Dexamethasone - instructions for use, dose, side effects, contraindications

Excipients: glycerol 22.50 mg, disodium edetate dihydrate 0.10 mg, sodium hydrogen phosphate dihydrate 0.80 mg, water for injection q.s. up to 1.00 ml.

Description:

Transparent, colorless or slightly yellowish liquid.

Pharmacotherapeutic group:Glucocorticosteroid

ATX: & nbsp

H.02.A.B.02 Dexamethasone

S.01.B.A.01 Dexamethasone

H.02.A.B Glucocorticoids

S.01.B.A Corticosteroids

Pharmacodynamics:

Dexamethasone is a synthetic hormone of the adrenal cortex with glucocorticosteroid action (GCS). It has anti-inflammatory and immunosuppressive effects, and also affects energy metabolism, homeostasis of glucose and (through negative feedback) on the secretion of the hypothalamic activating factor and adrenocorticotropic hormone of the pituitary gland.

GCS are fat-soluble substances and therefore easily penetrate into target cells through cell membranes.Binding of the hormone to the receptor causes conformational changes in the receptor and increases its affinity for DNA. The hormone receptor complex penetrates the cell nucleus and binds to the regulatory site of the DNA molecule, also known as the element of the glucocorticoid response (GRE).

The activated receptor binds to GRE or specific genes and regulates the transcription of the template RNA (mRNA). The newly formed mRNA is transported to the ribosomes, which then participate in the formation of new proteins. Depending on the type of target cells and cellular processes, the formation of new proteins can both be enhanced (for example, synthesis of tyrosine transaminase in liver cells), and suppressed (eg, IL-2 synthesis in lymphocytes). Since the receptors for GCS are found in all tissues, the realization of their action is carried out in most cells of the body.

Influence on energy metabolism and glucose homeostasis: dexamethasone, along with insulin, glucagon and catecholamines, regulates the accumulation and consumption of energy. In the liver, it stimulates the formation of glucose from pyruvate and amino acids and the formation of glycogen. AT peripheral tissues, in particular in muscles, reduces glucose consumption and mobilizes amino acids (from proteins), which are the substrate of gluconeogenesis in the liver. Immediate effects on the metabolism of fats are manifested by a central redistribution of adipose tissue and increased lipolysis in response to the effects of catecholamines.

Through the receptors in the proximal tubules of the kidneys dexamethasone stimulates renal blood flow and glomerular filtration, suppresses the formation and secretion of vasopressin and improves the ability of the kidneys to excrete acids.

Increases the sensitivity of vessels to pressor agents.

In high doses dexamethasone suppresses the formation of type I and III collagen fibroblasts and the formation of glycosaminoglycans; due to the inhibition of the formation of extracellular collagen and matrix, they slow the healing of wounds. Long-term use of high doses It causes progressive bone resorption both mediated effect, and directly reduces its formation (stimulates parathyroid hormone secretion and suppresses the secretion of calcitonin). In addition, it leads to a negative balance of calcium,reduces calcium absorption in the intestine and strengthens its excretion by the kidneys. This usually leads to secondary hyperparathyroidism and phosphaturia.

Action on the hypothalamus and pituitary: dexamethasone has a 30-fold more pronounced effect than endogenous cortisol. Therefore, it is a more potent inhibitor of the secretion of corticotropin-releasing factor (CRF) and adrenocorticotropic hormone (ACTH). In pharmacological doses depresses the hypothalamic-pituitary-adrenal system, promotes the development of secondary adrenal insufficiency.

Insufficiency of the adrenal cortex can develop as early as the 5-7th day of dexamethasone administration in daily doses equivalent to 20-30 mg of prednisone or after 30 days of therapy with small doses. After abolishing the short course of therapy (up to 5 days) with high doses, the function of the adrenal cortex can be restored in one week; after a long course, normalization occurs later, usually this process takes up to 1 year. Some patients may develop an irreversible atrophy of the adrenal cortex.

Anti-inflammatory and immunosuppressive action glucocorticosteroids is associated with their molecular and biochemical effects.Molecular anti-inflammatory effect is the result of the interaction of glucocorticosteroids with glucocorticoid receptors and changes in the expression of a number of genes that regulate the formation of a variety of information molecules, proteins and enzymes involved in the inflammation process. This leads to a decrease or prevention of a tissue response to inflammation: suppression of cumulation of macrophages and leukocytes, suppression of phagocytosis and release of lysosomal enzymes, synthesis of inflammatory mediators, blockage of macrophage inhibitory factor.

Dexamethasone reduces the expansion and permeability of capillaries, reduces the adhesion of leukocytes to the endothelium, inhibits the synthesis of Pg, leukotrienes, thromboxanes.

Dexamethasone reduces the formation of leukotrienes by reducing the release of arachidonic acid of their cellular phospholipids, which is the result of suppression of the activity of phospholipase A₂. The effect on phospholipase is mediated by an increase in the concentration of lipocortin (macrocortin), which is an inhibitor of phospholipase A₂. The suppressive effect of dexamethasone on the synthesis of prostaglandins and thromboxane is the result of a decrease in the synthesis of a specific mDNA encoding the formation of cyclooxygenase.

Dexamethasone prevents or inhibits cellular immune responses (delayed-type hypersensitivity reactions), reduces the number of T-lymphocytes (type I helper cells), monocytes and eosinophils, binds immunoglobulins to their receptors, inhibits the synthesis of interleukins: reduces T-lymphocytic blastogenesis and reduces primary immune answer. Activates humoral immunity by stimulating T-helper type II - increases the production of antibodies. A significant effect is the reduction in the formation of tumor necrosis factor (TNF) and IL-1.

Pharmacokinetics:

Maximum concentration dexamethasone is achieved in blood plasma already after 5 minutes after intravenous administration (in / in) and 1 hour after intramuscular injection (in / m). With local administration to the joints or soft tissues (in the lesion), absorption is slower than with the / m application. With the / in application, the effect develops rapidly, with the / m application, the clinical effect develops after 8 hours. The effect is long-lasting: from 17 to 28 days after the intravenous use and from 3 days to 3 weeks after topical application. Transition of dexamethasone phosphate in dexamethasone in blood plasma and synovial fluid occurs quickly,

In blood plasma, approximately 77% Dexamethasone binds to proteins, mainly albumin. Only a small amount of dexamethasone binds to non-albumin proteins. Penetrates into the extra- and intracellular spaces. In the central nervous system (hypothalamus, pituitary gland) its effects are due to binding to membrane receptors. AT peripheral tissues binds to cytoplasmic receptors. Disintegration occurs in the place of its action, i.e. in the cell. Metabolized mainly in the liver (mainly by conjugation with glucuronic and sulfuric acids) to inactive metabolites, as well as in the kidneys and other tissues. It is excreted mainly by the kidneys. The half-life (T₁_/₂) - 190 min.

Indications:

A drug Dexamethasone is used intravenously or intramuscularly in acute cases or when oral therapy is not possible:

- endocrine diseases: acute insufficiency of the adrenal cortex, primary or secondary insufficiency of the adrenal cortex, congenital hyperplasia of the adrenal cortex, subacute thyroiditis;

- shock (burn, traumatic, operational, toxic) - with ineffectiveness of vasoconstrictive agents, plasma-substituting drugs and other symptomatic therapy;

- cerebral edema (tumors brain, cerebral trauma, neurosurgical intervention, cerebral hemorrhage, encephalitis, meningitis, radiation damage);

- asthmatic status, severe bronchoconstriction bronchial asthma, chronic obstructive bronchitis);

- 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, with the impossibility of oral treatment;

- blood diseases: acute hemolytic anemia, agranulocytosis, idiopathic thrombocytopenic purpura in adults;

- severe infectious diseases (in combination with antibiotics);

- ophthalmology (subconjunctival, retrobulbar or parabulbar injection): allergic conjunctivitis, 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 field of pathological education): keloids, discoid lupus erythematosus, annular gRanulema.

Contraindications:

Hypersensitivity to the active substance or auxiliaries of the drug, acute viral, bacterial or systemic fungal infections (if adequate adequate therapy is not provided), Itenko-Cushing syndrome, vaccination with live vaccines; intramuscular administration is contraindicated in patients with severe hemostasis disorders.

For topical use (optional) - an introduction to unstable joints, septic arthritis.

Carefully:

Systemic infections (against adequate antimicrobial therapy), latent tuberculosis, herpetic infection of the eyes (risk of corneal perforation), diabetes mellitus, chronic heart failure (CHF), recent myocardial infarction, chronic renal failure (CRF), diverticulitis,hypertension, keratitis, epilepsy, ulcerative colitis (with the threat of perforation or infectious complications), newly established intestinal anastomosis, peptic ulcer (including in history), osteoporosis, myasthenia gravis gravis, elderly age (increased risk of osteoporosis and arterial hypertension), hypothyroidism / hepatic insufficiency, steroid myopathy, severe affective disorders (including history, especially steroid psychosis), pregnancy, breastfeeding period, children's age .

Pregnancy and lactation:

It is impossible to exclude the negative impact on the fetus and the newborn. Dexamethasone slows the fetal development of the fetus. In pregnancy dexamethasone It is used only in individual urgent cases, if the expected benefit for the mother justifies the existing risk to the fetus. In eclampsia, pregnant women use the lowest doses to ensure effective control of the concomitant disease.

Glucocorticosteroids penetrate the placenta and can reach high concentrations in the fetus. Dexamethasone less intensely metabolized in the placenta compared, for example, with prednisone,so the fetus can be determined by high concentrations of dexamethasone. Therapeutic doses of glucocorticosteroids may increase the risk of placental insufficiency, oligohydramnion, growth and fetal growth retardation and fetal death, increase in the number of leukocytes (neutrophils) in a child, and the risk of developing adrenal insufficiency. There is no evidence of a teratogenic effect of glucocorticosteroids.

If a woman received during pregnancy dexamethasone, additional glucocorticosteroid administration is recommended in labor. If labor activity is delayed or planned by cesarean section, in pericarpal the period is recommended to inject intravenously 100 mg of hydrocortisone every 8 hours.

A small amount of glucocorticosteroids are secreted into breast milk. Therefore, mothers who receive dexamethasone, breastfeeding is not recommended, especially when using supraphysiological doses (about 1 mg), as this can delay the growth of the baby and reduce the secretion of its endogenous corticosteroids.

Dosing and Administration:

Doses are set individually for each patient, depending on the nature of the disease, the expected duration of treatment, the tolerability of glucocorticosteroids and the patient's response to ongoing therapy:

Solution for injections can be administered intravenously (as injections or infusions with glucose solution or saline solution), intramuscularly and locally (intraarticularly, into the foci of skin lesions, into soft tissues).

Parenteral administration

Parenterally dexamethasone is administered in acute cases when oral therapy is not possible and under the conditions described in the "Indications for use" section.

The recommended average initial daily dose for iv or in / m use varies from 0.5 mg to 9 mg and, if necessary, up to 24 mg (equivalent to 1 / 3-1 / 2 oral doses). The initial dose of dexamethasone should be applied until the clinical effect has been achieved; then the dose gradually decreases to the minimum effective. If high doses are used for more than a few days, the dose should gradually decrease over the next few days or longer.Long-term treatment should be carried out at a dose not exceeding 0.5 mg / day.

Local application

The recommended single dose of dexamethasone for intraarticular administration is 0.4 mg to 4 mg. The dose depends on the size of the affected joint. The usual dose of dexamethasone is from 2 mg to 4 mg for large joints and from 0.8 mg to 1 mg for small joints.

Intra-articular administration can be repeated after 3-4 months. More frequent administration of dexamethasone can damage the intraarticular cartilage and necrosis of the bone.

The usual dose of dexamethasone for insertion inside the joint bag is from 2 mg to 3 mg, for insertion into the vagina of the tendon - from 0.4 mg to 1 mg, and for the tendons - from 1 mg to 2 mg.

With the introduction of limited lesions, the same dose of dexamethasone is used as for intraarticular administration. The drug can be administered simultaneously at a maximum of two foci.

The recommended dose of dexamethasone for inflammation of soft tissues (periarticular administration) is from 2 mg to 6 mg.

Use in children

With the / m application, the dose for replacement therapy is 0.02 mg / kg body weight or 0.67 mg / m² body surface area, which is divided into 3 injections with an interval of 2 days, or from 0.008 mg to 0.01 mg / kg body weight or from 0.2 mg to 0.3 mg / m² body surface area daily. For other indications, the recommended dose is from 0.02 mg to 0.1 mg / kg body weight or from 0.8 mg to 5 mg / m² body surface area, every 12-24 hours.

Urgent situations

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 achieving a therapeutic effect dexamethasone Enter 2-4 mg, if necessary, followed by a gradual withdrawal of the drug. To maintain a long-term effect, the drug is injected every 3-4 hours or as a continuous drip infusion. After arresting the acute condition of the patient is transferred to the reception of dexamethasone inside.

At a shock enter strictly in / in a bolus in a dose of 2-6 mg / kg. If necessary, repeat doses are administered every 2-6 h or in the form of a prolonged IV infusion at a dose of 3 mg / kg / day. Treatment with dexamethasone should be performed as part of a complex therapy of shock. The use of pharmacological doses is permissible only with life-threatening conditions and, as a rule, this time does not exceed 48-72 hours.

When the brain is swollen, the initial dose of 10 mg is given IV, then 4 mg every 6 hours before the symptomatic relief (usually within 12-24 hours).After 2-4 days, the dose is reduced and the drug is gradually stopped for 5-7 days.

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

With acute edema of the brain, short-term intensive therapy is performed: loading dose for adults is 50 mg IV, then on day 1-3, 8 mg is administered every 2 hours, on the 4th day - 4 mg every 2 hours, on 5-8 days - 4 mg every 4 hours, then the daily dose is reduced at 4 mg / day until complete withdrawal. For children weighing over 35 kg the loading dose is 25 mg IV, then on day 1-3, 4 mg every 2 hours, on the 4th day - 4 mg every 4 hours, on 5-8 days - 4 mg every 6 hours, then daily The dose is reduced by 2 mg / day until it is completely canceled. Children with body weight less than 35 kg the loading dose is 20 mg IV, then on day 1-3, 4 mg are administered every 3 hours, on the 4th day - 4 mg every 6 hours, for 5-8 days - 2 mg every 6 hours, then daily the dose is reduced by 1 mg / day until the drug is completely discontinued.

In acute chronic allergic diseases, parenteral and oral administration of dexamethasone is combined: 1st day - iv 4-8 mg, 2-3 days - inside 1 mg 2 times a day, 4-5 days - inside 0.5 mg 2 times per day, 6-7 days - inside 0.5 mg once. On the 8th day evaluate the effectiveness of therapy.

Equivalent doses of glucocorticosteroids

dexamethasone 0.75 mg	Prednisone 5 mg
cortisone 25 mg	methylprednisolone 4 mg
hydrocortisone 20 mg	triamcinolone 4 mg
prednisolone 5 mg	betamethasone 0.75 mg

Side effects:

Classification of the frequency of development of side effects of the World Health Organization (WHO):

Often - >1/10

often from> 1/100 to < 1/10

infrequently - from> 1/1000 to <1/100

rarely from> 1/10000 to <1/1000

very rarely - from <1/10000, including individual messages

frequency is unknown - can not be estimated from the available data.

Infectious and parasitic diseases:

frequency unknown: disguise infections, activation of strongyloidiasis, opportunistic infection.

Violations from the blood and lymphatic system:

rarely reducing the number of monocytes and / or lymphocytes, leukocytosis, eosinopenia, thrombocytopenia purpura and netrombotsitopenicheskaya:

frequency unknown: polycemia.

Immune system disorders:

infrequently: allergic reactions (including reactions of hypersensitivity), a decrease in the immune response and an increase in susceptibility to infections;

rarely: dermal rash, bronchospasm, anaphylactoid reactions.

Heart Disease:

very rarely: polyfocal ventricular extrasystoles, transient bradycardia, decreased myocardial contractility, heart failure, rupture myocardium after a recent acute infarction.

Vascular disorders:

infrequently: increased blood pressure;

very rarely: vasculitis, thromboembolism.

Disorders from the psyche:

often: mental disorders;

infrequently: changes in personality and behavior, insomnia, irritability, depression;

rarely: psychosis;

frequency unknown: suicidal thoughts, hallucinations, euphoria, anxiety, lability of mood.

Impaired nervous system:

infrequently: edema of the papillae of the optic nerve and increased intracranial pressure (pseudotumor of the brain) after the abolition of therapy, dizziness, headache, vertigo, neuropathy, hyperkinesia;

very rarely: convulsions;

frequency unknown: manifestation of latent epilepsy.

Disorders from the endocrine system:

often: adrenal insufficiency, pituitary insufficiency (especially on the background of stress), Itenko-Cushing's syndrome, irregularities in the regularity of the menstrual cycle, hirsutism, suppression of growth in children.

Disorders from the metabolism and nutrition:

often: weight gain, obesity, a decrease in glucose tolerance, "steroid" diabetes, hyperglycemia, the transition of latent diabetes mellitus to a clinically manifested, increased need for insulin or oral hypoglycemic drugs in patients with diabetes mellitus, sodium and water retention, increased potassium loss;

infrequently: hypertriglyceridemia;

very rarely: hypokalemic alkalosis, negative nitrogen balance;

frequency unknown: increase appetite, hypercholesterolemia, epidural lipomatosis.

Disorders from the digestive system:

infrequently: nausea, hiccough, stomach ulcer or duodenal ulcer;

very rarely: esophagitis, perforation of the ulcer and bleeding of the gastrointestinal tract (hematemesis, melena), pancreatitis, perforation of the gallbladder and intestines (especially in patients with chronic inflammatory diseases of the large intestine);

frequency is unknown: discomfort in epigastric region.

Disturbances from the musculoskeletal and connective tissue:

often: mouse atrophy, osteoporosis, muscle weakness, "steroid" myopathy (muscle weakness due to catabolism of muscle tissue);

infrequently: aseptic necrosis of bones;

rarely; compression fractures of the vertebrae, tendon ruptures (especially when certain quinolones are used together), articular cartilage damage and bone necrosis (associated with frequent intraarticular injections).

Disturbances from the skin and subcutaneous tissues:

often: delayed healing of wounds, striae, petechiae and ecchymosis, increased sweating, acne, suppression of skin reaction during allergological tests, erythema, thinning of the skin;

very rarely: angioedema, allergic dermatitis, urticaria;

frequency unknown: telangiectasia.

Disorders from the side of the organ of vision:

infrequently: a "steroidal" cataract, especially the posterior subcapsular cataract, glaucoma, increased intraocular pressure;

very rarely: exophthalmos, secondary eye infections, retinopathy;

The frequency is unknown: ptosis, mydriasis, chemosis, corneal perforation with keratitis therapy, iatrogenic scleral perforation.

Violations of the genitals and breast:

rarely: impotence;

frequency unknown: amenorrhea.

General disorders and disorders at the site of administration:

very rarely: edema, hyper- or hypopigmentation of the skin, atrophy of the skin or subcutaneous tissues, "sterile" abscesses and redness of the skin, burning sensation at the injection site, arthropathy, Sharko's arthropathy.

The "cancellation" syndrome

If a patient taking long-term glucocorticosteroids rapidly decreases the dose of the drug, signs of adrenal insufficiency may develop, arterial hypotension and death. It is also possible to develop a withdrawal syndrome that is not associated with adrenal insufficiency (anorexia, nausea, vomiting, lethargy, headache, fever, arthralgia, desquamation of the epithelium, myalgia, weight loss, lowering blood pressure).

In some cases, the symptoms of the "cancellation" syndrome may be similar to the symptoms and signs of an exacerbation or relapse of the disease, for which the patient was receiving treatment.

With the development of severe adverse events, treatment should be discontinued.

Overdose:

Symptoms: increased blood pressure, edema, peptic ulcer, hyperglycemia, impaired consciousness.

Treatment: symptomatic.

There is no specific antidote. Hemodialysis is ineffective.

Interaction:

The simultaneous use of dexamethasone and non-steroidal anti-inflammatory drugs increases the risk of ulceration in the gastrointestinal tract.

Indomethacin, displacing dexamethasone from association with albumin, increases the risk of developing its side effects.

The effect of dexamethasone decreases with simultaneous application of isoenzyme inducers CYP3A4 (eg, phenytoin, phenobarbital, carbamazepine, primidon, rifabutin, rifampicin) or drugs, raising metabolic clearance of glucocorticosteroids (ephedrine and aminoglutethimide), in such cases it is necessary to increase doses dexamethasone.

Interactions between dexamethasone and the above drugs may distort the results of dexamethasone compressed samples. If samples with dexamethasone should be taken during therapy with one of these drugs, then this interaction should be taken into account in interpreting results of the samples.

Simultaneous use of dexamethasone and inhibitors of isoenzyme CYP3A4 (eg, ketoconazole, macrolide antibiotics) can lead to an increase in the concentration of dexamethasone in the blood.

Dexamethasone is mild inducer of isoenzyme CYP3A4. Simultaneous use of drugs that are metabolized by isoenzyme CYP3A4 (indinavir, erythromycin) can increase their clearance, which can be accompanied by a decrease in their concentration in the plasma blood.

By suppressing activity isoenzyme CYP3A4 ketoconazole may increase plasma concentrations of dexamethasone. On the other hand, ketoconazole can suppress the synthesis of glucocorticosteroids in the adrenal glands, therefore, during the reduction of doses of dexamethasone may develop adrenal insufficiency.

Dexamethasone reduces the therapeutic effect of hypoglycemic drugs, antihypertensive drugs, praziquantel and thiazide diuretics (necessary increase doses of these drugs), increases the activity of heparin, albendazole and potassium-sparing diuretics (if necessary, doses of these drugs are reduced).

Dexamethasone may alter the action of coumarin anticoagulants, so more frequent monitoring of prothrombin time is recommended during therapy.

Weaken the influence of vitamin D on the absorption of calcium ions in the lumen of the intestine. Ergocalciferol and parathyroid hormone interfere with the development of osteopathy caused by dexamethasone.

Simultaneous use of high doses of glucocorticosteroids with β-adrenoblockers, thiazide diuretics, furosemide, ethacrynic acid, carbonic anhydrase inhibitors, amphotericin B increases the risk of hypokalemia.

In patients with hypokalemia, arrhythmogenic and toxic effect of cardiac glycosides.

Hypokalemia caused by glucocorticosteroids may increase the severity and duration of muscle blockade against the background of the use of nondepolarizing muscle relaxants.

Antacids reduce absorption dexamethasone in the stomach.

The pharmacokinetic interaction of dexamethasone with food or alcohol has not been studied, however, simultaneous consumption of food and preparations with high potassium content is not recommended.

Smoking does not affect the pharmacokinetics of dexamethasone.

Simultaneous application with Cyclosporine increases the risk of seizures in children.

Immunosuppressants increase the risk of infection and lymphoma or otherlymphoproliferative disorders caused by the Epstein-Barr virus.

Dbenocorticosteroids increase the renal clearance of salicylates, so it is sometimes difficult to achieve therapeutic concentrations of salicylates in plasma blood. It is necessary with caution and gradually reduce the dose of glucocorticosteroids, since it can increase the concentration of salicylates in the blood plasma and intoxication with these drugs.

With the simultaneous use of oral contraceptives, antithyroid drugs may increase the period floordejection glucocorticosteroids, with appropriate strengthening of their biological effects and increased frequency of adverse side effects.

With the simultaneous use with pirretinom release thyroid-stimulating hormone can decrease.

Contraindicated simultaneous the use of ritodrine and dexamethasone in the period of labor, as this can lead to the death of the mother due to the development of pulmonary edema.

The simultaneous use of dexamethasone and thalidomide can cause toxic epidermal necrolysis.

Simultaneous administration with m-holinoblokatorami (including antihistamine medicinal means, tricyclic antidepressants), nitrates promotes the development of increased intraocular pressure.

With simultaneous use with fluoroquinolones, the risk of tendonitis increases (predominantly Achilles tendon) in elderly patients and in patients with diseases of tendons.

Potential therapeutically beneficial interactions: one-timeennth use of dexamethasone and metoclopramide, diphenhydramine, prochlorperazine or antagonists of 5-HT₃-receptors (serotonin or 5-hydroxytryptamine receptors of type 3), such as ondansetron or granisetron, effectively to prevent nausea and vomiting caused by chemotherapy (cisplatin, cyclophosphamide, methotrexate, fluorouracil).

Special instructions:

Against the backdrop of parenteral therapy, glucocorticosteroids may develop (albeit rarely) reactions of increased sensitivity. Therefore, before starting treatment, care must be taken (especially in patients with a heightened sensitivity to other drugs in the anamnesis).

In patients who need long-term therapy with dexamethasone,after the cessation of therapy, withdrawal syndrome (also without distinct signs of adrenal insufficiency) may develop: fever, nasal discharge, conjunctival hyperemia, headache, dizziness, drowsiness and irritability, muscle and joint pain, vomiting, weight loss, weakness, convulsions. therefore dexamethasone it is necessary to cancel by gradual reduction of doses. Rapid cancellation of the drug can be fatal for the patient.

If during the period of application or during the period of drug withdrawal the patient is exposed to severe stress (trauma, surgery or serious disease), the dose of dexamethasone should be increased or introduced hydrocortisone or cortisone.

In patients who received long-term therapy with dexamethasone and underwent stress after its withdrawal, it is necessary to resume the use of dexamethasone due to the fact that induced adrenal insufficiency can persist for several months after drug discontinuation.

Dexamethasone therapy can mask signs of infectious processes and signs of intestinal perforation.

Dexamethasone can aggravate the course of fungal infections, latent amoebiasis or pulmonary tuberculosis. Patients with acute pulmonary tuberculosis dexamethasone can be prescribed (together with antituberculosis drugs) only in the case of fulminant or severe disseminated process. Patients with inactive pulmonary tuberculosis receiving therapy with Dexamethasone, or patients with positive tuberculin samples should receive parallel therapy with anti-tuberculosis drugs.

Particular attention and careful medical supervision is necessary for patients with osteoporosis, arterial hypertension, heart failure, tuberculosis, glaucoma, hepatic or renal insufficiency, diabetes mellitus, active peptic ulcers, fresh intestinal anastomoses, ulcerative colitis and epilepsy. With caution, it is necessary to apply dexamethasone in the first weeks after acute myocardial infarction, as well as patients with thromboembolism, myasthenia, glaucoma, hypothyroidism, psychosis or psychoneuroses, as well as patients of advanced age.

During therapy with dexamethasone, decompensation of diabetes mellitus or a transition from latent toclinically manifested diabetes mellitus.

With prolonged use, it is necessary to control the potassium level in the blood serum.

During therapy with dexamethasone, vaccination with live vaccines is contraindicated.

Immunization with killed viral or bacterial vaccines does not give the expected growth in the titer of specific antibodies and therefore does not provide the necessary protective action. Dexamethasone usually not applied 8 weeks before vaccination and within 2 weeks after vaccination.

Dexamethasone may increase susceptibility or mask the symptoms of infectious diseases. Veterinary pox, measles and other infections can be more severe and even fatal in non-immune individuals. Immunosuppression often develops with long-term use of SCS, but it can also occur with short-term treatment.

Patients taking high doses of dexamethasone for a long time should avoid contact with infectious patients; In case of accidental contact, preventive treatment with immunoglobulin is recommended.

Care should be taken when treating patients who have recently undergone surgery or bone fractures, since dexamethasone can slow the healing of wounds and fractures.

The effect of glucocorticosteroids is increased in patients with cirrhosis or hypothyroidism.

Intra-articular administration of glucocorticosteroids may be accompanied by local and systemic effects.

Frequent use leads to destruction of articular cartilage and necrosis of bone tissue.

Before intraarticular injection from the joint, the synovial fluid must be pumped out and examined (for the presence of an infectious process). It is necessary to avoid the introduction of glucocorticosteroids into the infected joint. If an injection of septic inflammation develops in the joint, appropriate antibiotic therapy is necessary. Patients should avoid loading on the joint into which the injection was made, until the inflammatory process is completely stopped.

Do not recommend injections in unstable joints.

Glucocorticosteroids can change the results of skin allergic tests.

Dexamethasone is used in children and adolescents only on strict indications. During the treatment, strict control of the growth and development of the child or adolescent is necessary.

Specific information on certain components of the drug

The drug contains less than 1 mmol (23 mg) of sodium per dose.

Effect on the ability to drive transp. cf. and fur:

Dexamethasone does not affect the ability to drive vehicles and work with other technical devices that require an increased concentration of attention and speed of psychomotor reactions.

Form release / dosage:

Solution for injection, 4 mg / ml.

Packaging:

1 ml per ampoule of dark glass (type I). A colored dot is placed on the ampoule, indicating the ampoule break line and the color coding ring.

5 ampoules per blister of PVC-aluminum foil.

For 5 blisters together with the instructions for use are placed in a pack of cardboard.

Storage conditions:

At a temperature of no higher than 25 ° C.

Keep out of the reach of children.

Shelf life:

5 years.

Do not use the drug after the expiration date.

Terms of leave from pharmacies:On prescription

Registration number:П N012237 / 02

Date of registration:28.04.2011 / 14.05.2015

Expiration Date:Unlimited

The owner of the registration certificate:KRKA, dd, Novo mesto, AOKRKA, dd, Novo mesto, AO

Manufacturer: & nbsp

KRKA, d.d. Slovenia

KRKA-RUS, LLC Russia

VECTOR-MEDICA, CJSC Russia

Representation: & nbspKRKA, dd, Novo mesto, AOKRKA, dd, Novo mesto, AO

Information update date: & nbsp21.03.2017

Illustrated instructions

Instructions

Dexamethasone (Dexamethasone)