Prednisolone for rheumatoid arthritis: treatment features, recommended dosage, patient reviews

Description of the drug

Prednisolone for arthritis is used as part of symptomatic therapy.
As an independent remedy, the medicine is ineffective; it must be taken only in combination with other drugs. Features of the drug:

• stops the inflammatory process;
• has antihistamine activity;
• inhibits immune activity;
• has antishock and antitoxic effects.

The main active ingredient is the corticosteroid prednisolone sodium phosphate. The drug is available in tablets and ampoules and is intended for systemic use. Each tablet contains 5 mg of active ingredient, as well as lactose, starch and magnesium stearate.

Each ampoule of the drug contains 30 mg of prednisolone and a number of excipients, including ethanol. The drug has a large list of indications and is used for almost any complicated inflammatory diseases of the skin and joints. Taking Prednisolone for rheumatoid arthritis should be agreed with your doctor, as the drug is unsafe.

Forms of release of the drug Prednisolone

GLUCOCORTICOID DRUGS

Toolkit

Indications for use

The list of indications for the drug is very large and includes more than 15 different diseases and conditions. Prednisolone tablets are prescribed as part of complex therapy for the following diseases:

• rheumatic disorders;
• chronic pathologies affecting connective tissue (lupus, scleroderma);
• multiple sclerosis;
• acute joint pathologies;
• chronic inflammation of the joints;
• adrenal insufficiency;
• hepatitis;
• hypoglycemia;
• autoimmune disorders affecting the epidermis;
• diseases of the hematopoietic system.

Any form of the drug can be used to treat rheumatoid arthritis with Prednisolone. The tablets are intended for oral administration and have a simple regimen of administration and understandable dosages. Treatment with this form of the drug is easy to carry out at home. The drug in ampoules is intended for injection only. Indications:

• systemic lupus erythematosus;
• scleroderma;
• Bekhterev's disease;
• anemia;
• leukemia;
• psoriasis;
• alopecia;
• inflammatory dermatological diseases;
• inflammatory pathologies of joints;
• acute adrenal insufficiency;
• Crohn's disease.

Injections are given either intravenously or intramuscularly. In the treatment of rheumatoid arthritis, it is proposed to treat exacerbation of this disease with prednisone, and treatment is carried out by injecting the drug directly into the joint capsule.

When arthritis worsens, an injection is given directly into the joint.

Prednisolone-Ferein solution for IV and IM administration 30 mg/ml in 1 ml ampoules No. 5x2

Name

Prednisolone-Ferein

Main active ingredient

Prednisolone

Release form

solution for intravenous and intramuscular administration 1 ml of the drug in glass ampoules or glass ampoules with a break ring. 3, 5 or 10 ampoules of the drug, together with instructions for medical use and a ceramic cutting disc for opening the ampoules, are placed in a pack of cardboard boxes with partitions or a corrugated insert, or with a polymer insert made of polyvinyl chloride film for placing and fixing the ampoules. 1 ml of the drug in glass ampoules with a break ring of 1 ml. 5 ampoules of the drug are placed in a blister made of polyvinyl chloride film, which is covered with a pack of boxed cardboard (chrome-ersatz).

Dosage

30 mg / 1 ml 1 ml

Pharmacodynamics

It has anti-inflammatory, antiallergic, immunosuppressive, antishock and antitoxic effects. In relatively large doses, it inhibits the activity of fibroblasts, the synthesis of collagen, reticuloendothelium and connective tissue (inhibition of the proliferative phase of inflammation), delays synthesis and accelerates protein catabolism in muscle tissue, but increases its synthesis in the liver. The antiallergic and immunosuppressive properties of the drug are due to inhibition of the development of lymphoid tissue with its involution with long-term use, a decrease in the number of circulating T- and B-lymphocytes, inhibition of mast cell degranulation, and suppression of antibody production. The antishock effect of the drug is due to an increase in the vascular response to endo- and exogenous vasoconstrictor substances, with restoration of the sensitivity of vascular receptors to catecholamines and an increase in their hypertensive effect, as well as a delay in the excretion of sodium and water from the body. The antitoxic effect of the drug is associated with the stimulation of protein synthesis processes in the liver and the acceleration of inactivation of endogenous toxic metabolites and xenobiotics in it, as well as with an increase in the stability of cell membranes, incl. hepatocytes. Enhances the deposition of glycogen in the liver and the synthesis of glucose from the products of protein metabolism. An increase in blood glucose levels activates the release of insulin. Inhibits the uptake of glucose by fat cells, which leads to activation of lipolysis. However, due to increased insulin secretion, lipogenesis is stimulated, which promotes fat accumulation. Reduces calcium absorption in the intestine, increases its leaching from bones and excretion by the kidneys. Suppresses the release of adrenocorticotropic hormone and β-lipotropin by the pituitary gland, and therefore, with long-term use, the drug can contribute to the development of functional insufficiency of the adrenal cortex. The main factors limiting long-term prednisone therapy are osteoporosis and Cushing's syndrome. Prednisolone inhibits the secretion of thyroid-stimulating and follicle-stimulating hormones. In high doses, it can increase the excitability of brain tissue and help lower the threshold for convulsive readiness. Stimulates excessive secretion of hydrochloric acid and pepsin in the stomach, and therefore may contribute to the development of peptic ulcers.

Pharmacokinetics

When administered intramuscularly, it is absorbed into the blood quickly, however, compared to reaching the maximum level in the blood, the pharmacological effect of the drug is significantly delayed and develops within 2-8 hours. In the blood plasma, most of prednisolone binds to transcortin (cortisol-binding globulin), and when the process is saturated, to albumin. With a decrease in protein synthesis, a decrease in the binding capacity of albumin is observed, which can cause an increase in the free fraction of prednisolone and, as a consequence, the manifestation of its toxic effect when using normal therapeutic doses. The half-life in adults is 2-4 hours, in children it is shorter. It is biotransformed by oxidation mainly in the liver, as well as in the kidneys, small intestine, and bronchi. Oxidized forms are glucuronidated or sulfated and excreted by the kidneys in the form of conjugates. About 20% of prednisolone is excreted from the body unchanged by the kidneys; a small part is excreted in bile. In liver diseases, the metabolism of prednisolone slows down and the degree of its binding to plasma proteins decreases, which leads to an increase in the half-life of the drug.

Indications for use

Intramuscular, intravenous administration: systemic connective tissue diseases: systemic lupus erythematosus, dermatomyositis, scleroderma, periarteritis nodosa, ankylosing spondylitis; hematological diseases: acute hemolytic anemia, lymphogranulomatosis, granulocytopenia, thrombocytopenic purpura, agranulocytosis, various forms of leukemia; skin diseases: eczema vulgaris, exudative erythema multiforme, pemphigus vulgaris, erythroderma, exfoliative dermatitis, seborrheic dermatitis, psoriasis, alopecia, adrenogenital syndrome; replacement therapy: Addison's 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 reactions; Intra-articular administration: chronic polyarthritis, osteoarthritis of large joints, rheumatoid arthritis, post-traumatic arthritis, arthrosis; For infectious diseases and latent forms of tuberculosis, the drug should be prescribed only in combination with antibiotics and anti-tuberculosis drugs. If it is necessary to use prednisolone while taking oral hypoglycemic drugs or anticoagulants, it is necessary to adjust the dosage regimen of the latter. In patients with thrombocytopenic purpura, the drug should be used only intravenously. After cessation of treatment, withdrawal syndrome, adrenal insufficiency, and exacerbation of the disease for which prednisolone was prescribed may occur. If, after finishing treatment with prednisolone, functional adrenal insufficiency is observed, use of the drug should be resumed immediately, and the dose reduction should be carried out very slowly and with caution (for example, the daily dose should be reduced by 2-3 mg over 7-10 days). Because of the risk of developing hypercortisolism, a new course of treatment with cortisone, after a previous long-term treatment with prednisone over several months, should always be started with low initial doses (except in acute life-threatening conditions). Electrolyte balance should be especially carefully monitored when prednisolone is used in combination with diuretics. With long-term treatment with prednisolone to prevent hypokalemia, it is necessary to prescribe potassium supplements and an appropriate diet due to a possible increase in intraocular pressure and the risk of developing subcapsular cataracts. During treatment, especially long-term treatment, observation by an ophthalmologist is necessary. If there is a history of psoriasis, use prednisolone in high doses with extreme caution. If there is a history of psychosis or seizures, prednisolone should be used only in minimal effective doses. Particular caution should be taken when prescribing the drug for migraines or a history of certain parasitic diseases (especially amoebiasis). Prednisolone should be prescribed to children with special caution. Prescribe with particular caution in immunodeficiency states (including AIDS or HIV infection). Also prescribe with caution after a recent myocardial infarction (in patients with acute, subacute myocardial infarction, expansion of the focus of necrosis, slowdown in the formation of scar tissue, and rupture of the heart muscle are possible). It is prescribed with particular caution for liver failure, conditions that cause the occurrence of hypoalbuminemia, and obesity of III-IV degree. Women during menopause need to undergo research regarding the possible occurrence of osteoporosis. In case of liver use of glucocorticoids for a long time, it is recommended to regularly monitor blood pressure, determine the level of glucose in urine and blood, perform a fecal occult blood test, blood clotting tests, and x-ray monitoring of the spine. Before starting treatment with glucocorticoids, a thorough examination of the gastrointestinal tract should be performed to exclude gastric and duodenal ulcers.

Directions for use and doses

The dose of the drug and the duration of treatment are determined by the doctor individually depending on the indications and severity of the disease. Prednisolone is administered intravenously (drip or stream) or intramuscularly. Intravenously, the drug is usually administered first as a stream, then as a drip. In case of acute adrenal insufficiency, a single dose of the drug is 100-200 mg, a daily dose is 300-400 mg. For severe allergic reactions, Prednisolone is administered in a daily 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 mg 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 or more with a gradual dose reduction. For status asthmaticus, Prednisolone is administered at a dose of 500-1200 mg per day, followed by a reduction to 300 mg per day and switching to maintenance doses. In case of 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. In case of shock that is resistant to standard therapy, Prednisolone is usually administered as a bolus at the beginning of therapy, after which it is switched to drip administration. If blood pressure does not increase within 10-20 minutes, repeat the infusion of the drug. After recovery from the shock state, drip administration 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). In case of acute hepatic-renal failure (in acute poisoning, 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 drug intake at a dose of 75-125 mg per day for no more than 7-10 days. In acute hepatitis, Prednisolone is administered at a dose of 75-100 mg/day for 7-10 days. For poisoning with cauterizing liquids 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 not possible, Prednisolone is administered intramuscularly in the same doses. After relief of the acute condition, Prednisolone tablets are prescribed orally, followed by a gradual reduction in the dose. When taking the drug for a long time, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly! Children: Use in children over 6 years of age only as directed and under the supervision of a physician. The doctor determines the dose and duration of therapy individually, depending on the age and severity of the disease. Long-term use in children may cause growth retardation, so it is necessary to limit the use of minimal doses for certain indications for the shortest possible time. The benefit of treatment must outweigh the possible risk of adverse reactions.

Use during pregnancy and lactation

Do not use the drug during pregnancy. If it is necessary to use the drug during lactation, it is recommended to stop breastfeeding.

Precautionary measures

The ability to influence the speed of reaction when driving vehicles or other mechanisms. Patients treated with prednisone should refrain from potentially hazardous activities that require increased attention to the speed of mental and motor reactions. Special groups of patients Elderly During long-term therapy, muscle atrophy, muscle pain or weakness, delayed wound healing, atrophy of the protein matrix of the bone leading to osteoporosis, vertebral compression fractures, avascular necrosis of the femoral head or humeral head, and pathological fractures of long tubular bones may be observed. Particularly serious complications may occur in elderly and debilitated patients. Before initiating glucocorticoid therapy in postmenopausal women, it is necessary to take into account that such patients are especially prone to osteoporosis. Use with caution in patients with osteoporosis. Liver dysfunction In patients with cirrhosis, an increased effect of glucocorticoids is observed. Renal dysfunction. Use with caution.

Interaction with other drugs

Anticoagulants: when used simultaneously with glucocorticoids, the effect of anticoagulants may be increased or decreased. Parenteral administration of prednisolone causes the thrombolytic effect of vitamin K antagonists (fluindione, acenocoumarol). Salicylates and other non-steroidal anti-inflammatory drugs: Concomitant use of salicylates, indomethacin and other non-steroidal anti-inflammatory drugs may increase the likelihood of gastric ulceration. Prednisolone reduces the level of salicylates in the blood serum, increasing their renal clearance. Caution is necessary when reducing the dose of prednisolone during long-term concomitant use. Hypoglycemic drugs: Prednisolone partially inhibits the hypoglycemic effect of oral hypoglycemic agents and insulin. Hepatic enzyme inducers, for example, barbiturates, phenytoin, pyramidone, carbamazepine and rifampicin increase the systemic clearance of prednisolone, thereby reducing the effect of prednisolone by almost 2 times. CYP3A4 inhibitors, such as erythromycin, clarithromycin, ketoconazole, diltiazem, aprepitant, itraconazole and oleandomycin, increase the elimination and plasma levels of prednisolone, which increases the therapeutic and side effects of prednisolone. Estrogen may potentiate the effect of prednisolone by slowing its metabolism. It is not recommended to adjust the dose of prednisolone for women using oral contraceptives, which contribute not only to an increase in the half-life, but also to the development of the atypical immunosuppressive effect of prednisolone. Fluoroquinolones: Concomitant use may cause tendon damage. Amphotericin, diuretics and laxatives: Prednisolone may increase potassium excretion in patients receiving these drugs concomitantly. Immunosuppressants: Prednisolone has active immunosuppressive properties, which may cause an increase in therapeutic effects or the risk of developing various adverse reactions when used simultaneously with other immunosuppressants. Only some of them can be explained by pharmacokinetic interactions. Glucocorticoids increase the antiemetic effectiveness of antiemetic drugs that are used in parallel during therapy with anticancer drugs that cause vomiting. Corticosteroids can increase the concentration of tacrolimus in the blood plasma when used simultaneously; when they are withdrawn, the concentration of tacrolimus in the blood plasma decreases. Immunization: Glucocorticoids may reduce the effectiveness of immunization and increase the risk of neurological complications. The use of therapeutic (immunosuppressive) doses of glucocorticoids with live viral vaccines may increase the risk of developing viral diseases. Emergency vaccines may be used during drug therapy. Anticholinesterase agents: In patients with myasthenia gravis, the use of glucocorticoids and anticholinesterase agents may cause muscle weakness, especially in patients with myasthenia gravis. Cardiac glycosides: the risk of developing glycoside intoxication increases. Others: Two serious cases of acute myopathy have been reported in elderly patients who took doxocarium chloride and high-dose prednisolone. With long-term therapy, glucocorticoids may reduce the effect of somatotropin. Cases of acute myopathy have been described with the use of corticosteroids in patients who are simultaneously receiving treatment with neuromuscular transmission blockers (for example, pancuronium). Cases of seizures have been reported with the simultaneous use of prednisolone and cyclosporine. Because coadministration of these drugs causes mutual inhibition of metabolism, it is likely that seizures and other side effects associated with the use of each of these drugs as monotherapy may occur more frequently when administered concomitantly. Concomitant use may cause an increase in the concentration of other drugs in the blood plasma. Antihistamines reduce the effect of prednisolone. When prednisolone is used simultaneously with antihypertensive drugs, the effectiveness of the latter may be reduced. Prednisolone should not be mixed or used simultaneously with other drugs in the same infusion system or syringe. When mixing a solution of prednisolone with heparin, a precipitate forms. Incompatible with aerosols of sympathomimetic drugs for the treatment of bronchial asthma in children (risk of respiratory paralysis).

Contraindications

Hypersensitivity to the components of the drug; peptic ulcer of the stomach and duodenum, osteoporosis, Itsenko-Cushing's disease, tendency to thromboembolism, renal failure, arterial hypertension, viral infections (including viral lesions of the eyes and skin), decompensated diabetes mellitus, vaccination period (at least 14 days before and after preventive immunization), lymphadenitis after BCG vaccination, active form of tuberculosis, glaucoma, cataracts, productive symptoms in mental illness, psychosis, depression; systemic mycosis, herpetic diseases, syphilis, severe myopathy (except for myasthenia gravis), poliomyelitis (except for the bulbar-encephalitic form), pregnancy and lactation. For intra-articular injections - infections at the injection site.

Compound

active ingredient: 1 ml of solution contains prednisotokg for prednisolone - 30 mg; excipients: sodium hydrogen phosphate anhydrous, sodium dihydrogen phosphate dihydrate, propylene glycol, water for injection. Basic physical and chemical properties: transparent, colorless or almost colorless solution.

Overdose

In case of overdose, nausea, vomiting, bradycardia, arrhythmia, increased symptoms of heart failure, cardiac arrest are possible; hypokalemia, increased blood pressure, muscle cramps, hyperglycemia, thromboembolism, acute psychosis, dizziness, headache, possible development of symptoms of hypercortisolism: weight gain, development of edema, arterial hypertension, glucosuria, hypokalemia. In children with an overdose, suppression of the hypothalamic-pituitary-adrenal system, Itsenko-Cushing syndrome, decreased excretion of growth hormone, and increased intracranial pressure is possible. There is no specific antidote. Treatment: discontinuation of the drug, symptomatic therapy, and, if necessary, correction of electrolyte balance.

Side effect

The development of severe adverse reactions depends on the dose and duration of treatment. Adverse reactions usually develop with long-term treatment with the drug. Over a short period, the risk of their occurrence is unlikely. Infections and invasions: increased sensitivity to bacterial, viral, fungal infections, their severity with masking of symptoms, opportunistic infections. From the blood and lymphatic system: an increase in the total number of leukocytes with a decrease in the number of eosinophils, monocytes and lymphocytes. The mass of lymphoid tissue decreases. Blood clotting may increase, which leads to thrombosis and thromboembolism. From the endocrine system and metabolism: suppression of the hypothalamic-pituitary-adrenal system, growth retardation in children and adolescents, menstrual irregularities, impaired secretion of sex hormones (amenorrhea), postmenopausal bleeding, Cushingoid face, hirsutism, weight gain, decreased tolerance to carbohydrates , increased need for insulin and oral hypoglycemic drugs, hyperlipidemia, negative balance of nitrogen and calcium, increased appetite, disturbance of mineral metabolism and electrolyte balance, hypokalemic alkalosis, hypokalemia, possible fluid and sodium retention in the body. Mental disorders: irritability, euphobia, depression, suicidal tendencies, insomnia, labile mood, 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, which is accompanied by nausea and swelling of the optic disc in children. From the nervous system: increased intracranial pressure, epileptic seizures, peripheral neuropathies, paresthesia, dizziness, headache, autonomic disorders. From the organs of vision: increased intraocular pressure, glaucoma, swelling of the optic nerve, cataracts, thinning of the cornea and sclera, exacerbation of ocular viral and fungal infections, exophthalmos. From the cardiovascular system: myocardial rupture due to myocardial infarction, arterial hypo- or hypertension, bradycardia, combined ventricular arrhythmia, asystole (due to rapid administration of the drug), atherosclerosis, thrombosis, vasculitis, heart failure, peripheral edema. In patients with acute myocardial infarction, the necrosis focus spreads, scar formation slows down. From the immune system: allergic reactions that cause anaphylactic shock with a fatal outcome, angioedema, allergic dermatitis, changes in the reaction to skin tests, relapse of tuberculosis, immunosuppression, hypersensitivity reactions, including rash, itching of the skin. From the gastrointestinal tract: nausea, bloating, unpleasant taste in the mouth, dyspepsia, peptic ulcers with perforation and bleeding, esophageal ulcer, esophageal candidiasis, pancreatitis, gallbladder perforation, gastric bleeding, local ileitis and ulcerative colitis. During the use of the drug, an increase in ALT, AST and alkaline phosphatase may be observed, which is usually not significant and is reversible after discontinuation of the drug. From the skin: slower regeneration, skin atrophy, formation of hematomas and atrophic stripes of the skin (striae), telangiectasia, acne, acne, hirsutism, microhemorrhages, ecchymosis, purpura, hypo- or hyperpigmentation, post-steroid panniculitis, which is characterized by the appearance of erythematosis, hot subcutaneous thickenings for 2 weeks after discontinuation of the drug, Kaposi's sarcoma. From the musculoskeletal system: proximal myopathy, osteoporosis, tendon rupture, muscle weakness, atrophy, myopathy, fractures of the spine and long bones, aseptic osteonecrosis. From the urinary system: increased risk of urolith formation and the content of leukocytes and red blood cells in the urine without obvious kidney damage. General: malaise, persistent hiccups when using the drug in high doses, adrenal insufficiency leading to hypotension, hypoglycemia and death in stressful situations such as surgery, trauma or infection if the dose of prednisolone is not increased. With abrupt withdrawal of the drug, withdrawal syndrome is possible, the severity of symptoms depends on the degree of adrenal atrophy, headache, nausea, abdominal pain, dizziness, anorexia, weakness, mood changes, lethargy, fever, myalgia, arthralgia, rhinitis, conjunctivitis, skin pain, weight loss. In more severe cases - severe mental disorders and increased intracranial pressure, steroid pseudorheumatism in patients with rheumatism, death. Reactions at the injection site: pain, burning, changes in pigmentation (depigmentation, leucoderma), skin atrophy, sterile abscesses, rarely - lipoatrophy.

Storage conditions

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

Buy Prednisolone-Ferein solution for IV and IM administration. 30 mg/ml in amp. 1 ml in pack No. 5x2 in the pharmacy

Price for Prednisolone-Ferein solution for intravenous and intramuscular injection. 30 mg/ml in amp. 1 ml in pack No. 5x2

Instructions for use for Prednisolone-Ferein solution for IV and IM administration. 30 mg/ml in amp. 1 ml in pack No. 5x2

When to take it for arthritis?

Rheumatoid arthritis is characterized by periodic exacerbations, during which swelling of the joints occurs, which is accompanied by acute pain and severe impairment of mobility of the affected area.

When and how to take Prednisolone for rheumatoid arthritis - only a rheumatologist can answer this question. This drug is a potent synthetic hormonal drug, which causes a large number of side effects and contraindications to the use of the drug.

Properties of Prednisolone for rheumatoid arthritis:

• quickly relieves swelling of the joint capsule;
• has an immunosuppressive effect, stopping the autoimmune process;
• relieves inflammation;
• relieves pain;
• stimulates the elimination of toxins.

The drug in tablets has lower bioavailability, therefore it is effective for moderate symptoms of arthritis. It is taken in a short course to quickly reduce the inflammatory response and improve overall well-being.

Treatment with glucocorticosteroid injections is one of the most effective ways to quickly stop the inflammatory process. Therapy with such drugs rarely takes more than three days. During this time, it is possible to get rid of severe symptoms and relieve swelling of the joints, returning them to their previous mobility.

Thus, Prednisolone is effective in quickly relieving the symptoms of rheumatoid arthritis.

The medicine suppresses the activity of the immune system, stopping the pathological process. Due to its systemic effect, Prednisolone cannot be taken continuously; therapy is carried out only in short courses and only as prescribed by a doctor.

Most often, Prednisolone therapy is carried out in a hospital, under the constant supervision of medical professionals. This measure is associated with a high risk of complications during treatment with this drug.

SYSTEMIC USE OF HA IN RHEUMATIC DISEASES

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Despite the long history of using GCs for rheumatic diseases, many questions still remain regarding the most adequate doses and dosage forms of drugs, routes of administration, duration of therapy, and ways to prevent side effects.
For rheumatic diseases, all the main options for GC therapy are widely used: 1. Local (intra-articular, rectal administration, etc.) 2. Local (ointments, drops, aerosol) 3. Systemic: low doses high doses alternating therapy pulse therapy “mini- pulse" therapy combined (primarily with cytotoxics).
When prescribing GCs for rheumatic disease, it is necessary to take into account several general principles of pharmacotherapy, the observance of which can improve the effectiveness and safety of treatment.
In the treatment of GC, 5 main phases are conventionally distinguished: • Induction: short-acting GC (prednisolone or methylprednisolone) at a dose approximately corresponding to 1 mc/kg/day with an 8-hour interval. • Consolidation: transition to a single dose of GC in the morning • Decrease: the rate of reduction depends on the dose; it is possible to switch to alternating therapy • Maintenance treatment: the minimum effective dose of the drug • Prevention of complications of GK therapy (starts from the induction phase ).
Typically, the dose of GC varies from 40 mg to 100 mg (0.5 mg/kg/day - 1.5 mg/kg/day in terms of prednisolone).
At the beginning, the daily dose of the drug is divided into 3 doses, then they switch to a single dose of the drug in the morning. Treatment with GC should be carried out only according to strict indications. At the same time, not only the doctor, but also the patient should be informed in detail about all the advantages and disadvantages of GC therapy. During treatment, the physician should strive to use short-acting GCs at the optimal dose and, if possible, not prescribe these drugs for a period longer than necessary to control disease activity. However, if there are clear indications, GCs should be prescribed as early as possible, without first trying to use “softer” methods of treatment. If long-term use of GCs is necessary, one should strive to switch as quickly as possible to a single dose of the entire dose in the morning, and then to an alternating regimen of GC therapy. Selection of the initial dose of GC, duration of therapy and rate of dose reduction should not be done empirically, but based on standardized clinical and laboratory parameters of disease activity. During the treatment process, it is necessary to remember that inhibition of the hypothalamic-pituitary-adrenal axis persists in patients receiving GC, even in a small dose (10 mg/day for 3 weeks or more), for a long time (up to 1 year) after discontinuation of the drug. With the development of severe intercurrent diseases or the need for surgical interventions, these patients should receive GC replacement therapy. Table 1. Main indications for systemic use of GCs in rheumatic diseases

The initial and especially maintenance dose of prednisolone and the timing of the drug may be of great importance. There is evidence that there is no significant inhibition of the hypothalamic-pituitary-adrenal axis

, if the dose of prednisolone does not exceed 5 mg/day.
The development of adverse reactions during GC treatment develops significantly more often in patients receiving more than 10 mg of prednisolone per day. It can be assumed that reducing the total dose of prednisolone and optimal timing of drug administration may reduce the risk of side effects, such as suppression of osteoblast (OB) function, since GCs suppress OB in a dose-dependent manner. For example, there is evidence that taking GC at night (at 2 a.m.) can reduce the level of IL-6 (an important mediator of inflammation and bone resorption in RA) to the same extent as administering 15–20 mg of GC in the morning over 24 hours before the study. These data suggest that low-dose GC treatment may reduce the potential risk of osteoporosis by inhibiting IL-6 synthesis. Currently, there is evidence that chronic inflammation in patients with RA, and possibly other autoimmune diseases, may be associated with defects at the level of the HPA axis. When studying an experimental model of arthritis in rats, it was found that chronic erosive arthritis can be induced only in female Lewis rats, while in related strains of Fisher rats minimal transient inflammatory changes in the joint develop. The only difference between these mouse strains is the disruption in the HPA axis. Thus, in Lewis mice, in contrast to Fisher rats, a decrease in the level of corticotropin-releasing hormone and RNA in the hypothalamus was detected, as well as a weakening of the synthesis of corticotropin-releasing hormone, corticotropin and cortisol in response to immunization with the streptococcal membrane. At the same time, the administration of cortisol to Lewis rats after antigenic stimulation prevents the development of arthritis, and the administration of a corticoid receptor inhibitor to Fisher rats causes the development of severe inflammatory joint damage in the latter. Similar disorders were found in RA. We describe a patient with RA who, after removal of a cortisol-secreting adenoma, experienced an exacerbation of the disease. In patients with PA, there was an absence of daily fluctuations in the concentration of cortisol in the blood serum, inadequate synthesis of cortisol in response to stress stimuli, and a low basal level of this hormone, which does not correspond to the severity of the inflammatory process. In patients with active untreated RA, there is a weakening of basal and corticotropin-stimulated cortisol synthesis. Moreover, approximately 10% of RA patients show signs of adrenal insufficiency. Obviously, in these patients we can expect a higher effectiveness of low doses of GC than in patients without a defect in the HPA axis. Interesting results were recently obtained when studying the relationship between the clinical effectiveness of GCs and the timing of drug administration
, taking into account their pharmacokinetics and daily fluctuations in the levels of cortisol and cytokines.
Until recently, it was believed that taking GC in the morning inhibits the synthesis of ACTH and cortisol to a lesser extent than at night and in the evening. Normally, cortisol levels begin to increase at 2 a.m. with a peak at 8 a.m. and return to basal levels by 12 p.m. Symptoms of RA (stiffness, inflammatory activity) usually decrease a few hours after waking up at the peak of cortisol synthesis. It is also suggested that a circadian increase in IL-6 levels may also be associated with an increase in RA activity in the morning. Daily fluctuations in IL-6 are observed in normal conditions and in patients with PA. Normally, the peak concentration of IL-6 occurs slightly earlier than ACTH and cortisol between 1 and 4 am. However, in RA, the peak of IL-6 is delayed and occurs between 2 and 7 am and the concentration of IL-6 is significantly higher than normal. On the other hand, judging by pharmacokinetic studies, the peak concentration of prednisolone in plasma is achieved after 1 - 3 hours, the half-life is 2 - 3.5 hours, and the maximum biological effect develops in approximately 6 hours. Recently, evidence has appeared that the use of GCs ( 5 - 7.5 mg) at night (at approximately 2 am) is more preferable from the point of view of suppression of IL-6 secretion and is associated with a significantly more pronounced reduction in the duration of morning stiffness, joint pain, Lansbury index, Ritchie index and morning concentrations of IL- 6, compared with standard GC intake in the morning. Systemic use of
GCs is one of the most effective methods of pharmacotherapy for some rheumatic diseases, which has significantly improved the prognosis and life expectancy of patients. The main indications for the systemic use of GCs in rheumatology are summarized in Table 1. There are a number of rheumatic diseases or syndromes in which the systemic use of GCs is not advisable due to low efficiency or the possibility of developing severe complications. These include osteoarthritis, degenerative spinal lesions, fibromyalgia, osteonecrosis, spondyloarthropathy, infectious arthritis, as well as Raynaud's phenomenon and scleroderma fibrosis.

Table 2. Indications for pulse therapy for rheumatic diseases

Pulse therapy

In the early 70s, reports appeared about the possibility of suppressing kidney transplant rejection by intravenously administering very large doses (“megadoses”) of GC to patients. This method is called “pulse therapy”. Although a clear definition of this term still does not exist, it usually means rapid (within 30–60 minutes) intravenous administration of large doses of GC (about 1000 mg in terms of MP) once a day for three days. Most often, when conducting pulse therapy, MP is used in the form of a solution of sodium hemisuccinate, and less commonly, dexamethasone. When studying pharmacokinetics

It was found that the level of MP in plasma, when administered intravenously, reaches a maximum within 1 hour and rapidly decreases over the next 6-7 hours. After 4 days, only trace amounts of active methylprednisolone are found in the peripheral blood, clearly insufficient for depot effects.
However, when studying the metabolism of isotope-labeled MP, it was shown that the latter accumulates very actively in various tissues, especially erythrocytes, some visceral tissues and the brain. At the same time, based on some indirect data, it was suggested that MP has the ability to be deposited to a greater extent in inflamed tissues than in normal tissues. These pharmacological properties of MP, as well as minimal mineralocorticoid activity, allow us to consider it as a means of choice when performing pulse therapy. Pulse therapy results in a decrease in cortisol levels, reflecting adrenal suppression, but adrenal function returns within approximately 4 weeks. The first report of pulse therapy for rheumatic diseases is usually attributed to E. Cathcart et al., who in 1976 used this method for lupus nephritis. The basis for conducting pulse therapy was the similarity of morphological changes in the kidneys of a patient with lupus nephritis with the picture observed during kidney transplant rejection. This allowed the authors to apply to the treatment of lupus nephritis a protocol previously developed for patients with acute transplant rejection, that is, GC pulse therapy. It must be emphasized that in patients with the most severe forms of rheumatic diseases, such as lupus nephritis, central nervous system lupus, rheumatoid vasculitis, systemic necrotizing vasculitis, GC pulse therapy must be combined with active cytotoxic therapy
, primarily CP, since only Combination therapy can actually improve the prognosis of the disease. There have been reports of the effectiveness of pulse therapy with dexamethasone in patients with RA, as well as resistant thrombocytopenic purpura. Indications for GC pulse therapy are given in Table. 2.

Alternative therapy

Alternating GC therapy is a treatment method that consists of prescribing short-acting GCs without significant mineralocorticoid activity once, in the morning (about 8 hours) every 48 hours. The goal of alternating therapy is to reduce the severity of the side effects of GCs while maintaining therapeutic effectiveness. It is believed that the possibility of alternating GC therapy should be discussed in all patients who are planning long-term GC treatment (more than several weeks). It has been shown that an alternating regimen at the onset of the disease can be successfully used in ulcerative colitis, chronic dermatoses, myasthenia gravis, and bronchial asthma. However, for systemic rheumatic diseases, such treatment tactics are usually not effective. Table 3. One of the possible schemes for switching to alternating GC intake

The development of this treatment was based on the assumption that the anti-inflammatory effects of GC last longer than the unwanted metabolic effects

. Therefore, there may be a rhythm of taking GCs in which, during the break between doses of drugs, their anti-inflammatory effect is maintained, but the risk of developing side effects is reduced. It is also assumed that intermittent administration of GC sets a certain rhythm of fluctuations in the level of GC in the blood, stimulating the normal diulnar cycle, which can prevent the development of Cushing's syndrome and suppression of the hypothalamic-pituitary axis. However, it is possible that a decrease in the severity of side effects with alternating administration of GC is associated only with a decrease in the total dose of the drug, which is determined by the characteristics of the bioavailability of GC. Indeed, there is evidence that the bioavailability of oral prednisolone is lower when administered as a single dose than when administered in several divided doses. At the same time, it is difficult to explain the decrease in the number of side effects while maintaining the effectiveness of this option of GC therapy only from this point of view. The use of short-acting GS and a 48-hour interval between doses is not empirical. There is evidence that the 36-, 24- and 12-hour intervals are associated with suppression of adrenal function, and the 72-hour interval reduces the therapeutic effectiveness of GCs. It has been established that the alternating regimen of GC therapy to a certain extent reduces the severity of clinical manifestations of Cushing's syndrome (some somatic and psychotic reactions, hypertension, growth retardation in children, increased sensitivity to infection, etc.) and to a lesser extent suppresses adrenal function. The positive properties of alternating therapy appear only with long-term treatment with GC. Therefore, it should not be used in patients who plan to use these drugs for a short time, as well as in the initial stage of treatment or during an exacerbation of the disease. It must be borne in mind that the alternating regimen does not in all cases prevent the development of Cushing's syndrome or suppression of the hypothalamic-pituitary-adrenal axis. In addition, in many patients, alternative therapy is difficult due to the deterioration of the patients’ well-being on the day of taking a low dose of GC. In table Figure 3 shows one of the possible schemes for switching to alternating GC intake.

Tactics of dose reduction and GC withdrawal

Short-term use of small doses of GC (less than 20 mg/day) for 3 weeks allows you to quickly stop treatment without developing withdrawal syndrome. However, in patients taking GCs for a long time, drug withdrawal is a long and difficult process (see Table 4).

GC for some rheumatic diseases Rheumatoid arthritis

GCs have been used to treat RA for almost 50 years and continue to be one of the most commonly used antirheumatic drugs. Thus, in the mid-80s, 24% of patients with RA in the UK and 15% in Denmark received GCs. However, results regarding the effectiveness of GCs in RA are difficult to interpret because they were obtained from poorly controlled (or short-term) studies, some of which used too high doses of drugs. Thus, according to K. Saag et al. (1996), who conducted a meta-analysis of 34 studies of GC in RA, only 9 were controlled and suitable for subsequent analysis. Overall, there is reason to believe that GC therapy provides adequate control of rheumatoid inflammation compared with placebo and other treatments. At the same time, according to J. Fries et al. (1996), who studied disease outcomes in 2888 patients with RA using the ARAMIS database, taking GCs is associated with a more unfavorable prognosis than taking basic antirheumatic drugs. However, it is not clear whether this is due to the effect of the GCs themselves or to the fact that GC treatment was prescribed to more severely affected RA patients. Table 4. Scheme of gradual dose reduction and discontinuation of GC from an initial dose of 40 mg (according to ES Shiom, 1992)

Early studies showed that prednisolone at a daily dose of 30 - 40 mg/day has a more pronounced anti-inflammatory activity than aspirin at a dose of 6 g. However, the development of a large number of side effects during treatment with such high doses of GCs suspended further study of the effectiveness of high doses of GCs with RA. Since 1964, several small open-label studies have been conducted regarding the effectiveness of low doses of GC.

(5 - 10 mg prednisolone).
A positive effect of low doses on such parameters as morning stiffness, hand grip strength, and ESR was noted. In early 1980, E. Harris et al. (1983) proposed the use of low doses of GC in RA as the so-called “bridge” therapy until the basic antirheumatic drugs begin to act, especially in those patients whose symptoms are not controlled by NSAIDs. They conducted the only double-blind controlled study (18 and 16 patients) of low doses of prednisolone (5 mg/day), which demonstrated a decrease in the number of painful joints by 12 months, but not by 24 months of therapy. There was no effect on the number of swollen joints or other parameters. After discontinuation of GC, all patients developed an exacerbation. Similar data on exacerbation of RA with a minimal reduction in the dose of GC (by an average of 3.5 mg/day) were noted by W. Buchanan et al. (1983), which indirectly confirms the anti-inflammatory activity of even low doses of GC. However, according to other authors, this largely reflects not the exacerbation of arthritis, but the development of GC withdrawal syndrome. Overall, there is good reason to believe that prednisolone doses ranging from 7 to 15 mg/day have optimal anti-inflammatory activity comparable to current NSAIDs and an acceptable toxicity profile. Table 5. Indications for the use of low doses of GCs in RA

For many years, the question of whether low doses of GCs affect the progression of joint destruction in RA has been studied, that is, do they have the basic antirheumatic activity that was demonstrated during treatment with high doses of GCs back in the early sixties? Of great interest are the data of J. Kirvan et al. (1995), who conducted a randomized, double-blind, controlled study of fixed doses of prednisolone (7.5 mg per day) in combination with basic therapy for RA. All patients were divided into 2 groups: 61 patients received prednisolone, 67 received placebo. Prednisolone 7.5 mg given over a 2-year period was found to reduce the rate of ren

Effect of Prednisolone for arthritis

Rheumatoid arthritis is an autoimmune disease. This pathology develops due to a specific immune reaction to human connective tissue cells, which results in inflammation in small joints. Since the exact causes of the development of this disease have not yet been identified, treatment is carried out using drugs that quickly relieve symptoms while simultaneously suppressing the activity of immune cells.

The main purpose of taking Prednisolone for rheumatoid arthritis is the immunosuppressive effect of the drug with a simultaneous anti-inflammatory effect. Thus, the glucocorticosteroid simultaneously reduces the activity of the mechanisms that cause inflammation and stops this inflammatory reaction, reducing discomfort.

Despite such a profound effect, Prednisolone does not cure arthritis, but only temporarily alleviates its course. Some time after taking the medicine, its activity decreases, the immune system continues to work as before, and the autoimmune attack on the joints resumes.

Prednisolone relieves unpleasant symptoms, but does not fight the disease

Description of substances and actions

The composition of Prednisolone contains synthetic hormones - replicas of cortisone and its derivative. In the human body, with rheumatoid arthritis, there is no significant change in the production of hormones, but increased dosages help relieve all the symptoms of the pathology.

The correct doses of Prednisolone for rheumatoid arthritis help relieve inflammation, remove harmful substances, and prevent shock and allergic reactions. However, with long-term use, disruption of the kidneys, liver and other massive side effects is possible.

Unpleasant symptoms appear after taking the medicine, even if the doctor prescribes a limited dosage.

Tablets and injections are used to treat rheumatoid arthritis during exacerbation, as well as in cases of severe forms of the disease. The drug is used to eliminate complicated types of pathology (vasculitis, for example).

A doctor should prescribe Prednisolone injections or tablets, since despite all its effectiveness, this substance often leads to severe side effects.

Application and dosage regimens

The dosage of Prednisolone for arthritis is selected individually for each patient. The amount of the drug taken depends on the patient’s weight, general health and the intensity of the inflammatory reaction.

The standard dosage for an adult patient when taking tablets is 20 mg per day. In severe cases, this amount can be increased to 30 mg. In this case, the daily dosage is divided into two doses - in the morning you need to take 2/3 of the dose, and in the evening the remaining amount. This is due to the peculiarities of drug metabolism in the human body.

The regimen for taking Prednisolone for rheumatoid arthritis includes another important condition - proper withdrawal of the drug. High-dose therapy lasts literally several days, and then the number of tablets is reduced in such a way as to reach a maintenance dose of 5 mg of the drug per day.

In particular cases, the dosage can be reduced or increased, but only as prescribed by a doctor. It is prohibited to independently adjust the treatment regimen.

The maximum permissible dosage of the drug in ampoules is 30 mg per day for large joints and 10 mg for small ones. For rheumatoid arthritis, the injection is given directly into the inflamed joint. It is impossible to perform such a manipulation on your own, so treatment is carried out in a hospital. Injections are given twice a week, not more often. The maximum duration of treatment is 3 weeks. In the vast majority of cases, three injections are enough for the exacerbation of the disease to subside.

PRINCIPLES OF LONG-TERM THERAPY

1. Prescribe glucocorticoids only when a therapeutic effect has not been achieved during treatment with other, less active drugs. The exceptions are adrenal insufficiency, adrenogenital syndrome, and life-threatening diseases.
2. Start with the lowest effective dose
   of glucocorticoids, which can be increased if necessary to achieve the desired effect.
3. Select the dose of glucocorticoids individually
   , depending more on the nature of the disease and the patient’s response to treatment than on age or body weight.
4. After obtaining the desired effect, the dose should be gradually reduced to the minimum
   at which the clinical effect is maintained.
5. Use intermediate-acting glucocorticoids.
6. take glucocorticoids taking into account the circadian rhythm
   , once a day.
7. When the patient's condition stabilizes, switch to alternating therapy.

CHRONOTHERAPY APPROACH

Considering the circadian physiological rhythm of glucocorticoid secretion, during continuous treatment the daily dose of glucocorticoids cannot be divided into 3-4 parts and taken at regular intervals, since this increases the risk of suppression of the hypothalamic-pituitary-adrenal system. At the same time, taking glucocorticoids in the morning reduces the risk of [1] suppression of the hypothalamic-pituitary-adrenal system and [2] the development of osteoporosis, since in the morning the hypothalamic-pituitary-adrenal system is least sensitive to the suppressive effect of exogenous glucocorticoids. In most cases, glucocorticoid medications should be taken as one morning dose

, which especially applies to long-acting drugs. The second option is to take most of the drug (2/3-3/4) in the morning and the remaining smaller portion around noon.

ALTERNATING THERAPY

Alternative therapy can be used in patients who are planning a long course of oral glucocorticoids. Alternative therapy consists of prescribing the drug every other day in a single dose. This dose should be 2 times higher than that that was used before transferring to alternative therapy. An example of transferring a patient to alternative therapy is given in Table 6.

Advantages of alternating therapy:

• less suppression of the hypothalamic-pituitary-adrenal system, reducing the risk of developing adrenal insufficiency;
• reducing the risk of developing infectious complications;
• reducing growth retardation in children.

It should be noted that alternating therapy does not reduce the risk of developing osteoporosis [2].

The transition from daily use to alternating therapy should be gradual and only after the condition has stabilized

sick. However, for a number of diseases, for example, nephrotic syndrome in children, treatment can be started immediately with alternative therapy.

Only glucocorticoids of intermediate duration of action

(prednisolone, methylprednisolone, prednisone), after taking one dose of which the hypothalamic-pituitary-adrenal system is suppressed for 12-36 hours. Long-acting glucocorticoids (triamcinolone, dexamethasone, betamethasone) should not be used, since even when they are prescribed every other day, the risk of suppression of the hypothalamic-pituitary-adrenal system does not decrease. Natural glucocorticoids (cortisone and hydrocortisone), which have a pronounced mineralocorticoid effect, as discussed above, are used mainly for replacement therapy.

Alternative therapy is not effective enough

in the treatment of hematological diseases, ulcerative colitis, malignant tumors, and in severe conditions. Sometimes patients with bronchial asthma or rheumatoid arthritis may experience an exacerbation of symptoms of the disease on the second “hormonal-free” day. In these cases, you can increase the dose of the drug, take a small additional dose on the second day, or, for bronchial asthma, prescribe inhaled glucocorticoids.

Table 6.

Scheme of transition to alternating therapy followed by gradual withdrawal of glucocorticoids (Avery's Drug Treatment, 1987) [4]

The starting dose of prednisolone is suggested to be 50 mg per day.

Contraindications

The list of contraindications for Prednisolone is quite impressive. You should familiarize yourself with them before starting treatment. Absolute contraindications:

• intolerance to the active substance;
• infectious diseases;
• viruses, fungi, parasites in the body;
• stomach ulcer;
• recent heart attack;
• diabetes;
• renal and liver failure;
• glaucoma;
• immunodeficiency due to HIV.

The drug should not be taken for several weeks after vaccination. In case of gastritis in the acute stage, it is necessary to stop using this medicine, as it can aggravate the symptoms.

A complete list of contraindications, precautions and drug interactions is given in the official instructions for the drug. This information should be read before starting treatment. The patient must notify the doctor about all medications that he takes on an ongoing basis. This is necessary to avoid dangerous drug interactions.

In the presence of fungal and infectious diseases, the drug is not prescribed

Prohibition on the use of the drug

Before taking Prednisolone for rheumatoid arthritis, you need to make sure there are no contraindications and also assess the possible risks. If contraindications are not observed, organ diseases that can be fatal may develop:

• the drug is prohibited for severe hypertension;
• You can’t take pills if you have diabetes;
• prohibited during pregnancy;
• do not take medicine for Itsenko-Cushing's disease;
• inflammation of the kidneys and inner walls of the heart is a direct contraindication;
• You should not take pills for psychosis and mental disorders;
• Therapy is prohibited for circulatory deficiency of the 3rd degree;
• you cannot take pills over the age of 80;
• stomach and intestinal ulcers – a complete ban on taking the drug;
• syphilis and tuberculosis;
• internal operations.

For you: Differences between gout and rheumatoid arthritis: what the tests will tell
You are prohibited from taking Prednisolone if a person has increased aggressiveness and excitability.

Side effects

When treating rheumatoid arthritis with a drug in the dosage form of tablets or ampoules, it should be noted that Prednisolone causes severe side effects. In this regard, therapy is recommended to be carried out under the supervision of the attending physician.

The most common reactions of the body to the action of Prednisolone:

• development of superinfection when taken against the background of bacterial, viral or fungal diseases;
• increased blood sugar levels;
• menstrual irregularities;
• decreased concentration of sex hormones;
• mental disorders, including delirium;
• paresthesia;
• migraine and vertigo;
• seizures;
• blood pressure surges;
• heart rate disturbances.

With long-term drug therapy, metabolic disorders and weight gain are possible. The drug can cause menstrual disorders in women and erectile dysfunction in men.

The drug is dangerous due to the risk of developing severe forms of an allergic reaction. When taking Prednisolone, anaphylactic shock and Quincke's edema were observed.

When taking the drug in tablets, digestive disorders are often observed, accompanied by vomiting, diarrhea, and disturbances in the acidity of gastric juice, and therefore it is not advisable to take the medicine for patients with chronic gastrointestinal diseases.

Prednisolone

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

The lowest dose of Prednisolone that provides a sufficient therapeutic effect should be used; if necessary, the dose should be reduced gradually.

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

If prolonged spontaneous remission occurs, treatment should be discontinued.

During long-term treatment, the patient should undergo regular examination (chest x-ray, plasma glucose concentration 2 hours after meals, urinalysis, blood pressure, body weight control, preferably an x-ray or endoscopic examination if there is a history of gastrointestinal ulcers). intestinal tract).

The growth and development of children on long-term therapy with Prednisolone should be carefully monitored. Growth retardation may occur in children receiving long-term, daily, multi-dose therapy. Daily use of prednisolone for a long time in children is possible only for absolute indications. Taking the drug every other day may reduce the risk of developing this side effect or avoid it altogether.

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

Patients receiving drugs that suppress the immune system are more susceptible to infections. For example, chickenpox, genus, and measles can be more severe and even fatal in unimmunized 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 strongyloid 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 death.

During prednisolone therapy, susceptibility to infections may increase, some infections may occur in an erased form, and new infections may develop. In addition, 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 the drug Prednisolone, both as monotherapy and in combination with other immunosuppressants that affect on cellular immunity, humoral immunity or neutrophil function. These infections may not be severe, but in some cases they can be severe and even fatal. Moreover, the higher doses of the drug are used, the higher the likelihood of developing infectious complications.

In patients receiving treatment with Prednisolone in doses that have an immunosuppressive effect, the administration of live or live attenuated vaccines is contraindicated, but killed or inactivated vaccines can be administered, however, the response to the administration of such vaccines may be reduced or even absent. Patients receiving treatment with Prednisolone in doses that do not have an immunosuppressive effect may be immunized according to appropriate 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 the drug 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 drug therapy, such patients should receive appropriate preventive treatment.

There have been cases of the development of Kaposi's sarcoma in patients receiving GCS therapy. When the drug is discontinued, clinical remission may occur.

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 is individual for each patient and depends on the dose, frequency of use, time of administration 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 can continue for several months after the end of treatment, so in case of any stressful situations during this period, Prednisolone should be re-prescribed. If the drug is abruptly discontinued, acute adrenal insufficiency may develop, leading to death.

GCS 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 low blood pressure. It is assumed that these effects occur due to sharp fluctuations in the concentration of prednisolone in the blood plasma, and not due to its decrease.

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

Since the secretion of mineralocorticosteroids may be impaired, concomitant administration of electrolytes or mineralocorticosteroids is necessary.

Moderate to large doses of hydrocortisone or cortisone may 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. It is necessary to limit the consumption of table salt with food and prescribe potassium supplements. All corticosteroids increase calcium excretion.

The use of Prednisolone may lead to an increase in the concentration of glucose in the blood plasma and a worsening of existing diabetes mellitus. Patients receiving long-term therapy with Prednisolone may be predisposed to developing diabetes mellitus.

For patients who may be exposed to stress during treatment with Prednisolone, an increase in the dose of the drug is indicated before, during and after a stressful situation.

During therapy with Prednisolone, the development of various mental disorders is possible: from euphoria, insomnia, mood swings and depression to acute mental manifestations. In addition, existing emotional instability or psychotic tendencies may be exacerbated.

Potentially severe mental disorders may occur when using Prednisolone. Symptoms usually appear within a few days to weeks after starting therapy. Most reactions disappear either after reducing the dose or after discontinuation of the drug. Despite this, specific treatment may be required. Patients and/or their relatives should be warned that if changes occur in the patient's psychological status (especially with the development of depression and suicidal attempts), they should seek medical help. Patients or their relatives should also be warned about the possibility of developing mental disorders during or immediately after reducing the dose of the drug or completely stopping it.

There are reports of the development of epidural lipomatosis in patients receiving GCS. Usually with long-term therapy at high doses.

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

Due to the existing risk of corneal perforation, GCS should be prescribed with caution when treating eye infections caused by the herpes simplex virus (ophthalmoherpes).

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

Therapy with Prednisolone may mask the symptoms of a peptic ulcer, in which case perforation or bleeding may develop without significant pain.

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

Careful monitoring of patients receiving systemic corticosteroids and those who have recently suffered a myocardial infarction is necessary.

Patients taking Prednisolone should be prescribed acetylsalicylic acid-based analgesics and non-steroidal anti-inflammatory drugs with caution.

Allergic reactions are possible. Due to the fact that phenomena such as skin irritation and anaphylactic or pseudoanaphylactic reactions have rarely been observed in patients receiving GCS, the necessary measures should be taken before prescribing GCS, especially if the patient has a history of allergic reactions to drugs.

High doses of corticosteroids can cause acute pancreatitis.

Therapy with high doses of GCS can cause acute myopathy; In this case, the disease is most susceptible to patients with disorders of neuromuscular transmission (for example, myasthenia gravis), as well as patients receiving concomitant therapy with quinolytics, for example, blockers of neuromuscular transmission. This kind of myopathy is generalized; it can affect the muscles of the eyes or respiratory system and even lead to paralysis of all limbs. In addition, creatine kinase levels may increase. In such cases, clinical recovery may take weeks or even years.

Osteoporosis is a common (but rarely detected) complication of long-term therapy with high doses of corticosteroids.

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

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

Since prednisolone can enhance the clinical manifestations of Itsenko-Cushing syndrome. Prednisolone should be avoided in patients with this disease. Careful monitoring of patients with a history or current history of thrombosis or thromboembolic complications is necessary.