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Methylprednisolone-FS tablet 8 mg in container pack No. 10x3

Name

Methylprednisolone-fs t

Release forms

pills

INN

Methylprednisolone

FTG

Glucocorticosteroid

Basic physical and chemical properties

tablets are white or almost white, round, flat-cylindrical, with a notch in the form of a cross.

Compound

active ingredient: methylprednisolone; 1 tablet contains: methylprednisolone 4 mg or 8 mg; excipients: lactose monohydrate, potato starch, sodium starch glycolate (type A), magnesium stearate, colloidal anhydrous silicon dioxide.

Drug classification code

Corticosteroids for systemic use. Glucocorticosteroids. Methylprednisolone. ATX code: N02AB04.

Pharmacological properties

Pharmacodynamics

Methylprednisolone is a synthetic glucocorticosteroid. Glucocorticoids penetrate cell membranes and form complexes with specific cytoplasmic receptors that penetrate the cell nucleus, bind to DNA (chromatin), stimulate mRNA transcription and further synthesis of various enzymes, which explains the effect of systemic use of glucocorticoids. Methylprednisolone is an analogue of prednisolone. It is similar in activity to prednisolone, but has virtually no mineralocorticoid activity, which ensures better tolerability. Glucocorticoids not only have a significant effect on the inflammatory process and the immune response, but also affect carbohydrate, protein and fat metabolism, the cardiovascular system, skeletal muscles and the central nervous system.

Effect on inflammation and immune response

Methylprednisolone has anti-inflammatory, desensitizing and angiallergic effects. It has antishock, antitoxic and immunosuppressive properties. Unlike cytostatics, the immunosuppressive properties of methylprednisolone are not associated with a mitostatic effect, but are the result of suppression of various stages of immunogenesis: migration of bone marrow stem cells, migration of B cells and interaction of T and B lymphocytes. Like other corticosteroids, methylprednisolone inhibits the release of cytokines (interleukins 1 and 2, γ-interferon) from lymphocytes and macrophages, inhibits the release of inflammatory mediators by eosinophils, reduces the metabolism of arachidonic acid, thereby achieving the following therapeutic effects: reducing the number of immunoactive cells near the site of inflammation; decreased vasodilation; stabilization of lysosomal membranes; inhibition of phagocytosis; decreased production of prostaglandins and related compounds. A dose of 4 mg of methylprednisolone has the same glucocorticosteroid (anti-inflammatory) effect as 20 mg of hydrocortisone. Methylprednisolone has only minimal mineralocorticoid effects (200 mg methylprednisolone is equivalent to 1 mg deoxycorticosterone). Effect on protein and carbohydrate metabolism Glucocorticoids exhibit a catabolic effect on proteins: they delay the synthesis and accelerate the breakdown of proteins. By stimulating steroid receptors, they induce the formation of a special class of proteins - lipocortins, which have an anti-edematous effect. The amino acids that are released are converted by the process of gluconeogenesis in the liver into glucose and glycogen. The absorption of glucose in peripheral tissues is reduced, which can lead to hyperglycemia and glycosuria, especially in patients prone to diabetes. Effect on fat metabolism Glucocorticoids have lipolytic activity, which manifests itself primarily in the tissues of the extremities, and lipogenetic activity, which is most pronounced in the chest, neck and head, which leads to the redistribution of fat deposits. In relatively high doses, it inhibits the development of lymphoid and connective tissue, including reticuloendothelium; reduces the number of mast cells, which are the site of formation of hyaluronic acid; inhibits the activity of hyaluronidase and helps reduce capillary permeability. The maximum pharmacological activity of corticosteroids occurs when peak plasma concentrations have already passed, so it is believed that the vast majority of therapeutic effects of drugs are due primarily to modification of enzyme activity, and not to direct action of the drug.

Pharmacokinetics

The pharmacokinetics of methylprednisolone is linear, regardless of the route of administration. Absorption The bioavailability of methylprednisolone in healthy people after oral administration is generally high (82-89%). After oral administration, methylprednisolone is rapidly absorbed and the maximum concentration of methylprednisolone in the blood plasma is achieved within 1.5-2.3 hours (depending on the dose) after taking this drug in healthy people. The level of absorption in the distal region is approximately 50% of the level of absorption in the proximal region. Distribution Methylprednisolone is widely distributed in tissues, penetrates the blood-brain barrier and is excreted into breast milk. Forms weak dissociated bonds with albumin and transcortin. Plasma protein binding of methylprednisolone in humans is approximately 77%. The volume of distribution of methylprednisolone is approximately 1/2 kg. Metabolism Methylprednisolone is metabolized in the liver to inactive metabolites. The main metabolites are 20-α-hydroxymethylprednisolone and 20-β-hydroxymethylprednisolone. Its metabolism in the liver occurs primarily with the participation of the CYP3A4 enzyme (for a list of drug interactions based on metabolism mediated by CYP3A isoenzymes, see the section “Interaction with other drugs and other types of interactions”). Conjugation reactions occur mainly in the liver, and to a lesser extent in the kidneys. Excretion Metabolites are excreted mainly in the urine in the form of glucuronides, sulfates and unconjugated compounds. The half-life of total methylprednisolone is 1.8 to 5.2 hours. The total clearance is about 5-6 ml/min/kg. Methylprednisolone is eliminated by hemodialysis.

Indications for use

Endocrine diseases Primary and secondary adrenal insufficiency (in this case, the first-line drugs are hydrocortisone or cortisone; if necessary, synthetic analogues can be used in combination with mineralocorticoids; simultaneous use of mineralocorticoids is especially important for the treatment of children); congenital adrenal hyperplasia; non-purulent thyroiditis; hypercalcemia in malignant tumors. Non-endocrine diseases Rheumatic diseases As an additional therapy for short-term use (to remove a patient from an acute condition or during an exacerbation of the process) for the following diseases: psoriatic arthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis (in some cases, low-dose maintenance therapy may be required); ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; acute gouty arthritis; post-traumatic osteoarthritis; synovitis in osteoarthritis; epicondylitis. Collagenoses During the period of exacerbation or in some cases as maintenance therapy for the following diseases: systemic lupus erythematosus; acute rheumatic carditis; systemic dermatomyositis (polymyositis); polymyalgia rheumatica with giant cell arteritis. Skin diseases Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme (Stevens-Johnson syndrome); mycosis fungoides; severe forms of psoriasis; exfoliative dermatitis; severe seborrheic dermatitis. Allergic diseases Control of severe or allergic conditions for which conventional therapy is ineffective: bronchial asthma; dermatitis (contact, atopic); serum sickness; seasonal or persistent allergic rhinitis; drug allergy. Ophthalmological diseases Severe acute and chronic allergic and inflammatory processes with eye damage, such as: allergic marginal corneal ulcers; eye lesions caused by Herpes zoster, inflammation of the anterior segment of the eye; diffuse posterior uveitis and choroiditis; sympathetic ophthalmia; allergic conjunctivitis; keratitis; chorioretinitis; iritis and iridocyclitis; Optic neuritis. Respiratory diseases Symptomatic sarcoidosis; Lefler's syndrome, refractory to treatment with other methods; berylliosis; focal or disseminated pulmonary tuberculosis (together with appropriate anti-tuberculosis chemotherapy); aspiration pneumonitis. Blood diseases Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; acquired (autoimmune) hemolytic anemia; erythroblastopenia (erythrocyte anemia); congenital (erythroid) hypoplastic anemia. Oncological diseases, as palliative therapy: leukemia and lymphoma in adults; acute leukemia in children. Edema syndrome For induction of diuresis or treatment of proteinuria with nephrotic syndrome without uremia, idiopathic type or caused by systemic lupus erythematosus. Diseases of the digestive tract To remove the patient from a critical condition with the following diseases: ulcerative colitis; Crohn's disease. Diseases of the nervous system: multiple sclerosis in the acute phase; swelling of the brain caused by a brain tumor. Diseases of other organs and systems: tuberculous meningitis with subarachnoid block or with the threat of block development, in combination with appropriate anti-tuberculosis chemotherapy; trichinosis with damage to the nervous system or myocardium. Organ transplantation.

Directions for use and doses

The initial dose for adults can vary from 4 to 48 mg of methylprednisolone per day, depending on the indication. It is necessary to use the lowest dose of corticosteroids to control the course of the disease. For less severe illnesses, low doses are usually sufficient, although individual patients may require higher starting doses. High doses can be used for diseases and conditions such as multiple sclerosis (200 mg per day), cerebral edema (200-1000 mg per day), organ transplantation (up to 7 mg/kg per day). If satisfactory clinical effect is not achieved after an appropriate period of time, therapy with methylprednisolone tablets should be discontinued and the patient should be given alternative therapy. If after long-term therapy the drug needs to be discontinued, it is recommended that this be done gradually rather than suddenly. If a satisfactory effect is achieved as a result of therapy, an individual maintenance dose should be selected for the patient by gradually reducing the initial dose at certain intervals until the lowest dose is found that will maintain the achieved clinical effect. It should be remembered that constant monitoring of the dosage of the drug is necessary. Situations in which it may be necessary to adjust the dose of the drug include: changes in clinical condition due to the onset of remission or exacerbation of the disease; individual patient response to the drug; exposure to stressful situations on the patient are not directly related to the underlying disease that the therapy is aimed at. In the latter case, it may be necessary to increase the dose of methylprednisolone for a certain period of time, depending on the patient's condition. It should be emphasized that the required dose may vary and should be selected individually depending on the nature of the disease and the patient's response to therapy. Alternating therapy (AT) Alternating therapy is a corticosteroid dosing regimen in which a double dose of glucocorticoids should be prescribed every other day, in the morning. The goal of this type of therapy is to provide the patient who requires long-term therapy with the maximum benefits of corticosteroids while minimizing some of the undesirable effects such as pituitary-adrenal suppression, Cushingoid condition, corticosteroid withdrawal syndrome, and growth suppression in children. Diseases Loading dose Maintenance dose Rheumatic diseases - severe rheumatoid arthritis, moderate, mild children - systemic lupus erythematosus - acute rheumatic fever 12-16 mg 8-10 mg 6-8 mg 6-10 mg 20-40 mg 6-12 mg 4-8 mg 2-6 mg2-8 mg8-20 mg 0.5 mg for every 450 g of body weight until serum mucoproteins reach 6 mg% and erythrocyte sedimentation rate remains normal for a week Allergic diseases - severe seasonal asthma - hay fever in severe form - exfoliative dermatitis (erythroderma) - contact dermatitis - asthma - allergic rhinitis not responding to standard therapy - generalized atopic dermatitis - generalized eczema in children 16-40 mg 16-40 mg 16-40 mg 16-40 mg 12-40 mg 12-40 mg 12- 40 mg8-12 mg 4-16 mg4-16 mg4-16 mg Diseases and inflammatory processes of the eye-acute-chronic 12-40 mg12-40 mg 2-12 mg Other diseases-adrenal-genital syndrome-ulcerative colitis-leukemia-nephrotic syndrome 16-60 mg 12-16 mg 20-60 mg (10-14 days or until diuresis appears) 4-12 mg 12-40 mg (3 days a week in a row for 6-12 months)

Adverse reactions

The development of severe adverse reactions depends on the dose and duration of treatment. Adverse reactions usually develop with long-term use of the drug; during a short period of use, the risk of their occurrence is unlikely. The following are adverse reactions associated with methylprednisolone therapy, listed according to organ system class, frequency, and severity. In each group, the frequencies of adverse reactions are indicated in order of decreasing severity. The frequency of adverse reactions is shown as: often (from ≥1/100 to

Contraindications

hypersensitivity to methylprednisolone or other components of the drug; systemic infections in cases where specific antimicrobial therapy is not intended; systemic fungal infections; Administration of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.

Overdose

No clinical syndrome of acute corticosteroid overdose has been reported. Case reports of acute toxicity and/or death following corticosteroid overdose are rare. In case of overdose, there is no specific antidote; supportive and symptomatic treatment is provided. Methylprednisolone is eliminated by dialysis.

Precautionary measures

Corticosteroids should be used with caution and under strict medical supervision in patients with arterial hypertension, congestive heart failure, diabetes mellitus (or a family history of diabetes), pancreatitis, and diseases of the digestive tract (peptic ulcer, local ileitis, ulcerative colitis or other inflammatory diseases of the digestive tract or diverticulitis with an increased risk of bleeding and perforation), ocular herpes (as corneal perforation is possible), hypothyroidism, history of corticosteroid-induced myopathy, liver failure, cirrhosis, epilepsy, abscess or other pyogenic infections, glaucoma, prone to thrombophlebitis and with mental disorders disorders. Caution must also be exercised when prescribing the drug to patients who have recently suffered a myocardial infarction, with recent intestinal anastomoses and renal failure. Patients with bleeding disorders should be under medical supervision. Immunosuppressive effects/increased susceptibility to infections Corticosteroids may increase susceptibility to infections and mask some symptoms of infections; In addition, new infections may develop during corticosteroid therapy. When using corticosteroids, resistance to infections may decrease and the body may be unable to localize the infection. There is a risk of developing secondary infections caused by bacteria, fungi, viruses, protozoa or helminths from any location in the body, which may occur during the use of corticosteroids as monotherapy or in combination with other immunosuppressive agents that affect the state of cellular and humoral immunity and neutrophil function . These infections can be mild, but can sometimes be severe and even fatal. As the dose of corticosteroids increases, the incidence of infectious complications increases. Patients taking drugs that suppress the immune system are more susceptible to infections than healthy people. Chickenpox and measles, for example, can have more serious or even fatal outcomes in unimmunized children or adults who take corticosteroids. The use of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Patients receiving immunosuppressive doses of corticosteroids can be vaccinated with killed or inactivated vaccines, but their response to such vaccines may be reduced. These immunization procedures can be performed in patients receiving corticosteroids in doses that do not have an immunosuppressive effect. The use of corticosteroids for active tuberculosis should be prescribed only in cases of fulminant or disseminated tuberculosis, when corticosteroids must be used in combination with appropriate anti-tuberculosis therapy. If corticosteroids are indicated for patients with latent tuberculosis or during the period of tuberculin testing, treatment should be carried out under strict medical supervision, since reactivation of the process is possible. During long-term corticosteroid therapy, such patients should be given appropriate prophylactic treatment. Cases of Kaposi's sarcoma have been reported in patients receiving corticosteroid therapy. In such cases, discontinuation of corticosteroid therapy may result in clinical remission. There is no consensus on the role of corticosteroids in the treatment of patients with septic shock. Previous studies have reported both positive and negative effects of corticosteroid use in this clinical setting. Later studies showed that corticosteroids as adjunctive therapy had a beneficial effect in patients with septic shock due to adrenal insufficiency. However, routine use of these drugs in patients with septic shock is not recommended. A systematic review of the data concluded that there was no benefit from short courses of high-dose corticosteroids in these patients. However, a meta-analysis and one review have shown that longer (5-11 days) courses of low-dose corticosteroids may reduce mortality, especially in patients with vasopressor-dependent septic shock. In addition, corticosteroids should be used with great caution in patients with known or suspected parasitic infections, such as strongyloidiasis (acne infestation). In these patients, corticosteroid-induced immunosuppression can lead to strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. Effect on the immune system Allergic reactions (eg, angioedema) may occur. Since skin reactions and anaphylactic/anaphylactoid reactions have been reported in rare cases in patients receiving corticosteroid therapy, appropriate precautions should be taken before use, especially if the patient has a history of allergy to any drug. Effects on the endocrine system In patients receiving corticosteroid therapy and who are exposed to stress, increasing the dose of rapid-acting corticosteroids before, during and after a stressful situation is indicated. Long-term use of glucocorticoids can lead to suppression of the hypothalamic-pituitary-adrenal axis (the development of secondary adrenal insufficiency) and contribute to the exacerbation of diseases and the development of complications in various conditions, for example, during acute injuries, diseases or surgery. The degree and duration of adrenocortical insufficiency varies between patients and depends on the dose, frequency, timing of use, and duration of glucocorticoid therapy. This effect can be minimized by using alternating therapy (see section "Dosage and Administration"). High doses of methylprednisolone significantly reduce the risk of developing these complications. If glucocorticoids are suddenly withdrawn, acute adrenal insufficiency may develop, which can be fatal. Adrenocortical insufficiency caused by the use of the drug can be minimized by gradually reducing the dose. This type of relative deficiency can be recorded for several months after discontinuation of therapy, therefore, if stressful situations arise during this period, hormonal therapy must be reinstated. Since mineralocorticoid secretion may be impaired, electrolytes and/or mineralocorticoids should be administered concomitantly. With long-term use of glucocorticoids, therapy should be discontinued gradually over several weeks to avoid “withdrawal syndrome” and serious complications. This syndrome includes symptoms such as anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, desquamation, myalgia, weight loss and/or hypotension. These effects are thought to result from a sudden change in glucocorticoid concentrations rather than from low corticosteroid levels. Long-term therapy should not be stopped suddenly, also in case of pregnancy. Because corticosteroids may cause or worsen Cushing's syndrome, their use should be avoided in patients with Cushing's disease. Particular attention should be paid to the use of corticosteroids in patients with hypothyroidism, which requires frequent monitoring of their condition. Patients with hypothyroidism or severe liver disease should have their dose reduced due to the increased effect of methylprednisolone. Metabolic and nutritional disorders Corticosteroids, including methylprednisolone, may increase blood glucose, worsen the condition of patients with a history of diabetes mellitus, and also contribute to the development of diabetes mellitus in patients using corticosteroids long-term. Mental disorders When using corticosteroids, various mental disorders are possible: from euphoria, insomnia, mood changes, personality changes to severe depression with the expression of psychotic manifestations. In addition, while taking corticosteroids, existing emotional instability and a tendency to psychotic reactions may increase. Particular attention should be paid to the systemic use of corticosteroids in both patients and their first-degree relatives with pre-existing severe affective mental disorders. These disorders include depressive or manic-depressive illness or pre-existing steroid psychosis. Symptoms usually occur within a few days or weeks of starting therapy. Most reactions disappear after reducing the dose or discontinuing the drug, although special treatment may be necessary. Mental reactions have been observed during corticosteroid withdrawal; their frequency is unknown. Patients and their caregivers should be advised to seek medical attention if the patient develops any mental health problems, especially if the patient is suspected of being depressed or having suicidal thoughts. Patients and their caregivers should be alert to possible psychiatric disorders that may occur during or immediately following tapering or discontinuation of systemic steroids. Nervous system disorders Patients with seizures, as well as myasthenia gravis, should use corticosteroids with caution (see information about myopathy in the “Adverse reactions” section). Although controlled clinical trials have demonstrated the effectiveness of corticosteroids in accelerating the reduction of acute symptoms of exacerbations of multiple sclerosis, they have not demonstrated the effect of corticosteroids on the outcome or natural history of this disease. According to the results of these studies, relatively high doses of corticosteroids must be used to demonstrate a significant effect (see section "Dosage and Administration"). Epidural lipomatosis has been reported in patients taking corticosteroids, usually in high doses over a long period of time. Visual disorders In case of eye damage caused by glaucoma (or if close relatives have this disease) or herpes simplex virus, corticosteroids should be used with caution, as this may cause perforation of the cornea. With long-term use of corticosteroids, posterior subcapsular cataracts and nuclear cataracts (especially in children), proptosis, or increased intraocular pressure may develop, which can lead to glaucoma with possible damage to the optic nerve. Patients taking glucocorticoids are at increased risk of developing secondary eye infections caused by fungi and viruses. Corticosteroid therapy has been associated with the development of retinal detachment. Cardiac disorders The negative effects of glucocorticoids on the cardiovascular system, such as dyslipidemia and hypertension, when used long-term in high doses, may contribute to the occurrence of additional cardiovascular adverse events in patients with pre-existing cardiovascular risk factors. In this regard, corticosteroids should be used rationally in such patients, and also take into account the modification of risk factors and, if necessary, additionally monitor cardiac activity. Low doses and alternating therapy may reduce the incidence of complications during corticosteroid therapy. In patients with congestive heart failure, systemic corticosteroids should be used with caution and only when absolutely necessary. Particular caution is required when using systemic corticosteroids in patients with recent myocardial infarction (myocardial rupture has been reported), and frequent monitoring of the patient's condition is necessary. Caution should be exercised in patients receiving cardioactive drugs such as digoxin due to steroid-induced electrolyte imbalance/potassium loss. Vascular disorders Cases of thrombosis, including thromboembolism, have been reported with the use of corticosteroids. Caution should be exercised when prescribing corticosteroids to patients who have or may be susceptible to thromboembolic disorders. Corticosteroids should be used with caution in patients with hypertension. Gastrointestinal disorders High doses of corticosteroids can cause the development of acute pancreatitis. There is no consensus that corticosteroids themselves cause the development of gastric ulcers during therapy. Corticosteroids may make it difficult to diagnose gastrointestinal complications because they reduce pain and may also mask the symptoms of peptic ulcers. In combination with NSAIDs, the risk of developing gastrointestinal ulcers increases. Therefore, aspirin and nonsteroidal anti-inflammatory drugs should be used with caution in combination with corticosteroids. Corticosteroids should be used with caution in ulcerative colitis if there is a risk of gastrointestinal wall perforation, abscess formation, or other purulent infection; with diverticula; in the case of recently performed intestinal anastomoses; with active or latent peptic ulcer. Hepatobiliary disorders Particular attention should be paid to the use of systemic corticosteroids in patients with cirrhosis and liver failure. Isolated hepatobiliary disorders have been reported, most of which were reversible after discontinuation of the drug. Careful monitoring is required. Musculoskeletal disorders Cases of acute myopathy have been reported with the use of high-dose corticosteroids, most often in patients with disorders of neuromuscular transmission (eg, myasthenia gravis) or in patients receiving therapy with anticholinergic drugs that block neuromuscular transmission ( e.g. pancuronium). This acute myopathy is generalized and can affect the eye and respiratory muscles and lead to tetraparesis. An increase in creatine kinase levels may occur. It may take several weeks to several years for clinical improvement or recovery after discontinuation of corticosteroids. Osteoporosis is one of the adverse reactions that is often observed, but rarely diagnosed, and develops with long-term use of high doses of glucocorticoids. During long-term therapy with methylprednisolone, it is necessary to consider prescribing bisphosphonates in patients with osteoporosis or with risk factors for its development. Risk factors for osteoporosis include age over 65 years, a history or family history of frequent fractures, early menopause (before 45 years), premenopausal amenorrhea, and low body weight. The risk of developing osteoporosis can be minimized by adjusting the dose of methylprednisolone to the lowest therapeutic level. Kidney disorders and