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Buy Dexamethasone online. Free worldwide shipping.

Solution for intravenous and intramuscular administration 4 mg ampoule 1 ml 25 pcs

Brand: SHREYA LIFE SCIENCES, Pvt. Ltd.

Drug form: Solution

Manufacturers: Slovenia

Active substance: Dexamethasone

Group: Endocrinology

Expiration date: 3 years

 

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Dexamethasone solution

$29.00Price
  • Indications for use of Dexamethasone are:

    Diseases requiring the introduction of fast-acting corticosteroids, as well as cases when oral administration of the drug is impossible:

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

    shock (burn, traumatic, operational, toxic) - with ineffectiveness of 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;

    rheumatic diseases;

    systemic connective tissue diseases;

    acute severe dermatoses;

    malignant diseases: palliative treatment of leukemia and lymphoma in adult patients; acute leukemia in children; hypercalcemia in patients with malignant tumors, 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.

    Pharmachologic effect:

    Synthetic glucocorticoid (GCS), a methylated derivative of fluoroprednisolone. 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 the plasma, increases the synthesis of albumin in the liver and kidneys (with an increase in the albumin / globulin ratio), reduces the synthesis and enhances the catabolism of protein 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.), the synthesis of "proinflammatory 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 the proliferation of lymphocytes (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; gamma-interferon) 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 diseases of the respiratory tract, the action is mainly due to the inhibition of inflammatory processes, the prevention or decrease in the severity of edema of the mucous membranes, a decrease in eosinophilic infiltration of the submucous 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.

    Pharmacokinetics

    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.

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