I N S T R U C T I O N for medical use of the medicinal product PREDNISOLONE (Prednisolone)

Composition:

Active substance: 1 ml of solution contains 30 mg of prednisolone sodium phosphate calculated as prednisolone;

Excipients: anhydrous sodium hydrogen phosphate, sodium dihydrogen phosphate dihydrate, propylene glycol, water for injections.

Pharmaceutical form. Solution for injection.

Main physicochemical properties: clear colorless or slightly yellow solution.

Pharmacotherapeutic group. Corticosteroids for systemic use. Glucocorticoids. ATC code H02AB06.

Pharmacological properties.

Pharmacodynamics.

The medicinal product exerts anti-inflammatory, antiallergic, immunosuppressive, anti-shock, and antitoxic effects.

At relatively high doses, it inhibits fibroblast activity, collagen synthesis, reticuloendothelial system, and connective tissue (inhibition of the proliferative phase of inflammation), delays protein synthesis and accelerates protein catabolism in muscle tissue, while increasing protein synthesis in the liver.

The antiallergic and immunosuppressive properties of the drug are due to inhibition of lymphoid tissue development with its involution during prolonged use, reduction in the number of circulating T- and B-lymphocytes, inhibition of mast cell degranulation, and suppression of antibody production.

The anti-shock effect of the drug is due to increased vascular response to endogenous and exogenous vasoconstrictive substances, restoration of vascular receptor sensitivity to catecholamines, enhancement of their hypertensive effect, as well as retention of sodium and water in the body.

The antitoxic effect of the drug is associated with stimulation of protein synthesis in the liver and acceleration of inactivation of endogenous toxic metabolites and xenobiotics in the liver, as well as increased stability of cellular membranes, including hepatocytes.

Enhances glycogen deposition and glucose synthesis from products of protein metabolism in the liver. Increased blood glucose levels stimulate insulin secretion. The drug inhibits glucose uptake by adipocytes, leading to activation of lipolysis. However, due to increased insulin secretion, lipogenesis is stimulated, promoting fat accumulation.

Reduces calcium absorption in the intestine, increases its leaching from bones, and enhances renal excretion. Inhibits pituitary release of adrenocorticotropic hormone and β-lipotropin, thus prolonged use of the drug may lead to functional insufficiency of the adrenal cortex.

The main factors limiting long-term therapy with prednisolone are osteoporosis and Cushing's syndrome. Prednisolone inhibits secretion of thyroid-stimulating hormone and follicle-stimulating hormone.

At high doses, it may increase excitability of brain tissues and reduce the seizure threshold.

Stimulates excessive secretion of hydrochloric acid and pepsin in the stomach, thereby promoting the development of peptic ulcer.

Pharmacokinetics.

After intramuscular administration, the drug is rapidly absorbed into the blood, but the pharmacological effect develops significantly later than the achievement of maximum blood concentration, typically within 2–8 hours. In blood plasma, the majority of prednisolone binds to transcortin (cortisol-binding globulin), and when this binding capacity is saturated, it binds to albumin. When protein synthesis is reduced, the binding capacity of albumins decreases, potentially increasing the free fraction of prednisolone and consequently causing toxic effects even at usual therapeutic doses. The elimination half-life in adults is 2–4 hours, and is shorter in children. Prednisolone is metabolized primarily via oxidation in the liver, as well as in the kidneys, small intestine, and bronchi. Oxidized forms are conjugated via glucuronidation or sulfation and excreted by the kidneys as conjugates. Approximately 20% of prednisolone is excreted unchanged by the kidneys; a small portion is excreted in bile.

In liver disease, prednisolone metabolism is slowed and its binding to plasma proteins is reduced, resulting in prolonged elimination half-life.

Clinical characteristics.

Indications.

Intramuscular, intravenous administration: systemic connective tissue diseases: systemic lupus erythematosus, dermatomyositis, scleroderma, polyarteritis nodosa, Bechterew's disease;

hematological disorders: acute hemolytic anemia, lymphogranulomatosis, granulocytopenia, thrombocytopenic purpura, agranulocytosis, various forms of leukemia;

skin diseases: common eczema, erythema multiforme, pemphigus vulgaris, erythroderma, exfoliative dermatitis, seborrheic dermatitis, psoriasis, alopecia, adrenogenital syndrome;

replacement therapy: Addisonian crisis;

emergency conditions: severe forms of nonspecific ulcerative colitis and Crohn's disease, shock (burn, traumatic, surgical, anaphylactic, toxic, transfusion), status asthmaticus, acute adrenal insufficiency, hepatic coma, severe allergic and anaphylactic reactions, hypoglycemic conditions;

Intra-articular administration: chronic polyarthritis, osteoarthritis of large joints, rheumatoid arthritis, post-traumatic arthritis, arthroses.

Contraindications.

Hypersensitivity to the components of the medicinal product.

Parasitic and infectious diseases of viral, fungal, or bacterial etiology, either currently present or recently resolved: herpes simplex, herpes zoster (viremic phase), syphilis, varicella, measles; amebiasis, strongyloidiasis (confirmed or suspected); systemic mycosis; active tuberculosis.

Post-vaccination period (duration of 10 weeks: 8 weeks before and 2 weeks after vaccination with live vaccines), lymphadenitis following BCG vaccination.

Gastrointestinal disorders: peptic ulcer of the stomach and duodenum.

Cardiovascular diseases: recent myocardial infarction, decompensated chronic heart failure, arterial hypertension, viral infections (including viral eye and skin infections), predisposition to thromboembolic disease.

Endocrine disorders: decompensated diabetes mellitus, Cushing's disease.

Severe chronic renal and/or hepatic insufficiency (except in such emergency conditions as hepatic coma).

Systemic osteoporosis. Severe myopathy (except in myasthenia gravis). Productive symptoms in psychiatric disorders, psychoses, depression. Poliomyelitis (except bulbar encephalitis form). Open-angle and closed-angle glaucoma, cataract. Pregnancy and breastfeeding period.

For intra-articular injections – infections at the injection site.

Interaction with other medicinal products and other types of interactions.

Anticoagulants: concomitant use with glucocorticoids may enhance or reduce the effect of anticoagulants. Parenteral administration of prednisolone potentiates the thrombolytic effect of vitamin K antagonists (fluindione, acenocoumarol).

Salicylates and other nonsteroidal anti-inflammatory drugs (NSAIDs): concomitant use of salicylates, indomethacin, and other NSAIDs may increase the risk of gastric mucosal ulceration. Prednisolone reduces serum salicylate levels by increasing renal clearance. Caution is required when tapering prednisolone doses after prolonged concomitant use.

Hypoglycemic agents: prednisolone partially suppresses the hypoglycemic effect of oral antidiabetic agents and insulin.

Steroids may reduce the efficacy of anticholinesterase agents in myasthenia gravis.

The effectiveness of coumarin anticoagulants and warfarin may be enhanced when used concomitantly with corticosteroids, requiring careful monitoring of the international normalized ratio or prothrombin time to avoid spontaneous bleeding.

Enzyme inducers of the liver, e.g., barbiturates, phenytoin, pyrimidone, carbamazepine, rifampicin, and rifabutin, increase the systemic clearance of prednisolone, thereby reducing its effect by almost half.

Mifepristone may reduce the effect of corticosteroids for 3–4 days.

Erythromycin and ketoconazole may inhibit the metabolism of certain corticosteroids.

CYP3A4 inhibitors, e.g., erythromycin, clarithromycin, ketoconazole, diltiazem, aprepitant, itraconazole, and oleandomycin, increase the elimination and plasma levels of prednisolone, thereby enhancing both therapeutic and adverse effects of prednisolone. Cases of Cushing's syndrome and adrenal suppression have been reported. It is recommended to avoid such combinations unless the benefit outweighs the increased risk of systemic adverse reactions; in such cases, patients require monitoring for systemic corticosteroid-related adverse effects.

Estrogens may potentiate the effect of prednisolone by slowing its metabolism. Dose adjustments of prednisolone in women taking oral contraceptives are not recommended, as this may not only prolong the half-life but also lead to atypical immunosuppressive effects of prednisolone.

Hypokalemic effects of acetazolamide, loop diuretics, thiazide diuretics, and carbenoxolone are enhanced by corticosteroids. The risk of hypokalemia is increased with theophylline and amphotericin. Corticosteroids should not be used concomitantly with amphotericin.

The risk of hypokalemia is also increased when high doses of corticosteroids are used with high doses of bambuterol, fenoterol, formoterol, ritodrine, salbutamol, salmeterol, and terbutaline. The toxicity of cardiac glycosides is increased in hypokalemia caused by corticosteroids.

Concomitant use with methotrexate increases the risk of hematological toxicity.

Fluoroquinolones: concomitant use may lead to tendon damage.

Amphotericin, diuretics, and laxatives: prednisolone may increase potassium excretion in patients receiving these drugs concomitantly.

Immunosuppressants: prednisolone has additive immunosuppressive properties, which may lead to increased therapeutic effects or risk of various adverse reactions when used concomitantly with other immunosuppressants. Only some of these interactions can be explained by pharmacokinetic interactions. Glucocorticoids enhance the antiemetic efficacy of antiemetic agents used concurrently in chemotherapy-induced nausea and vomiting.

Corticosteroids may increase the plasma concentration of tacrolimus when used concomitantly; upon discontinuation of corticosteroids, the plasma concentration of tacrolimus decreases.

Immunization: glucocorticoids may reduce the effectiveness of immunization and increase the risk of neurological complications. Administration of therapeutic (immunosuppressive) doses of glucocorticoids with live viral vaccines may increase the risk of developing viral infections. (See Special precautions).

Emergency-type vaccines may be administered during treatment with this drug.

Anticholinesterase agents: in patients with myasthenia, the use of glucocorticoids and anticholinesterase agents may cause muscle weakness, especially in patients with myasthenia gravis.

Cardiac glycosides: increased risk of glycoside intoxication.

Others: two serious cases of acute myopathy have been reported in elderly patients receiving high-dose doxorubicin and prednisolone. Long-term therapy with glucocorticoids may reduce the effect of somatotropin.

Cases of acute myopathy have been described with corticosteroid use in patients simultaneously receiving neuromuscular blocking agents (e.g., pancuronium).

Seizures have been reported with concomitant use of prednisolone and cyclosporine. Since simultaneous administration of these drugs causes mutual inhibition of metabolism, it is likely that seizures and other adverse effects associated with each drug used as monotherapy may occur more frequently with combined use. Concurrent use may also lead to increased plasma concentrations of other drugs.

Antihistamines reduce the effect of prednisolone.

Concomitant use of prednisolone with antihypertensive agents may reduce the effectiveness of the latter.

Special precautions for use.

In patients who have received systemic corticosteroids in doses exceeding physiological levels (approximately 7.5 mg of prednisolone or equivalent) for more than three weeks, discontinuation of the drug should not be abrupt. The rate of dose reduction depends entirely on whether the disease may relapse when systemic corticosteroid dosage is decreased. In such cases, careful monitoring for clinical signs of disease activity is required. If disease relapse is not expected upon discontinuation of systemic corticosteroids, but hypothalamic-pituitary-adrenal system (HPA) suppression remains uncertain, the systemic corticosteroid dose may be rapidly reduced to a physiological level. Once the daily dose is equivalent to 7.5 mg of prednisolone, dose reduction should proceed more slowly to allow recovery of the HPA axis.

Rapid dose reduction of systemic corticosteroids administered for less than three weeks is appropriate if disease relapse is considered unlikely. Rapid tapering (up to 40 mg of prednisolone or equivalent) administered for less than three weeks is unlikely to result in clinically significant HPA axis suppression in most patients.

Gradual dose reduction of systemic corticosteroids is recommended in the following patient groups, even if the treatment course lasted three weeks or less:

Patients who have undergone repeated courses of systemic corticosteroids, especially if treatment lasted more than three weeks.
If a short course was initiated within one year after discontinuation of long-term therapy (months or years).
Patients with other causes of adrenocortical insufficiency besides exogenous corticosteroid therapy; therapy withdrawal should be prolonged, as longer HPA axis recovery is expected.
Patients receiving systemic corticosteroid doses exceeding 40 mg per day of prednisolone (or equivalent).
Patients who repeatedly take doses in the evening.

HPA axis suppression and other adverse effects can be minimized by using the lowest effective dose for the shortest possible duration, preferably administered in the morning or on alternate days. Patients should be regularly reviewed for appropriate dose titration according to disease activity.

Adrenocortical insufficiency may develop during prolonged corticosteroid therapy and may persist for years after treatment cessation. Discontinuation of corticosteroids after long-term therapy should be gradual to avoid acute adrenal insufficiency; the dose should be tapered over weeks or months depending on the dose and duration of treatment. During prolonged therapy, any intercurrent illness, trauma, or surgical procedure may require temporary dose escalation; if corticosteroids have been discontinued after prolonged therapy, temporary re-initiation may be necessary.

In infectious diseases and latent forms of tuberculosis, the drug should be prescribed only in combination with antibiotics and antituberculosis agents. During corticosteroid therapy, clinical manifestations of infections may be atypical, and serious infections such as septicemia or tuberculosis may progress significantly before diagnosis.

Varicella (chickenpox) may have severe consequences in immunosuppressed patients. Patients receiving systemic corticosteroids should avoid contact with individuals infected with varicella or measles.

In case of exposure to measles, prophylaxis with intramuscular normal immunoglobulin may be required.

Live vaccines should not be administered to patients with immunosuppression caused by high-dose corticosteroid therapy, as this increases the risk of infection development. Immune response to other vaccines may be diminished.

There have been reports of Kaposi's sarcoma development in patients receiving corticosteroid therapy. Discontinuation of corticosteroids leads to clinical remission.

Since corticosteroid therapy may cause fluid retention, this should be considered in patients with renal insufficiency, hypertension, and heart failure.

When administering prednisolone concomitantly with oral hypoglycemic agents or anticoagulants, dosage adjustments of the latter may be necessary. In patients with thrombocytopenic purpura, the drug should be administered intravenously only.

After discontinuation of treatment, withdrawal syndrome, adrenal insufficiency, and exacerbation of the underlying disease for which prednisolone was prescribed may occur. If adrenal insufficiency is observed after completion of prednisolone therapy, drug administration should be immediately resumed, and dose reduction should proceed very slowly and cautiously (e.g., daily dose reduced by 2–3 mg every 7–10 days). Due to the risk of hypercorticism, a new course of cortisone therapy after prior prolonged prednisolone treatment over several months should always begin with low initial doses (except in life-threatening acute conditions).

Electrolyte balance should be carefully monitored when prednisolone is used concomitantly with diuretics. During prolonged prednisolone therapy, potassium supplements and an appropriate diet should be prescribed to prevent hypokalemia and due to the possible increase in intraocular pressure and risk of subcapsular cataract development.

Corticosteroids may worsen the course of diabetes mellitus, osteoporosis, hypertension, glaucoma, and epilepsy; therefore, patients with these conditions or a family history thereof require careful monitoring.

Patients with severe affective disorders (especially steroid-induced psychosis), steroid myopathy, peptic ulcer, hypothyroidism, recent myocardial infarction, or a history of tuberculosis require frequent and careful monitoring. In such clinical situations, prednisolone should be used at the lowest effective doses.

In patients with hepatic insufficiency, blood levels of corticosteroids may increase because they are metabolized in the liver.

During prolonged glucocorticoid therapy, regular monitoring of blood pressure, urine and blood glucose levels, fecal occult blood testing, coagulation parameters, and radiological spine examination is recommended. Before initiating glucocorticoid therapy, a thorough gastrointestinal examination should be performed to exclude peptic ulcer disease of the stomach and duodenum.

Ophthalmological monitoring is necessary during therapy, especially during prolonged treatment. Prednisolone should be used with particular caution in patients with a history of psoriasis.

If there is a history of psychosis or seizures, prednisolone should be used only at the lowest effective doses.

The drug should be prescribed with special caution in patients with migraine or a history of certain parasitic diseases (especially amebiasis).

Prednisolone should be prescribed to children with special caution.

Use with caution in immunodeficiency states (including AIDS or HIV infection). Also use with caution after recent myocardial infarction (in patients with acute or subacute myocardial infarction, possible extension of the necrotic area, delayed scar formation, or cardiac muscle rupture may occur).

Prescribe with special caution in hepatic insufficiency, conditions predisposing to hypoalbuminemia, and obesity grade III–IV.

Postmenopausal women should undergo evaluation for possible osteoporosis development.

Pediatric population: Corticosteroids cause dose-dependent growth retardation in children and adolescents, which may be irreversible.

Use in elderly patients: Common adverse reactions of systemic corticosteroids may have more serious consequences in elderly patients, particularly osteoporosis, hypertension, hypokalemia, diabetes, infections, and skin thinning. Patients require careful monitoring to prevent and detect life-threatening adverse reactions early.

Patients and/or their caregivers should be warned about the possibility of developing severe psychiatric adverse reactions during systemic steroid therapy (see Adverse Reactions). Symptoms usually appear within days or weeks after starting treatment. The risk is higher with high doses, although dose levels do not reliably predict onset, type, severity, or duration of reactions. Most psychiatric adverse reactions resolve after dose reduction or discontinuation of the drug, although specific treatment may be required.

Patients/caregivers should be advised to seek medical help if disturbing psychological symptoms occur, especially depressive mood or suicidal thoughts. Psychiatric disorders may also occur during or immediately after dose reduction/discontinuation of systemic steroids, although such reactions have been infrequently reported.

Elderly patients with depression or manic-depressive disorders in their history require careful monitoring during systemic steroid therapy.

Visual disturbances

Ocular adverse events have been reported with systemic or local corticosteroid use. If a patient complains of blurred vision or other visual disturbances, an ophthalmological examination should be performed to exclude cataract, glaucoma, or rare conditions such as central serous chorioretinopathy (CSCR), which may develop after use of systemic or local corticosteroids.

Renal crisis in scleroderma

In patients with systemic scleroderma, regular monitoring of blood pressure and creatinine levels is necessary, as corticosteroid use (15 mg prednisolone or more) increases the risk of scleroderma renal crisis (potentially fatal), which may lead to oliguria.

Use during pregnancy or breastfeeding

The medicinal product should not be used during pregnancy.

If use of the drug is necessary during lactation, breastfeeding should be discontinued.

Ability to influence reaction speed when driving or operating machinery

Patients undergoing prednisolone treatment should refrain from potentially hazardous activities requiring heightened attention and rapid mental and motor responses.

Dosage and Administration.

It is not allowed to mix prednisolone with other medicinal products or to administer them simultaneously in the same infusion system or syringe!

The drug is intended for intravenous, intramuscular, or intra-articular administration. The dose of prednisolone depends on the severity of the disease.

For treatment of adults, the daily dose is 4–60 mg administered intravenously or intramuscularly.

In children, the drug should be administered intramuscularly (deeply into the gluteal muscle) strictly according to indications and under physician supervision: for children aged 6–12 years – 25 mg/day, for children aged 12 years and older – 25–50 mg/day. The duration of treatment and number of injections are determined individually.

In Addison's disease, the daily dose for adults is 4–60 mg administered intravenously or intramuscularly.

In severe forms of non-specific ulcerative colitis – 8–12 mL/day (240–360 mg of prednisolone) for 5–6 days; in severe forms of Crohn's disease – 10–13 mL/day (300–390 mg of prednisolone) for 5–7 days.

In emergency conditions, prednisolone is administered intravenously slowly (approximately over 3 minutes) or by drip infusion at a dose of 30–60 mg. If intravenous administration is difficult, the drug may be administered deeply intramuscularly. With this route of administration, the effect develops more slowly. If necessary, the drug may be re-administered intravenously or intramuscularly at a dose of 30–60 mg after 20–30 minutes.

In individual cases, an increase in the specified dose may be permitted, as determined by the physician on an individual basis.

For adults, the dose of prednisolone for intra-articular administration is 30 mg for large joints, 10–25 mg for medium-sized joints, and 5–10 mg for small joints. The drug is administered every 3 days. The treatment course lasts up to 3 weeks.

Children. The drug should be used in children aged 6 years and older only as prescribed and under physician supervision.

The physician determines the dose and duration of therapy individually, depending on age and severity of the disease. With prolonged use in children, growth retardation is possible (see Special Warnings and Precautions for Use); therefore, treatment should be limited to the minimum effective doses for the shortest possible duration indicated. The benefit of therapy must outweigh the potential risk of adverse reactions.

Overdose. In case of overdose, nausea, vomiting, bradycardia, arrhythmia, worsening of heart failure symptoms, cardiac arrest, hypokalemia, increased blood pressure, muscle cramps, hyperglycemia, thromboembolism, acute psychosis, dizziness, headache may occur. Symptoms of hypercorticism may develop: weight gain, edema, arterial hypertension, glucosuria, hypokalemia. In children, overdose may lead to suppression of the hypothalamic-pituitary-adrenal system, Cushing's syndrome, reduced growth hormone excretion, and increased intracranial pressure.

There is no specific antidote.

Treatment: discontinue the drug, provide symptomatic therapy, and, if necessary, correct electrolyte imbalances.

Side effects

The development of severe adverse reactions, including suppression of the hypothalamic-pituitary-adrenal (HPA) axis, depends on both the dose and duration of treatment. Adverse reactions usually occur during prolonged therapy. The risk of their occurrence is unlikely during short-term use.

Infections and infestations: Increased susceptibility to bacterial, viral, fungal infections; increased severity of infections with masking of symptoms; opportunistic infections; tuberculosis relapse.

Benign and malignant neoplasms (including cysts and polyps): Kaposi's sarcoma. Discontinuation of corticosteroids may lead to clinical remission.

Blood and lymphatic system disorders: Increased total leukocyte count with decreased eosinophils, monocytes, and lymphocytes. Lymphoid tissue mass decreases. Increased blood coagulability may lead to thrombosis and thromboembolism.

Endocrine and metabolic disorders: Suppression of the hypothalamic-pituitary-adrenal system; growth retardation in children and adolescents; menstrual cycle disturbances; impaired sex hormone secretion (amenorrhea); postmenopausal bleeding; Cushingoid facies; hirsutism; weight gain; decreased carbohydrate tolerance; increased insulin and oral hypoglycemic agent requirements; hyperlipidemia; negative nitrogen and calcium balance; increased appetite; disturbances in mineral metabolism and electrolyte balance; hypokalemic alkalosis; hypokalemia; possible fluid and sodium retention; adrenal insufficiency leading to arterial hypotension, hypoglycemia, and fatal outcomes in stressful situations such as surgery, trauma, or infection if the prednisolone dose is not increased.

Psychiatric disorders: Irritability, euphoria, depression, suicidal tendencies, insomnia, mood lability, increased concentration, psychological dependence, mania, hallucinations, exacerbation of schizophrenia, dementia, psychosis, anxiety, sleep disturbances, epileptic seizures, cognitive dysfunction (including amnesia and impaired consciousness), increased intracranial pressure accompanied by vomiting and optic disc edema in children.

Nervous system disorders: Increased intracranial pressure accompanied by vomiting, epileptic seizures, peripheral neuropathies, paresthesia, dizziness, headache, autonomic disturbances.

Eye disorders: Increased intraocular pressure, glaucoma, optic disc edema, cataract, exacerbation of ocular viral and fungal infections, exophthalmos, central serous choroidopathy, scleral and corneal thinning.

Ear and labyrinth disorders: Vertigo.

Cardiovascular disorders: Myocardial rupture following myocardial infarction, arterial hypotension or hypertension, bradycardia, combined ventricular arrhythmia, asystole (due to rapid administration), atherosclerosis, thrombosis, vasculitis, heart failure, peripheral edema. In patients with acute myocardial infarction – extension of the necrotic area, delayed scar formation.

Immune system disorders: Allergic reactions causing anaphylactic shock with fatal outcome, angioneurotic edema, allergic dermatitis, altered skin test reactions, tuberculosis relapse, immunosuppression, hypersensitivity reactions including rash and skin pruritus.

Respiratory, thoracic and mediastinal disorders: Hiccups.

Gastrointestinal disorders: Nausea, vomiting, bloating, abdominal pain, diarrhea, unpleasant taste in mouth, dyspepsia, peptic ulcers with perforation and hemorrhage, esophageal ulcer, esophageal candidiasis, pancreatitis, gallbladder perforation, gastrointestinal bleeding, localized ileitis, and ulcerative colitis.

During treatment, transient elevations in alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase may occur, which are usually not clinically significant and reversible upon discontinuation of the drug.

Skin and subcutaneous tissue disorders: Delayed regeneration, skin atrophy, bruising and development of atrophic skin streaks (striae), telangiectasia, hyperhidrosis, pruritus, urticaria, acneiform eruptions, acne, hirsutism, petechiae, ecchymosis, purpura, hypo- or hyperpigmentation, post-steroid panniculitis characterized by erythematous, hot subcutaneous nodules appearing within 2 weeks after discontinuation, Kaposi's sarcoma.

Musculoskeletal and connective tissue disorders: Proximal myopathy, osteoporosis, tendon rupture, muscle weakness, atrophy, myopathy, myalgia, avascular osteonecrosis, vertebral and long bone fractures, aseptic necrosis.

Renal and urinary disorders: Renal crisis in scleroderma, increased risk of urolithiasis, increased leukocytes and erythrocytes in urine without apparent kidney damage.

Reproductive system and breast disorders: Menstrual cycle disturbances, impaired sex hormone secretion (amenorrhea), postmenopausal bleeding.

General disorders: Malaise, increased appetite, pain, burning sensation, pigmentation changes (depigmentation, leukoderma), skin atrophy, sterile abscesses, rarely lipodystrophy, persistent hiccups with high-dose therapy, adrenal insufficiency leading to arterial hypotension, hypoglycemia, and fatal outcomes in stressful situations such as surgery, trauma, or infection if the prednisolone dose is not increased.

Upon abrupt discontinuation of the drug, withdrawal syndrome may occur; severity of symptoms depends on the degree of adrenal atrophy. Symptoms include hypotension, headache, nausea, abdominal pain, dizziness, anorexia, weakness, mood changes, lethargy, fever, myalgia, arthralgia, rhinitis, conjunctivitis, pruritic skin lesions, weight loss. In more severe cases: severe psychiatric disturbances, increased intracranial pressure, steroid-induced pseudorheumatism in patients with rheumatic disease, and potentially fatal outcomes. In some cases, withdrawal symptoms may either occur or mimic a clinical relapse of the disease for which the patient was treated.

Injection site reactions: Pain, burning, pigmentation changes (depigmentation, leukoderma), skin atrophy, sterile abscesses, rarely lipodystrophy.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after drug authorization is of great importance. It enables ongoing monitoring of the benefit-risk balance of the medicinal product. Healthcare professionals should report any suspected adverse reactions in accordance with applicable legislation.

Shelf life. 2 years.

Storage conditions. Store in the original packaging to protect from light at a temperature not exceeding 25 °C. Keep out of reach of children.

Incompatibilities. Prednisolone must not be mixed or administered simultaneously with other medicinal products in the same infusion system or syringe.

When prednisolone solution is mixed with heparin, a precipitate forms.

Incompatible with aerosols of sympathomimetic agents used in the treatment of bronchial asthma in children (risk of respiratory paralysis).

Packaging. 1 ml of solution in ampoules. 5 ampoules per blister; 1 blister per cardboard box.

Prescription category. By prescription only.

Manufacturer. LLC "FZ "STADA", Ukraine.

Manufacturer's address and place of business.
Ukraine, 09100, Kyiv region, Bila Tserkva, Kyivska str., 37.