Universal reference book for medicines

Active substance: dexamethasone

Type: GCS for oral administration

Manufacturer: KRKA (Slovenia)
Composition, form of production and packaging
1 tab.

dexamethasone 500 Ојg

10 pieces.
- packings of cellular contour (1) - packs cardboard.
10 pieces.
- bottles of dark glass (1) - packs of cardboard.

Description of the drug approved by the manufacturer for the printed edition of 2011.


Glucocorticosteroid (GCS) is a methylated derivative of fluoride prednisolone, inhibits the release of interleukin-1 and interleukin-2, interferon gamma from lymphocytes and macrophages.
Has anti-inflammatory, antiallergic, desensitizing, anti-shock, antitoxic and immunosuppressive action.
Suppresses pituitary adrenocorticotropic hormone release (ACTH) and beta-lipotropin, but does not reduce the content of circulating beta-endorphin.
Oppressing the secretion of thyroid-stimulating hormone (TSH) and follicle-stimulating hormone (FSH).
Increases the excitability of the central nervous system (CNS), reduces the number of lymphocytes and eosinophils, increases erythrocytes (stimulates the production of erythropoietins).

Interacts with specific cytoplasmic receptors, forms a complex penetrating the nucleus of the cell, stimulates the synthesis of mRNA, which induces the formation of proteins, including.
lipocortin, which mediate cellular effects. Lipocortin depresses phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, Pg, leukotrienes, which promote inflammation, allergies, etc.
Protein metabolism: reduces the amount of protein in the plasma (due to globulins) with an increase in the albumin / globulin ratio, increases the synthesis of albumins in the liver and kidneys;
enhances protein catabolism in muscle tissue.
Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides (TG), redistributes fat (accumulation of fat mainly in the area of ​​the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.

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

Water-electrolyte metabolism: retards Na + and water in the body, stimulates the excretion of K + (MCS activity), reduces the absorption of Ca2 + from the gastrointestinal tract, "cleanses" Ca2 + from the bones, increases the excretion of Ca2 + by the kidneys.

The anti-inflammatory effect is associated with the inhibition of eosinophil release by inflammatory mediators;
inducing lipocortin formation and reducing the number of mast cells producing hyaluronic acid; with a decrease in the permeability of capillaries; stabilization of cell membranes and membranes of organelles (especially lysosomal).
The antiallergic effect develops as a result of suppression of the synthesis and secretion of mediators of allergy, inhibition of release from sensitized mast cells and basophils of histamine and other biologically active substances, a decrease in the number of circulating basophils, suppression of lymphoid and connective tissue development, reduction in the number of T- and B-lymphocytes, cells, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody formation, changes in the immune response of the body.

In chronic obstructive pulmonary disease (COPD), the effect is mainly based on inhibition of inflammatory processes, inhibition of development or prevention of edema of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of bronchial epithelium, deposition of circulating immune complexes in the mucosa of the bronchi, and inhibition of erosion and desquamation of the mucosa .
Increases the sensitivity of beta-adrenergic receptors of small and medium-sized bronchial tubes to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus due to oppression or reduction of its production.
The anti-shock and antitoxic effect is associated with an increase in blood pressure (by increasing the concentration of circulating catecholamines and restoring the sensitivity of adrenoreceptors to them, as well as vasoconstriction), reducing the permeability of the vascular wall, membrane-protective properties, activation of liver enzymes involved in endo- and xenobiotic metabolism.

Immunosuppressive effect is due to inhibition of the release of cytokines (interleukin1, interleukin2, interferon gamma) from lymphocytes and macrophages.

Suppresses the synthesis and secretion of ACTH, and again - the synthesis of endogenous GCS.
It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
The peculiarity of the action is a significant inhibition of the pituitary function and almost complete absence of MKS activity.
Doses of 1-1.5 mg / day inhibit the adrenal cortex; biological T 1/2 - 32-72 h (the duration of oppression of the hypothalamic-pituitary-cortical adrenal gland system).
The strength of the glucocorticosteroid activity of 0.5 mg of dexamethasone corresponds to approximately 3.5 mg of prednisone (or prednisolone), 15 mg of hydrocortisone or 17.5 mg of cortisone.


Dexamethasone is rapidly and almost completely absorbed after ingestion.
The bioavailability of dexamethasone tablets is approximately 80%. C max in blood plasma and the maximum effect after ingestion are achieved after 1-2 hours; After taking a single dose, the effect persists for approximately 2.75 days.
In blood plasma, approximately 77% of dexamethasone binds to proteins, mainly albumin.
An insignificant amount of dexamethasone binds to non-albumin proteins.Dexamethasone is a fat-soluble substance that can penetrate into extra- and intracellular spaces. In the central nervous system (hypothalamus, pituitary gland), its effects are due to binding to membrane receptors. In peripheral tissues, it binds to cytoplasmic receptors. Its disintegration takes place in the place of its action, i.e. in a cage. Metabolized mainly in the liver until the formation of inactive metabolites. It is excreted by the kidneys.

On the part of the endocrine system: substitution therapy of primary and secondary (pituitary) adrenal insufficiency, congenital adrenal hyperplasia, subacute thyroiditis and severe forms of post-radiation thyroiditis.
Rheumatic diseases: rheumatoid arthritis (including juvenile chronic arthritis) and extra-articular lesions in rheumatoid arthritis (lungs, heart, eyes, skin vasculitis).
Systemic connective tissue diseases, vasculitis and amyloidosis (as part of combination therapy): systemic lupus erythematosus (treatment of polyserositis and internal lesions), Sjogren's syndrome (treatment of lung, kidney and brain lesions), systemic sclerosis (treatment of myositis, pericarditis and alveolitis) , polymyositis, dermatomyositis, systemic vasculitis, amyloidosis (replacement therapy with adrenal insufficiency), scleroderma.

Skin diseases: pemphigoid, bullous dermatitis, herpetiform dermatitis, exfoliative dermatitis, exudative erythema (severe forms), nodular erythema, seborrheic dermatitis (severe forms), psoriasis (severe forms), lichen, fungoid mycoses, Quincke edema, bronchial asthma, contact dermatitis , atopic dermatitis, serum sickness, allergic rhinitis, drug disease (hypersensitivity to drugs), urticaria after a blood transfusion, systemic immune diseases (sarcoidosis, temporal arteritis).

Eye diseases: proliferative changes in the orbit (endocrine ophthalmopathy, pseudotumor), sympathetic ophthalmia, immunosuppressive therapy for corneal transplantation.

Diseases of the gastrointestinal tract: ulcerative colitis (severe exacerbations), Crohn's disease (severe exacerbations), chronic autoimmune hepatitis, rejection reaction after liver transplantation.

Blood diseases: congenital or acquired acute pure aplastic anemia, autoimmune hemolytic anemia, secondary thrombocytopenia in adults, erythroblastopenia, acute lymphoblastic leukemia (induction therapy), myelodysplastic syndrome, angioimmunoblast malignant T-cell lymphoma (in combination with cytostatics), plastocytoma (in combination with cytostatics), anemia after myelofibrosis with myeloid metaplasia or lymphoplasmacytoid immunocytoma, systemic histiocytosis (systemic process).

Kidney diseases: primary and secondary glomerulonephritis (Goodpasture's syndrome), kidney damage in systemic connective tissue diseases (systemic lupus erythematosus, Sjogren's syndrome), systemic vasculitis (usually in combination with cyclophosphamide), glomerulonephritis with nodular polyarteritis, Chang-Strauss syndrome, Wegener's granulomatosis purplish Shonlein-Genocha, mixed cryoglobulinemia, kidney damage in arteritis Takayasu, interstitial nephritis, immunosuppressive therapy after kidney transplantation, diuresis and
and reducing proteinemii idiopathic nephrotic syndrome (without uremia) and renal lesions associated with systemic lupus erythematosus.
Malignant diseases: palliative therapy of leukemia and lymphoma in adults, acute leukemia in children, hypercalcemia in malignant neoplasms.

Other indications: tubercular meningitis with subarachnoid blockade (in combination with adequate anti-tuberculosis therapy), trichinosis with neurologic or myocardial manifestations.


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

The recommended starting dose for adults is 0.5 mg to 9 mg / day.

The usual maintenance dose is from 0.5 mg to 3 mg / day.

The minimum effective daily dose is 0.5-1 mg.

The maximum daily dose is 10-15 mg.

The daily dose can be divided into 2-4 receptions.

After reaching the therapeutic effect, the dose is gradually reduced (usually by 0.5 mg every 3 days until a maintenance dose is reached).

With prolonged use of high doses inside, the drug is recommended to be taken during meals, and in the intervals between meals it is necessary to take antacids.
The duration of dexamethasone 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).
- with bronchial asthma , rheumatoid arthritis, ulcerative colitis - 1.5-3 mg / day;

- with systemic lupus erythematosus - 2-4.5 mg / day;

- with hematological 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;
2 day - inside, 4 mg 3 times a day; 3, 4 day - inside, 4 mg 2 times a day; 5, 6 day - 4 mg / day, inside; Day 7 - cancellation of the drug.
Dosing in children

Children (depending on age) are prescribed 2.5-10 mg / m 2 body surface area / day, dividing the daily dose by 3-4 doses.

Diagnostic tests for hyperfunction of the adrenal cortex

Short 1-mg dexamethasone test: 1 mg dexamethasone inside at 11.00;
blood sampling for determination of serum cortisol at 8.00 the next day.
Special 2-day test with 2 mg of dexamethasone: 2 mg of dexamethasone every 6 hours for 2 days;
24-hour urine is collected to determine the concentration of 17-hydroxycorticosteroids.

Classification of the incidence of adverse events (WHO): very often> 1/10, often> 1/100 to <1/10, infrequently from> 1/1000 to <1/100, rarely> 1/10000 to <1 / 1000, very rarely from <1/10000, including individual messages.

On the part of the immune system: infrequently, reactions of increased sensitivity, a decrease in the immune response, and an increase in susceptibility to infections.

On the part of the endocrine system: often - transient adrenal insufficiency, growth retardation in children and adolescents, adrenal insufficiency and atrophy (reduction of response to stress), Itenko-Cushing syndrome, menstrual cycle disorder, hirsutism, transition of latent diabetes to clinically manifested, increase the need for insulin or oral hypoglycemic drugs in patients with diabetes mellitus, sodium and water retention, increased potassium loss;
very rarely - hypokalemic alkalosis, negative nitrogen balance due to protein catabolism.
Disorders of metabolism and nutrition: often - reduced tolerance to carbohydrates, increased appetite and weight gain, obesity;
infrequently hypertriglyceridemia.
From the nervous system: often - mental disorders;
infrequently - edema of the papillae of the optic nerve and increased intracranial pressure (pseudotumor brain) after the abolition of therapy, dizziness, headache; very rarely - convulsions, euphoria, insomnia, irritability, hyperkinesia, depression; rarely - psychosis.
On the part of the digestive system: infrequently - peptic ulcers, acute pancreatitis, nausea, hiccups, stomach ulcers or 12 duodenal ulcer;
very rarely - esophagitis, perforation of the ulcer and bleeding of the gastrointestinal tract (hematomasis, melena), pancreatitis, perforation of the gallbladder and intestine (especially in patients with chronic inflammatory diseases of the large intestine).
From the sense organs: infrequently - posterior subcapsular cataract, increased intraocular pressure, propensity to develop secondary bacterial, fungal or viral infections of the eyes, trophic corneal changes, exophthalmos.

From the cardiovascular system: infrequently - arterial hypertension, hypertensive encephalopathy;
very rarely - polyfocal ventricular extrasystoles, transient bradycardia, heart failure, myocardial rupture after a recent acute infarction.
From the skin: often erythema, thinning and fragility of the skin, delayed healing of wounds, striae, petechiae and ecchymosis, excessive sweating, steroid acne, suppression of skin reaction during allergological tests;
very rarely - anginaurotic edema, allergic dermatitis, urticaria.
From the musculoskeletal system: often - muscle atrophy, osteoporosis, muscle weakness, steroid myopathy (muscle weakness due to catabolism of muscle tissue);infrequently - aseptic necrosis of bones;
very 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).
On the part of the hematopoiesis system: rarely - thromboembolic complications, a decrease in the number of monocytes and / or lymphocytes, leukocytosis, eosinophilia (as in other glucocorticosteroids), thrombocytopenia and netrombocytopenic purpura.

Allergic reactions: rarely - skin rash, itching, angioedema, bronchospasm, anaphylactic shock.

From the genitourinary system: rarely - impotence.

Signs and symptoms of glucocorticosteroid withdrawal syndrome

If a patient taking long-term glucocorticosteroids quickly decreases the dose of the drug, signs of adrenal insufficiency, arterial hypotension, and death may develop.

In some cases, the withdrawal symptoms may be similar to the symptoms and signs of an exacerbation or relapse of the disease, for which the patient is receiving treatment.
With the development of severe undesirable phenomena, treatment with Dexamethasone should be stopped.

For short-term use according to "vital" indications, the only contraindication is increased sensitivity to the active substance or auxiliary components of the drug.

The drug Dexamethasone is contraindicated in patients with galactosemia, lactase deficiency and glucose-galactose malabsorption syndrome, due to the fact that the composition of the drug includes lactose.

Parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently transferred, including recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chicken pox, measles; amebiasis, strongyloidiasis (established or suspected); systemic mycosis; active and latent tuberculosis, pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination, immunodeficiency (including AIDS or HIV infection).
Diseases of the gastrointestinal tract: peptic ulcer of stomach and duodenum, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with threat of perforation or abscess formation, diverticulitis.

Diseases of the cardiovascular system, incl.
recently suffered myocardial infarction (in patients with acute and subacute myocardial infarction, the spread of the necrosis foci, slowing the formation of scar tissue and, as a result, rupture of the heart muscle), decompensated chronic heart failure, hypertension, hyperlipidemia.
Endocrine diseases: diabetes mellitus (including a violation of carbohydrate tolerance), thyrotoxicosis, hypothyroidism, Itenko-Cushing's disease.

Severe chronic kidney and / or liver failure, nefrourolitiaz; hypoalbuminemia and conditions predisposing to its occurrence; systemic osteoporosis, myasthenia gravis, acute psychosis, obesity (III-IV v.), polio (except bulbar form of encephalitis), open-and-closure glaucoma, lactation.

During pregnancy (especially in the first trimester) drug Dexamethasone can be used only if the expected therapeutic effect outweighs the potential risk to the fetus. When long-term therapy with dexamethasone during pregnancy does not exclude the possibility of fetal growth. In the case of the drug Dexamethasone in the last 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 a woman during pregnancy received glyukortikosteroidy, during childbirth recommend the additional use of glucocorticosteroids. If labors delayed or planned caesarean section in the peripartum period recommended intravenously administered 100 mg of hydrocortisone every 8 hours.
If necessary, drug therapy Dexamethasone breastfeeding should be discontinued.

Contraindicated in severe renal insufficiency, nefrourolitiaze.

Contraindicated in severe chronic liver failure.

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

Patients requiring long-term therapy with dexamethasone after discontinuation of therapy may develop a "cancellation" syndrome (also without of distinct signs of adrenal insufficiency): fever, nasal discharge, conjunctival hyperemia, headache, dizziness, drowsiness and irritability, pain in muscles and joints , vomiting, weight loss, weakness, cramps. Therefore, it is necessary to cancel the dexamethasone by gradually reducing the dose. Rapid removal of the drug can be fatal.
Patients receiving long-term therapy with dexamethasone and after it is subjected to stress cancel, it is necessary to resume the use of dexamethasone, due to the fact that the induced adrenal insufficiency may persist for several months after discontinuation of therapy.
Dexamethasone therapy may mask the signs of existing or new infections and signs of bowel perforation in patients with ulcerative colitis. Dexamethasone can exacerbate systemic fungal infections, latent amoebiasis or pulmonary tuberculosis.
Patients with acute pulmonary tuberculosis dexamethasone can be administered (together with the anti-TB drugs) only in the case of heavy or fulminant metastatic process. Patients with inactive pulmonary tuberculosis receiving dexamethasone, or patients with a positive tuberculin skin test should be parallel to receive TB chemoprophylaxis.
Particular attention and close medical supervision is necessary for patients with osteoporosis, hypertension, congestive heart failure, tuberculosis, glaucoma, liver or kidney disease, diabetes, active peptic ulcers, fresh intestinal anastomosis, ulcerative colitis and epilepsy. With careful preparation is administered in the first few weeks after acute myocardial infarction in patients with venous thromboembolism, with myasthenia gravis, glaucoma, hypothyroidism, psychosis or psychoneurosis, and patients older than 65 years.
During therapy with dexamethasone is possible decompensation of diabetes or latent transition in clinically overt diabetes.
Prolonged treatment is necessary to monitor the level of potassium in serum.
During therapy with dexamethasone contraindicated vaccination with live vaccines.
Immunization with killed viral or bacterial vaccines do not give the expected growth titer of specific antibody and therefore does not provide the necessary protective action. Dexamethasone not usually prescribed for 8 weeks prior to vaccination and at 2 weeks following vaccination.
Patients taking high dose of dexamethasone for a long time, should avoid contact with patients with measles; in the event of accidental contact may prophylactic treatment immunoglobulin.
Care should be taken when treating patients who have recently undergone surgery or broken bones as dexamethasone can slow the healing of wounds and fractures.
The action of corticosteroids is enhanced in patients with liver cirrhosis or hypothyroidism.
Dexamethasone is used in children and adolescents only on strict conditions. During treatment requires strict control of the growth and development of the child or adolescent.
Specific information about some of the ingredients of the drug
in the drug Dexamethasone includes lactose, and therefore, its application in patients with galactosemia, lactase deficiency and syndrome of glucose-galactose malabsorption contraindicated.
The effect on the ability of road management and other complex mechanisms
Dexamethasone did not affect the ability to control and road work with technical devices that require concentration and psychomotor speed reactions.

A single application of a large number of tablets does not cause clinically significant toxicity.
Symptoms may increase dose-related side effects. In this case, the dose should be reduced.
Treatment: supportive and symptomatic.
There is no specific antidote.

Hemodialysis is ineffective.


The simultaneous use of dexamethasone and non-steroidal anti-inflammatory drugs (NSAIDs) and increases the risk of formation of ulcers of the gastrointestinal tract.
Action dexamethasone decreases while applying CYPZA4 isoenzyme inducers (e.g., phenytoin, phenobarbitone, carbamazepine, primidone, rifabutin, rifampicin), or agents that increase the metabolic clearance of glucocorticoids (ephedrine and aminoglutethimide); in such cases it is necessary to increase the dose of dexamethasone.
The interaction between dexamethasone and the above drugs can distort the results of dexamethasone supressionnyh samples. If tests with dexamethasone should be conducted during therapy with one of these drugs, this interaction should be considered when interpreting the results of the samples.
The simultaneous use of dexamethasone and inhibitors CYPZA4 isoenzyme (e.g., ketoconazole, macrolide antibiotics) may lead to increased blood concentrations of dexamethasone.
Concomitant use of drugs that are metabolized CYPZA4 (e.g., indinavir, erythromycin) can increase their ride height, which may be accompanied by a reduction in their serum concentrations.
Dexamethasone reduces the effectiveness of hypoglycemic drugs, antihypertensives, praziquantel and natriyuretikov (need to increase the dose of these drugs); It increases the activity of heparin, albendazole and potassium-sparing diuretics (if required dose of these drugs decrease).
Dexamethasone can change the effect of coumarin anticoagulants, so during therapy is recommended more frequent monitoring of prothrombin time. Antacids reduce the absorption of dexamethasone in the stomach. Smoking did not affect the pharmacokinetics of dexamethasone.
With simultaneous use of oral contraceptives may increase T 1/2 glucocorticosteroids with corresponding increase their biological effects, and increased frequency of adverse side effects.
Concomitant use of ritodrine and dexamethasone during labor, as this may result due to pulmonary edema to the mother's death. The combined use of thalidomide and dexamethasone can induce toxic epidermal necrolysis.
Potential therapeutically beneficial interactions: the simultaneous use of dexamethasone and metoclopramide, diphenhydramine, prochlorperazine or antagonists of 5-HT 3 receptor antagonists (serotonin or 5-hydroxytryptamine receptors of 3 types), such as ondansetron or granisetron, is effective in the prevention of nausea and vomiting caused by chemotherapy (cisplatin , cyclophosphamide, methotrexate, fluorouracil).

The drug is released by prescription.


The drug is stored at a temperature not higher than 25 В° C, in the original package.
Keep out of the reach of children.
Shelf life -
5 years. Do not use the drug after the expiration date.
Alphabetical index of medicines:
A  B  V  G  D  E  J
Z  I  Y  K  L  M  N
O  P  R  S  T  U  F
H  C  CH  SH  E  U  Y

Privacy policy:
Copyright 2009 - 2017. Universal reference book of medicines. All rights reserved.
When using site materials, an active hyperlink is required!