Active substanceDexamethasoneDexamethasone
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  • Dosage form: & nbsppills
    Composition:

    One tablet contains:

    active substance: dexamethasone in terms of 100% substance 0.5 mg;

    Excipients: sucrose (sugar), potato starch, stearic acid.

    Description:

    Tablets of white color, flat-cylindrical, with a facet.

    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:

    Synthetic glucocorticosteroid - 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, immunosuppressive, anti-shock and antitoxic action.

    Suppresses the release of pituitary adrenocorticotropic hormone and beta-lipotropin, but does not reduce the level of circulating beta-endorphin. Oppressing 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 quantitative content of erythrocytes (stimulates the production of erythropoietins).

    Interacts with specific cytoplasmic receptors and forms a complex penetrating the nucleus of the cell, stimulates the synthesis of mRNA; the latter induces the formation of proteins, incl. lipocortin, mediating cellular effects. Lipocortin depresses phospholipase A2, inhibits the release of arachidonic acid, and suppresses the synthesis of endoperoxides, prostaglandins, leukotrienes, which promote inflammation, allergies, and others.

    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, 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; increases the activity of glucose-6-phosphatase,leading to an increase in the intake of glucose from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases leading to the activation of gluconeogenesis.

    Water-electrolyte exchange: detains 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, "removes" calcium ions from the bones, increases the excretion of calcium ions by the kidneys.

    Anti-inflammatory effect is associated with 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).

    Antiallergic effect develops as a result of suppression of synthesis and secretion of mediators of allergy, inhibition of release from sensitized mast cells and basophils of histamine and other biologically active substances, reduction in the number of circulating basophils, suppression of lymphoid and connective tissue development,reducing the number of T- and B-lymphocytes, mast cells, reducing the sensitivity of effector cells to mediators of allergy, suppressing antibody formation, changing the immune response of the body.

    In chronic obstructive pulmonary disease, the action 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 the bronchial epithelium, deposition of circulating immune complexes in the mucous membrane of 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.

    Anti-shock and antitoxic action 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), a decrease in the permeability of the vascular wall, membrane-protective properties, activation of liver enzymes involved in the metabolism of endo- and xenobiotics.

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

    Suppresses the synthesis and secretion of ACTH and, again, the synthesis of endogenous glucocorticosteroids. 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 a virtually complete absence of mineralocorticosteroid activity. Doses of 1-1.5 mg / day inhibit the adrenal cortex; the biological half-life is 32-72 h (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 for oral dosage forms.

    Pharmacokinetics:

    After oral intake quickly and completely absorbed, the maximum concentration of dexamethasone in the blood plasma - 1-2 hours. In the blood binds (60-70%) with specific carrier protein - transcortin. Easily passes through gistogematicheskie barriers (incl.through blood-brain and placental barriers). Metabolised in the liver (mainly by conjugation with glucuronic and sulfuric acids) to inactive metabolites. It is excreted by the kidneys (a small part by the lactating glands). Half-life is 3-5 hours.

    Indications:

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

    Acute and chronic inflammatory joint diseases: gouty and psoriatic arthritis, osteoarthritis (including posttraumatic), polyarthritis, humeropathy periarthritis, ankylosing spondylitis (Bechterew's disease), juvenile arthritis, Still's syndrome in adults, bursitis, nonspecific tenosynovitis, synovitis and epicondylitis .

    Rheumatic fever, acute rheumatic heart disease.

    Acute and chronic allergic diseases: allergic reactions to medicines and food products, serum sickness, urticaria, allergic rhinitis, angioedema, drug exanthema, pollinosis.

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

    A cerebral edema (including on the background of a brain tumor or associated with surgery, radiation therapy or head trauma) after previous parenteral administration.

    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 hyperplasia of the adrenal glands.

    Kidney disease of autoimmune genesis (including acute glomerulonephritis); nephrotic syndrome.

    Subacute thyroiditis.

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

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

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

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

    Lung cancer (in combination with cytostatics).

    Multiple sclerosis.

    Diseases of the gastrointestinal tract: ulcerative colitis, Crohn's disease, local enteritis.

    Hepatitis.

    Prevention of graft rejection in combination therapy.

    Hypercalcemia on the background of cancer, nausea and vomiting during cytostatic therapy.

    Myeloma disease.

    Conduct a sample in the differential diagnosis of hyperplasia (hyperfunction) and adrenal cortex tumors.

    Contraindications:

    For short-term use according to "vital" indications, the only contraindication is hypersensitivity.

    Carefully:

    Parasitic and infectious diseases of viral, fungal or bacterial origin (currently or recently transferred, including the recent contact with the patient) - herpes simplex, herpes zoster (viremicheskaya phase), chicken pox, measles; amoebiasis, strongyloidiasis (or suspected); systemic mycosis; active and latent tuberculosis. The use in severe infectious diseases is permissible only against the background of specific therapy.

    Pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination.

    Immunodeficiency conditions (including AIDS or HIV infection).

    Diseases of the gastrointestinal tract: peptic ulcer of stomach and duodenum, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with perforation or abscessing, 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 (including a violation of tolerance to carbohydrates), thyrotoxicosis, hypothyroidism, Itenko-Cushing's disease.

    Severe chronic renal and / or hepatic insufficiency, nephrourolythiasis.

    Hypoalbuminemia and conditions predisposing to its occurrence.

    Systemic osteoporosis, myasthenia gravis gravis, acute psychosis, obesity (III-IV st), poliomyelitis (with the exception of the form of bulbar encephalitis), open and closed angle glaucoma, lactation period.

    Pregnancy and lactation:

    During pregnancy (especially in the first trimester), the drug can be used only for life indications. With prolonged therapy during pregnancy, the possibility of impaired fetal growth is not ruled out. In the case of use in the III 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, then breastfeeding should be discontinued.

    Dosing and Administration:

    Inside, in individually selected doses, the magnitude of which is determined by the type of disease; the degree of his activity and the nature of the patient's response.

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

    Children (depending on the age) 83.3-333.3 μg / kg or 2.5-10 mg / sq. m / day in 3 4 reception.

    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 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; 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.

    A trial with dexamethasone (Liddell test). It is conducted in the form of small and large tests.

    With a small test dexamethasone give the patient 0.5 mg every 6 hours during the day (ie at 8 am, at 14:00, 20:00 and 2:00 in the morning). Urine to determine 17-oxycorticosteroids or free cortisol is collected from 8:00 am to 8:00 am 2 days before the appointment 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 practically healthy individuals. Six hours after the last dose of dexamethasone, the cortisol content in the plasma is lower than 135-138 nmol / l (less than 4.5-5 μg / 100 ml). Reducing the excretion of 17-hydroxycorticosteroids below 3 mg / day, and free cortisol below 54-55 nmol / day (below 19-20 μg / day) excludes hyperfunction of the adrenal cortex. In individuals with a disease or with Isenko-Cushing syndrome, there is no change in the secretion of corticosteroids during a small test.

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

    Side effects:

    The frequency of development and severity of side effects depend on the duration of application, the amount of dose used and the possibility of observing the circadian rhythm of the appointment. Usually dexamethasone well tolerated. It has a low mineralocorticoid activity, i.e. its effect on water-electrolyte exchange is small. As a rule, low and medium doses of dexamethasone do not cause delays in sodium and water in the body, increased excretion of potassium.

    The following side effects are described:

    From the endocrine system: depression of glucose tolerance, steroid diabetes mellitus or manifestation of latent diabetes mellitus, oppression of the adrenal gland function, Itenko-Cushing syndrome (lunar face, obesity of the pituitary type, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia, striae), delay in sexual development in children.

    From the digestive system: nausea, vomiting, pancreatitis, steroid ulcer of the stomach and duodenum, erosive esophagitis, bleeding and perforation of the gastrointestinal tract, increase or decrease in appetite, flatulence, hiccough. In rare cases - increased activity of "liver" transaminases and alkaline phosphatase.

    From the cardiovascular system: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or increased severity of chronic heart failure, ECG changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread of the focus of necrosis, slowing the formation of scar tissue, which can lead to rupture of the heart muscle.

    From the nervous system: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, pseudotumor, cerebral palsy, headache, convulsions.

    From the sense organs: posterior subcapsular cataract,increased intraocular pressure with possible damage to the optic nerve, a tendency to develop secondary bacterial, fungal or viral infections of the eyes, trophic changes in the cornea, exophthalmos.

    From the side of metabolism: increased excretion of calcium ions, hypocalcemia, weight gain, negative nitrogen balance (increased protein breakdown), increased sweating.

    Caused by mineralocorticosteroid activity - fluid retention and sodium ions (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).

    From the side of the musculoskeletal system: slowing the growth and processes of ossification in children (premature closure of epiphyseal growth zones), osteoporosis (very rarely - pathological bone fractures, aseptic necrosis of the head of the humerus and thigh bone), rupture of muscle tendons, steroid myopathy, muscle loss (atrophy).

    From the skin and mucous membranes: delayed healing of wounds, petechiae, ecchymosis, thinning of the skin, atrophy of the skin and subcutaneous tissue, hyper- or hypopigmentation, steroid acne, striae, propensity to develop pyoderma and candidiasis. Allergic reactions: generalized (skin rash, skin itching, anaphylactic shock), local allergic reactions.

    Other: development or exacerbation of infections (the emergence of this side effect is facilitated by jointly used immunosuppressants and vaccination), leukocyturia, withdrawal syndrome.

    Overdose:

    It is possible to strengthen the above described side effects, except for allergic reactions. It is necessary to reduce the dose of dexamethasone. Treatment is symptomatic.

    Interaction:

    Dexamethasone increases the toxicity of cardiac glycosides (because of the resulting hypokalemia, the risk of arrhythmias increases).

    Accelerates the removal of acetylsalicylic acid, reduces its level in the blood (with the dexamethasone abolition, the concentration of salicylates in the blood increases and the risk of side effects increases).

    With simultaneous use with live antiviral vaccines and against other types of immunizations, increases the risk of virus 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 hepatotoxic effects of paracetamol (induction of "liver" enzymes and the formation of a toxic metabolite of paracetamol).

    Increases (with prolonged therapy) the content of folic acid.

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

    In high doses reduces the effect of somatropin.

    Antacids reduce the absorption of glucocorticosteroid agents.

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

    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 glucocorticosteroids.

    Reduces the concentration of praziquantel in the blood.

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

    Thiazide diuretics, inhibitors of carbonic anhydrase, other glucocorticosteroids 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 ulceration of the gastrointestinal mucosa, bleeding, in combination with non-steroidal anti-inflammatory drugs for the treatment of arthritis, it is possible to reduce the dose of glucocorticosteroids due to the summation of the therapeutic effect.

    Indomethacin, displacing dexamethasone from 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 glucocorticosteroids decreases under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of "hepatic" microsomal enzymes (an increase in metabolic rate).

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

    The clearance of glucocorticosteroids rises against the background of thyroid hormones.

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

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

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

    Tricyclic antidepressants can increase the severity of depression caused by taking glucocorticosteroids (not shown for the therapy of these side effects).

    The risk of developing cataracts increases with other glucocorticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine.

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

    Special instructions:

    Before and during the course of glucocorticosteroid therapy, it is necessary to monitor the general blood test, the level of glycemia and the content of electrolytes in the plasma. Assigning dexamethasone with intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously treat with bactericidal antibiotics.

    With daily administration to 5 months of treatment, atrophy of the adrenal cortex develops. Can mask some symptoms of infections; during treatment it is useless to carry out immunization.

    With the sudden abolition of glucocorticosteroids, especially in the case of previous use of high doses, there is a syndrome of "cancellation" of glucocorticosteroids (not due to hypocorticism): decreased appetite, nausea, inhibition, generalized musculoskeletal pain, asthenia, and possibly the emergence and acute adrenal insufficiency arterial pressure, arrhythmia, sweating, weakness, oligoanuria, vomiting, abdominal pain, diarrhea, hallucinations, fainting, coma).

    After the abolition, the relative adrenocortical cortex remains relatively insignificant for several months. If during this period there are stressful situations, prescribe (for indications) for a time glucocorticosteroids, if necessary in combination with mineralocorticosteroids.

    Children during prolonged treatment need careful monitoring of the dynamics of growth and development. Children who were in contact with sick measles or chickenpox during the treatment period prophylactically prescribe specific immunoglobulins.

    During treatment with dexamethasone (especially long-term) it is necessary to observe the oculist, control blood pressure and water-electrolyte balance, as well as patterns of peripheral blood and glycemia.

    In order to reduce side effects, it is possible to prescribe anabolic steroids, antacids, and also increase the intake of potassium ions into the body (diet, potassium preparations). Food should be rich in potassium ions, proteins, vitamins, containing a small amount of fats, carbohydrates and salt.

    In children during growth, glucocorticosteroids should be used only in absolute indications and under the close supervision of the treating physician.

    Form release / dosage:

    Tablets, 0.5 mg.

    Packaging:

    For 10 tablets in a planar cell package.

    5 contour mesh packages together with instructions for use in a pack of cardboard.
    Storage conditions:

    In a dry, the dark place at a temperature of no higher than 25 ° C.

    Keep out of the reach of children.

    Shelf life:

    4 years.

    Do not use after the expiration date.

    Terms of leave from pharmacies:On prescription
    Registration number:P N002537 / 01
    Date of registration:14.07.2008
    Expiration Date:Unlimited
    The owner of the registration certificate:AKRIKHIN HFK, JSC AKRIKHIN HFK, JSC Russia
    Manufacturer: & nbsp
    Representation: & nbspAKRIKHIN OJSC AKRIKHIN OJSC Russia
    Information update date: & nbsp21.03.2017
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