Medopred, 30 mg/ml, solution for injection, 1 ml, 10 pcs.
There may be pharmaceutical incompatibility of prednisolone with other intravenously administered drugs - it is recommended to administer it separately from other drugs (iv bolus, or through another dropper, as a second solution).
When mixing a solution of prednisolone with heparin, a precipitate forms.
Prednisolone with long-term therapy can increase the content of folic acid.
Simultaneous administration of prednisolone with:
- inducers of microsomal liver enzymes (phenobarbital, rifampicin, phenytoin, theophylline, ephedrine) leads to a decrease in its concentration;
- diuretics (especially thiazide and carbonic anhydrase inhibitors) and amphotericin B can lead to increased excretion of potassium from the body and an increased risk of developing heart failure;
- sodium-containing drugs can lead to the development of edema and increased blood pressure;
- cardiac glycosides - their tolerability worsens and the likelihood of developing ventricular extrasystole increases (due to hypokalemia);
- indirect anticoagulants - weakens (less often enhances) their effect (dose adjustment required);
- anticoagulants and thrombolytics - increases the risk of bleeding from ulcers in the gastrointestinal tract;
- ethanol and nonsteroidal anti-inflammatory drugs (NSAIDs) - increases the risk of erosive and ulcerative lesions in the gastrointestinal tract and the development of bleeding (in combination with NSAIDs in the treatment of arthritis, it is possible to reduce the dose of GCS due to the summation of the therapeutic effect);
- paracetamol - the risk of developing hepatotoxicity increases (induction of liver enzymes and the formation of a toxic metabolite of paracetamol);
- acetylsalicylic acid - accelerates its elimination and reduces its concentration in the blood (when prednisolone is discontinued, the concentration of salicylates in the blood increases and the risk of side effects increases);
- insulin and oral hypoglycemic drugs, antihypertensive drugs - their effectiveness decreases;
- vitamin D - its effect on calcium absorption in the intestine is reduced;
- growth hormone - reduces the effectiveness of the latter, and with praziquantel - its concentration in the blood;
- m-anticholinergic blockers (including antihistamines and tricyclic antidepressants) and nitrates - increases intraocular pressure;
- tricyclic antidepressants - can increase the severity of depression caused by taking glucocorticosteroids (not indicated for the treatment of these side effects);
- isoniazid and mexiletine - increases their metabolism (especially in “slow” acetylators), which leads to a decrease in their plasma concentrations.
Carbonic anhydrase inhibitors and loop diuretics may increase the risk of osteoporosis.
Indomethacin, displacing prednisolone from its connection with albumin, increases the risk of developing its side effects.
ACTH enhances the effect of prednisolone.
Ergocalciferol and parahormone prevent the development of osteopathy caused by prednisolone.
Cyclosporine and ketoconazole, by slowing down the metabolism of prednisolone, can in some cases increase its toxicity.
The simultaneous administration of androgens and steroidal anabolic drugs with prednisolone promotes the development of peripheral edema and hirsutism, and the appearance of acne.
Estrogens and oral estrogen-containing contraceptives reduce the clearance of prednisolone, which may be accompanied by an increase in the severity of its action. When used simultaneously with live antiviral vaccines and against the background of other types of immunization, it increases the risk of viral activation and the development of infections.
Antipsychotics (neuroleptics) and azathioprine increase the risk of developing cataracts when prednisolone is prescribed.
The simultaneous administration of antacids reduces the absorption of prednisolone.
When used simultaneously with antithyroid drugs, the clearance of prednisolone decreases and with thyroid hormones increases.
Hypokalemia caused by glucocorticosteroids can increase the severity and duration of muscle blockade due to muscle relaxants.
Mitotane and other inhibitors of adrenal function may necessitate an increase in the dose of prednisolone.
Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders caused by the Epstein-Barr virus.
Medopred®
There may be pharmaceutical incompatibility of prednisolone with other intravenously administered drugs - it is recommended to administer it separately from other drugs (iv bolus, or through another dropper, as a second solution).
When mixing a solution of prednisolone with heparin, a precipitate forms.
Prednisolone with long-term therapy can increase the content of folic acid.
Simultaneous administration of prednisolone with:
- inducers of microsomal liver enzymes (phenobarbital, rifampicin, phenytoin, theophylline, ephedrine) leads to a decrease in its concentration;
- diuretics (especially thiazide and carbonic anhydrase inhibitors) and amphotericin B can lead to increased excretion of potassium from the body and an increased risk of developing heart failure;
- sodium-containing drugs can lead to the development of edema and increased blood pressure;
- cardiac glycosides - their tolerability worsens and the likelihood of developing ventricular extrasystole increases (due to hypokalemia);
- indirect anticoagulants - weakens (less often enhances) their effect (dose adjustment required);
- anticoagulants and thrombolytics - increases the risk of bleeding from gastrointestinal ulcers;
- ethanol and nonsteroidal anti-inflammatory drugs (NSAIDs) - increases the risk of erosive and ulcerative lesions in the gastrointestinal tract and the development of bleeding (in combination with NSAIDs in the treatment of arthritis, it is possible to reduce the dose of GCS due to the summation of the therapeutic effect);
- paracetamol - the risk of developing hepatotoxicity increases (induction of liver enzymes and the formation of a toxic metabolite of paracetamol);
- acetylsalicylic acid - accelerates its elimination and reduces its concentration in the blood (when prednisolone is discontinued, the concentration of salicylates in the blood increases and the risk of side effects increases);
- insulin and oral hypoglycemic drugs, antihypertensive drugs - their effectiveness decreases;
- vitamin D - its effect on calcium absorption in the intestine is reduced;
- growth hormone - reduces the effectiveness of the latter, and with praziquantel - its concentration in the blood;
- m-anticholinergics (including antihistamines and tricyclic antidepressants) and nitrates - helps increase intraocular pressure;
- tricyclic antidepressants - can increase the severity of depression caused by taking glucocorticosteroids (not indicated for the treatment of these side effects);
- isoniazid and mexilegane - increases their metabolism (especially in “slow” acetylators), which leads to a decrease in their plasma concentrations.
Carbonic anhydrase inhibitors and loop diuretics may increase the risk of osteoporosis. Indomethacin, displacing prednisolone from its connection with albumin, increases the risk of developing its side effects.
ACTH enhances the effect of prednisolone.
Ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by prednisolone.
Cyclosporine and ketoconazole, by slowing down the metabolism of prednisolone, can in some cases increase its toxicity.
The simultaneous administration of androgens and steroidal anabolic drugs with prednisolone promotes the development of peripheral edema and hirsutism, and the appearance of acne.
Estrogens and oral estrogen-containing contraceptives reduce the clearance of prednisolone, which may be accompanied by an increase in the severity of its action. When used simultaneously with live antiviral vaccines and against the background of other types of immunization, it increases the risk of viral activation and the development of infections.
Antipsychotics (neuroleptics) and azathioprine increase the risk of developing cataracts when prednisolone is prescribed.
The simultaneous administration of antacids reduces the absorption of prednisolone.
When used simultaneously with antithyroid drugs, the clearance of prednisolone decreases and with thyroid hormones increases.|
Hypokalemia caused by glucocorticosteroids can increase the severity and duration of muscle blockade due to muscle relaxants.
Mitotane and other inhibitors of adrenal function may necessitate an increase in the dose of prednisolone.
Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders caused by the Epstein-Barr virus.
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Medopred - tablets
GCS is a dehydrated analogue of hydrocortisone, inhibits the release of interleukin1, interleukin2, interferon gamma from lymphocytes and macrophages. It has anti-inflammatory, antiallergic, desensitizing, antishock, antitoxic and immunosuppressive effects.
Suppresses the release of ACTH and beta-lipotropin by the pituitary gland, but does not reduce the concentration of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.
Increases the excitability of the central nervous system, reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (stimulates the production of erythropoietins).
Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus and stimulates the synthesis of mRNA; the latter induces the formation of proteins, incl. lipocortin, mediating cellular effects. Lipocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, Pg, leukotrienes, which contribute to inflammation, allergies, etc.
Protein metabolism: reduces the amount of protein in 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 TG, redistributes fat (fat accumulation 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, leading to an increase in the flow 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 metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (MCS activity), reduces the absorption of Ca2+ from the gastrointestinal tract, “washes out” Ca2+ from the bones, increases the excretion of Ca2+ by the kidneys.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; inducing the formation of lipocortin and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes and organelle membranes (especially lysosomal ones).
The antiallergic effect develops as a result of suppression of the synthesis and secretion of allergic 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, suppression of the development of lymphoid and connective tissue, a decrease in the number of T- and B-lymphocytes, mast cells, reducing the sensitivity of effector cells to allergy mediators, inhibiting antibody formation, changing the body's immune response.
In COPD, the action is based mainly on inhibition of inflammatory processes, inhibition of development or prevention of swelling of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of the bronchial epithelium, deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of beta-adrenergic receptors of small and medium-caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by inhibiting or reducing its production.
Antishock and antitoxic effects are associated with an increase in blood pressure (due to an increase in the concentration of circulating catecholamines and restoration of the sensitivity of adrenergic receptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane protective properties, and activation of liver enzymes involved in the metabolism of endo- and xenobiotics.
The 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, secondarily, the synthesis of endogenous corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
