Prednisol ampoules 30mg 1ml №3

Packaging

3 amp. on 1 ml.

Mechanism of action

Prednisol is a synthetic glucocorticoid drug, a dehydrated analogue of Hydrocortisone. 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 glucocorticosteroids (GCS) exist in all tissues, especially in the liver) with the formation of 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 ratio of albumin / globulin), 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 (increased glucose uptake from the liver into the bloodstream); increases phosphoenolpyruvate carboxylase activity and aminotransferase synthesis (activation of gluconeogenesis); contributes to the development of hyperglycemia.
Water-electrolyte metabolism: retains Na + and body water, stimulates the excretion of K + (mineralocorticoid activity), reduces the absorption of Ca2 + from the gastrointestinal tract, reduces the mineralization of bone tissue.
The anti-inflammatory effect is associated with inhibition of release of inflammatory mediators by eosinophils and mast cells; 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. It acts on all stages of the inflammatory process: inhibits prostaglandin synthesis at the level of arachidonic acid (lipocortin inhibits phospholipase A2, inhibits arachidonic acid liberation and inhibits the biosynthesis of endopereas, leukotrienes, contributing to the processes of inflammation, allergies, etc.), synthesis of "proinflammatory cytokines". tumor necrosis factor alpha and others); increases the resistance of the cell membrane to the action of various damaging factors.
The immunodepression effect is caused by the involution of lymphoid tissue,inhibition of lymphocyte proliferation (especially T-lymphocytes), suppression of B-cell migration and interaction of T- and B-lymphocytes, inhibition of release of cytokines (interleukin-1, 2; gamma-interferon) from lymphocytes and macrophages and reduction of antibody formation.
Antiallergic effect develops as a result of reduced synthesis and secretion of allergy mediators, inhibition of release from sensitized mast cells and histamine basophils and other biologically active substances, reduction in the number of circulating basophils, suppression of lymphoid and connective tissue, reduction in the number of T and B lymphocytes, fat cells, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody production, changes in the immune response of the body.
In obstructive airway diseases, the effect is mainly due to the inhibition of inflammatory processes, prevention or reduction of the mucosal edema, decreased eosinophilic infiltration of the submucous layer of the bronchial epithelium and deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of eroding and desquamation of the mucous membrane. Increases the sensitivity of beta-adrenoreceptors of the bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production.
Inhibits the synthesis and secretion of ACTH and secondary synthesis of endogenous corticosteroids.
It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.

Indications and usage

Acute conditions in which parenteral administration of glucocorticoids is indicated:
- Shock resistant to standard therapy (burn, traumatic, transfusion, toxic, as well as anaphylactic shock, cardiogenic shock resulting from myocardial infarction, asthmatic status).
- Toxic state, which arose against the background of infectious diseases (in this case, long-term treatment with corticosteroids should be carried out with simultaneous treatment with antibiotics).
- Acute insufficiency of the adrenal cortex (for example, the crisis in Addison's disease, Waterhouse-Friedrichsen syndrome).
- Prevention or elimination of arterial hypotension during general anesthesia during operations in patients with chronic adrenal insufficiency, requiring prolonged use of steroid drugs.
- Hepatic coma.

Contraindications

Hypersensitivity, peptic ulcer in the acute phase, decompensated diabetes mellitus, severe hypertension, osteoporosis, Itsenko – Cushing disease, active form of tuberculosis, glaucoma, systemic mycoses, acute viral infection, productive symptoms in mental diseases. Viral and bacterial diseases of the eye, primary glaucoma, corneal diseases with epithelial damage.Bacterial, fungal, viral skin lesions, tuberculosis, syphilis, skin tumors, pregnancy. Newborn due to the presence in the composition of benzyl alcohol. Vaccination period (increases the risk of infections, especially in children).

Dosage and administration

The recommended single dose for adults is 30-45 mg, which must be slowly injected intravenously or deeply into the gluteus. However, with intramuscular administration, the slower development of the effect must be taken into account. If necessary, you can re-enter 30-60 mg into a vein or into a muscle. In case of shock, higher doses should be administered - 150-300 mg, slowly intravenously or in the form of drip infusion (in case of cardiogenic shock, doses of the drug can reach 1 g or more). When referring to the history of the presence of mental illness, the administration of large doses requires special care. As the acute condition improves, it is advisable to continue treatment with prednisone pill form. Single dose for children: at the age of 2-12 months, 2-3 mg / kg of body weight intravenously or deeply into the gluteal muscle at the age of 1-14 years, 1-2 mg / kg of body weight in / in, slowly (for 3 min. ) or deep into the gluteus muscle. If necessary, the drug can be re-entered after 20-30 minutes.

Special notes

During treatment with Prednisolone (especially long-term), it is necessary to observe an oculist, monitor blood pressure, water and electrolyte balance, as well as pictures of peripheral blood and blood glucose levels.
In order to reduce side effects, you can prescribe antacids, as well as increase the intake of K + in the body (diet, potassium supplements). Food should be rich in proteins, Vitamins, with a restriction of the content of fats, carbohydrates and salt.
The effect of the drug is enhanced in patients with hypothyroidism and liver cirrhosis. The drug may exacerbate existing emotional instability or psychotic disorders. When referring to a history of psychosis, Prednisolone in high doses is prescribed under the strict supervision of a physician.
It should be used with caution in acute and subacute myocardial infarction - the spread of necrosis, slowing the formation of scar tissue and rupture of the heart muscle may occur.
In stressful situations during maintenance treatment (for example, surgery, trauma or infectious diseases), the dose of the drug should be adjusted due to the increased need for glucocorticosteroids.
It should be carefully monitored for patients during the year after the end of long-term therapy with Prednisone due to the possible development of relative insufficiency of the adrenal cortex in stressful situations.
With a sudden cancellation, especially in the case of the previous use of high doses, the development of the "cancellation" syndrome (anorexia, nausea, lethargy, generalized musculoskeletal pain, general weakness), as well as exacerbation of the disease, about which Prednisolone was prescribed, are possible.
During treatment with Prednisolone, vaccination should not be given due to a decrease in its efficacy (immune response).
When prescribing Prednisolone for intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously treat antibiotics with a bactericidal effect.
In children during long-term treatment with Prednisolone, careful monitoring of the dynamics of growth and development is necessary. Children who were in contact with measles or chicken pox during the treatment period are prescribed specific immunoglobulins prophylactically.
Due to the weak mineralocorticoid effect for replacement therapy for adrenal insufficiency, Prednisolone is used in combination with mineralocorticoid.
In patients with diabetes, blood glucose should be monitored and, if necessary, correct therapy.
X-ray monitoring of the osteo-articular system is shown (pictures of the spine, hand).
Prednisone in patients with latent infectious diseases of the kidneys and urinary tract can cause leukocyturia, which may have diagnostic value.
Prednisolone increases the content of metabolites 11 - and 17 - oxyketocorticosteroids.

Prednisolone increases the toxicity of cardiac glycosides (due to the resulting hypokalemia increases the risk of arrhythmias). Accelerates the elimination of ASA, reduces its concentration in the blood (with the abolition of prednisone, the concentration of salicylates in the blood increases and increases the risk of side effects).When applied simultaneously with live antiviral vaccines and against the background of other types of immunizations, it increases the risk of virus activation and the development of infections. Increases the metabolism of isoniazid, meksiletin (especially in "fast" acetylators), which leads to a decrease in their plasma concentrations. Increases the risk of hepatotoxic reactions of Paracetamol (induction of "liver" enzymes and the formation of a toxic metabolite of paracetamol). Increases (with long-term therapy) the content of folic acid. Hypokalemia caused by GCS can increase the severity and duration of muscle blockade on the background of muscle relaxants. In high doses, reduces the effect of somatropin. Antacids reduce the absorption of corticosteroids. Prednisolone reduces the effect of hypoglycemic drugs; enhances the anticoagulant action of coumarin derivatives. Weakens the effect of vitamin D on the absorption of Ca2 + in the intestinal lumen. Ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by GCS. Reduces the concentration of praziquantel in the blood. Cyclosporine (inhibits metabolism) and Ketoconazole (decreases clearance) increase toxicity. Thiazide diuretics, carbonic anhydrase inhibitors, other GCS and amphotericin B increase the risk of hypokalemia, Na + -containing drugs - edema and increase blood pressure. NSAIDs and ethanol increase the risk of ulceration of the mucous membrane of the gastrointestinal tract and bleeding, in combination with NSAIDs for the treatment of arthritis may reduce the dose of corticosteroids due to the sum of the therapeutic effect.Indomethacin, displacing prednisone from its association with albumin, increases the risk of its side effects. Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis. The therapeutic effect of corticosteroids is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin, and other inducers of "liver" microsomal enzymes (increased metabolic rate). Mitotan and other inhibitors of the function of the adrenal cortex may necessitate an increase in the dose of GCS. Clearance of GCS increases due to thyroid hormones. Immunosuppressants increase the risk of developing infections and lymphomas or other lymphoproliferative disorders associated with Epstein-Barr virus. Estrogens (including oral estrogen-containing contraceptives) reduce GC clearance, lengthen T1 / 2 and their therapeutic and toxic effects. The emergence of hirsutism and acne contributes to the simultaneous use of other steroid hormonal drugs - androgens, estrogens, anabolic steroids, oral contraceptives. Tricyclic antidepressants may increase the severity of GCS-induced depression (not indicated for the treatment of these side effects). The risk of developing cataracts is increased when applied against the background of other corticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine. The simultaneous appointment with m-anticholinergics (including antihistamine drugs, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.

In the dark place at a temperature of no higher than 25 ° C. Keep out of the reach of children.