Prednisolone (Tablets, Solution, Ointment) Instructions for Use

ATC Code

H02AB06 (Prednisolone)

Active Substance

Prednisolone (Rec.INN registered by WHO)

Clinical-Pharmacological Group

Corticosteroids for oral administration

Pharmacotherapeutic Group

Corticosteroids for systemic use. Glucocorticoids

Pharmacological Action

Prednisolone is a synthetic glucocorticoid drug, a dehydrogenated analogue of hydrocortisone. It exerts anti-inflammatory, antiallergic, immunosuppressive, and antishock actions, and increases the sensitivity of beta-adrenergic receptors to endogenous catecholamines.

It interacts with specific cytoplasmic receptors (glucocorticoid receptors are present in all tissues, especially abundant in the liver) to form a complex that induces the production of proteins (including enzymes that regulate vital processes in cells).

The anti-inflammatory effect is associated with the inhibition of the release of inflammatory mediators from eosinophils and mast cells; induction of lipocortin formation and reduction of the number of mast cells producing hyaluronic acid; decreased capillary permeability; stabilization of cell membranes (especially lysosomal) and organelle membranes. It acts on all stages of the inflammatory process: inhibits the synthesis of prostaglandins (Pg) at the level of arachidonic acid (lipocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes, which contribute to inflammation, allergy, and other processes), synthesis of “pro-inflammatory cytokines” (including interleukin 1, TNFα); increases the resistance of the cell membrane to various damaging factors.

Effect on protein metabolism: reduces the amount of globulins in blood plasma, increases the synthesis of albumin in the liver and kidneys (with an increase in the albumin/globulin ratio), reduces the synthesis and enhances the catabolism of protein in muscle tissue.

Effect on 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.

Effect on carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase (increasing the release of glucose from the liver into the blood); increases the activity of phosphoenolpyruvate carboxykinase and the synthesis of aminotransferases (activation of gluconeogenesis); contributes to the development of hyperglycemia.

Effect on water-electrolyte metabolism: retains sodium ions (Na⁺) and water in the body, stimulates the excretion of potassium ions (K⁺) (mineralocorticoid activity), reduces the absorption of calcium ions (Ca²⁺) from the gastrointestinal tract, causes “leaching” of calcium ions from bones and increases its renal excretion, reduces bone tissue mineralization.

The immunosuppressive effect is due to the induced 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 the release of cytokines (interleukin-1, 2; gamma-interferon) from lymphocytes and macrophages, and a decrease in antibody formation.

The antiallergic effect develops as a result of a decrease in the synthesis and secretion of allergy mediators, inhibition of the release of histamine and other biologically active substances from sensitized mast cells and basophils, a reduction 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, a decrease in the sensitivity of effector cells to allergy mediators, inhibition of antibody formation, and a change in the body’s immune response.

In obstructive respiratory diseases, the action is mainly due to the inhibition of inflammatory processes, prevention or reduction of the severity of mucosal edema, reduction of eosinophilic infiltration of the submucosal layer of the bronchial epithelium, and deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucosa. It increases the sensitivity of beta-adrenergic receptors of small and medium caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces mucus viscosity by reducing its production. It suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous glucocorticoids.

Pharmacokinetics

Absorption

When taken orally, Prednisolone is well absorbed from the gastrointestinal tract. C_max in the blood is reached 1-1.5 hours after oral administration.

Distribution

Up to 90% of prednisolone binds to blood plasma proteins: transcortin (cortisol-binding globulin) and albumin.

Metabolism

Prednisolone is metabolized in the liver, partially in the kidneys and other tissues, mainly by conjugation with glucuronic and sulfuric acids. The metabolites are inactive.

Excretion

It is excreted in the bile and by the kidneys through glomerular filtration and is 80-90% reabsorbed by the tubules. 20% of the dose is excreted by the kidneys unchanged. T_1/2 from blood plasma after oral administration is 2-4 hours.

Indications

Systemic connective tissue diseases

• Systemic lupus erythematosus;
• Scleroderma;
• Polyarteritis nodosa;
• Dermatomyositis;
• Rheumatoid arthritis.

Acute and chronic inflammatory joint diseases

• Gouty and psoriatic arthritis;
• Osteoarthritis (including post-traumatic);
• Polyarthritis;
• Scapulohumeral periarthritis;
• Ankylosing spondylitis (Bekhterev’s disease);
• Rheumatoid arthritis, including juvenile rheumatoid arthritis;
• Adult-onset Still’s disease;
• Bursitis;
• Nonspecific tenosynovitis;
• Synovitis;
• Epicondylitis.

Acute rheumatism, acute rheumatic carditis.

Bronchial asthma.

Acute and chronic allergic diseases including

• Allergic reactions to drugs and food;
• Serum sickness;
• Urticaria;
• Allergic rhinitis;
• Drug exanthema;
• Hay fever, etc.

Skin diseases

• Pemphigus;
• Psoriasis;
• Eczema;
• Atopic dermatitis (widespread neurodermatitis);
• Contact dermatitis (with large skin surface involvement);
• Toxidermia;
• Seborrheic dermatitis;
• Exfoliative dermatitis;
• Toxic epidermal necrolysis (Lyell’s syndrome);
• Bullous herpetiform dermatitis;
• Stevens-Johnson syndrome.

Cerebral edema (only after confirmation of symptoms of increased intracranial pressure by magnetic resonance or computed tomography results), caused by a brain tumor and/or associated with surgery or radiation therapy, after parenteral use of prednisolone.

Allergic eye diseases

• Allergic forms of conjunctivitis.

Inflammatory eye diseases

• Sympathetic ophthalmia;
• Severe sluggish anterior and posterior uveitis;
• Optic neuritis.

Primary or secondary adrenal insufficiency (including the condition after adrenalectomy). The drugs of choice are hydrocortisone or cortisone; if necessary, synthetic analogues can be used in combination with mineralocorticosteroids; the addition of mineralocorticosteroids is especially important in children.

Congenital adrenal hyperplasia.

Autoimmune kidney diseases (including acute glomerulonephritis); nephrotic syndrome (including against the background of lipoid nephrosis).

Subacute thyroiditis.

Diseases of the blood and hematopoietic system

• Agranulocytosis;
• Pannyelopathy;
• Autoimmune hemolytic anemia;
• Lymphoid and myeloid leukemias;
• Lymphogranulomatosis;
• Thrombocytopenic purpura;
• Secondary thrombocytopenia in adults;
• Erythroblastopenia (erythrocytic anemia);
• Congenital (erythroid) hypoplastic anemia.

Interstitial lung diseases

• Acute alveolitis;
• Pulmonary fibrosis;
• Stage II-III sarcoidosis.

Tuberculous meningitis, pulmonary tuberculosis, aspiration pneumonia (in combination with specific chemotherapy).

Berylliosis, Loeffler’s syndrome (not amenable to other therapy), lung cancer (in combination with cytostatics).

Multiple sclerosis.

Gastrointestinal diseases

• Ulcerative colitis;
• Crohn’s disease;
• Regional enteritis.

Hepatitis.

Prevention of transplant rejection reaction during organ transplantation.

Hypercalcemia associated with cancer.

Multiple myeloma.

ICD codes

Dosage Regimen

Tablets

The drug is taken orally with a small amount of water.

The dose and duration of treatment are selected by the doctor individually depending on the indications and severity of the disease. The selection of the dose and duration of treatment is determined based on the individual response to therapy.

The entire daily dose of the drug is recommended to be taken once, or the double daily dose – every other day, taking into account the circadian rhythm of endogenous glucocorticosteroid secretion in the interval from 6 to 8 a.m. The daily dose of Prednisolone should be taken after a meal (breakfast). A high daily dose can be divided into 2-4 doses, with a larger dose to be taken in the morning.

For acute conditions and as replacement therapy, adults are prescribed an initial dose of 20-30 mg/day, the maintenance dose is 5-10 mg/day. If necessary, the initial dose can be 15-100 mg/day, the maintenance dose 5-15 mg/day.

For children from 3 years and older, the initial dose is 1-2 mg/kg of body weight per day in 4-6 doses, the maintenance dose is 0.3-0.6 mg/kg/day.

Upon achieving a therapeutic effect, the dose is gradually reduced by 5 mg, then by 2.5 mg at intervals of 3-5 days, first discontinuing the later doses.

With long-term use of the drug, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly. The withdrawal of the maintenance dose is carried out more slowly the longer the glucocorticoid therapy has been used.

During stressful exposures (infection, allergic reaction, trauma, surgery, nervous stress), to avoid exacerbation of the underlying disease, the dose of prednisolone should be temporarily increased (by 1.5-3 times, and in severe cases – by 5-10 times).

Solution

The dose of Prednisolone and the duration of treatment are established by the doctor individually depending on the indications and severity of the disease.

Prednisolone is administered intravenously (by drip or bolus) or intramuscularly. The intravenous route is usually administered first as a bolus, then by drip.

For acute adrenal insufficiency, a single dose of 100-200 mg for 3-16 days.

For bronchial asthma, the drug is administered depending on the severity of the disease and the effectiveness of complex treatment from 75 to 675 mg per course of treatment from 3 to 16 days; in severe cases, the dose can be increased to 1400 mg per course of treatment and more with a gradual dose reduction.

For status asthmaticus, Prednisolone is administered at a dose of 500-1200 mg/day with subsequent reduction to 300 mg/day and transition to maintenance doses.

For thyrotoxic crisis, 100 mg of the drug is administered in 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.

For shock resistant to standard therapy, Prednisolone is usually administered initially as a bolus, then switched to drip infusion. If blood pressure does not increase within 10-20 minutes, the bolus administration of the drug is repeated. After recovery from shock, drip infusion is continued until blood pressure stabilizes. A single dose is 50-150 mg (in severe cases – up to 400 mg). The drug is re-administered after 3-4 hours. The daily dose can be 300-1200 mg (with subsequent dose reduction).

For acute hepatic-renal failure (in acute poisonings, in the postoperative and postpartum periods, etc.), Prednisolone is administered at 25-75 mg/day; if indicated, the daily dose can be increased to 300-1500 mg/day and higher.

For rheumatoid arthritis and systemic lupus erythematosus, Prednisolone is administered in addition to systemic administration of the drug at a dose of 75-125 mg/day for no more than 7-10 days.

For acute hepatitis, Prednisolone is administered at 75-100 mg/day for 7-10 days.

For poisoning with caustic fluids with burns of the digestive tract and upper respiratory tract, Prednisolone is prescribed at a dose of 75-400 mg/day for 3-18 days.

If intravenous administration is impossible, Prednisolone is administered intramuscularly in the same doses. After relief of the acute condition, Prednisolone tablets are prescribed orally, followed by a gradual dose reduction.

With long-term use of the drug, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly!

Ointment

For external use, apply a thin layer to the affected skin surface. The duration of application depends on the nature of the disease and can be 6-14 days, if necessary and as prescribed by a doctor – up to 20 days.

In children over 1 year of age, the area of application of the preparation containing Prednisolone should be limited, the minimum effective doses should be used for the shortest possible course, and manipulations that may lead to increased skin resorption of prednisolone (warming, fixing and occlusive dressings) should be excluded.

Adverse Reactions

The frequency of development and severity of side effects depend on the duration of use, the magnitude of the dose used, and the possibility of observing the circadian rhythm of prednisolone administration.

Infectious and parasitic diseases opportunistic infection, masking of clinical symptoms of infections, candidal esophagitis.

From the immune system skin rash, itching, anaphylactic shock.

From the endocrine system decreased glucose tolerance, “steroid” diabetes mellitus or manifestation of latent diabetes mellitus, suppression of adrenal function, Itsenko-Cushing syndrome (moon face, pituitary-type obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, muscle weakness, striae), hirsutism, delayed sexual development in children, increased need for insulin or oral hypoglycemic drugs in patients with diabetes mellitus.

From metabolism and nutrition increased excretion of calcium ions, hypocalcemia, weight gain, negative nitrogen balance (increased protein breakdown), increased sweating, increased or decreased appetite.

Disorders due to mineralocorticoid activity retention of fluid and sodium ions in the body (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).

Mental disorders suicidal thoughts, inappropriate behavior, irritability, confusion, mood swings, delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, nervousness or anxiety, insomnia.

From the nervous system amnesia, increased intracranial pressure, cerebellar pseudotumor, headache, convulsions, cognitive disorders, epidural lipomatosis.

From the organ of vision posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, tendency to develop secondary bacterial, fungal or viral infectious eye diseases, trophic changes of the cornea, exophthalmos, central serous chorioretinopathy, glaucoma.

From the ear and labyrinthine disorders dizziness, vertigo.

From the heart arrhythmia, bradycardia (up to cardiac arrest); development (in predisposed patients) or progression of chronic heart failure, ECG changes characteristic of hypokalemia, thromboses. In acute and subacute myocardial infarction, spread of the necrosis focus, slowing of scar tissue formation is possible, which can lead to rupture of the heart muscle.

From the vessels increased blood pressure, hypercoagulation, thromboembolism (including pulmonary embolism), telangiectasias.

From the gastrointestinal tract nausea, vomiting, pancreatitis, “steroid” ulcer of the stomach and duodenum, erosive esophagitis, gastrointestinal bleeding and perforation of the gastrointestinal tract wall, indigestion, flatulence, hiccups.

From the liver and biliary tract increased activity of liver transaminases and alkaline phosphatase.

From the skin and subcutaneous tissues delayed wound healing, petechiae, ecchymoses, thinning of the skin, hyper- or hypopigmentation, acne, striae, tendency to develop pyoderma and candidiasis.

From the musculoskeletal system and connective tissue slowing of growth and ossification processes in children (premature closure of epiphyseal growth zones), osteoporosis (pathological bone fractures, aseptic necrosis of the head of the humerus and femur), muscle tendon rupture, “steroid” myopathy, decrease in muscle mass (atrophy).

General disorders malaise.

Other increased susceptibility to infections, exacerbation of infections (this adverse reaction is facilitated by co-administered immunosuppressants and vaccination), leukocyturia, “glucocorticoid withdrawal” syndrome, frequent urination at night, urolithiasis.

Contraindications

• Hypersensitivity to prednisolone or to any of the excipients;
• Lactase deficiency, lactose intolerance, glucose-galactose malabsorption;
• Systemic mycosis;
• Simultaneous use of live and attenuated vaccines with immunosuppressive doses of the drug;
• Eye infection caused by the herpes simplex virus (due to the risk of corneal perforation);
• Breastfeeding period;
• Children under 3 years of age.

The use of the drug in patients with acute or subacute myocardial infarction is not recommended due to the risk of spreading the necrosis focus, slowing the formation of scar tissue, and, as a consequence, rupture of the heart muscle.

With caution

The drug should be used with caution in the following diseases and conditions

Gastrointestinal diseases

• Gastric and duodenal ulcer;
• Esophagitis, gastritis;
• Acute or latent peptic ulcer;
• Recently created intestinal anastomosis;
• Ulcerative colitis with threat of perforation or abscess formation;
• Diverticulitis.

Parasitic and infectious diseases of viral, fungal or bacterial nature (current or recently suffered, including recent contact with a sick person)

• Herpes simplex;
• Herpes zoster (viremic phase);
• Chickenpox;
• Measles;
• Amebiasis;
• Strongyloidiasis;
• Active or latent tuberculosis.

Use in severe infectious diseases is permissible only against the background of specific antimicrobial therapy.

Pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination. Immunodeficiency states (including AIDS or HIV infection).

Diseases of the cardiovascular system, including chronic heart failure, arterial hypertension, hyperlipidemia.

Endocrine diseases

• Diabetes mellitus (including impaired carbohydrate tolerance);
• Thyrotoxicosis;
• Hypothyroidism;
• Obesity (grade III-IV).

Severe chronic renal or hepatic failure, nephrourolithiasis.

Hypoalbuminemia and conditions predisposing to its occurrence (liver cirrhosis, nephrotic syndrome).

Convulsive syndrome.

Elderly patients (high risk of osteoporosis and arterial hypertension).

Thromboembolic complications in history or predisposition to the development of these conditions.

History of mental disorders, acute psychosis.

Systemic osteoporosis, myasthenia gravis, poliomyelitis (except for the form of bulbar encephalitis), open-angle and closed-angle glaucoma.

Pregnancy.

In children during the growth period, glucocorticosteroids should be used only for absolute indications and under the especially careful supervision of the attending physician.

Use in Pregnancy and Lactation

Pregnancy

Prednisolone easily penetrates the placental barrier.

During pregnancy (especially in the first trimester) or in women planning pregnancy, the use of the drug is indicated only when the expected therapeutic effect outweighs the risk of the negative effect of prednisolone on the mother and fetus. Glucocorticosteroids should be prescribed during pregnancy only for absolute indications. With long-term therapy during pregnancy, fetal growth is impaired. In the third trimester of pregnancy, there is a danger of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in the newborn. Children born to mothers who received Prednisolone during pregnancy should be carefully examined to timely identify possible symptoms of adrenal insufficiency. There have been cases of cataract development in newborns whose mothers took glucocorticosteroids during pregnancy.

Careful monitoring of pregnant women with gestosis in the second half of pregnancy, including preeclampsia, while taking glucocorticosteroids is necessary.

The effect of glucocorticosteroids on the course and outcome of labor is unknown.

Breastfeeding period

Since glucocorticosteroids penetrate into breast milk, if it is necessary to use the drug, breastfeeding should be discontinued.

Use in Hepatic Impairment

The drug should be prescribed with caution in severe hepatic insufficiency.

The drug has a more pronounced effect in patients with liver cirrhosis.

Use in Renal Impairment

The drug should be prescribed with caution in chronic renal failure.

Pediatric Use

The use of the drug is contraindicated in children under 3 years of age.

In children during the growth period, glucocorticosteroids should be used only for absolute indications and under the especially careful supervision of the attending physician.

Geriatric Use

The drug should be prescribed with caution to elderly patients (high risk of osteoporosis and arterial hypertension).

Special Precautions

Since complications of prednisolone therapy depend on the dose and duration of treatment, in each specific case, based on an analysis of the benefit-risk ratio, a decision is made on the need for such treatment, and the duration of treatment and frequency of administration are determined.

The smallest dose of prednisolone that provides sufficient therapeutic effect should be used; if necessary, the dose reduction should be carried out gradually.

Due to the risk of arrhythmia, the use of prednisolone in high doses should be carried out in a hospital equipped with the necessary equipment (electrocardiograph, defibrillator).

If a long-term spontaneous remission occurs, treatment should be discontinued.

With long-term treatment, the patient should undergo regular examination (chest X-ray, determination of blood glucose concentration 2 hours after a meal, general urinalysis, blood pressure, body weight control, it is advisable to perform X-ray or endoscopic examination if there is a history of ulcerative gastrointestinal diseases).

The growth and development of children on long-term prednisolone therapy should be carefully monitored. Growth retardation can be observed in children receiving long-term daily, divided-dose therapy. Daily use of prednisolone for a long time in children is possible only for absolute indications. The use of the drug every other day may reduce the risk of developing this adverse reaction or allow it to be avoided altogether.

Children receiving long-term prednisolone therapy are at increased risk of developing intracranial hypertension.

Patients receiving drugs that suppress the immune system are more susceptible to infections. For example, chickenpox and measles can have a more severe course, even fatal, in non-immunized children or in adults receiving Prednisolone.

Prednisolone should also be prescribed with great caution to patients with confirmed or suspected parasitic infections, such as strongyloidiasis. Prednisolone-induced immunosuppression in such patients leads to strongyloides hyperinfection and dissemination of the process with widespread migration of larvae, often with the development of severe forms of enterocolitis and gram-negative septicemia with possible fatal outcome.

During prednisolone therapy, susceptibility to infections may increase, some infections may occur in an erased form, and new infections may develop. Also, the body’s ability to localize the infectious process is reduced. The development of infections caused by various pathogenic organisms, such as viruses, bacteria, fungi, protozoa or helminths, which are localized in various systems of the human body, may be associated with the use of prednisolone, both as monotherapy and in combination with other immunosuppressants that affect cellular immunity, humoral immunity or neutrophil function. These infections may be mild, but in some cases, severe course and even death are possible. The higher the doses of the drug used, the higher the likelihood of infectious complications.

Patients receiving prednisolone therapy at doses that have an immunosuppressive effect are contraindicated from receiving live or live attenuated vaccines, but killed or inactivated vaccines may be administered; however, the response to such vaccines may be reduced or even absent. Patients receiving prednisolone therapy at doses that do not have an immunosuppressive effect may be immunized according to the relevant indications.

The use of prednisolone in active tuberculosis should be limited to cases of fulminant and disseminated tuberculosis, when Prednisolone is used to treat the disease in combination with appropriate anti-tuberculosis chemotherapy. If Prednisolone is prescribed to patients with latent tuberculosis or with positive tuberculin tests, then treatment should be carried out under strict medical supervision, since reactivation of the disease is possible. During long-term therapy with the drug, such patients should receive appropriate prophylactic treatment.

Cases of Kaposi’s sarcoma development have been reported in patients receiving corticosteroid therapy. Clinical remission may occur upon discontinuation of the drug.

When using the drug Prednisolone in therapeutic doses for a long period, suppression of the hypothalamic-pituitary-adrenal system (secondary adrenal insufficiency) may develop. The degree and duration of adrenal insufficiency are individual for each patient and depend on the dose, frequency of use, administration time, and duration of therapy.

The severity of this effect can be reduced by using the drug every other day or by gradually reducing the dose. This type of relative adrenal insufficiency may persist for several months after the end of treatment; therefore, during any stressful situations in this period, Prednisolone should be re-prescribed.

Abrupt withdrawal of the drug may lead to the development of acute adrenal insufficiency, which can be fatal.

“Corticosteroid withdrawal” syndrome (not related to adrenal insufficiency) can also occur due to abrupt drug withdrawal. This syndrome includes symptoms such as anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, skin peeling, myalgia, weight loss, and decreased blood pressure. It is assumed that these effects occur due to a sharp fluctuation in the plasma concentration of prednisolone, not because of its decrease.

Patients with hypothyroidism or liver cirrhosis exhibit a more pronounced effect of prednisolone.

Since mineralocorticoid secretion may be impaired, concomitant administration of electrolytes and/or mineralocorticoids is necessary.

Medium and large doses of hydrocortisone or cortisone can cause increased blood pressure, sodium and water retention, and increased potassium excretion. These effects are less likely with the use of synthetic corticosteroids (including prednisolone), except when they are used in high doses. Dietary salt restriction and potassium supplementation are necessary. All corticosteroids increase calcium excretion.

The use of prednisolone can lead to an increase in plasma glucose concentration and worsening of pre-existing diabetes mellitus. Patients receiving long-term prednisolone therapy may be predisposed to developing diabetes mellitus.

Patients who may be exposed to stress while on prednisolone therapy are indicated for an increase in the drug dose before, during, and after the stressful situation.

During prednisolone therapy, various mental disorders may develop: from euphoria, insomnia, mood swings, and depression to acute psychotic manifestations. Furthermore, pre-existing emotional lability or a tendency to psychotic reactions may be exacerbated.

Potentially severe mental disorders may occur with the use of prednisolone. Symptoms usually appear within several days or weeks of starting therapy. Most reactions disappear either after dose reduction or after drug discontinuation. Despite this, specific treatment may be required. Patients and/or their relatives should be warned that if changes in the patient’s psychological status occur (especially with the development of depression and suicide attempts), medical help should be sought. Patients or their relatives should also be warned about the possibility of mental disorders occurring during or immediately after dose reduction or complete discontinuation of the drug.

There are reports of the development of epidural lipomatosis in patients receiving corticosteroids (usually with long-term high-dose therapy).

Long-term use of prednisolone can lead to the occurrence of posterior subcapsular cataracts, exophthalmos, or glaucoma with possible damage to the optic nerve and can provoke the addition of a secondary ocular fungal or viral infection.

Due to the existing risk of corneal perforation, corticosteroids should be prescribed with caution for the treatment of eye disease caused by the herpes simplex virus (ophthalmic herpes).

Prednisolone therapy can lead to the development of central serous chorioretinopathy, which in turn can lead to retinal detachment.

Prednisolone therapy can mask the symptoms of a peptic ulcer, and in this case, perforation or bleeding can develop without significant pain.

Prednisolone should be used with caution in patients with risk factors for cardiovascular diseases, including hyperlipidemia and patients predisposed to increased blood pressure, since prednisolone intake can provoke new reactions in case of high doses and long-term treatment. Regular monitoring of heart function is necessary. The use of low doses of prednisolone every other day may reduce the severity of these reactions.

Close monitoring is required for patients receiving systemic corticosteroids who have recently experienced myocardial infarction.

Analgesics based on acetylsalicylic acid and NSAIDs should be prescribed with caution to patients taking Prednisolone.

Allergic reactions are possible. Due to the fact that patients treated with corticosteroids have rarely experienced phenomena such as skin irritation and anaphylactic or pseudo-anaphylactic reactions, necessary measures should be taken before prescribing corticosteroids, especially if the patient’s history includes a history of allergic reactions to drugs.

High doses of corticosteroids can cause acute pancreatitis.

High-dose corticosteroid therapy can cause acute myopathy; patients with impaired neuromuscular transmission (e.g., myasthenia gravis) are most susceptible to this disease, as well as patients receiving concomitant therapy with anticholinergics, such as neuromuscular blocking agents. This type of myopathy is generalized; it can affect the muscles of the eyes or respiratory system and even lead to paralysis of all limbs. Furthermore, creatine kinase activity may increase. In such cases, clinical recovery may take weeks or even years.

Osteoporosis is a common (but rarely detected) complication of long-term high-dose corticosteroid therapy.

Corticosteroids are prescribed with caution for long-term therapy in elderly patients due to an increased risk of osteoporosis and fluid retention, which potentially causes increased blood pressure.

Concomitant treatment with methylprednisolone and fluoroquinolones increases the risk of tendon rupture, especially in elderly patients.

Since Prednisolone can enhance the clinical manifestations of Cushing’s syndrome, the use of prednisolone should be avoided in patients with this disease.

Close monitoring is necessary for patients with a history of or current thrombosis or thromboembolic complications.

Effect on the ability to drive vehicles and machinery

During the period of taking the drug, it is necessary to refrain from driving vehicles and engaging in potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Overdose

Symptoms possible intensification of dose-dependent adverse reactions, which require a reduction in the dose of prednisolone. With long-term use of the drug, the development of Cushing’s syndrome is possible.

Treatment symptomatic. In case of a single intake of an excessive dose of the drug, gastric lavage should be performed; activated charcoal may be taken.

Drug Interactions

Simultaneous use of prednisolone with

• inducers of hepatic microsomal enzymes (phenobarbital, rifampicin, phenytoin, theophylline, ephedrine, carbamazepine, aminoglutethimide, primidone, rifabutin) – leads to a decrease in its plasma concentration;
• mifepristone – reduces the effect of prednisolone for 3-4 days after taking mifepristone;
• methotrexate – increases the toxicity of methotrexate due to reduced metabolism of prednisolone;
• etoposide – increases the effectiveness and enhances the toxic effect of etoposide due to inhibition of its metabolism in the liver under the influence of prednisolone;
• diuretics (especially thiazide and carbonic anhydrase inhibitors) and amphotericin B – may lead to increased excretion of potassium ions (K⁺) from the body;
• sodium-containing drugs – may lead to the development of edema and increased blood pressure;
• amphotericin B – increases the risk of heart failure;
• cardiac glycosides – their tolerance worsens and the likelihood of ventricular extrasystoles increases (due to induced hypokalemia);
• indirect anticoagulants – weakens (less often enhances) their effect (dose adjustment is required);
• anticoagulants and thrombolytics – increases the risk of bleeding from ulcers in the gastrointestinal tract;
• ethanol and NSAIDs – increases the risk of erosive and ulcerative lesions in the gastrointestinal tract and the development of bleeding (in combination with NSAIDs for the treatment of arthritis, it is possible to reduce the dose of corticosteroids due to the summation of the therapeutic effect);
• paracetamol – increases the risk of hepatotoxicity (induction of liver enzymes and formation of a toxic metabolite of paracetamol);
• acetylsalicylic acid – accelerates its excretion and reduces its concentration in the blood (upon discontinuation of prednisolone, the concentration of salicylates in the blood increases and the risk of adverse reactions increases);
• insulin and oral hypoglycemic drugs, antihypertensive agents – their effectiveness is reduced;
• vitamin D – reduces its effect on the absorption of calcium ions (Ca²⁺) in the intestine;
• somatotropic hormone – reduces its effectiveness;
• praziquantel – reduces its concentration;
• m-anticholinergics (including antihistamines and tricyclic antidepressants with m-anticholinergic activity) and nitrates – contributes to increased intraocular pressure;
• 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, by displacing Prednisolone from its binding to albumin, increases the risk of its adverse reactions.

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.

Simultaneous use of androgens and steroid anabolic drugs with prednisolone contributes to 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.

Mitotane and other inhibitors of adrenal cortex function may necessitate an increase in the dose of prednisolone.

When used simultaneously with live antiviral vaccines and against the background of other types of immunizations – increases the risk of virus activation and the development of infections.

Antipsychotic agents (neuroleptics) and azathioprine increase the risk of cataract development when using prednisolone.

Immunosuppressants increase the risk of infections and lymphoma or other lymphoproliferative disorders caused by the Epstein-Barr virus.

Simultaneous use of antacids reduces the absorption of prednisolone.

When used simultaneously with antithyroid drugs, the clearance of prednisolone decreases, and with thyroid hormones – increases.

Storage Conditions

The drug should be stored out of the reach of children at a temperature not exceeding 25°C (77°F).

Shelf Life

The shelf life is 5 years. Do not use after the expiration date printed on the packaging.

Dispensing Status

The drug is dispensed by prescription.

Important Safety Information

This information is for educational purposes only and does not replace professional medical advice. Always consult your doctor before use. Dosage and side effects may vary. Use only as prescribed.