Review of instructions for Prednisolone for rheumatoid arthritis: preventing treatment errors

Doctors often prescribe Prednisolone for rheumatoid arthritis, especially when severe symptoms and aggressive inflammation develop. With the development of additional autoimmune effects, the medicine becomes the No. 1 assistant, which can significantly make the patient’s life easier.

In most cases, patients take the drug in tablet form, but in particularly severe situations, doctors prescribe injections. The drug Prednisolone is widely used in the treatment of various arthritis, but it has some limitations and side effects that can become critical for certain groups of people. The medicine is especially dangerous for those who suffer from liver and kidney pathologies.

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.

Prednisolone 30 mg/ml 1ml No. 3 solution d/in.amp. i.v. and i.m.

Instructions for use of the drug for specialists PREDNISOLE Trade name Prednisolone International nonproprietary name Prednisolone Dosage form Solution for intravenous and intramuscular administration 30 mg/ml Composition 1 ml of solution contains the active substance - prednisolone sodium phosphate, equivalent to prednisolone phosphate - 30 mg, excipients: disodium edetate, sodium hydrogen phosphate, sodium dihydrogen phosphate dihydrate, propylene glycol, water for injection. Description Transparent solution, colorless or with a greenish-yellow tint. Pharmacotherapeutic group Corticosteroids for systemic use. Glucocorticosteroids. Prednisolone ATX code H02AB06 Pharmacological properties Pharmacokinetics Up to 90% of the drug binds to blood plasma proteins: transcortin (cortisol-binding globulin) and albumin. Prednisolone is metabolized in the liver, partially in the kidneys and other tissues, mainly through conjugation with glucuronic and sulfuric acids. Metabolites are inactive. It is excreted in bile and urine via glomerular filtration and is 80-90% reabsorbed by the renal tubules. 20% of the dose is excreted unchanged by the kidneys. The half-life from blood plasma after intravenous administration is 2-3 hours. Pharmacodynamics Prednisolone is a synthetic glucocorticoid drug, a dehydrogenated analogue of hydrocortisone. It has anti-inflammatory, antiallergic and immunosuppressive effects, increases the sensitivity of beta-adrenergic receptors to endogenous catecholamines. Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) are found in all tissues, especially in the liver) to form a complex that induces the formation of proteins (including enzymes that regulate vital processes in cells). The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils and mast cells; inducing the formation of lipocortins and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes (especially lysosomal) and organelle membranes. 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 liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes, which contribute to inflammation, allergies, etc.), the synthesis of “proinflammatory cytokines” ( interleukin 1, tumor necrosis factor alpha, etc.); increases the resistance of the cell membrane to the action of various damaging factors. Protein metabolism: reduces the amount of globulins in the blood plasma, increases the synthesis of albumins in the liver and kidneys (with an increase in the albumin/globulin ratio), reduces the synthesis and enhances protein catabolism in muscle tissue. 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. Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase (increasing the flow of glucose from the liver into the blood); increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases (activation of gluconeogenesis); promotes the development of hyperglycemia. Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (mineralocorticoid activity), reduces the absorption of Ca2+ from the gastrointestinal tract, causes “leaching” of calcium from the bones and increases its renal excretion, reduces bone mineralization. The immunosuppressive effect is caused by the involution of lymphoid tissue, inhibition of the proliferation of lymphocytes (especially T lymphocytes), suppression of the migration of B cells and the interaction of T and B lymphocytes, inhibition of the release of cytokines (interleukin-1, 2; interferon gamma) from lymphocytes and macrophages and decreased 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 decrease 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, reducing the sensitivity of effector cells to allergy mediators, inhibiting antibody formation, changing the body's immune response. In obstructive diseases of the respiratory tract, the effect is mainly due to inhibition of inflammatory processes, prevention or reduction of the severity of swelling of the mucous membranes, 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. Increases the sensitivity of beta-adrenergic receptors of small and medium-sized bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production. Suppresses the synthesis and secretion of adrenocorticotropic hormone and, secondarily, the synthesis of endogenous corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation. Indications for use Urgent conditions requiring a rapid increase in the concentration of glucocorticosteroids in the body: - shock conditions (burn, traumatic, surgical, toxic) - in case of ineffectiveness of vasoconstrictors, plasma replacement drugs and other symptomatic therapy - allergic reactions (acute severe forms), blood transfusion shock, anaphylactic shock, anaphylactoid reactions - cerebral edema (including against the background of a brain tumor or associated with surgery, radiation therapy or head injury) - bronchial asthma (severe form), status asthmaticus - systemic connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis) - acute adrenal insufficiency - thyrotoxic crisis - acute hepatitis, hepatic coma - reduction of inflammation and prevention of cicatricial contractions (in case of poisoning with acids and alkalis). Method of administration and dosage 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. The drug is usually administered intravenously, first as a stream, then as a drip. In case of acute adrenal insufficiency, a single dose of the drug is 100-200 mg, daily 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 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 use 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. A single dose is 50-150 mg (in severe cases - up to 400 mg). The drug is re-administered after 3-4 hours. After recovery from the shock state, drip administration is continued until blood pressure stabilizes. 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 per day; if indicated, the daily dose can be increased to 300-1500 mg per day or 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 per day for no more than 7-10 days. For acute hepatitis, Prednisolone is administered at a dose of 75-100 mg per day for 7-10 days. For poisoning with acids and alkalis with burns of the digestive tract and upper respiratory tract, Prednisolone is prescribed at a dose of 75-400 mg per 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. With long-term use of the drug, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly! Children from 2 to 12 months. - 2-3 mg/kg/day, from 1 to 14 years -1-2 mg/kg/day, IM, IV administered slowly (over 3 minutes). If necessary, this dose can be repeated after 20-30 minutes. Side effects Very common (>1/10); often (>1/100, <1/10); uncommon (>1/1000, <1/100); rare (>1/10000, <1/1000); very rare (<1/10,000. In general, the incidence of predicted adverse effects, including suppression of the hypothalamic-pituitary-adrenal axis, depends on the dose, timing of administration and duration of treatment. Adverse effects can be minimized by using the lowest effective dose during as short as possible.Very often - increased susceptibility to infection, worsening of an existing infection, activation of a latent infection and masking of symptoms of infection due to the immunosuppressive and anti-inflammatory effect of prednisolone - decrease in the number of eosinophils and lymphocytes - immunosuppressive and anti-inflammatory effect leading to masking or worsening of an existing diseases - adrenal insufficiency (starting with inhibition of the hypothalamus and ending with true atrophy of the adrenal cortex) with long-term oral use of prednisolone, withdrawal syndrome due to adrenal insufficiency (headache, nausea, dizziness, anorexia, weakness, changes in emotional state, apathy and inadequate response to stressful situations , “steroid diabetes mellitus” with low insulin sensitivity, increased blood sugar levels in patients already suffering from diabetes mellitus (100%). Growth retardation in children as a result of impaired secretion of growth hormone and decreased sensitivity to growth hormone - increased intraocular pressure (up to 40% of patients treated with an oral drug), cataracts in 30% of patients with long-term treatment with the drug orally. - lung abscess in patients suffering from lung cancer (12%). - osteoporosis with symptoms such as back pain, decreased mobility, acute pain, vertebral compression fractures and decreased vertebral height, long bone fractures (25% with long-term treatment with the drug for oral administration, see section 4.4). Myopathy (10%) when treated with high doses. Often - increased white blood cell and platelet counts - Cushing's syndrome, including changes in fat deposition (moon face, central obesity, bull's hump) with long-term oral doses above physiological (usually more than 50 mg per day), hypokalemia due to retention of sodium instead of potassium, amenorrhea in women of childbearing age, increased cholesterol, triglycerides and lipoproteins when treated with high doses taken orally - euphoria, depression, corticosteroid-induced psychosis - hypertension (due to sodium retention, which leads to fluid retention), worsening congestive heart failure (as a result of sodium) - increased risk of developing tuberculosis - oral candidiasis, increased symptoms with colitis, ileitis, diverticulitis - fungal infection of the mucous membranes, stretch marks, acne, bruising, dermatitis, ecchymosis, facial erythema, atrophy, hirsutism, slow wound healing, increased sweating, telangiectasia and thinning of the skin, masking or worsening existing skin diseases. - nocturnal polyuria Uncommon - allergic reactions - diabetes mellitus (<1%) with low oral doses, increased cholesterol, triglycerides and lipoproteins with low oral doses - insomnia, mood swings, personality changes, mania and hallucinations - respiratory muscle myopathy - stomach ulcers or colon ulcers, gastrointestinal hemorrhages (0.5%), perforation of the stomach, intestines - aseptic necrosis of bone tissue - urinary stones due to increased excretion of calcium and phosphate, impaired secretion of sex hormones (menstruation disorders, hirsutism, impotence) , vasculitis Rarely - risk of thrombosis due to blood clotting - changes in thyroid function - with cerebral malaria, the coma state may last, dementia. - high risk of destruction of the cornea with simultaneous herpes eye infection (due to masking of this infection), glaucoma (long-term treatment with the drug orally). Very rarely - ketoacidosis and hyperosmolar coma, manifestation of latent hyperparathyroidism, accelerated development of porphyria - tumor lysis syndrome - manifestation of latent epilepsy, pseudotumor cerebri (benign intracranial hypertension with symptoms such as headache, blurred vision and visual impairment) - exophthalmos (after prolonged oral treatment with the drug) - cardiomyopathy with an increased risk of decreased cardiac output, arrhythmia due to hypokalemia - pancreatitis after long-term treatment with high doses - epidermal necrolysis, Steven-Johnson syndrome Contraindications For short-term use for health reasons, the only contraindication is hypersensitivity to Prednisolone or the components of the drug. In children during the growth period, GCS should be used only according to absolute indications and under the particularly careful supervision of the attending physician. The drug should be prescribed with caution for the following diseases and conditions: - peptic ulcer of the stomach and duodenum, esophagitis, gastritis, acute or latent peptic ulcer, recently created intestinal anastomosis, ulcerative colitis with the threat of perforation or abscess formation, diverticulitis, chronic hepatitis with HbsAg positive reaction - parasitic and infectious diseases of a viral, fungal or bacterial nature (currently occurring or recently suffered, including recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chicken pox, measles; amebiasis, strongyloidiasis; systemic mycosis; active and latent tuberculosis. Use for severe infectious diseases is permissible only against the background of specific therapy - pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination, immunodeficiency conditions (including AIDS or HIV infection) - recent heart attack myocardium (in patients with acute and subacute myocardial infarction, the necrosis focus may spread, the formation of scar tissue may slow down and, as a result, the heart muscle will rupture), severe chronic heart failure, arterial hypertension, hyperlipidemia - diabetes mellitus (including impaired carbohydrate tolerance ), thyrotoxicosis, hypothyroidism, Itsenko-Cushing's disease, obesity (III-IV stage) - severe chronic renal and/or liver failure, nephrourolithiasis - hypoalbuminemia and conditions predisposing to its occurrence - systemic osteoporosis, myasthenia gravis - acute psychosis, poliomyelitis (for except for the form of bulbar encephalitis) - open- and closed-angle glaucoma - pregnancy - lymphadenitis after BCG vaccination Drug interactions Pharmaceutical incompatibility of Prednisolone with other intravenously administered drugs is possible - it is recommended to administer it separately from other drugs (iv bolus, or through another dropper, such as second solution). When mixing a solution of prednisolone with heparin, a precipitate forms. Simultaneous administration of Prednisolone with: - inducers of “liver” microsomal enzymes (phenobarbital, phenytoin, theophylline, rifampicin, ephedrine) leads to a decrease in its concentration. - diuretics (especially “thiazide” and carbonic anhydrase inhibitors) and amphotericin B can lead to increased excretion of K+ from the body; with sodium-containing drugs - edema and increased blood pressure. - amphotericin B increases the risk of developing heart failure. - cardiac glycosides worsen their tolerability and increase the likelihood of developing ventricular extrasystole (due to hypokalemia caused). - indirect anticoagulants weaken (less often enhance) their effect (dose adjustment required). - anticoagulants and fibrinolytics increase the risk of bleeding from ulcers in the gastrointestinal tract. - ethanol and non-steroidal anti-inflammatory drugs (NSAIDs) increase the risk of erosive and ulcerative lesions in the gastrointestinal tract and the development of bleeding (in combination with NSAIDs in the treatment of arthritis, it is possible to reduce the dose of glucocorticosteroids due to the summation of the therapeutic effect). - paracetamol increases the risk of developing hepatotoxicity (induction of liver enzymes and the formation of a toxic metabolite of paracetamol). - acetylsalicylic acid accelerates its elimination and reduces its concentration in the blood (when prednisolone is discontinued, the level of salicylates in the blood increases and the risk of side effects increases). - insulin and oral hypoglycemic drugs, antihypertensive drugs reduce their effectiveness. — vitamin D reduces its effect on the absorption of Ca2+ in the intestine. - growth hormone, reduces the effectiveness of the latter, and with praziquantel - its concentration. - M-anticholinergics (including antihistamines and tricyclic antidepressants) and nitrates increase intraocular pressure. - isoniazid and mexelitine 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, displacing Prednisolone from its connection with albumin, increases the risk of developing its side effects. — ACTH enhances the effect of Prednisolone. - ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by Prednisolone. - cyclosporine and ketoconazole, slowing down the metabolism of Prednisolone, can in some cases increase its toxicity. - simultaneous administration of androgens and steroidal anabolic drugs with Prednisolone promotes 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 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 immunization, it increases the risk of viral activation and the development of infections. - antipsychotics (neuroleptics) and azathioprine increase the risk of developing cataracts when Prednisolone is prescribed. - when used simultaneously with antithyroid drugs, the clearance of Prednisolone decreases, and with thyroid hormones, the clearance of Prednisolone increases. Special instructions Before starting treatment (if impossible due to the urgency of the condition, during treatment), the patient should be examined to identify possible contraindications. Clinical examination should include examination of the cardiovascular system, x-ray examination of the lungs, examination of the stomach and duodenum, urinary system, and visual organs; control of blood formula, glucose and electrolytes in blood plasma. During treatment with Prednisolone (especially long-term), observation by an ophthalmologist, monitoring of blood pressure, water and electrolyte balance, as well as peripheral blood patterns and blood glucose levels are necessary. In order to reduce side effects, the intake of K+ into the body should be increased (diet, potassium supplements). Food should be rich in proteins, vitamins, and limit the content of fats, carbohydrates and table salt. The effect of the drug is enhanced in patients with hypothyroidism and liver cirrhosis. The drug may worsen existing emotional instability or psychotic disorders. If a history of psychosis is indicated, Prednisolone in high doses is prescribed under the strict supervision of a physician. In stressful situations during maintenance treatment (for example, surgery, trauma or infectious diseases), the dose of the drug should be adjusted due to an increased need for glucocorticosteroids. With sudden withdrawal, especially in the case of previous use of high doses, the development of withdrawal syndrome (anorexia, nausea, lethargy, generalized musculoskeletal pain, general weakness) is possible, as well as an exacerbation of the disease for which Prednisolone was prescribed. During treatment with Prednisolone, vaccination should not be carried out due to a decrease in its effectiveness (immune response). When prescribing Prednisolone for intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously treat with bactericidal antibiotics. In patients with diabetes mellitus, blood glucose levels should be monitored and therapy adjusted if necessary. X-ray monitoring of the osteoarticular system (images of the spine, hand) is indicated. In patients with latent infectious diseases of the kidneys and urinary tract, Prednisolone can cause leukocyturia, which may have diagnostic value. Prednisolone increases the content of 11- and 17-hydroxyketocorticosteroid metabolites. Use in pediatrics In children during long-term treatment with Prednisolone, careful monitoring of the dynamics of growth and development is necessary. Children who during the treatment period were in contact with patients with measles or chickenpox are prescribed specific immunoglobulins prophylactically. Due to the weak mineralocorticoid effect, Prednisolone is used in combination with mineralocorticoids for replacement therapy for adrenal insufficiency. Pregnancy and lactation During pregnancy (especially in the first trimester) it is used only for health reasons. With long-term therapy during pregnancy, the possibility of impaired fetal growth cannot be ruled out. In the case of the use in the III trimester of pregnancy, there is a danger of the occurrence of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in a newborn. Features of the effect of the drug on the ability to drive a vehicle or potentially dangerous mechanisms do not affect the ability to drive a car and work with equipment. An overdose symptoms: it is possible to strengthen the side effects described above. Treatment: It is necessary to reduce the dose of prednisolone. Symptomatic therapy. The release form and packaging of 1 ml of the drug is placed in a dark glass ampoule. 3 ampoules are placed in a plastic tray or in a contour cell package of aluminum and transparent PVC film foil. A plastic tray or contour cell packaging, along with instructions for medical use in the state and Russian languages, are placed in a cardboard box. Storage conditions are stored in a place protected from light at a temperature of not higher than 250 C. Do not freeze! Keep out of the reach of children! The shelf life of 2 years is not used after expiration of the shelf life. Conditions of the vacation from pharmacies according to the recipe Manufacturer Adjio Pharmacetals LTD A-38, Nandizhot industrial estate, saffedpool, Kurla-Andhery Road, Mumbai-400 072 Tel: +91-22-28518206/ 42319000 FACE: +91-22-28518204 [email pro-PROTEDEDEDE ] The owner of the registration certificate of Adjio Pharmacetalz LTD address of the organization that accepts in the territory of the Republic of Kazakhstan claims from consumers on the quality of products: representative office of Ajio Pharmaceuticals Limited Almaty, st. Shevchenko, d. 118, office 228 Tel: +7 (727) 2240402

The effect of Prednisolone on arthritis

The glucocorticosteroid drug has several powerful effects, which is why it is prescribed for the treatment of arthritis:

• almost completely eliminates swelling and inflammation during periods of exacerbation , prevents their progression for a long time;
• slows down the development of the disease , with early treatment it promotes regression of the disease (complete cure of arthritis is impossible);
• normalizes joint mobility - temporarily, for up to 6 months after the course;
• completely blocks or significantly limits autoimmune processes caused by arthritis;
• almost completely eliminates pain in the joints;
• increases the effectiveness of other anti-inflammatory drugs , including traditional recipes;
• slows down the process of joint destruction.

The effectiveness of therapy is maximum if the patient does not abuse the drug. Incorrect use “when necessary”, violation of courses lead to the formation of insensitivity of the body to therapy.

This medicine has a persistent effect, is chemically synthesized and is prescribed only by the attending physician. In this case, self-medication is not acceptable.

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.

Indications for use of Prednisolone

Taking Prednisolone for rheumatoid arthritis is indicated if processes intensify or autoimmune reactions appear:

• painful sensations increase greatly, up to loss of performance;
• inflammatory processes accelerate, covering more tissues of the joint and muscles next to it;
• the risk of autoimmune reactions increases;
• the formation of complications with the threat of the formation of dangerous pathologies of a systemic nature (organ vasculitis);
• the process of joint destruction accelerates, or all the symptoms of the disease intensify;
• serious disabilities up to and including disability, partial or complete immobility of joints;
• long-term use of NSAIDs and the need to replace them with other medications.

But there are situations when taking Prednisolone for rheumatoid arthritis is completely contraindicated.

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.

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How to understand It is prohibited to take Prednisolone if a person has increased aggressiveness and excitability.

Rules for the use of tablets and injections

The doctor prescribes a regimen for taking Prednisolone for rheumatoid arthritis:

• low doses - from 5 to 15 mg per day;
• average – from 20 to 40 mg per day;
• high – from 50 to 60 or more;
• pulse therapy – 1000 mg per day for a maximum of 3 days.

The very next day after the first use of the product, a sharp reduction in symptoms is observed. When injections are administered, relief from an acute attack occurs within 3-5 hours.

If the dosage is reduced quickly, withdrawal symptoms may occur.

With withdrawal syndrome, the symptoms of the pathology sometimes intensify, up to severe stiffness and arthralgia.

Taking low doses

An amount of up to 15 mg per day is prescribed to eliminate inflammation; therapy using non-steroidal drugs is comparable. Minimal toxicity protects against severe side effects. If you take the drug 7.5 mg per day, then within 2 years the rate of disease progression is noticeably reduced.

When starting treatment, the drug is taken 2-3 times a day, then you can take the tablets once in the morning. The duration of the course directly depends on the severity of symptoms, sometimes lasting several months.

If you take the drug at 1-2 am, then in the morning the painful sensation is reduced and the stiffness of the joints is reduced.

Application of pulse therapy

The maximum doses of Prednisolone are prescribed during exacerbation of the disease. They are administered intravenously when diluted in 150 ml of isotonic solution over 40 minutes. Such treatment guarantees active deposition of the drug in the organs and brain.

When using pulse therapy, even in such small courses, severe side effects may develop: hypertension, osteoporosis, problems with the adrenal glands. Reception is carried out only under the supervision of a specialist.

The prescription of loading doses of the drug must be strictly justified, but it is impossible to regularly resort to therapy in this way.

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

Side effects from Prednisolone

Unpleasant reactions to taking the drug develop from almost all body systems. They can be combined or be an independent phenomenon:

• problems with the endocrine system , including menstrual irregularities and deterioration of adrenal function, diabetes, developmental delay in children;
• gastrointestinal problems: ulcers, gastritis, pancreatitis, as well as many other pathologies;
• metabolism: low nitrogen balance, calcium excretion, weight gain, increased sweating;
• heart: arrhythmia, diseases of different parts of the heart, hypertension.

When taking Prednisolone, both the skeletal system and the central nervous system suffer, as well as the immune system, vision and other organs.

Prednisolone is very effective in eliminating severe symptoms of arthritis. But taking it is a big risk for other organs.