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|Decadron 0.5 mg|
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Pharmacological action of Decadron
Synthetic glucocorticoid (GCS), methylated fluoroprednisolone derivative. It has anti-inflammatory, anti-allergic, immunosuppressive effects, increases the sensitivity of beta-adrenergic receptors to endogenous catecholamines.
It interacts with specific cytoplasmic receptors (receptors for GCS are present in all tissues, especially in the liver) to form a complex that induces the formation of proteins (including enzymes that regulate vital processes in cells.)
Protein metabolism: reduces the amount of globulins in plasma, increases the synthesis of albumin in the liver and kidneys (with an increase in the albumin / globulin ratio), reduces the synthesis and enhances protein catabolism in muscle tissue.
Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation occurs mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.
Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase (increasing the flow of glucose from the liver into the blood); increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases (activation of gluconeogenesis); promotes the development of hyperglycemia.
Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (mineralocorticoid activity), reduces the absorption of Ca+ from the gastrointestinal tract, and reduces bone mineralization.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils and mast cells; by 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 (especially lysosomal) and organelle membranes. Acts at all stages of the inflammatory process: inhibits the synthesis of prostaglandins (Pg) at the level of arachidonic acid (lipocortin inhibits phospholipase A2, inhibits the liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes that promote inflammation, allergies, etc.), synthesis of "pro-inflammatory" cytokines interleukin 1, tumor necrosis factor alpha, etc.); increases the resistance of the cell membrane to the action of various damaging factors.
The immunosuppressive effect is due to the involution of lymphoid tissue caused by the inhibition of lymphocyte proliferation (especially T-lymphocytes), suppression of the migration of B-cells and the interaction of T- and B-lymphocytes, inhibition of the release of cytokines (interleukin-1, 2; interferon gamma) from lymphocytes and macrophages and decreased antibody production.
The antiallergic effect develops as a result of a decrease in 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, T and B lymphocytes, and mast cells; suppressing the development of lymphoid and connective tissue, reducing the sensitivity of effector cells to allergy mediators, suppressing antibody production, changing the body's immune response.
In obstructive respiratory diseases, the action is mainly due to the inhibition of inflammatory processes, the prevention or reduction of the severity of edema of the mucous membranes, a decrease in eosinophilic infiltration of the submucosal layer of the bronchial epithelium and the deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucosa. Increases the sensitivity of beta-adrenergic receptors of the bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production.
Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous GCS.
It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
A feature of the action is a significant inhibition of the function of the pituitary gland and an almost complete absence of mineralocorticosteroid activity.
Doses of 1-1.5 mg / day inhibit the function of the adrenal cortex; biological half-life - 32-72 hours (duration of inhibition of the hypothalamus-pituitary-adrenal cortex).
In terms of the strength of glucocorticoid activity, 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.
In the blood it binds (60-70%) with a specific carrier protein - transcortin. Easily passes through the histohematological barriers (including through the hemato-encephalic and placental).
It is metabolized 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). T1/2 of dexamethasone from plasma - 3-5 hours.
Indications of the drug Dexamethasone
Diseases requiring the introduction of fast-acting GCS, as well as cases when oral administration of the drug is not possible:
endocrine diseases: acute adrenal insufficiency, primary or secondary adrenal cortex insufficiency, congenital hyperplasia adrenal cortex, subacute thyroiditis;
shock (burn, traumatic, operational, toxic) - with ineffectiveness of vasoconstrictors, plasma-substituting drugs and other symptomatic therapy;
edema of the brain (with a brain tumor, traumatic brain injury, neurosurgical intervention, cerebral hemorrhage, encephalitis, meningitis, radiation injury);
asthmatic status; severe bronchospasm (exacerbation of bronchial asthma, chronic obstructive bronchitis);
severe allergic reactions, anaphylactic shock;
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, when oral treatment is impossible;
blood diseases: acute hemolytic anemia, agranulocytosis, idiopathic thrombocytopenic purpura in adults;
severe infectious diseases (in combination with antibiotics);
in ophthalmic practice (subconjunctival, retrobulbar or parabulbar treatment): allergic conjunctivitis, keratitis, keratoconjunctivitis without damage to the epithelium, iritis, iridocyclitis, blepharitis, blepharoconjunctivitis, scleritis, inflammatory process of the eyes, immunosuppression of the eyes, episclanitis cornea;
local application (in the field of pathological education): keloids, discoid lupus erythematosus, annular granuloma.
Method of administration and dosage Decadron tablets
The dose is set individually, depending on the disease and the patient's condition. Inside (during or after a meal) once, in the morning (small dose) or in 2-3 doses (large dose): 2-3 mg to 4-6 mg (10-15 mg) per day, after achieving the effect, the dose is gradually reduced up to supporting - 0.5-1 mg, (2-4.5 mg and more) per day; treatment is stopped gradually (at the end, several injections of corticotropin are prescribed. Children - 0.25-25 mg, or 0.0833-0.3333 mg / kg or 0.0025-0.0001 mg / m2 per day in 3-4 doses depending on age.
Hypersensitivity, mycoses, vaccination with live viral vaccine.
It is possible to change the effects when used simultaneously with acetylsalicylic acid, phenytoin, phenobarbital, ephedrine, rifampin, indomethacin, coumarin anticoagulants, diuretics.
Treatment: with the development of undesirable phenomena - symptomatic, Itsenko-Cushing's syndrome - the appointment of aminoglutethimide.
Use with caution in ulcerative colitis, intestinal diverticulitis, hypoalbuminemia. The appointment in the case of intercurrent infections, tuberculosis, septic conditions requires preliminary and subsequent simultaneous antibacterial therapy. It is necessary to take into account the strengthening of the action in hypothyroidism and cirrhosis of the liver, aggravation of psychotic symptoms and emotional lability at their high baseline level, masking of some symptoms of infections, the likelihood of persisting for several months (up to a year) relative adrenal insufficiency after discontinuation of dexamethasone (especially in the case of prolonged use) ... Breastfeeding is stopped for the period of treatment. With a long course, the dynamics of the growth and development of children is carefully monitored, an ophthalmological examination is systematically carried out, the state of the hypothalamic-pituitary-adrenal system, and the level of glucose in the blood are monitored. Discontinue therapy only gradually. It is recommended to be careful when carrying out any kind of operations, the occurrence of infectious diseases, injuries, to avoid immunization, to exclude the use of alcoholic beverages. In children, in order to avoid overdose, the dose is calculated based on the surface area of the body. In case of contact with patients with measles, chickenpox and other infections, appropriate preventive therapy is prescribed.
Violations of water and electrolyte balance, musculoskeletal system, gastrointestinal tract, endocrine and cardiovascular systems; dermatological, neurological, ophthalmic, metabolic and other disorders.