Universal reference book for medicines
Name of the drug: PREDNISOL (PREDNISOL)

Active substance: prednisolone

Type: GCS for injection

Manufacturer: AGIO PHARMACEUTICALS (India)
Composition, form of production and packaging
The solution for intravenous and / or injections is
clear, colorless or with a greenish-yellow hue.

1 ml

prednisolone (in the form of sodium phosphate) 30 mg

Excipients: disodium edetate - 500 Ојg, sodium hydrophosphate anhydrous - 2.3 mg, sodium dihydrogen phosphate dihydrate - 340 Ојg, propylene glycol - 250 Ојg, water q / u - up to 1 ml.

1 ml - dark glass ampoules (3) - plastic trays (1) - cardboard packs.

1 ml - ampoules of dark glass (3) - blisters (1) - packs of cardboard.

1 ml - ampoules of dark glass (3) - blisters (20) - packs of cardboard.

1 ml - ampoules of dark glass (5) - blisters (1) - packs of cardboard.

1 ml - ampoules of dark glass (5) - blisters (20) - packs of cardboard.


Description of the drug approved by the manufacturer for the printed edition of 2011.


Prednisol is a synthetic glucocorticoid drug, a dehydrogenated analog of hydrocortisone.
Has anti-inflammatory, antiallergic, immunosuppressive action, increases the sensitivity of beta-adrenoreceptors to endogenous catecholamines.
Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) are present in all tissues, especially in the liver), with the formation of a complex inducing the formation of proteins (including enzymes that regulate vital processes in cells.)

Protein metabolism: reduces the number of globulins in plasma, increases the synthesis of albumins in the liver and kidneys (with increasing albumin / globulin ratio), reduces synthesis and enhances protein catabolism in muscle tissue.

Lipid metabolism: increases synthesis of higher fatty acids and triglycerides, redistributes fat (accumulation of fat occurs mainly in the area of ​​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 intake 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-electrolytic metabolism: retards Na + and water in the body, stimulates the excretion of K + (mineralocorticoid activity), reduces the absorption of Ca 2+ from the gastrointestinal tract, reduces the mineralization of bone tissue.

The anti-inflammatory effect is associated with the suppression of the release of eosinophils and mast cells by inflammatory mediators;
inducing the formation of lipocortins and reducing the number of mast cells that produce hyaluronic acid; with a decrease in the permeability of capillaries; stabilization of cell membranes (especially lysosomal) and membranes of organelles. It acts on all stages of the inflammatory process: it inhibits the synthesis of prostaglandins at the level of arachidonic acid (lipocortin depresses phospholipase A2, suppresses the liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes, promoting inflammation, allergies, etc.), the 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.
Immunosuppressive effect is caused by induced lymphoid tissue involution, suppression 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 a decrease in the formation of antibodies.

The antiallergic effect develops as a result of a decrease in the synthesis and secretion of mediators of allergy, inhibition of release from sensitized mast cells and basophils of histamine and other biologically active substances, a decrease in the number of circulating basophils, T- and B-lymphocytes, mast cells;
suppression of the development of lymphoid and connective tissue, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody formation, changes in the immune response of the body.
In obstructive airway diseases, the effect is mainly due to inhibition of inflammatory processes, prevention or reduction of mucosal edema, a decrease in the 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 small and medium-sized bronchial tubes to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production.
Suppresses the synthesis and secretion of ACTH and, again, the synthesis of endogenous GCS.
It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.

Up to 90% of the drug binds to plasma proteins: transcortin (cortisol-binding globulin) and albumins.
Prednisolone is metabolized in the liver, partially in the kidneys and other tissues, mainly by conjugation with glucuronic and sulfuric acids. Metabolites are inactive. It is excreted with bile and urine by glomerular filtration and is reabsorbed by tubules by 80-90%. 20% of the dose is excreted by the kidneys unchanged. T 1/2 from the plasma after intravenous administration for 2-3 hours.

Prednisol is used for emergency therapy in conditions requiring a rapid increase in the concentration of glucocorticosteroids in the body:

- shock conditions (burn, traumatic, operational, toxic, cardiogenic) - with ineffectiveness of vasoconstrictors, plasma-substituting drugs and other symptomatic therapy;

- Allergic reactions (acute severe forms), hemotransfusion shock, anaphylactic shock, anaphylactoid reactions;

- edema of the brain (including against the background of a brain tumor or associated with surgery, radiation therapy or head trauma);

- bronchial asthma (severe form), asthmatic status;

- systemic connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis);

acute adrenal insufficiency;

- thyrotoxic crisis;

acute hepatitis, hepatic coma;

- Reduction of inflammatory phenomena and prevention of cicatricial narrowing (when poisoning with cauterizing fluids).


The dose of the drug and the duration of treatment is determined by the doctor individually, depending on the indications and severity of the disease.
Prednisol is administered intravenously (by drip or jet) or by intramuscular injection. Intravenously, the drug is usually injected first with a stream, then drip.
In acute adrenal insufficiency, a single dose of the drug is 100-200 mg, daily 300-400 mg.

In severe allergic reactions Prednisol is administered in a daily dose of 100-200 mg for 3-16 days.

In bronchial asthma, the drug is administered depending on the severity of the disease and the effectiveness of complex treatment from 75 to 675 mg for a course of treatment of 3 to 16 days;
in severe cases, the dose may be increased to 1,400 mg per treatment course and more with a gradual dose reduction.
With asthmatic status Prednisol is administered at a dose of 500-1200 mg per day, followed by a decrease to 300 mg per day and transition to maintenance doses.

In thyrotoxic crisis , 100 mg of the drug are administered at a daily dose of 200-300 mg;
if necessary, the daily dose can be increased to 1000 mg. The duration of administration depends on the therapeutic effect, usually up to 6 days.
In the case of shock resistant to standard therapy , Prednisol is usually injected at the start of therapy, after which it becomes drip.
If the arterial pressure does not increase within 10-20 minutes, repeat the injection. After excretion from the shock state, drip administration continues until blood pressure stabilizes. Single dose is 50-150 mg (in severe cases - up to 400 mg). Repeated drug is administered after 3-4 hours. The daily dose can be 300-1200 mg (with a subsequent dose reduction).
In acute liver-kidney failure (with acute poisoning, in the postoperative and postpartum periods, etc.), Prednisol is administered at 25-75 mg per day;
in the presence of indications, the daily dose can be increased to 300-1500 mg per day or more.
In rheumatoid arthritis and systemic lupus erythematosus Prednisol is administered in addition to the systemic administration of the drug at a dose of 75 -125 mg per day for not more than 7-10 days.

In acute hepatitis, prednisol is administered at 75-100 mg per day for 7-10 days.

When poisoning with cauterizing liquids with burns of the digestive tract and upper respiratory tract Prednisol is prescribed in a dose of 75-400 mg per day for 3-18 days.

If intravenous administration is not possible, Prednisol is administered intramuscularly in the same doses.
After arresting the acute condition, prescribe inside Prednisol in tablets, followed by a gradual decrease in the dose. With prolonged use of the drug, the daily dose should be reduced gradually. Long-term therapy can not be stopped suddenly!

The frequency of development and severity of side effects depends on the duration of application, the amount of dose used and the possibility of observing the circadian rhythm of prescribing Prednisol.

When applying Prednisol may be noted:

On the part of the endocrine system: a decrease in glucose tolerance, steroid diabetes mellitus or manifestation of latent diabetes mellitus, oppression of the adrenal gland function, Itenko-Cushing syndrome (lunar face, obesity of the pituitary type, hirsutism, increased arterial pressure, dysmenorrhea, amenorrhea, muscle weakness, striae) , delay in sexual development in children.

On the part of the digestive system: nausea, vomiting, pancreatitis, steroid ulcer of the stomach and duodenum, erosive esophagitis, gastrointestinal bleeding and perforation of the gastrointestinal wall, increased or decreased appetite, digestive disorders, flatulence, hiccough.
In rare cases - increased activity of "liver" transaminases and alkaline phosphatase.
From the cardiovascular system: arrhythmias, bradycardia (up to cardiac arrest);
development (in predisposed patients) or increased manifestation of heart failure, changes in ECG, characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread of the focus of necrosis, slowing the formation of scar tissue, which can lead to rupture of the heart muscle.
From the nervous system: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, pseudotumor, cerebral palsy, headache, convulsions.

From the sensory organs: posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, propensity to develop secondary bacterial, fungal or viral eye infections, trophic corneal changes, exophthalmos, sudden loss of vision (for parenteral administration in the head, neck, nasal shells, scalp, possibly the deposition of drug crystals in the vessels of the eye).

On the part of metabolism: increased excretion of calcium, hypocalcemia, weight gain, negative nitrogen balance (increased protein breakdown), increased sweating.

Caused by mineralocorticoid activity: fluid retention and sodium (peripheral edema), pshernatriemia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).

On the part of the musculoskeletal system: slowing growth and ossification processes in children (premature closure of the epiphyseal growth zones), osteoporosis (very rarely - pathological bone fractures, aseptic necrosis of the head of the humerus and thigh bone), rupture of the tendons of muscles, steroid myopathy, (atrophy).

On the part of the skin and mucous membranes: delayed healing of wounds, petechiae, ecchymosis, thinning of the skin, hyper- or hypopigmentation, steroid acne, striae, propensity to develop pyoderma and candidiasis.

Allergic reactions: skin rash, itching, anaphylactic shock, local allergic reactions.

Local with parenteral administration: burning, numbness, pain, tingling at the injection site, infection at the injection site, rarely - necrosis of surrounding tissues, scar formation at the injection site;
atrophy of the skin and subcutaneous tissue with the / m introduction (especially dangerous is the introduction to the deltoid muscle).
Other: development or exacerbation of infections (the emergence of this side effect is facilitated by jointly used immunosuppressants and vaccination), leukocyturia, withdrawal syndrome.


- hypersensitivity to prednisolone or the components of the drug.

In children during the growth period, SCS should be used only in absolute indications and under the strictest supervision of the attending physician.


- gastrointestinal diseases - peptic ulcer of stomach and duodenum, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with perforation or abscessing threat, diverticulitis;

- parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently transferred, including recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chicken pox, measles;
amebiasis, strongyloidiasis; systemic mycosis; active and latent tuberculosis. The use in severe infectious diseases is permissible only against the background of specific therapy;
- pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination;

- immunodeficiency conditions (including AIDS or HIV infection);

- diseases of the cardiovascular system (including recently transferred myocardial infarction - in patients with acute and subacute myocardial infarction it is possible to spread the focus of necrosis, slow the formation of scar tissue and, as a result, break the heart muscle), severe chronic heart failure, hypertension, hyperlipidemia);

- Endocrine diseases - diabetes mellitus (including a violation of carbohydrate tolerance), thyrotoxicosis, hypothyroidism, Itenko-Cushing's disease, obesity (III-IV century);

- severe chronic renal and / or hepatic insufficiency, nephrourolythiasis;

- hypoalbuminemia and conditions predisposing to its occurrence;

- systemic osteoporosis, myasthenia gravis, acute psychosis, poliomyelitis (except for the form of bulbar encephalitis), open and closed angle glaucoma;

- Pregnancy.


When pregnancy (especially in the first trimester) is used only for life indications.

Since glucocorticosteroids penetrate into breast milk, if it is necessary to use the drug during breastfeeding, it is recommended to stop breastfeeding.


Use with caution in severe chronic kidney failure, nephrourolythiasis.


Use with caution in severe chronic liver failure.


In children during the growth period, SCS should be used only in absolute indications and under the strictest supervision of the attending physician.


During treatment with prednisol (especially long-term), it is necessary to observe the oculist, monitor blood pressure, the state of water-electrolyte balance, as well as patterns of peripheral blood and blood glucose levels.

In order to reduce side effects, antacids can be prescribed, as well as increase the intake of K + into the body (diet, potassium preparations).
Food should be rich in proteins, vitamins, with a restriction of fat, carbohydrates and table salt.
The effect of the drug is enhanced in patients with hypothyroidism and liver cirrhosis.
The drug can enhance existing emotional instability or psychotic disorders.When referring to psychosis in an anesthesia, prednisol is given in high doses under the strict supervision of a doctor.
With caution should be used in acute and subacute myocardial infarction - possibly spreading the focus of necrosis, slowing the formation of scar tissue and rupture of the heart muscle.

In stressful situations during maintenance treatment (for example, surgical operations, trauma or infectious diseases), a correction of the dose of the drug should be made in connection with an increase in the need for glucocorticosteroids.

In case of sudden cancellation, especially in case of prior application of high doses, it is possible to develop a withdrawal syndrome (anorexia, nausea, block, generalized musculoskeletal pain, general weakness), as well as an exacerbation of the disease for which Prednisol was prescribed.

During treatment Prednisol should not be vaccinated due to a decrease in its effectiveness (immune response).

When prescribing prednisol for intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously perform antibiotic treatment with bactericidal action.

In children during prolonged treatment with prednisol, careful monitoring of the dynamics of growth and development is necessary.
Babies that during treatment in contact with patients with measles or chickenpox, specific immunoglobulins administered prophylactically.
Due to the weak mineralocorticoid effect for replacement therapy for adrenal insufficiency Prednizol used in combination with a mineralocorticoid.
Patients with diabetes should monitor blood glucose content and correct treatment if necessary.
Shows the X-ray control of the osteo-articular system (spine images, brushes).
Prednizol patients with latent infectious diseases of the urinary tract can cause pyuria, which may be of diagnostic value.
Prednizol increases the content of 11- and 17-metabolites oksiketokortikosteroidov.

May increase the side effects described above. It is necessary to reduce the dose Prednizola. Treatment - symptomatic.

Possible pharmaceutical incompatibility Prednizola intravenously administered with other drugs - it is recommended to be administered separately from other drugs (in / bolus or through a dropper, etc., as a second solution.). When mixing the solution with heparin Prednizola precipitate formed.
Simultaneous administration Prednizola from:
- inducer "liver" microsomal 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 K + and increase the risk of heart failure;
- a sodium-containing drugs - to the development of edema and high blood pressure;
- cardiac glycosides - worsening their tolerance and increases the likelihood of ventricular ekstrasitolii (due to induced hypokalemia);
- indirect anticoagulants - weakens (less amplifies) their effect (dose adjustment is required);
- anticoagulants and thrombolytics • increased risk of bleeding from ulcers in the gastrointestinal tract;
- ethanol and NSAID - enhanced risk of erosive ulcerous lesions in the gastrointestinal tract and of bleeding (in combination with NSAIDs for the treatment of arthritis may be reduced dose glucocorticosteroids for therapeutic effect summation);
- paracetamol - increases the risk of hepatotoxicity (liver enzyme induction and formation of a toxic metabolite of acetaminophen);
- acetylsalicylic acid - accelerates its excretion and lowers blood concentration (cases Prednizola salicylates blood increases, and increases the risk of side effects);
- insulin and oral hypoglycemic agents, antihypertensive agents - their efficiency is reduced;
- Vitamin D - decreases its effect on Ca2 + absorption in the intestine;
- STH - reduces the effectiveness of the latter, and with praziquantel - its concentration;
- M-holinoblokatorami (including antitistaminnye drugs and tricyclic antidepressants) and nitrate - contributes to the intraocular pressure;
- isoniazid and mexiletine - increases their metabolism (especially in "fast acetylators"), which leads to a decrease in their plasma concentrations.
Carbonic anhydrase inhibitors, and "loop" diuretics may increase the risk of osteoporosis.
Indomethacin, displacing Prednizol from its association with albumin, increases the risk of its side effects.
ACTH increases the effects Prednizola.
Ergocalciferol and parathyroid hormone hinder the development of osteopathy caused Prednizolom.
Cyclosporine and ketoconazole, slowing metabolism Prednizola, can in some cases increase its toxicity.
Simultaneous with the appointment of androgens and anabolic steroid drugs with Prednizolom contributes to the development of peripheral edema and hirsutism, acne.
Estrogens and estrogen-containing oral contraceptives reduce Prednizola clearance, which may be accompanied by increased severity of his actions.
Mitotane and other inhibitors of adrenocortical function may necessitate increasing the dose Prednizola.
While the use of live virus vaccines and immunization compared to other types of activation increases the risk of viruses and the development of infections.
Antipsychotic drugs (neuroleptics) and azathioprine increases the risk of developing cataracts in the appointment Prednizola.
While the use of antithyroid drugs decreases, and a thyroid hormone - increased clearance Prednizola.
Hypokalemia caused Prednizolom may increase the severity and duration of muscle blockade on the background of muscle relaxants.
Immunosuppressants increase the risk of injection and lymphoma or other. Lymphoproliferative disorders associated with Epstein-Barr virus.
Tricyclic antidepressants may increase the severity of depression caused by the intake Prednizola (not shown for the therapy of side-effects data).

On prescription.


Store at a temperature not higher than 25 В° C, protected from light.
Do not freeze. Keep out of the reach of children. Shelf life - 2 years.
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