dexamethasone.

Taking the drug may mask the symptoms of “peritoneal irritation” in patients with perforation of the stomach or intestinal wall.

Against the background of the use of corticosteroids, it is possible to change the motility and number of spermatozoa.

Children who have been in contact with measles or chickenpox patients during treatment are prescribed specific immunoglobulins as a preventive measure. In children, during long-term treatment with dexamethasone, careful monitoring of the dynamics of growth and development is necessary.

Influence on the ability to drive vehicles and mechanisms During treatment, it is not recommended to drive vehicles, as well as engage in potentially dangerous activities that require rapid psychomotor reactions and increased concentration of attention.

Storage conditions

In a dark place at a temperature not exceeding 25 °C. Keep out of reach of children.

Shelf

life is 2 years.Do not use the product after the expiration date indicated on the package.

Active ingredient

Dexamethasone

Conditions of release from pharmacies

By prescription

Dosage form

solution for injection