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oral primobolan

Prednisolone Nycomed – a synthetic glucocorticosteroid preparation, dehydrated analogue of hydrocortisone.Anti-inflammatory, antiallergic, immunosuppressive action, increases beta-adrenoceptor sensitivity to endogenous catecholamines. Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) in all tissues, especially many of them in oral primobolan¬†the liver) to form a complex that induces the formation of proteins (including .ch enzymes that regulate cells in the vital processes).. The protein sharing reduces the amount of globulin in plasma, increases the synthesis of albumin in the liver and kidneys (with increase of albumin / globulin ratio) decreases protein synthesis and increases in muscle catabolism. Lipid metabolism : higher increases the synthesis of fatty acids and triglycerides, it redistributes fat (fat accumulation occurs mainly in the shoulder belt, the face, abdomen), leads to the development of hypercholesterolemia. carbohydrate metabolism: increases carbohydrate absorption from the gastrointestinal tract; It increases the activity of glucose-6-phosphatase (increase of glucose from the liver into the blood); fosfoenolpiruvatkarboksilazy increases the activity and synthesis of aminotransferases (activation of gluconeogenesis); contributes to the development of hyperglycemia. Water-eletrolitny sharing delay sodium and water in the body, stimulate the excretion of potassium (mineralocorticoid activity) reduces the absorption of calcium from the digestive tract, reduced mineralization of bone tissue. The anti-inflammatory effect is due to inhibition of the release of eosinophils and mast cells of mediators of inflammation ;lipokortinov inducing formation and reduce the number of mast cells that produce hyaluronic acid; with decreasing capillary permeability; stabilization of cell membranes (particularly lysosomal) membranes and organelles. Acts on all phases of the inflammatory process: inhibits prostaglandin synthesis for arachidonic acid level (Lipokortin inhibits phospholipase A2 suppresses liberatiou arachidonic acid inhibits the biosynthesis endoperekisey, leukotrienes promoting inflammation, allergies, etc.), Synthesis of “proinflammatory cytokine” (interleukin 1, tumor necrosis factor alpha, and others).; increases the stability of the cell membrane to the action of various damaging factors. Immunosuppressive effect is due to the called involution of lymphoid tissue, inhibition of lymphocyte proliferation (especially T cells), suppression of the migration of B cells, and the interaction of T and B lymphocytes, inhibition of the release of cytokines (IL-1, 2;. gamma interferon) of lymphocytes and macrophages and the decrease in antibody formationAntiallergic effect is due to a decrease of synthesis and secretion of mediators of allergy, inhibition of release from sensitized mast cells and basophils, histamine and other biologically active substances, reducing the number of circulating basophils, T. and B lymphocytes, mast cells; suppression of lymphoid and connective tissue, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody production, changes in the immune response of the body.

When obstructive airway diseases effect is due, mainly, inhibition of inflammatory processes, preventing or reducing the severity of mucosal edema, reduction of eosinophil infiltration submucosal bronchial epithelium layer and deposition in the bronchial mucosa of circulating immune complexes, as well as braking and erozirovaniya desquamation mucosa. It increases the sensitivity of the beta-adrenergic receptors of the bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetic, reduces the viscosity of mucus by reducing its production. It suppresses the synthesis and secretion of ACTH and secondary -. The synthesis of endogenous corticosteroids Stops connective tissue reaction in the course of the inflammatory process and reduces the possibility oral primobolan of the formation of scar tissue.
Ingestion prednisone is well absorbed from the gastrointestinal tract. The maximum blood concentration is reached after 1-1.5 hours after oral administration. Up to 90% of the drug binds to plasma proteins: transcortin (kortizolsvyazyvayuschim globulin) and albumin. Prednisolone is metabolized in the liver and kidneys and partly in other tissues, mainly by conjugation with glucuronic acid and sulfuric acid. The metabolites are inactive.
It is deduced with bile and in the urine by glomerular filtration and 80-90% is reabsorbed tubules. 20% of the dose excreted by the kidneys in an unmodified form.
The half-life period of the plasma after oral administration is 2-4 hours after intravenous administration of 2-3.5 hours.

testimony

For oral administration:

 

  • Systemic connective tissue diseases (systemic lupus erythematosus, scleroderma, periarteritis nodosa, dermatomyositis, rheumatoid arthritis).
  • Acute and chronic inflammatory arthritic joint disease and psoriatic arthritis, osteoarthritis (including post-traumatic), polyarthritis (including senile), frozen shoulder, ankylosing spondylitis (ankylosing spondylitis), juvenile arthritis, Still’s syndrome in adults, bursitis , nonspecific tenosynovitis, synovitis and epicondylitis.
  • Acute rheumatic fever, rheumatic carditis, chorea.
  • Bronchial asthma, asthmatic status.
  • Acute and chronic allergic diseases – including Allergic reactions to medicines and foods, serum sickness, urticaria, allergic rhinitis, angioedema, drug rash, hay fever and others.
  • Skin diseases oral primobolan¬†– pemphigus, psoriasis, eczema, atopic dermatitis (common neurodermatitis), contract dermatitis (with the defeat of a large surface of the skin), drug reaction, seborrheic dermatitis, exfoliative dermatitis, toxic epidermal necrolysis (Lyell’s syndrome), bullous dermatitis herpetiformis, Stevens-Johnson syndrome .
  • Cerebral edema (including on the background of a brain tumor or associated with surgery, radiation therapy, or head injury) after a preliminary parenteral use.
  • Allergic eye disease – allergic form of conjunctivitis.
  • Inflammatory diseases of the eye – sympathetic ophthalmia, severe lingering front and rear uveitis, optic neuritis.
  • Primary or secondary adrenocortical insufficiency (including the state after the removal of the adrenal glands).
  • Congenital adrenal hyperplasia.

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