Prednisolone is a synthetic glucocorticosteroid drug, a dehydrated hydrocortisone analog. It has anti-inflammatory, anti-allergic, immunosuppressive effect, increases sensitivity of beta-adrenoreceptors to endogenous catecholamines.
Interacts with cytoplasmic glucocorticosteroid receptors (GCS receptors are present in all tissues, especially in liver) to form a complex, inducing the formation of proteins (including enzymes regulating vital processes in cells).
Anti-inflammatory effect is associated with inhibition of release of inflammatory mediators by eosinophils and mast cells, induction of lipocortin formation and reduction of mast cells producing hyaluronic acid, reduction of capillary permeability, stabilization of cell membranes and organelle membranes (especially lysosomal).
Acts on all stages of the inflammatory process: inhibits the synthesis of prostaglandins at the level of arachidonic acid (Lipokortin inhibits phospholipase A2, inhibits the release of arachidonic acid and inhibits the synthesis of endoperoxins, leukotrienes, contributing to inflammation processes, allergies, etc.).); synthesis of “pro-inflammatory cytokines” (interleukin-1, tumor necrosis factor alpha, etc.); increases the resistance of cell membranes.The basic elements of the immune system are the following: > Immunodeficiency Virus (immunoenzyme), > Immunodeficiency Virus (immunoenzyme), > Immunoassay (immunoassay).
Immunosuppressive effect is caused by involution of lymphoid tissue, inhibition of lymphocyte proliferation (especially T-lymphocytes), suppression of B-lymphocyte migration and interaction between T- and B-lymphocytes, inhibition of cytokine release (interleukin-1, interleukin-2, gamma interferon) from lymphocytes and macrophages and reduction of antibody formation.
The anti-allergic action is caused by decrease of synthesis and secretion of allergy mediators, inhibition of histamine and other bioactive substances release from sensitized mast cells and basophils, reduction of circulating basophils number, decrease of T- and B-lymphocytes and mast cells quantity, suppression of lymphoid and connective tissue development, reduction of effector cells sensitivity to allergy mediators, suppression of antibodies formation, change of the body immune response.
In obstructive airways diseases the action is mainly caused by inhibition of inflammatory processes, prevention or reduction of bronchial mucous membrane edema severity, decrease of eosinophilic infiltration of submucous layer of bronchial epithelium and deposition of circulating immune complexes in bronchial mucosa, and also inhibition of mucous membrane erosion and desquamation. It increases sensitivity of small and medium caliber bronchial beta-adrenoreceptors to endogenous catecholamines and exogenous sympathomimetics, decreases mucus viscosity by reducing its production.
Inhibits the synthesis and secretion of adrenocorticotropic hormone (ACTH) and secondary to the synthesis of endogenous GCS.
Inhibits connective tissue reactions in the inflammatory process and reduces the possibility of scar tissue formation.
Effect on protein metabolism: reduces the number of globulins in the blood plasma, increases the synthesis of albumins in the liver and kidneys (with an increase in albumin/globulin ratio), reduces synthesis and increases the catabolism of protein in muscle tissue.
Effect on lipid metabolism: increases the synthesis of higher fatty acids and triglycerides; redistributes fat (mobilization from the subcutaneous tissue of the extremities and accumulation of fat mainly in the shoulder girdle, face, abdomen); leads to hypercholesterolemia.
Effect on carbohydrate metabolism: increases absorption of carbohydrates from the gastrointestinal tract (GIT), increases the activity of glucose-6-phosphatase (increased flow of glucose from the liver into the blood), increases the activity of phosphoenolpyruvate carboxylase and aminotransferase synthesis (activation of gluconeogenesis), promotes the development of hyperglycemia.
Effect on water-electrolyte metabolism: retains sodium and water in the body; stimulates potassium excretion (mineralocorticoid activity); reduces absorption of calcium from gastrointestinal tract; causes “washout” of calcium from bones and its increased renal excretion; reduces bone mineralization.
Absorption during injection into thigh muscles is faster than gluteal muscles. Maximal concentration in plasma is reached after 0.5 hour after intravenous injection. With intramuscular administration maximum concentration is reached after 0.5-1 hours.
Up to 90% of prednisolone is bound to plasma proteins: transcortin (corticosteroid-binding globulin) and albumin.
Prednisolone is metabolized primarily in the liver, partially in the kidneys and other tissues, mainly by conjugation with glucuronic and sulfuric acids. Metabolites are inactive.
The elimination half-life of prednisolone from blood plasma is about 3 hours.
Excreted through the intestine and kidneys by glomerular filtration and is 80-90 % reabsorbed by the renal tubules. 20% of the dose is excreted unchanged by the kidneys.
It is used for emergency therapy in conditions requiring rapid increase in the concentration of glucocorticosteroids in the body:
- shock conditions (burn, traumatic, surgical, toxic, cardiogenic) – when vasoconstrictors, plasma substitute drugs and other symptomatic therapy are ineffective;
- Brain edema (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 scarring (in poisoning with cauterizing fluids).
Prednisolone sodium phosphate – 40.32 mg
(in terms of prednisolone) – 30.00 mg
Sodium hydrophosphate (sodium phosphate displaced) – 0.91 mg
dinatrium edetate dihydrate (trilon B) – 0.50 mg
sodium dihydrophosphate dihydrate
(disodium phosphate disubstituted 2-water) – 0.34 mg
propylene glycol – 0.25 ml
water for injection – up to 1 ml
How to take, the dosage
V/v (by trickle, then dropwise) or intramuscularly. The dose of Prednisolone and duration of treatment shall be determined by the physician individually, depending on the indication and severity of the disease.
In acute adrenal insufficiency a single dose of the drug is 100-200 mg and daily 300-400 mg.
In severe allergic reactions, Prednisolone is given 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 the complex treatment of 75 to 675 mg for a treatment course of 3 to 16 days; in severe cases the dose may be increased to 1400 mg per course of treatment or more with gradual reduction of the dose.
In asthmatic status, Prednisolone is given in a dose of 500-1200 mg per day with subsequent reduction to 300 mg per day and transition to maintenance doses.
In thyrotoxic crisis, 100 mg of the drug is administered in a daily dose of 200-300 mg; if necessary, the daily dose may be increased to 1000 mg. The duration of administration depends on the therapeutic effect, usually up to 6 days.
In case of shock resistant to standard therapy, Prednisolone is usually administered by trickle at the beginning of therapy, after which it is switched to drip administration. If BP does not increase within 10-20 minutes, the drug is repeated by trickle administration. After recovery from shock continue drip administration until BP stabilizes. The single dose is 50-150 mg (in severe cases up to 400 mg). The drug shall be repeatedly administered after 3-4 hours. The daily dose may be 300-1200 mg (with subsequent dose reduction).
In acute hepatic and renal failure (in acute poisoning, in postoperative and postpartum periods), Prednisolone is administered in 25-75 mg per day; if indicated, the daily dose may be increased to 300-1500 mg per day and higher.
In rheumatoid arthritis and systemic lupus erythematosus Prednisolone is administered in addition to systemic administration of the drug in a dose of 75-125 mg daily for not more than 7-10 days.
In acute hepatitis, Prednisolone is administered at 75-100 mg daily for 7-10 days.
In cauterizing fluid poisoning with burns of the digestive tract and upper respiratory tract, Prednisolone is prescribed in a dose of 75-400 mg daily for 3-18 days.
If IV administration is not possible, Prednisolone is administered in m/m in the same doses. After the acute condition is resolved, oral Prednisolone tablets are prescribed, with subsequent gradual reduction of the dose.
In long-term use of the drug, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly!
Heart glycosides: increased risk of cardiac rhythm disturbances and glycoside toxicity associated with hypokalemia.
Barbiturates, antiepileptic drugs (phenytoin, carbamazepine), rifampicin, glutethimide accelerate the metabolism of GCS (through induction of microsomal enzymes), weaken their effects.
The antihistamines weaken the effects of prednisolone.
Amphotericin B, carbohydrase inhibitors: hypokalemia, left ventricular myocardial hypertrophy, circulatory failure.
Paracetamol: hypernatremia, peripheral edema, increased calcium excretion, risk of hypocalcemia and osteoporosis. Increased risk of hepatotoxicity of paracetamol.
Anabolic steroids, androgens: increased risk of peripheral edema, acne; use with caution, especially in liver and heart disease.
Estrogen-containing oral contraceptives: increased concentration of glucocorticosteroid-binding globulins in serum, slower metabolism, increased T1/2, increased effect of prednisolone.
Choline-blocking drugs (mainly atropine) – increase in intraocular pressure.
Anticoagulants (coumarin derivatives, indandion, heparin), streptokinase, urokinase:decreased, and in some patients increased effectiveness; dose should be determined based on SP; increased risk of ulceration and bleeding from the GI tract.
Tricyclic antidepressants may exacerbate psychiatric disorders associated with prednisolone administration. They should not be prescribed to treat these disorders.
The oral antidiabetic drugs, insulin: attenuation of hypoglycemic effect, increase in blood glucose concentration. Correction of the dose of antidiabetic drugs is possible.
Antithyroid drugs, thyroid hormones – changes in thyroid function (dose adjustment of these drugs or discontinuation of their use is possible).
Diuretics: weakening of the action of diuretics (potassium-saving), hypokalemia.
Laxatives: weakening of action, hypokalemia.
Ephedrine may accelerate the metabolism of GCS (correction of prednisolone dose is possible).
Immunosuppressive drugs: increased risk of infection, lymphoma and other lymphoproliferative diseases.
Isoniazid: decrease in plasma concentration of isoniazid, mainly in persons with rapid acetylation (possible change in dose).
Mexiletine: acceleration of metabolism of mexiletine and reduction of its concentration in blood serum.
Drugs that block neuromuscular conduction (depolarizing myorelaxants): hypocalcemia associated with the use of prednisolone may increase synaptic blockade, leading to increased duration of neuromuscular blockade.
NSAIDs, acetylsalicylic acid, alcohol: weakening of action, increased risk of peptic ulcer disease and bleeding from the gastrointestinal tract.
Drugs and food containing sodium: peripheral edema, arterial hypertension (it may be necessary to reduce sodium intake with food and medications with high sodium content; sometimes use of GCS requires additional sodium administration).
Vaccines containing live viruses: while using immunosuppressive doses of GCS, viral replication and viral disease may occur; decreased antibody production (concomitant use is not recommended).
Other vaccines: increased risk of neurological complications and decreased antibody production.
Folic acid: increased need for this drug.
Prednisolone is contraindicated in patients with systemic fungal infections because of the risk of increased infection. The drug may in some cases be used in fungal infections treated with amphotericin B to reduce its side effects, but in these cases it may cause circulatory failure and left ventricular myocardial hypertrophy and severe hypokalemia. Taking the drug with food may reduce gastrointestinal side effects.
The effectiveness of antacid drugs in preventing ulcer formation, bleeding from the digestive tract or intestinal perforation has not been confirmed. With long-term treatment, it may be necessary to limit sodium and increase potassium, and to increase protein in the diet.
If steroid myopathy develops, if therapy with prednisolone cannot be reversed, replacement with another GCS may alleviate the symptoms.
The risk of osteoporosis with prolonged use of GCS may be reduced by taking calcium and vitamin D or by exercise if the patient’s condition allows.
If psychosis or depression occurs, the dose should be reduced if possible, or the drug should be stopped. Phenothiazines or lithium compounds may be used if necessary.
Acetylsalicylic acid or other NSAIDs can be prescribed to alleviate some of the symptoms of GCS withdrawal (without suppressing the hypothalamic-pituitary-adrenal system).
For short-term use for vital indications, the only contraindications are hypersensitivity to prednisolone or drug components; systemic mycosis; epidural and intrathecal administration of the drug; cerebral edema due to craniocerebral injury; simultaneous use of live or weakened vaccines with immunosuppressive doses of the drug Herpes simplex virus infection of the eye (because of the risk of corneal perforation); The drug is not recommended for patients with acute or subacute myocardial infarction because of possible spread of necrosis, delayed scar tissue formation and, therefore, rupture of the heart muscle; in children during growth, GCS should be used only if absolutely indicated and under close supervision of the attending physician; breast-feeding period.
In gastrointestinal diseases: gastric and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with threat of perforation or abscessing, diverticulitis.
In parasitic and infectious diseases of viral, fungal or bacterial nature (current or recently suffered, including recent contact with a patient) – herpes simplex, herpes zoster (viremic phase), varicella, measles; amebiasis, strongyloidosis; active and latent tuberculosis. Application in severe infectious diseases is allowed only against the background of specific antimicrobial therapy.
In the pre- and post-vaccination period (period of 8 weeks before and 2 weeks after vaccination), with lymphadenitis after BCG vaccination. In immunodeficiency conditions (including AIDS or HIV infections).
In diseases of the cardiovascular system: recent myocardial infarction, chronic heart failure in decompensation stage, arterial hypertension, hyperlipidemia.
In endocrine diseases: diabetes (including impaired glucose tolerance), hyperthyroidism, hypothyroidism, obesity degree III-IV).
In chronic renal and/or hepatic insufficiency of severe degree, nephrourolithiasis. With hypoalbuminemia and the conditions predisposing to its occurrence (liver cirrhosis, nephrotic syndrome).
In systemic osteoporosis, myasthenia gravis, acute psychosis, poliomyelitis (except for bulbar encephalitis), open and closed angle glaucoma.
In patients with current thromboembolic complications or with a predisposition to develop these complications.
In patients with a history of severe affective disorders.
In case of seizure syndrome.
Prednisolone bufus should be used with caution in elderly patients because of the increased risk of osteoporosis and arterial hypertension.
In children during growth, GCS should be used only with absolute indications and under the close supervision of the attending physician.
In short-term use of prednisolone, like other GCSs, side effects are rare. When using prednisolone for a long time, the following side effects may develop:
Water-electrolyte metabolism disorders: sodium and fluid retention in the body, hypokalemia, hypokalemic alkalosis.
Cardiovascular system disorders: increase in BP, circulatory failure.
Musculoskeletal system disorders: muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, spinal compression fracture, aseptic necrosis of femoral and humeral heads, pathological fractures of long bones.
Gastrointestinal organs: steroid ulcer with possible perforation and bleeding, pancreatitis, flatulence, ulcerative esophagitis, digestive disorders, nausea, increased appetite.
Skin disorders: atrophic streaks, acne, delayed wound healing, skin thinning, petechiae and bruises, erythema, increased sweating, allergic dermatitis, urticaria, angioedema.
Nervous system and sensory organs: Increased intracranial pressure with optic nipple congestion syndrome (pseudotumor of the brain – more common in children, usually after reducing the dose too quickly, symptoms are headache, worsened visual acuity or double vision); seizures, dizziness, headache, sleep disturbance, posterior subcapsular cataracts, increased intraocular pressure, glaucoma; exophthalmos.
Endocrine status: Secondary adrenal and hypothalamic-pituitary insufficiency (especially during stressful situations such as illness, trauma, surgery); Cushing’s syndrome; growth suppression in children; menstrual disorders; decreased carbohydrate tolerance; manifestation of latent diabetes and increased need for insulin or oral antidiabetic drugs in diabetic patients, hirsutism.
Metabolic side: negative nitrogen balance as a result of protein catabolism, hyperglycemia, glucosuria.
Mental disorders: symptoms mimicking schizophrenia, mania or delirium syndrome (most often appear during the first two weeks of treatment). Women and lupus erythematosus patients are most susceptible to mental disorders.
Others: anaphylactic and hypersensitivity reactions, obliterating endarteritis, weight gain, masking of symptoms of infectious diseases, fainting.
The risk of overdose is increased with long-term use of prednisolone, especially in high doses.
Symptoms: increased BP, peripheral edema, increased adverse effects described above.
Treatment: The drug should be temporarily discontinued or the dose should be reduced.
Prednisolone penetrates through the placenta. During pregnancy (especially in the first trimester) or in women planning pregnancy, the use of Prednisolone bufus is indicated only if the expected treatment effect of Prednisolone bufus exceeds the risk of adverse effects on the mother and fetus. GCS should be administered during pregnancy only for absolute indications.
Malformations (cleft palate) and fetal hypotrophy may occur if prolonged therapy during pregnancy.
There is no data on the effect of GCS on the course and outcome of childbirth. Children born by mothers who received high doses of the drug during pregnancy should be closely monitored.
Since GCSs penetrate into breast milk, the child should not be breastfed if Prednisolone bufus is used.
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