Metipred tablets 16 mg No. 30

Instructions for use Metipred tablets 16 mg No. 30

Composition

active ingredient: 1 tablet contains methylprednisolone 4 mg or 16 mg;

excipients: lactose monohydrate, corn starch, gelatin, magnesium stearate, talc.

Dosage form

Pills.

Main physicochemical properties: white or almost white, round, flat tablets with beveled edges and a score.

Pharmacotherapeutic group

Corticosteroids for systemic use.

ATX code H02A B04.

Pharmacological properties

Pharmacodynamics

The effect of methylprednisolone, like other glucocorticoids, is realized through interaction with steroid receptors in the cytoplasm. The steroid receptor complex is transported into the cell nucleus, binds to DNA and changes the transcription of genes for most proteins. Glucocorticoids inhibit the synthesis of many proteins, various enzymes that cause joint destruction (in rheumatoid arthritis), as well as cytokines that play an important role in immune and inflammatory reactions. They induce the synthesis of lipocortin - a key protein in the neuroendocrine interaction of glucocorticoids, which leads to a decrease in the inflammatory and immune response.

Glucocorticoids, including methylprednisolone, suppress or prevent the development of tissue responses to a variety of thermal, mechanical, chemical, infectious, and immunological agents. Thus, glucocorticoids act symptomatically, reducing the symptoms of the disease without affecting the cause. The anti-inflammatory effect of methylprednisolone is at least five times greater than that of hydrocortisone.

The endocrine effects of methylprednisolone are to suppress ACTH secretion, inhibit endogenous cortisol production, and with prolonged use cause partial atrophy of the adrenal cortex. A single dose of 40 mg of methylprednisolone inhibits corticotropin secretion for about 36 hours. They affect calcium and vitamin D metabolism, carbohydrate, protein, and lipid metabolism, so patients taking methylprednisolone may experience an increase in blood glucose levels, decreased bone density, muscle atrophy, and dyslipidemia. Glucocorticoids also increase blood pressure, modulate behavior, and mood. Methylprednisolone has virtually no mineralocorticoid activity.

Pharmacokinetics

The bioavailability of oral methylprednisolone is usually greater than 80%, but may be reduced to 60% when high doses are used.

When methylprednisolone is taken orally, peak serum concentrations are observed after 1–2 hours.

Methylprednisolone is 77% bound to plasma proteins, binding to transcortin is negligible. The volume of distribution is 1–1.5 l/kg. Methylprednisolone is metabolized to inactive metabolites. The average clearance is 6.5 ml/kg/min. The duration of the anti-inflammatory effect is
18–36 hours. Approximately 5% of the drug is excreted in the urine. Methylprednisolone crosses the placenta and is excreted in breast milk. Methylprednisolone is removed by dialysis.

Indication

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 cancer.

Non-endocrine diseases.

Rheumatic diseases.

As an additional therapy for short-term use (to relieve the patient from an acute condition or during 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 tendosynovitis;

· 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;

· systemic dermatomyositis (polymyositis);

· acute rheumatic carditis;

· polymyalgia rheumatica with giant cell arteritis.

Skin diseases.

· Pemphigus;

· bullous dermatitis herpetiformis;

· severe erythema multiforme (Stevens-Johnson syndrome);

· exfoliative dermatitis;

· fungal mycosis;

· severe psoriasis;

· severe seborrheic dermatitis.

Allergic conditions.

For the treatment of the following severe and allergic conditions when standard treatment is ineffective:

· seasonal or perennial allergic rhinitis;

· serum sickness;

· bronchial asthma;

· drug allergy;

· contact dermatitis;

· atopic dermatitis.

Eye diseases.

Severe acute and chronic allergic and inflammatory processes with eye damage, such as:

Allergic marginal corneal 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.

Respiratory diseases.

Symptomatic sarcoidosis;

· Leffler syndrome, which is not amenable to treatment by other methods;

· berylliosis;

· fulminant or disseminated pulmonary tuberculosis (used 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 the induction of diuresis or treatment of proteinuria in nephrotic syndrome without uremia, idiopathic type or caused by systemic lupus erythematosus.

Diseases of the digestive tract.

To remove a patient from a critical condition with the following diseases:

ulcerative colitis;

Regional enteritis (Crohn's disease).

Diseases of the nervous system.

Multiple sclerosis in the exacerbation phase;

· brain swelling caused by a brain tumor.

Diseases of other organs and systems.

Tuberculous meningitis with subarachnoid block or at risk of developing a block, in combination with appropriate anti-tuberculosis chemotherapy;

Trichinosis with damage to the nervous system or myocardium.

Organ transplantation.

Contraindication

Tuberculosis and other acute or chronic bacterial or viral infections with insufficient antibiotic and chemotherapy, systemic fungal infections.

Hypersensitivity to methylprednisolone or to excipients.

Interaction with other medicinal products and other types of interactions

Methylprednisolone is a substrate of the cytochrome P450 (CYP) enzyme and is metabolized primarily by the CYP3A4 isoenzyme. CYP3A4 is the dominant enzyme of the most abundant CYP subtype in the liver of adult humans. It catalyzes 6-β-hydroxylation of steroids, which is 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 inhibitors – Drugs that inhibit CYP3A4 activity tend to decrease hepatic clearance and increase plasma concentrations of CYP3A4 substrate drugs, such as methylprednisolone. In the presence of a CYP3A4 inhibitor, the dose of methylprednisolone may need to be titrated to avoid steroid toxicity. CYP3A4 inhibitors include: grapefruit juice; macrolide antibiotics (troleandomycin).

CYP3A4 inducers – drugs that stimulate CYP3A4 activity tend to increase hepatic clearance, leading to decreased plasma concentrations of drugs that are CYP3A4 substrates. When these drugs are used concomitantly, an increase in the dose of methylprednisolone may be required to achieve the desired effect. Such drugs include the antibiotic, anti-tuberculosis
drug – rifampin; anticonvulsants – phenobarbital, phenytoin.

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 the immunosuppressants cyclophosphamide, tacrolimus.

CYP3A4 inducers and substrates – anticonvulsants: carbamazepine.

CYP3A4 inhibitors and substrates – antiemetics: aprepitant, fosaprepitant; antifungals: itraconazole, ketaconazole; calcium channel blockers: diltiazem; oral contraceptives: ethinyl estradiol/norethindrone; macrolide antibiotics: clarithromycin, erythromycin;

Immunosuppressants – cyclosporine:

- when cyclosporine is used concomitantly with methylprednisolone, mutual inhibition of metabolism may occur, resulting in increased plasma concentrations of one or both of these drugs. In this regard, it is possible that adverse events associated with the use of one of these drugs as monotherapy will be more likely when they are used concomitantly;

- the development of seizures has been reported with the simultaneous use of methylprednisolone and cyclosporine;

Antiviral drugs – HIV protease inhibitors:

- protease inhibitors such as indinavir and ritonavir may lead to increased plasma concentrations of corticosteroids;

- corticosteroids can induce the metabolism of HIV protease inhibitors, resulting in a decrease in their plasma concentrations.

Anticoagulants (for oral use). The effect of methylprednisolone on oral coagulants is variable, with simultaneous use of these drugs may develop both enhanced and weakened effects of oral coagulants. Therefore, to obtain the desired anticoagulant effect, blood coagulation parameters should be regularly monitored.

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.

Salicylates and other nonsteroidal anti-inflammatory drugs: Concomitant use of salicylates, indomethacin and other nonsteroidal anti-inflammatory drugs may increase the incidence of gastrointestinal bleeding and ulcers. Methylprednisolone may increase the clearance of acetylsalicylic acid with prolonged use in high doses, which may lead to a decrease in serum salicylates or an increased risk of salicylate intoxication when methylprednisolone is discontinued. Acetylsalicylic acid and nonsteroidal anti-inflammatory drugs in combination with corticosteroids should be used with caution in the treatment of patients with hypoprothrombinemia.

Hypoglycemic drugs: methylprednisolone partially inhibits the hypoglycemic effect of oral antidiabetic drugs and insulin.

Enzyme inducers, such as barbiturates, phenytoin, pyrimidone, carbamazepine and rifampicin, increase the systemic clearance of methylprednisolone, thus reducing the effect of methylprednisolone by almost 2 times.

Estrogens may potentiate the effects of methylprednisolone by slowing its metabolism. Estrogens reduce some of the immunosuppressive effects of methylprednisolone.

Amphotericin, diuretics and laxatives: methylprednisolone may increase potassium excretion in patients receiving these drugs concurrently.

There is also an increased risk of hypokalemia when corticosteroids are used with xanthine or β2 antagonists.

The hypokalemic effect of acetazolamide, loop and thiazide diuretics, and carbenoxolone is increased.

Cytostatics and immunosuppressants: methylprednisolone has additive immunosuppressive properties, which may increase the therapeutic effect or the risk of various adverse reactions when administered concomitantly with other immunosuppressants. Only some of these effects can be explained by pharmacokinetic interactions. Glucocorticoids enhance the antiemetic efficacy of other antiemetics used concomitantly with anticancer drugs that induce emesis.

Corticosteroids may increase tacrolimus plasma concentrations when used concomitantly; upon withdrawal, tacrolimus plasma concentrations increase.

Convulsions have been reported with the concomitant use of methylprednisolone and cyclosporine. Since the simultaneous administration of these drugs causes mutual inhibition of metabolism, it is likely that convulsions and other adverse effects associated with the use of each of these drugs as monotherapy may occur more frequently when they are used together. Concomitant use may lead to increased plasma concentrations of the other drugs.

Immunization: Glucocorticoids may reduce the effectiveness of immunization and increase the risk of neurological complications. The use of therapeutic (immunosuppressive) doses of glucocorticoids with live viral vaccines may increase the risk of viral diseases.

Fluoroquinolones: concomitant use may lead to tendon damage.

Others: Two serious cases of acute myopathy have been reported in elderly patients receiving doxacamine chloride and high doses of methylprednisolone.

With prolonged therapy, glucocorticoids may reduce the effect of somatotropin.

Application features

Methylprednisolone, like other glucocorticoids, may exacerbate certain underlying diseases.

Corticosteroids should be used with caution and under medical supervision in patients with arterial hypertension, congestive heart failure, mental disorders, diabetes mellitus, pancreatitis, gastrointestinal diseases (peptic ulcer, local ileitis, ulcerative colitis (or other inflammatory diseases of the intestinal tract) or diverticulitis with an increased risk of bleeding and perforation), osteoporosis, glaucoma. Patients with blood clotting disorders should be under close medical supervision. It is also necessary to be careful when prescribing the drug to patients who have recently suffered a myocardial infarction, with epilepsy, recent anastomoses and renal failure.

Metipred may potentiate the ulcerogenic effect of salicylates and other nonsteroidal anti-inflammatory drugs.

The risk of gastric ulceration and bleeding increases with the simultaneous use of methylprednisolone and anticoagulants. Glucocorticoids can also reduce the effect of anticoagulants. Therefore, the dosage regimen of anticoagulants must be accompanied by monitoring of prothrombin time, namely the international normalized ratio (INR).

Immunosuppressive effects/Increased susceptibility to infections

Corticosteroids may increase susceptibility to infections; they may mask some symptoms of infections; and new infections may develop during corticosteroid therapy. Corticosteroids may decrease resistance to infections and may result in an inability to control infection. Infections caused by any agent, including viruses, bacteria, fungi, protozoa, or helminths, from any site in the body, may be associated with the use of corticosteroids alone or in combination with other immunosuppressants that affect cellular immunity, humoral immunity, or neutrophil function. These infections may be mild, but they 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.

In addition, corticosteroids should be used with great caution in patients with confirmed 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. Early studies reported both positive and negative effects of corticosteroids in this clinical setting. Later studies have suggested 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 studies following the administration of short courses of high-dose corticosteroids in such patients concluded that there is no evidence to support such use. However, a meta-analysis and one review of studies have suggested that longer (5–11 days) courses of low-dose corticosteroids may reduce mortality, particularly in patients with vasopressor-dependent septic shock.

The use of live or live attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids is contraindicated. Patients receiving immunosuppressive doses of corticosteroids may be vaccinated with killed or inactivated vaccines, but their response to such vaccines may be attenuated. These immunization procedures may be performed in patients receiving non-immunosuppressive doses of corticosteroids.

The use of corticosteroids in active tuberculosis should be limited to cases of fulminant or disseminated tuberculosis, in which case corticosteroids should be used in combination with appropriate anti-tuberculosis chemotherapy. If corticosteroids are indicated in patients with latent tuberculosis or with a negative tuberculin test, treatment should be carried out under close medical supervision, since exacerbation of the disease is possible. During prolonged corticosteroid therapy, such patients should be prescribed chemoprophylactic drugs.

There is a risk of tuberculosis recurrence and complications from chickenpox and herpes zoster.

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.

Blood and lymphatic system

Aspirin and nonsteroidal anti-inflammatory drugs in combination with corticosteroids should be used with caution.

Immune system

Allergic reactions (e.g. angioedema) may develop.

Endocrine system

Sudden withdrawal of glucocorticoids can lead to acute adrenal insufficiency, which can be fatal.

Adrenal insufficiency caused by the use 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, hormone therapy should be resumed. Since mineralocorticoid secretion may be impaired, electrolytes and/or mineralocorticoids should be administered simultaneously.

Since glucocorticosteroids may induce or exacerbate Cushing's syndrome, their use should be avoided in patients with Cushing's disease.

A more pronounced effect of corticosteroids is noted in patients with hypothyroidism.

Metabolism and nutrition

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.

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 necessary. Psychiatric reactions have been reported with corticosteroid withdrawal; the frequency is unknown. Patients/caregivers should be advised to seek medical advice if the patient develops any psychiatric disorder, particularly if they suspect that they are depressed or have suicidal thoughts. 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 short-acting steroids should be increased before, during, and after the stressful situation.

Nervous system disorders

Patients with seizures, as well as those with myasthenia gravis, should use corticosteroids with caution.

Organs of vision

In eye infections caused by the herpes simplex virus, corticosteroids should be used with caution because of the possibility of corneal perforation.

Prolonged use of corticosteroids may cause posterior subcapsular cataracts and nuclear cataracts (especially in children), exophthalmos, or increased intraocular pressure, which can lead to glaucoma with possible damage to the optic nerve. Patients using glucocorticoids are at increased risk of developing secondary ocular infections caused by fungi and viruses.

Heart disorders

Systemic corticosteroids should be used with caution and only when absolutely necessary in patients with congestive heart failure.

Vascular disorders

Corticosteroids should be used with caution in patients with hypertension.

Gastrointestinal tract

There is no consensus on whether corticosteroids cause peptic ulcer development during therapy. However, glucocorticoid therapy may mask the symptoms of peptic ulcer, so perforation or bleeding may occur without significant pain.

Corticosteroids should be used with caution in nonspecific ulcerative colitis, if there is a risk of perforation, abscess formation, or other purulent infection; in diverticulitis; in the case of recently performed intestinal anastomoses; in active or latent peptic ulcer.

Hepatobiliary system

There is an increase in the effects of corticosteroids in patients with cirrhosis of the liver.

Musculoskeletal disorders

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.

Osteoporosis is a common (but rarely diagnosed) side effect associated with long-term use of high doses of glucocorticoids.

Concomitant use of fluoroquinolones and glucocorticoids increases the risk of tendon damage.

Kidneys and urinary system

Corticosteroids should be used with caution in patients with renal insufficiency.

Research results

When using hydrocortisone or cortisone in medium and high doses, an increase in blood pressure, salt and water retention, and increased potassium excretion are possible. These effects are observed less often when using synthetic derivatives of these drugs, except when high doses are used. It is recommended to prescribe a diet with a restriction of salt intake and take potassium supplements. All corticosteroids increase calcium excretion.

Injuries, poisonings and procedural complications

Systemic corticosteroids should not be used in high doses in the treatment of patients with traumatic brain injury.

Others

The drug contains lactose monohydrate, therefore patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.

Since the occurrence of complications during treatment with glucocorticoids depends on the dose of the drug and the duration of therapy, in each case, a careful assessment of the ratio of the benefit of using the drug and the potential risk should be carried out when determining both the dose and duration of treatment, and the choice of the regimen of use - daily or intermittent.

When treating with corticosteroids, the lowest dose that provides sufficient therapeutic effect should be prescribed, and when dose reduction becomes possible, this reduction should be carried out gradually.

Carcinogenic, mutagenic and reproductive effects

No carcinogenic and mutagenic effects of the drug, as well as its adverse effects on reproductive functions, were detected.

With prolonged use in children, growth retardation is possible, so it is necessary to limit the use of minimum doses according to specific indications for the shortest possible time.

Elderly patients should be treated with caution, as the elderly are more susceptible to side effects that may occur when taking glucocorticoids, such as stomach ulcers, osteoporosis, and skin atrophy.

Use during pregnancy or breastfeeding

Animal studies have shown that high doses of corticosteroids administered to females may cause fetal malformations. Despite the results of animal studies, the potential for harm to the fetus is unlikely when this drug is used during pregnancy. No studies have been conducted on the effects of corticosteroids on human reproduction. Since there is no adequate evidence of the safety of corticosteroids in pregnant women, these drugs should be prescribed during pregnancy only if clearly needed.

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. Although adrenal insufficiency is rare in infants exposed to corticosteroids in utero, infants born to mothers who received relatively high doses of corticosteroids during pregnancy should be closely monitored for signs of adrenal insufficiency.

The effect of corticosteroids on the course and outcome of labor is unknown.

When prescribing corticosteroids to pregnant and lactating women, or to women planning to become pregnant, the benefit of the drug to the mother should be carefully weighed against the potential risk to the fetus.

Corticosteroids are excreted in human milk. Corticosteroids excreted in human milk may suppress growth and affect endogenous glucocorticoid production in breastfed infants. Because adequate studies of the effects of corticosteroids on human reproduction have not been conducted, this drug should be used in nursing mothers only if the potential benefit justifies the potential risk to the infant.

Ability to influence reaction speed when driving vehicles or other mechanisms

The drug usually does not affect the reaction speed when driving or using other mechanisms, but there is a risk of mood disorders, which may affect the ability to drive or operate other mechanisms.

The effect of corticosteroids on the ability to drive or use machines has not been systematically evaluated. After treatment with corticosteroids, side effects such as dizziness, vertigo, visual disturbances, and fatigue may occur. In such cases, patients should not drive or use machines.

Method of administration and doses

The initial dose of Metipred for adults can range from 4 mg to 48 mg of methylprednisolone per day, depending on the nature of the disease. In less severe diseases, lower 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/day), cerebral edema (200-1000 mg/day) and organ transplantation (up to 7 mg/kg/day).

If a satisfactory effect is achieved as a result of therapy, the patient should be selected for an individual maintenance dose by gradually reducing the initial dose at certain intervals until the lowest dose is found that allows maintaining the achieved clinical effect. It should be remembered that constant monitoring of the dosage regimen of the drug is necessary. Situations may arise in which it is necessary to adjust the dose; these include changes in the clinical condition due to the onset of remission or exacerbation of the disease, the patient's individual response to the drug, as well as the impact on the patient of stressful situations not directly related to the underlying disease, which is the subject of therapy; in the latter case, it may be necessary to increase the dose of the drug for a certain period of time, depending on the patient's condition. The required dose may vary and should be selected individually, depending on the nature of the disease and the patient's response to therapy.

It should be emphasized that the dosage of the drug should be individual and based on an assessment of the course of the disease and the clinical effect.

The drug should not be discontinued suddenly, it should be done gradually.

Alternative therapy

Alternating therapy is a corticosteroid dosing regimen in which a double daily dose of corticosteroid is administered every other day, in the morning. The goal of this type of therapy is to achieve maximum clinical benefit in a patient requiring long-term therapy while minimizing some of the undesirable effects, such as pituitary-adrenal axis suppression, Cushing's syndrome, corticosteroid withdrawal syndrome, and growth suppression in children.

Children.

The drug is used in pediatric practice.

The development and growth of children, including infants, should be carefully monitored during long-term corticosteroid therapy.

Growth retardation may occur in children receiving daily glucocorticoids for prolonged periods of time. Therefore, this dosage regimen should be used only when absolutely necessary. The use of alternating therapy usually avoids or minimizes this side effect (see section "Method of administration and dosage").

Overdose

An overdose of methylprednisolone is not accompanied by acute intoxication. In chronic intoxication, which is manifested by suppression

adrenal glands, it is necessary to gradually reduce the dose. In case of overdose, gastric lavage and administration of activated charcoal are recommended.

Methylprednisolone is removed by dialysis. There is no antidote for methylprednisolone.

Adverse reactions

When taking methylprednisolone, the same side effects develop as when taking other glucocorticoids. The duration of therapy and dosage affect the occurrence of side effects. With long-term therapy, side effects occur frequently, with a short duration of treatment - rarely.

Methylprednisolone may cause fluid and salt retention.

Since methylprednisolone in high doses leads to insufficiency and atrophy of the adrenal cortex over a long period, in stressful conditions (for example, surgery or infection) arterial hypotension, hypoglycemia and even death may develop if not increased