Instructions for use Methylprednisolone-FS tablets 8 mg blister No. 30
Composition
active ingredient: methylprednisolone;
1 tablet contains 4 mg or 8 mg of methylprednisolone;
Excipients: lactose monohydrate, potato starch, sodium starch glycolate (type A), magnesium stearate, colloidal anhydrous silicon dioxide.
Dosage form
Pills.
main physicochemical properties: tablets of white or almost white color, round shape, flat-cylindrical, with a notch in the form of a cross.
Pharmacotherapeutic group
Simple corticosteroid preparations for systemic use. Glucocorticosteroids. Methylprednisolone. ATC code H02A B04.
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 subsequent synthesis of various enzymes, which explains the effect of systemic use of glucocorticoids.
Methylprednisolone is an analogue of prednisolone. It is close in activity to prednisolone, but has practically no mineralocorticoid activity, which provides better tolerability.
Effect on the inflammatory process and immune response. Methylprednisolone has anti-inflammatory, desensitizing and antiallergic effects. It has antishock, antitoxic and immunosuppressive properties. Unlike cytostatics, the immunosuppressive properties of methylprednisolone are not associated with mitostatic action, but are the result of inhibition 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, which achieves the following therapeutic effects: reduction in the number of immunoactive cells near the focus of inflammation; reduction of vasodilation; stabilization of lysosomal membranes; inhibition of phagocytosis; reducing the production of prostaglandins and related compounds.
Effect on carbohydrate and protein metabolism. Glucocorticoids have a catabolic effect on proteins: they inhibit synthesis and accelerate protein breakdown. By stimulating steroid receptors, they induce the formation of a special class of proteins – lipocortins, which have anti-edema activity. The duration of the anti-inflammatory effect is 18-36 hours.
The released amino acids are converted into glucose and glycogen in the liver by gluconeogenesis. Glucose uptake in peripheral tissues is reduced, which can lead to hyperglycemia and glycosuria, especially in patients predisposed to diabetes.
Effect on fat metabolism.
Glucocorticoids have lipolytic activity, which is primarily manifested 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 tissues, including reticuloendothelium; reduces the number of mast cells, which are the site of hyaluronic acid formation; inhibits hyaluronidase activity and helps reduce capillary permeability.
Pharmacokinetics.
After oral administration, methylprednisolone is rapidly absorbed mainly in the proximal small intestine. The level of absorption in the distal part is approximately 50% of the level of absorption in the proximal part. Forms weak dissociative bonds with albumin and transcortin. From 40% to 90% of the drug is in the bound state. The volume of distribution of methylprednisolone is 61 l. The drug is metabolized mainly in the liver. The main metabolites are 20-β-hydroxymethylprednisolone and 20-β-hydroxy-6-α-methylprednisolone. Metabolites are excreted mainly in the urine in the form of glucuronides, sulfates and unconjugated compounds. Conjugation reactions occur mainly in the liver, to a lesser extent in the kidneys. The clearance of methylprednisolone is 383 l/day; the half-life is 165 minutes. Approximately 5% of the drug is excreted from the body in the urine.
Indication
Endocrine diseases.
Primary and secondary adrenal cortical insufficiency (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.
Collagenoses. During the period of exacerbation or in some cases as a maintenance therapy for the following diseases: systemic lupus erythematosus; acute rheumatic carditis; systemic dermatomyositis (polymyositis); polymyalgia rheumatica in 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. For the treatment of the following severe and allergic conditions in case of ineffectiveness of standard treatment: bronchial asthma; dermatitis (contact, atopic); serum sickness; seasonal or perennial allergic rhinitis; drug allergy.
Eye diseases. Severe acute, chronic allergic and inflammatory processes with damage to the eyes and adnexa, such as: allergic corneal marginal ulcers; eye damage 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; Leffler syndrome, not amenable to other treatment methods; berylliosis; fulminant or disseminated pulmonary tuberculosis (use in combination with appropriate anti-tuberculosis chemotherapy); aspiration pneumonitis.
Hematological diseases. Idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; acquired (autoimmune) hemolytic anemia; erythroblastopenia (erythrocytic anemia); congenital (erythroid) hypoplastic anemia.
Oncological diseases. As palliative therapy for the following diseases: leukemias and lymphomas in adults; acute leukemia in children.
Edema syndrome. For induction of diuresis or treatment of proteinuria in nephrotic syndrome without uremia, idiopathic type or caused by systemic lupus erythematosus.
Digestive tract diseases. To bring the patient out of critical condition with the following diseases: ulcerative colitis; Crohn's disease.
Diseases of the nervous system. Multiple sclerosis in the acute phase; cerebral edema caused by a brain tumor.
Diseases of other organs and systems. Tuberculous meningitis with subarachnoid block or with the threat of block, in combination with appropriate anti-tuberculosis chemotherapy; trichinosis with damage to the nervous system or myocardium.
Organ transplantation.
Contraindication
The use of Methylprednisolone-FS is contraindicated in case of hypersensitivity to methylprednisolone or to other components of the drug in history; in acute and chronic bacterial or viral infections with insufficient antibiotic and chemotherapy; systemic fungal infections; in the period from 6 weeks before and 2 weeks after prophylactic vaccinations.
Administration of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Interaction with other medicinal products and other types of interactions
Methylprednisolone is a substrate of the cytochrome P450 (CYP) enzyme, metabolized primarily by the CYP3A4 isoenzyme, which is the dominant enzyme of the most abundant CYP subtype in the liver of adult humans. It catalyzes 6-β-hydroxylation of steroids, a key step in phase I metabolism for both endogenous and synthetic corticosteroids. Many other compounds are also substrates of CYP3A4, some of which (like other drugs) alter glucocorticoid metabolism by inducing (increasing activity) or inhibiting the CYP3A4 isoenzyme.
CYP3A4 inducers - drugs that stimulate CYP3A4 activity, as a rule, increase hepatic clearance and reduce plasma concentrations of drugs that are CYP3A4 substrates. With simultaneous use of these drugs, an increase in the dose of methylprednisolone may be required. With simultaneous use with rifampin, phenytoin, pyrimidone, phenobarbital, the effect of methylprednisolone is reduced.
CYP3A4 inhibitors – drugs that inhibit CYP3A4 activity generally reduce hepatic clearance, increase elimination and plasma levels of methylprednisolone, which may increase the therapeutic and side effects of methylprednisolone.
In the presence of a CYP3A4 inhibitor, it may be necessary to titrate the methylprednisolone dose to avoid steroid toxicity. CYP3A4 inhibitors include: grapefruit juice, macrolide antibiotics (troleandomycin), isoniazid.
CYP3A4 substrates - the presence of another CYP3A4 substrate may result in inhibition or induction of the hepatic clearance of methylprednisolone, requiring appropriate dose adjustment. Adverse reactions associated with the use of one of these drugs as monotherapy may be more likely when they are used concomitantly. These include immunosuppressants: cyclophosphamide, tacrolimus.
CYP3A4 inducers and substrates – anticonvulsants: carbamazepine.
Contraceptives (oral): ethinyl estradiol/norethindrone. It is recommended to adjust the dose of methylprednisolone in women using oral contraceptives, which contributes not only to an increase in the half-life, but also to the development of an atypical immunosuppressive effect of methylprednisolone.
Immunosuppressants: Cyclosporine. Convulsions have been reported with the concomitant use of methylprednisolone and cyclosporine. Since the simultaneous administration of these drugs causes mutual inhibition of metabolism, which may result in increased plasma concentrations of one or both of these drugs, it is likely that convulsions and other adverse effects associated with the use of either drug as monotherapy may occur more frequently with their concomitant use.
Antiviral drugs – HIV protease inhibitors:
Protease inhibitors such as indinavir and ritonavir may lead to increased plasma concentrations of corticosteroids;
Corticosteroids may induce the metabolism of HIV protease inhibitors, resulting in decreased plasma concentrations.
Aromatase inhibitors – aminoglutethimide. Adrenal suppression caused by aminoglutethimide may exacerbate endocrine changes caused by long-term glucocorticoid treatment.
Other interactions.
Salicylates and other nonsteroidal anti-inflammatory drugs: The use of methylprednisolone with salicylates, indomethacin, and other nonsteroidal anti-inflammatory drugs may increase the likelihood of gastric ulceration and increase the risk of gastrointestinal bleeding. Methylprednisolone may contribute to a decrease in serum salicylates by increasing their renal clearance. Caution is required when reducing the dose of methylprednisolone during prolonged concomitant use. Discontinuation of methylprednisolone may result in an increase in serum salicylate levels, which may increase the risk of salicylate toxicity.
Anticholinergics: Corticosteroids may interfere with the effects of anticholinergics:
Cases of acute myopathy have been reported with concomitant use of high-dose corticosteroids and anticholinergic agents that block neuromuscular transmission (see section "Special warnings and precautions for use");
Antagonism of the neuromuscular blocking effects of pancuronium and vecuronium has been reported in patients receiving corticosteroids. This interaction is expected for all competitive neuromuscular blocking agents;
Corticosteroids may reduce the therapeutic effect of anticholinesterase agents in patients with myasthenia gravis.
Anticoagulants: when used simultaneously with glucocorticoids, an increase or decrease in the effect of anticoagulants - coumarin derivatives may be noted. The dosage regimen of anticoagulants must be accompanied by monitoring of prothrombin time.
Hypoglycemic drugs: when used simultaneously with methylprednisolone, the effectiveness of oral antidiabetic drugs and insulin is reduced, since corticosteroids can increase blood glucose concentrations, so it may be necessary to adjust the dose of antidiabetic drugs.
Fluoroquinolones: concomitant use may lead to tendon damage.
Immunization: Glucocorticoids may reduce the immunizing efficacy of vaccines and increase the risk of neurological complications. The use of therapeutic (immunosuppressive) doses of glucocorticoids simultaneously with live viral vaccines may increase the risk of viral diseases. Emergency vaccines may be used during therapy with the drug.
During long-term therapy, glucocorticoids may reduce the effect of somatotropin.
The effect of cardiac glycosides is enhanced when used together with methylprednisolone.
Methylprednisolone with chloroquine, hydroxychloroquine, metloquine increases the risk of developing myopathy and cardiomyopathy.
When methylprednisolone is used concomitantly with praziquantel, the concentration of praziquantel in the blood may decrease.
When corticosteroids are used in conjunction with potassium-sparing drugs (such as diuretics), patients should be observed closely for hypokalemia. There is also an increased risk of hypokalemia when corticosteroids are used in conjunction with amphotericin B, xanthenes, or β2-antagonists. The therapeutic effect of antihypertensive drugs and diuretics is inhibited by corticosteroids. The hypokalemic effect of acetazolamide, loop and thiazide diuretics, and carbenoxolone is enhanced.
Application features
Methylprednisolone-FS can be used in two modes: as circadian therapy and alternating therapy. In circadian therapy, the drug should be taken after meals, preferably after breakfast, without chewing, with sufficient fluid. In some cases, for example, in the presence of morning and night attacks in patients with obstructive lung diseases, the daily dose can be divided into two doses: 2/3 of the dose in the morning and 1/3 of the dose in the evening (between 18.00 and 20.00).
Since complications of glucocorticoid treatment depend on the dose and duration of therapy, in any case, the benefit-risk ratio should be assessed with respect to both the dose and duration of treatment and the choice of daily or intermittent dosing regimen. To minimize adverse reactions, the full daily dose of methylprednisolone should be taken in the morning in accordance with the circadian rhythm of endogenous cortisol production. When treating with corticosteroids, the lowest dose that provides an adequate therapeutic effect should be prescribed, and when dose reduction becomes possible, this reduction should be carried out gradually.
If a satisfactory clinical effect is not achieved after a certain period of time, the drug should be discontinued and the patient should be prescribed another type of therapy.
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, gastrointestinal diseases (peptic ulcer, localized ileitis, ulcerative colitis (or other inflammatory diseases of the digestive tract) or diverticulitis with an increased risk of bleeding and perforation), herpes of the eye (since corneal perforation is possible), hypothyroidism, a history of corticosteroid-induced myopathy, liver failure, cirrhosis of the liver, epilepsy, abscess or other pyogenic infections, glaucoma, those prone to thrombophlebitis and those with mental disorders. Caution should also be exercised when prescribing the drug to patients who have recently suffered a myocardial infarction, with recently performed intestinal anastomoses and renal failure. Patients with blood clotting disorders should be under the supervision of a doctor.
The adverse cardiovascular effects of glucocorticoids, such as dyslipidemia and hypertension, may predispose patients with preexisting cardiovascular risk factors to additional cardiovascular effects when used at high doses and for prolonged periods. Therefore, corticosteroids should be used judiciously in such patients, with consideration of risk modification and, if necessary, additional cardiac monitoring.
Gastrointestinal tract.
Corticosteroids may complicate the diagnosis of gastrointestinal complications because they cause a decrease in pain and may mask symptoms of peptic ulcer, perforation, or bleeding without significant pain, and latent hyperparathyroidism. In combination with NSAIDs, the risk of gastrointestinal ulcers increases. Therefore, aspirin and nonsteroidal anti-inflammatory drugs should be used with caution in combination with corticosteroids.
High doses of corticosteroids can cause the development of acute pancreatitis.
Immune system.
Allergic reactions (e.g. angioedema) may occur. Since skin reactions and anaphylactic/anaphylactoid reactions have been reported rarely in patients receiving corticosteroid therapy, appropriate precautions should be taken before use, especially if the patient has a history of allergy to any drug.
Immunosuppressive effects/increased susceptibility to infections.
Corticosteroids may decrease resistance to infections and may result in an inability to localize infection. There is a risk of secondary infections caused by bacteria, fungi, viruses, protozoa, or helminths from any site in the body, which may occur during the use of corticosteroids or in combination with other immunosuppressive agents that impair cellular and humoral immunity and neutrophil function. Infections may be mild, but may also be severe, and in some cases fatal. The incidence of infectious complications increases with increasing corticosteroid doses.
Patients taking medications 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 consequences in unimmunized children or adults taking corticosteroids.
The drug 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 chemotherapy.
If corticosteroids are indicated in patients with latent tuberculosis or during the period of tuberculin test deviation, 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 prescribed appropriate prophylactic treatment.
In addition, corticosteroids should be used with great caution in patients with known or suspected parasitic infections, such as strongyloidiasis (pinworm infection). In such patients, corticosteroid-induced immunosuppression may lead to strongyloidiasis hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal septicemia caused by gram-negative organisms.
There is no consensus on the role of corticosteroids in the treatment of patients with septic shock. Earlier studies have reported both positive and negative effects of corticosteroids in this clinical setting. Later studies have shown that corticosteroids as adjunctive therapy have a beneficial effect in patients with septic shock who have adrenal insufficiency. However, routine use of these drugs in patients with septic shock is not recommended. A systematic review of the evidence following short courses of high-dose corticosteroids in such patients concluded that there is no evidence to support their use. However, a meta-analysis and one review have shown that longer (5–11 days) courses of low-dose corticosteroids may reduce mortality, particularly in patients with vasopressor-dependent septic shock.
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.
Mental disorders.
When using corticosteroids, various mental disorders are possible: from euphoria, insomnia, mood swings, personality changes to severe depression with psychotic manifestations. In addition, while taking corticosteroids, pre-existing emotional instability and a tendency to psychotic reactions may increase.
Potentially serious psychiatric disorders may develop with systemic corticosteroids (see section 4.8). Symptoms usually occur within a few days to weeks of initiating therapy. Most reactions resolve after dose reduction or discontinuation, although specific treatment may be required. Psychiatric reactions have been reported with corticosteroid withdrawal; the frequency is unknown. Patients/caregivers should be advised to seek medical advice if any psychiatric disorder develops in the patient, particularly if there is a suspicion of depression or suicidal ideation. Patients/caregivers should be alert to possible psychiatric disorders that may occur during or immediately after tapering or discontinuing systemic steroids. If a patient receiving steroid therapy is exposed to an unusual stressor, the dose of rapid-acting steroids should be increased before, during, and after the stressful situation.
Nervous system disorders.
Patients with seizures and myasthenia gravis should use corticosteroids with caution. Prolonged use of corticosteroids may cause posterior subcapsular and nuclear cataracts (especially in children), exophthalmos, or increased intraocular pressure, which can lead to glaucoma with possible optic nerve damage. Corticosteroids have been associated with central serous choriopathy, which can lead to retinal detachment. Patients taking glucocorticoids are at increased risk of secondary ocular infections caused by fungi and viruses.
Although controlled clinical trials have demonstrated the efficacy of corticosteroids in accelerating the resolution of acute symptoms of multiple sclerosis exacerbations, they have not demonstrated an effect of corticosteroids on the outcome or natural history of the disease. These trials have shown that relatively high doses of corticosteroids are required to demonstrate a significant effect (see Dosage and Administration).
Musculoskeletal disorders.
Osteoporosis is one of the frequently observed but rarely diagnosed adverse reactions that develops with prolonged use of high doses of glucocorticoids.
Acute myopathy has been reported with high-dose corticosteroids, most commonly in patients with neuromuscular disorders (e.g. myasthenia gravis) or in patients receiving concomitant anticholinergic therapy such as neuromuscular blocking agents (e.g. pancuronium). This acute myopathy is generalized, may involve the ocular and respiratory muscles, and may result in quadriparesis. Elevated creatine kinase levels may occur. Clinical improvement or recovery may take several weeks to several years after discontinuation of corticosteroids.
Endocrine system.
Corticosteroids, including methylprednisolone, may increase blood glucose levels, worsen the condition of patients with pre-existing diabetes, and predispose patients to diabetes mellitus who use corticosteroids long-term.
Patients receiving corticosteroid therapy and exposed to stress are advised to increase the dose of rapid-acting corticosteroids before, during, and after the stressful situation.
Prolonged use of glucocorticoids can suppress the hypothalamic-pituitary-adrenal axis (secondary adrenocortical insufficiency), which can contribute to the exacerbation of diseases and the development of complications in various conditions, for example, in acute injuries, diseases or surgery. The degree and duration of adrenocortical insufficiency vary in different patients and depend on the dose, frequency, time of use, as well as the duration of glucocorticoid therapy. This effect can be minimized by using alternating therapy. High doses of methylprednisolone significantly reduce the risk of developing the listed complications.
With prolonged use of glucocorticoids, therapy should be discontinued gradually, over several weeks, to avoid withdrawal syndrome and serious complications. Long-term therapy should not be stopped abruptly, also in case of pregnancy.
Sudden withdrawal of glucocorticoids can lead to acute adrenal insufficiency, which can be fatal.
Adrenal insufficiency caused by the administration of the drug can be minimized by gradually reducing the dose. This type of relative insufficiency can persist for several months after discontinuation of therapy; therefore, if stressful situations arise during this period, hormonal therapy should be resumed. Since mineralocorticoid secretion may be impaired, electrolytes and/or mineralocorticoids should be administered concurrently.
Since glucocorticosteroids may cause or exacerbate Cushing's syndrome, their use should be avoided in patients with Cushing's disease.
The effect of corticosteroids is more pronounced in patients with hypothyroidism. Patients with hypothyroidism or severe liver disease should reduce the dose due to the increased effect of methylprednisolone.
Others.
When hydrocortisone or cortisone is used in medium and high doses, it is possible to increase blood pressure, salt and water retention, and increase potassium excretion. These effects are observed less often with the use of synthetic derivatives of these drugs, except when high doses are used.
Pheochromocytoma crisis, which can be fatal, has been reported following the use of systemic corticosteroids. Corticosteroids should be administered to patients with suspected or established pheochromocytoma only after an appropriate risk/benefit assessment.
During long-term treatment with glucocorticoids, it is recommended to regularly monitor blood pressure, determine the level of glucose in urine and blood, conduct a fecal occult blood test, determine the erythrocyte sedimentation rate, and perform X-ray examination of the spine. Electrolyte balance should be carefully monitored when methylprednisolone is used in combination with diuretics. During long-term treatment with methylprednisolone, an appropriate diet with salt restriction and potassium supplements should be prescribed to prevent hypokalemia. All corticosteroids increase calcium excretion.
Glucocorticoids should be prescribed with caution to elderly patients due to the increased risk of side effects (peptic ulcer, osteoporosis, and skin ulcers).
Growth retardation may occur in children receiving glucocorticoids for prolonged periods of time, several times a day, and this dosage regimen should be used only when absolutely necessary. The use of alternating therapy usually avoids or minimizes this side effect.
No carcinogenic or mutagenic effects of the drug, as well as its adverse effects on reproductive functions, were detected.
Systemic corticosteroids should not be used in high doses in the treatment of patients with traumatic brain injury.
The drug contains lactose, therefore, patients with hereditary galactose intolerance, lactase deficiency or glucose-galactose malabsorption syndrome are not recommended to use Methylprednisolone-FS.
Use during pregnancy or breastfeeding
Pregnancy: Animal studies have shown that high doses of corticosteroids administered to pregnant women may cause fetal malformations. However, corticosteroids administered to pregnant women do not appear to cause congenital malformations.
Despite the results of animal studies, the use of this medicinal product during pregnancy is unlikely to cause harm to the fetus.
Adequate studies on the effects of corticosteroids on human reproductive function have not been conducted. Since there is no definitive evidence of the safety of corticosteroids during pregnancy, these drugs should be prescribed only if clearly needed. When deciding to prescribe Methylprednisolone-FS to pregnant and lactating women, or women who may become pregnant, a careful assessment of the benefit of the drug and the potential risk to the mother, fetus and child should be made.
Some corticosteroids readily cross the placental barrier. One retrospective study reported an increased incidence of low birth weight in infants born to mothers who had received corticosteroids. Infants whose mothers had received relatively high doses of corticosteroids during pregnancy should be closely monitored for signs of adrenal insufficiency, although adrenal insufficiency is rare in infants exposed to corticosteroids in utero.
The effect of corticosteroids on the course and outcome of labor is unknown.
Cataracts have been observed in infants whose mothers received long-term corticosteroid treatment during pregnancy.
Lactation. Methylprednisolone is excreted in human milk. Corticosteroids excreted in human milk may suppress growth and affect endogenous glucocorticoid production in breastfed infants. Since adequate studies of the effects of glucocorticoids on human reproduction have not been conducted, if necessary, the drug should be used in nursing mothers only if the potential benefit outweighs the potential risk to the infant.
Ability to influence reaction speed when driving vehicles or other mechanisms
Data on the effect of the drug on reaction speed have not been systematically evaluated, but after treatment with corticosteroids there is a risk of adverse reactions such as dizziness, vertigo, visual disturbances, fatigue, mood lability. In this case, patients should not drive or operate other mechanisms.
Method of administration and doses
The initial dose of the drug for adults may vary depending on the indication. In less severe diseases, low doses are usually sufficient, although individual patients may require higher starting doses. High doses can be used in 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 a satisfactory clinical effect is not achieved after an appropriate period of time, therapy with Methylprednisolone-FS tablets should be discontinued and the patient should be prescribed alternative therapy. If the drug needs to be discontinued after long-term therapy, it is recommended that this be done gradually rather than abruptly.
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 dose control is necessary.
