Instructions for use DEXAMETHASON solution

The hormonal agent shows antiallergic, anti-inflammatory and immunosuppressive activity. Injections are prescribed for antitoxic, desensitizing, antishock therapy. Due to the active components, the susceptibility of adrenergic receptors to endogenous catecholamines increases.

Composition and release form

Tablets - 1 tablet:

• Active ingredient: Dexamethasone – 0.0005 g
• Excipients: potato starch – 0.0340 g; sucrose (sugar) – 0.1140 g; stearic acid – 0.0015 g.

Tablets weighing 0.15 g.

Tablets 0.5 mg.

10, 14 tablets in a blister pack made of polyvinyl chloride film and aluminum foil.

5, 10 blister packs of 10 tablets each or 4 blister packs of 14 tablets each with instructions for use in a cardboard pack.

Description of the dosage form

Tablets are white, flat-cylindrical with a chamfer.

Pharmacokinetics

Absorption

After oral administration, it is quickly and completely absorbed, the maximum concentration of dexamethasone in the blood plasma is 1-2 hours.

Distribution

In the blood it binds (60–70%) to a specific carrier protein – transcortin. Easily passes through histohematic barriers (including the blood-brain and placental barriers).

Metabolism

Metabolized in the liver (mainly by conjugation with glucuronic and sulfuric acids) to inactive metabolites.

Removal

Excreted by the kidneys (a small amount of dexamethasone passes into breast milk). Half-life is 3-5 hours.

Pharmacodynamics

Dexamethasone is a synthetic glucocorticosteroid (GCS), a methylated derivative of fluoroprednisolone. It has anti-inflammatory, antiallergic, desensitizing, immunosuppressive, antishock and antitoxic effects.

Inhibits the secretion of thyroid-stimulating hormone and follicle-stimulating hormone.

Increases the excitability of the central nervous system, reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (stimulates the production of erythropoietin). Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus, stimulates the synthesis of matrix ribonucleic acid (mRNA); the latter induces the formation of proteins, including lipocortin, that mediate cellular effects. Lipocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, prostaglandins, leukotrienes, which contribute to inflammation, allergies and others.

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

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

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

Effect on water-electrolyte metabolism: retains sodium ions and water in the body, stimulates the excretion of potassium ions (mineralocorticosteroid activity), reduces the absorption of calcium ions from the gastrointestinal tract, “washes out” calcium ions from the bones, increases the excretion of calcium ions by the kidneys.

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

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

In chronic obstructive pulmonary disease, the effect is based mainly on inhibition of inflammatory processes, inhibition of development or prevention of swelling of the mucous membranes, 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 beta-adrenergic receptors of small and medium-caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of bronchial secretions due to inhibition or reduction of its production.

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

The immunosuppressive effect is due to inhibition of the release of cytokines (interleukin-1, interleukin-2; interferon gamma) from lymphocytes and macrophages. Suppresses the synthesis and secretion of adrenocorticotropic hormone (ACTH), and secondarily the synthesis of endogenous GCS.

The peculiarity of the action is significant inhibition of pituitary function and the almost complete absence of mineralocorticosteroid activity. Doses of 1-1.5 mg/day inhibit the adrenal cortex; biological half-life is 32-72 hours (duration of inhibition of the hypothalamic-pituitary-adrenal cortex system).

In terms of the strength of glucocorticoid activity, 0.5 mg of dexamethasone corresponds to approximately 3.5 mg of prednisolone, 15 mg of hydrocortisone or 17.5 mg of cortisone for oral dosage forms.

Dexamethasone

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, glucose homeostasis and (via negative feedback) the secretion of hypothalamic activating factor and pituitary adrenocorticotropic hormone.

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

The activated receptor binds to GREs or specific genes and regulates messenger RNA (mRNA) transcription. The newly formed mRNA is transported to 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 be either enhanced (for example, the synthesis of tyrosine transaminase in liver cells) or suppressed (for example, the synthesis of IL-2 in lymphocytes). Since receptors for GCS are found in all tissues, their action is realized in most cells of the body.

Effect on energy metabolism and glucose homeostasis:

Dexamethasone, along with insulin, glucagon and catecholamines, regulates the accumulation and expenditure of energy. In the liver, it stimulates the formation of glucose from pyruvate and amino acids and the formation of glycogen. In peripheral tissues, particularly in muscles, it reduces glucose consumption and mobilizes amino acids (from proteins), which are a substrate for gluconeogenesis in the liver. Direct effects on fat metabolism include central redistribution of adipose tissue and increased lipolysis in response to catecholamines.

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

Increases the sensitivity of blood vessels to pressor agents.

In high doses, dexamethasone suppresses the formation of collagen types I and III by fibroblasts and the formation of glycosaminoglycans; by inhibiting the formation of extracellular collagen and matrix, they slow down wound healing. Long-term use of high doses causes progressive bone tissue resorption as an indirect effect, and directly reduces its formation (stimulates the secretion of parathyroid hormone and suppresses the secretion of calcitonin). In addition, it leads to a negative calcium balance, reduces calcium absorption in the intestines and increases its excretion by the kidneys. This usually results in secondary hyperparathyroidism and phosphaturia.

Action on the hypothalamus and pituitary gland:

Dexamethasone has a 30 times 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, it inhibits the hypothalamic-pituitary-adrenal system and promotes the development of secondary adrenal insufficiency.

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

Anti-inflammatory and immunosuppressive effects

glucocorticosteroids is associated with their molecular and biochemical effects. The 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 many information molecules, proteins and enzymes involved in the process of inflammation. This leads to a decrease or prevention of the tissue response to inflammation: inhibition of the accumulation of macrophages and leukocytes, suppression of phagocytosis and release of lysosomal enzymes, synthesis of inflammatory mediators, blocking of the macrophage inhibitory factor.

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

Dexamethasone reduces the formation of leukotrienes by reducing the release of arachidonic acid from cellular phospholipids, which results from inhibition of phospholipase A2 activity. 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 specific mDNA encoding the formation of cyclooxygenase.

Dexamethasone prevents or inhibits cellular immune reactions (delayed hypersensitivity reactions), reduces the number of T-lymphocytes (T-helper type I), monocytes and eosinophils, the binding of 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 - enhances the production of antibodies. A significant effect is a decrease in the formation of tumor necrosis factor (TNF) and IL-1.

Indications for use of Dexamethasone

Systemic connective tissue diseases (systemic lupus erythematosus, scleroderma, periarteritis nodosa, dermatomyositis, rheumatoid arthritis).

Acute and chronic inflammatory diseases of the joints: gouty and psoriatic arthritis, osteoarthritis (including post-traumatic), polyarthritis, glenohumeral periarthritis, ankylosing spondylitis (ankylosing spondylitis), juvenile arthritis, syndrome

Stilla in adults, bursitis, nonspecific tenosynovitis, synovitis and epicondylitis.

Rheumatic fever, acute rheumatic carditis.

Acute and chronic allergic diseases: allergic reactions to drugs and foods, serum sickness, urticaria, allergic rhinitis, angioedema, drug exanthema, hay fever.

Skin diseases: pemphigus, psoriasis, eczema, atopic dermatitis, diffuse neurodermatitis, contact dermatitis (affecting a large surface of the skin), toxicerma, seborrheic dermatitis, exfoliative dermatitis, toxic epidermal necrolysis (Lyell's syndrome), bullous dermatitis herpetiformis, malignant exudative erythema (syndrome) Stevens-Johnson).

Brain edema (only after confirmation of symptoms of increased intracranial pressure by magnetic resonance or computed tomography) caused by a brain tumor and/or associated with surgery or radiation injury.

Allergic eye diseases: allergic corneal ulcers, allergic forms of conjunctivitis.

Inflammatory eye diseases: sympathetic ophthalmia, severe sluggish anterior and posterior uveitis, optic neuritis.

Primary or secondary adrenal insufficiency (including the condition after removal of the adrenal glands).

Congenital adrenal hyperplasia.

Kidney diseases of autoimmune origin (including acute glomerulonephritis); nephrotic syndrome.

Subacute thyroiditis.

Diseases of the hematopoietic organs - agranulocytosis, panmyelopathy, autoimmune hemolytic anemia, acute lymphoid and myeloid leukemia, lymphogranulomatosis, thrombocytopenic purpura, secondary thrombocytopenia in adults, erythroblastopenia (erythrocytic anemia), congenital (erythroid) hypoplastic anemia.

Lung diseases: acute alveolitis, pulmonary fibrosis, stage II-III sarcoidosis. Bronchial asthma (for bronchial asthma, the drug is prescribed only in severe cases, ineffectiveness or inability to take inhaled corticosteroids).

Tuberculous meningitis, pulmonary tuberculosis, aspiration pneumonia (in combination with specific chemotherapy).

Berylliosis, Loeffler's syndrome (not amenable to other therapy).

Lung cancer (in combination with cytostatics).

Multiple sclerosis.

Gastrointestinal diseases: ulcerative colitis, Crohn's disease, local enteritis.

Hepatitis.

Prevention of transplant rejection as part of complex therapy.

Hypercalcemia due to cancer, nausea and vomiting during cytostatic therapy.

Multiple myeloma.

Conducting a test for the differential diagnosis of hyperplasia (hyperfunction) and tumors of the adrenal cortex.

Contraindications to the use of Dexamethasone

• For short-term use for “life-saving” indications, the only contraindication is hypersensitivity; systemic mycosis;
• simultaneous use of live and attenuated vaccines with immunosuppressive doses of the drug;
• sucrose intolerance, isomaltase/sucrase deficiency, glucose-galactose malabsorption; breastfeeding period; children up to 3 years old.

Carefully:

Parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently suffered, including recent contact with a patient) –

• herpes simplex, herpes zoster (viremic phase), chicken pox, measles;
• amebiasis, strongyloidiasis (established or suspected);
• active and latent tuberculosis.

Use of Dexamethasone during pregnancy and children

Dexamethasone crosses the placenta (can reach high concentrations in the fetus) and into breast milk. During pregnancy, especially in the first trimester, or in women planning pregnancy, the use of Dexamethasone is indicated only if the expected therapeutic effect outweighs the risk of negative effects on the mother or fetus. GCS should be prescribed during pregnancy only for absolute indications. With long-term therapy during pregnancy, the possibility of fetal damage cannot be excluded. If used in the third trimester of pregnancy, there is a risk of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in the newborn. If it is necessary to carry out treatment with the drug during breastfeeding, breastfeeding should be stopped.

Side effects of Dexamethasone

The incidence and severity of side effects depend on the duration of use, the size of the dose used and the ability to comply with the circadian rhythm of the prescription. Dexamethasone is usually well tolerated. It has low mineralocorticoid activity, that is, its effect on water and electrolyte metabolism is small. As a rule, low and medium doses of dexamethasone do not cause sodium and water retention in the body or increased potassium excretion.

• Endocrine system disorders: decreased glucose tolerance, “steroidal” diabetes mellitus or manifestation of latent diabetes mellitus, suppressed adrenal function, Itsenko-Cushing syndrome (moon face, pituitary type obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis, striae), delayed sexual development in children.
• Blood and lymphatic system disorders: moderate leukocytosis, leukocyturia, lymphopenia, eosinopenia, polycythemia.
• Gastrointestinal tract disorders: nausea, vomiting, abdominal pain, discomfort in the epigastric region, pancreatitis, “steroid” gastric and duodenal ulcers, erosive esophagitis, bleeding and perforation of the stomach and intestinal wall, increased or decreased appetite , flatulence, hiccups. In rare cases, increased activity of liver transaminases and alkaline phosphatase.
• Disorders of the heart and blood vessels: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or progression of CHF, electrocardiographic changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis and thromboembolism, vasculitis, increased capillary fragility. In patients with acute and subacute myocardial infarction, the necrosis focus spreads, the formation of scar tissue slows down, which can lead to rupture of the heart muscle.
• Nervous system disorders: increased intracranial pressure, cerebellar pseudotumor, headache, convulsions.
• Mental disorders: nervousness or anxiety, insomnia, emotional lability, delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, suicidal tendencies.
• Visual disorders: 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, corneal perforation, central serous chorioretinopathy.
• Hearing and labyrinthine disorders: dizziness, vertigo.
• Metabolic and nutritional disorders: hypercholesterolemia, increased excretion of calcium ions, hypocalcemia, weight gain, negative nitrogen balance (increased protein breakdown), increased sweating, epidural lipomatosis. Caused by mineralocorticosteroid activity - fluid and sodium ion retention (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).
• Disorders of the musculoskeletal and connective tissue: slowing of growth and ossification processes in children (premature closure of the epiphyseal growth plates), 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).
• Disorders of the skin and subcutaneous tissues: delayed healing of wounds, petechiae, ecchymoses, thinning of the skin, atrophy of the skin and subcutaneous tissue, hyper- or hypopigmentation, “steroid” acne, stretch marks, a tendency to develop pyoderma and candidiasis, impaired skin pigmentation (hypo- or hyperpigmentation), telangiectasia.
• Immune system disorders: generalized (skin rash, skin itching, anaphylactic shock), local allergic reactions.
• Infectious and parasitic diseases: development or exacerbation of infections (the appearance of this side effect is facilitated by jointly used immunosuppressants and vaccination), masking of infections.
• General disorders and disorders at the injection site: withdrawal syndrome.

What does Dexamethasone help with, indications and contraindications

The drug is a synthetic corticosteroid, an analogue of the hormone of the adrenal cortex. The component composition of the medication helps:

• normalize the functioning of extracellular structures of cartilage and bone tissues;
• reduce the level of capillary permeability;
• stabilize membranes;
• slow down the processes of cytokine release from lymphocytes and macrophages;
• accelerate protein catabolism;
• slow down glucose utilization and calcium absorption;
• retain water and sodium ions in tissues.

The processing of components occurs in the liver, partially in the kidneys and other organs. Metabolic products are excreted through the genitourinary system.

The drug is used against pathologies amenable to systemic therapy, as an addition to the main course of treatment. Intravenous and intramuscular injections are given when tablets or local medications are ineffective.

Dexamethasone is prescribed to patients:

• with allergies and rheumatic diseases;
• swelling of brain tissue;
• shock states of various origins;
• individual kidney lesions;
• autoimmune disorders;
• diseases of the respiratory tract, blood;
• acute severe dermatoses.

The drug is prescribed for hormone replacement therapy and the fight against inflammatory bowel pathologies. Dexamethasone is contraindicated:

• with hypersensitivity to the component composition;
• infectious, parasitic diseases of bacterial and viral origin;
• systemic mycoses, osteoporosis, immunodeficiency;
• myasthenia gravis, ulcers, colitis and other gastrointestinal diseases;
• lesions of the cardiovascular department;
• diabetes mellitus, psychosis, acute renal or liver failure.

The medicine is not injected into the joints if they are unstable, spontaneous bleeding of the apparatus, fractures or infectious lesions. The ban includes periarticular osteoporosis, the postoperative period - after arthroplasty.

Drug interactions

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

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

When used simultaneously with live antiviral vaccines and against the background of other types of immunizations, it increases the risk of viral activation and the development of infections.

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

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

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

Hypokalemia caused by GCS can increase the severity and duration of muscle blockade due to muscle relaxants.

In high doses, it reduces the effect of somatropin.

Antacids reduce the absorption of corticosteroids.

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

Weakens the effect of vitamin D on the absorption of calcium ions in the intestinal lumen.

Ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by GCS.

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, sodium-containing drugs - edema and increased blood pressure.

Non-steroidal anti-inflammatory drugs and ethanol increase the risk of developing ulceration of the gastrointestinal mucosa and bleeding; in combination with non-steroidal anti-inflammatory drugs for the treatment of arthritis, it is possible to reduce the dose of GCS due to the summation of the therapeutic effect.

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

Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis.

The therapeutic effect of GCS is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of “liver” microsomal enzymes (increased metabolic rate).

Mitotane and other inhibitors of adrenal function may necessitate an increase in the dose of GCS.

The clearance of GCS increases against the background of thyroid hormones.

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

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

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

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

The risk of developing cataracts increases when used in conjunction with other corticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine.

Simultaneous administration with m-anticholinergics (including antihistamines, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.

When used simultaneously with fluoroquinolones, the risk of tendonopathy (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 and cardiomyopathy.

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

Instructions for use DEXAMETHASON solution

Allergic reactions may occur (although rarely) during parenteral use of corticoids. Appropriate measures should be taken before starting treatment, taking into account this possibility (especially in patients with a history of allergic reactions to any drugs).

Patients undergoing long-term treatment with dexamethasone may experience corticoid withdrawal syndrome. Therefore, the dosage of dexamethasone should be gradually reduced.

If during therapy or when discontinuing a drug the patient is exposed to unexpected stress (trauma, surgery or serious illness), then the dose of dexamethasone should be increased or hydrocortisone or cortisone prescribed. In patients who have experienced severe stress after discontinuation of long-term dexamethasone, dexamethasone should be restarted as induced adrenal insufficiency may persist for several months after discontinuation of treatment.

Treatment with dexamethasone or natural glucocorticoids may mask signs of existing or new infection and signs of interstitial perforation.

Dexamethasone can aggravate the course of systemic fungal infections, latent amebiasis and pulmonary tuberculosis.

In patients with active pulmonary tuberculosis, dexamethasone should be prescribed (in combination with antituberculosis therapy) in cases of fulminant or severe disseminated pulmonary tuberculosis. Patients with inactive tuberculosis who are taking dexamethasone or patients with a positive tuberculin test should receive chemoprophylaxis.

Particular caution and close medical monitoring should be performed in patients with osteoporosis, hypertension, heart failure, tuberculosis, glaucoma, liver failure, renal failure, diabetes, active gastric and duodenal ulcers, recent intestinal anastomosis, ulcerative colitis and epilepsy. Particular attention should be paid to patients in the first weeks after myocardial infarction, as well as patients with thromboembolism, asthenic bulbar palsy, glaucoma, hypothyroidism, psychosis or psychoneurosis, and elderly patients.

During treatment with dexamethasone, an exacerbation of diabetes or a transition from a latent form to the form of clinical manifestations of diabetes may occur.

During long-term treatment, it is necessary to monitor serum potassium levels. Vaccination with live vaccines is contraindicated during treatment with dexamethasone. Immunization with killed viral or bacterial vaccines does not lead to the expected increase in antibodies and does not have the expected protective effect. Dexamethasone is usually not prescribed 8 weeks before and 2 weeks after vaccination. Patients receiving or taking high doses of dexamethasone for a long time should avoid contact with people with measles; In case of accidental contact, prophylactic treatment with immunoglobulin is recommended. Caution is advised in patients recovering from recent surgery and a bone fracture, as dexamethasone may delay the healing of wounds and fractures.

The effect of glucocorticoids is potentiated in patients with liver cirrhosis or hypothyroidism. Intra-articular administration of corticoids can cause local and systemic effects. Frequent use may cause damage to articular cartilage and bone necrosis.

Before intra-articular injection, synovial fluid should be evacuated from the joint and examined (for possible infection). Injecting corticosteroids into infected joints should be avoided. If septic inflammation of the joint develops after the injection, then appropriate antibacterial treatment must be started.

Patients should be informed that it is necessary to avoid putting stress on the joints into which the injection was performed until the inflammatory process has completely resolved.

Injections into unstable joints are not recommended. Corticosteroids may interfere with allergy skin test results. Dexamethasone is used in children and adolescents only under strict indications. During treatment with dexamethasone, the growth and development of children and adolescents should be carefully monitored.

Special information about some of the ingredients of the drug.

This drug contains less than 1 mmol (23 mg) sodium per dose, which is a negligible amount.

Pregnancy and lactation.

Dexamethasone should be prescribed to pregnant women only in selected urgent cases when the expected benefit to the mother justifies the risk to the fetus.

Particular care should be taken in case of preeclampsia. According to general recommendations for glucocorticoid treatment during pregnancy, the lowest effective dose to control the underlying disease should be used.

Glucocorticoids are excreted in small quantities in breast milk. Therefore, breastfeeding is not recommended for mothers taking dexamethasone, especially when using high physiological doses (about 1 mg). This can lead to fetal growth retardation and decreased secretion of endogenous corticosteroids.

Impact on the ability to drive a car or use other machinery.

Dexamethasone does not affect the ability to drive a car or operate machinery.

Dexamethasone dosage

Orally, in individually selected doses, the amount of which is determined by the type of disease, the degree of its activity and the nature of the patient’s response.

The average daily dose is 0.75-9 mg. In severe cases, large doses can be used, divided into 3-4 doses. The maximum daily dose is usually 15 mg. After achieving a therapeutic effect, the dose is gradually reduced (usually by 0.5 mg every 3 days) to a maintenance dose of 2-4.5 mg/day. The minimum effective dose is 0.5-1 mg/day.

Children (depending on age) are prescribed 83.3-333.3 mcg/kg or 2.5-10 mg/sq.m/day in 3-4 doses.

The duration of dexamethasone use depends on the nature of the pathological process and the effectiveness of treatment and ranges from several days to several months or more. Treatment is stopped gradually (at the end several injections of corticotropin are prescribed).

For bronchial asthma, rheumatoid arthritis, ulcerative colitis – 1.5-3 mg/day; for systemic lupus erythematosus – 2-4.5 mg/day; for oncohematological diseases – 7.5-10 mg.

For the treatment of acute allergic diseases, it is advisable to combine parenteral and oral administration: 1 day – 4-8 mg parenterally; Day 2 – orally, 4 mg 3 times a day; 3, 4 days – orally, 4 mg 2 times a day; 5, 6 days – 4 mg/day, orally; Day 7 – drug withdrawal.

Dexamethasone test (Liddle test). It is carried out in the form of small and large tests. For a small test, dexamethasone is given to the patient 0.5 mg every 6 hours during the day (that is, at 8 a.m., 2 p.m., 8 p.m., and 2 a.m.). Urine for the determination of 17-hydroxycorticosteroids or free cortisol is collected from 8 a.m. to 8 a.m. 2 days before the administration of dexamethasone and also 2 days at the same time intervals after taking the indicated doses of dexamethasone. These doses of dexamethasone inhibit the formation of corticosteroids in almost all apparently healthy individuals. 6 hours after the last dose of dexamethasone, plasma cortisol levels are below 135-138 nmol/l (less than 4.5-5 mcg/100 ml). Reducing the excretion of 17-hydroxycorticosteroids below 3 mg/day, and free cortisol below 54-55 nmol/day (below 19-20 mcg/day) excludes hyperfunction of the adrenal cortex. In persons suffering from Cushing's disease or syndrome, no changes in the secretion of corticosteroids are observed during a small test.

When conducting a large test, dexamethasone is prescribed 2 mg every 6 hours for 2 days (that is, 8 mg dexamethasone per day). Urine is also collected to determine 17-hydroxycorticosteroids or free cortisol (if necessary, determine free cortisol in plasma). With Itsenko-Cushing's disease, there is a decrease in the excretion of 17-hydroxycorticosteroids or free cortisol by 50% or more, while with adrenal tumors or adrenocorticotropic-ectopic (or corticoliberin-ectopic) syndrome, the excretion of corticosteroids does not change. In some patients with adrenocorticotropic-ectopic syndrome, a decrease in the excretion of corticosteroids is not detected even after taking dexamethasone at a dose of 32 mg/day.

Instructions for use for Dexamethasone injections

The medication is administered intravenously or intramuscularly; it is recommended for emergency conditions. In difficult cases, the dosage is increased from 4 to 20 mg, injections are repeated until the required therapeutic effect is obtained, the daily dose does not exceed 80 mg. After stabilization of the condition, treatment continues at 2-4 mg, with a gradual decrease in volumes until the medication is discontinued.

To create a long-lasting effect, injections are administered every 3-4 hours; the use of droppers with a solution is allowed. The treatment regimen depends on the indications:

• shock states - from 2 to 6 mg per kilogram of body weight, repeated after 2-6 hours, for 3 days;
• swelling of brain tissue - the first dose is 10 mg, later to suppress symptoms - 4 mg every 6 hours, for 1-2 days, on days 2-4 the dosage is reduced, the total time of therapy does not exceed 1 week;
• oncology - maintenance treatment 2 mg 2-3 times a day;
• allergies – 4-8 mg once a day.

The dose of the drug and its changes depend on health indicators and relief of clinical signs of acute phases of pathologies.