Description of the drug MEDROL
GKS. When used systemically, it has anti-inflammatory, antiallergic, desensitizing, antishock, antitoxic and immunosuppressive effects.
When applied externally and locally, the therapeutic activity of methylprednisolone is due to its anti-inflammatory, antiallergic and antiexudative (due to the vasoconstrictor effect) effect.
Its anti-inflammatory activity is 5 times higher than that of hydrocortisone; it has virtually no mineralocorticoid activity.
Suppresses the functions of leukocytes and tissue macrophages. Inhibits the release of interleukin-1, interleukin-2, interferon gamma from lymphocytes and macrophages.
Methylprednisolone suppresses the pituitary release of ACTH (and secondarily the synthesis of endogenous corticosteroids) and β-lipotropin, but does not reduce the level of circulating β-endorphin. Inhibits the secretion of TSH and FSH.
Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus and stimulates the synthesis of mRNA; the latter induces the formation of proteins (including lipocortin) that mediate cellular effects. Lipocortin inhibits the activity of phospholipase A2, which leads to suppression of the release of arachidonic acid, inhibition of the synthesis of prostaglandins, endoperoxides, leukotrienes, which are factors of inflammation and allergic reactions. Suppresses the release of COX (mainly COX-2), which also helps to reduce the production of prostaglandins.
Helps stabilize lysosomal membranes, thereby reducing the concentration of proteolytic enzymes in the area of inflammation. Reduces capillary permeability due to the release of histamine.
Methylprednisolone has a pronounced dose-dependent effect on the metabolism of proteins, fats and carbohydrates.
Reduces the protein content in plasma (due to globulins) with an increase in the albumin/globulin ratio, increases the synthesis of albumins in the liver and kidneys.
It has a catabolic effect in lymphoid and connective tissue, muscles, adipose tissue, skin, bone tissue. Osteoporosis and Itsenko-Cushing syndrome are the main factors limiting long-term GCS therapy. As a result of the catabolic effect, growth suppression in children is possible.
Stimulates the synthesis of higher fatty acids and TG, redistributes adipose tissue (fat accumulates mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.
Increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase, which leads to increased flow of glucose from the liver into the blood; stimulates gluconeogenesis.
Retains sodium ions and water in the body, stimulates the excretion of potassium, reduces the absorption of calcium from the gastrointestinal tract, promotes the leaching of calcium from bones, increases the excretion of calcium by the kidneys.
In high doses, methylprednisolone can increase the excitability of brain tissue and help lower the seizure threshold.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; 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 and organelle membranes (especially lysosomal ones).
The antiallergic effect develops as a result of suppression of 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 circulating lymphocytes (T- and B-cells) , mast cells, decreased sensitivity of effector cells to allergy mediators, inhibition of antibody production, changes in the body’s immune response.
In COPD, the action is based mainly on inhibition of inflammatory processes, inhibition of development or prevention of swelling of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of the bronchial epithelium, deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of β-adrenergic receptors of small and medium caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by inhibiting or reducing its production.
Antishock and antitoxic effects are associated with an increase in blood pressure (due to an increase in the concentration of circulating catecholamines and restoration of the sensitivity of adrenergic receptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane protective properties, and activation of liver enzymes involved in the metabolism of endo- and xenobiotics.
The immunosuppressive effect is due to inhibition of the release of cytokines (interleukin-1, interleukin-2), interferon gamma from lymphocytes and macrophages.
Suppresses fibroblast activity and collagen formation, reduces the possibility of scar tissue formation.
Stimulates excess production of hydrochloric acid and pepsin in the stomach, which increases the risk of developing peptic ulcers.
Medrol®
— Since the complications of methylprednisolone therapy 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 also determined.
- The minimum effective dose of the drug should be used to ensure a sufficient therapeutic effect; if necessary, the dose should be reduced gradually.
— During therapy with methylprednisolone, the development of various mental disorders is possible: from euphoria, insomnia, mood instability, personality changes and severe depression to acute psychotic manifestations. In addition, existing emotional instability or psychotic tendencies may be exacerbated.
— Potentially severe mental disorders may occur when using MEDROL®. 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. Psychological effects have been reported in association with methylprednisolone discontinuation; the frequency of these effects is not known.
— 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), it is necessary to 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.
- For patients who may be exposed to stress during methylprednisolone therapy, an increase in the dose of the drug before, during and after a stressful situation is indicated.
— Although controlled clinical studies have shown that methylprednisolone is effective in accelerating the recovery process during exacerbation of multiple sclerosis, it has not been established that methylprednisolone affects the outcome and pathogenesis of this disease.
Studies have also shown that sufficiently high doses of methylprednisolone must be administered to achieve a significant effect.
— There are reports of the development of epidural lipomatosis in patients receiving methylprednisolone. Usually with long-term therapy at high doses.
- In patients receiving immunosuppressive doses of methylprednisolone, live or live attenuated vaccines are contraindicated, but killed or inactivated vaccines can be administered, although the response to such vaccines may be reduced. Patients receiving treatment with methylprednisolone in doses that do not have an immunosuppressive effect may be immunized according to appropriate indications.
— During therapy with methylprednisolone, some infections may occur in an erased form, in addition, new infections may develop. When using methylprednisolone, it is possible to reduce resistance to infections, and also reduce the body's ability to localize the infectious process. 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 methylprednisolone, both as monotherapy and in combination with other immunosuppressants affecting cellular immunity, humoral immunity or neutrophil function. These infections can be mild, but in some cases they can be severe and even fatal. Moreover, the higher doses of methylprednisolone are used, the higher the likelihood of developing infectious complications.
— The use of MEDROL® in active tuberculosis should be limited to cases of fulminant and disseminated tuberculosis, when GCS are used to treat the disease in combination with appropriate anti-tuberculosis chemotherapy. If the drug 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 process is possible. During long-term treatment with methylprednisolone, such patients should receive appropriate prophylactic treatment.
— The drug should be used with caution in case of eye damage caused by the herpes simplex virus, due to possible perforation of the cornea.
- GCS, including methylprednisolone, can lead to an increase in blood glucose concentrations, worsen the course of existing diabetes mellitus and, with long-term therapy, can lead to a predisposition to diabetes mellitus.
- Long-term use of methylprednisolone can lead to the occurrence of posterior subcapsular cataracts, glaucoma with possible damage to the optic nerve and provoke the addition of a secondary ocular fungal or viral infection.
- Methylprednisolone therapy can lead to the development of central serous chorioretinopathy, which in turn can lead to retinal detachment.
— Children receiving long-term therapy with MEDROL® are at increased risk of developing intracranial hypertension.
- The use of high doses of methylprednisolone can lead to the development of pancreatitis in children.
- Allergic reactions (for example, angioedema) may develop. When using methylprednisolone, precautions should be taken, especially in patients with a history of allergic reactions to drugs.
— The drug contains lactose produced from cow's milk. Caution should be exercised in patients with known or suspected hypersensitivity to cow's milk or its components or other dairy products as they may contain trace amounts of dairy ingredients.
- Medium and large doses of hydrocortisone or cortisone may cause increased blood pressure, sodium and water retention, and increased potassium excretion. These effects are less likely when using synthetic corticosteroids (including methylprednisolone), 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.
— Systemic corticosteroids, including the drug MEDROL®, are not indicated and should not be used for the treatment of traumatic brain injury. An increase in mortality was found at 2 weeks or 6 months after head injury in patients treated with methylprednisolone sodium succinate. There was no direct association with administration of methylprednisolone sodium succinate.
— Osteoporosis is a common and, at the same time, rarely diagnosed adverse reaction that develops with long-term use of high doses of methylprednisolone.
- Children receiving the drug for a long time daily, several times a day, may experience growth retardation, so this dosage regimen should be used only for absolute indications. The use of alternative therapy can usually avoid or minimize this adverse reaction. When using MEDROL® in children, patients should be carefully monitored for normal growth and development.
- Manifestations of secondary adrenal insufficiency that develop during methylprednisolone therapy can be minimized by gradually reducing the dose. This type of relative deficiency may persist for several months after the end of treatment, so methylprednisolone should be reintroduced during this period in any stressful situations. Since the secretion of mineralocorticosteroids may be impaired, electrolytes and/or mineralocorticosteroids should be administered simultaneously.
— There is a more pronounced effect of methylprednisolone in patients with hypothyroidism and cirrhosis of the liver.
— Patients receiving drugs that suppress the immune system are more susceptible to infections than healthy people. For example, chickenpox and measles may be more severe and even fatal in unimmunized children or in adults receiving MEDROL®.
— There is no consensus on the likelihood of developing peptic ulcers during methylprednisolone therapy. Methylprednisolone therapy may mask the symptoms of a peptic ulcer, which may result in perforation or bleeding without significant pain. GCS therapy may mask symptoms of peritonitis, as well as other signs and symptoms associated with gastrointestinal dysfunction, such as perforation, obstruction and pancreatitis. When used simultaneously with NSAIDs, the risk of gastrointestinal ulcers increases.
- The use of methylprednisolone in high doses can lead to the development of acute pancreatitis.
— There are reports of the development of reversible liver damage, which is relieved by discontinuation of therapy. In this regard, appropriate monitoring should be carried out.
— Undesirable reactions of the drug MEDROL® from the cardiovascular system, such as dyslipidemia, increased blood pressure, can provoke new reactions in predisposed patients when using high doses of the drug MEDROL® and long-term treatment. In this regard, methylprednisolone should be taken with caution in patients predisposed to cardiovascular diseases and special attention should be paid to additional monitoring of the state of the cardiovascular system.
- Cases of thrombosis, including venous thromboembolism, have been reported with the use of GCS. Therefore, GCS should be used with caution in patients with current thromboembolic complications or who are predisposed to developing these complications.
- Methylprednisolone should be prescribed with caution for ulcerative colitis, if there is a threat of perforation of the walls of the gastrointestinal tract, the development of an abscess or other purulent infection, as well as for diverticulitis, in the presence of fresh intestinal anastomoses, with active or latent peptic ulcers, renal failure, arterial hypertension, osteoporosis, myasthenia gravis.
— Cases (including fatalities) of the development of crises have been reported in patients suffering from pheochromocytoma receiving systemic therapy with corticosteroids, including methylprednisolone. In patients with suspected or confirmed pheochromocytoma. Methylprednisolone should only be used after a careful risk/benefit assessment.
— There have been cases of the development of Kaposi's sarcoma in patients receiving methylprednisolone therapy (if they are discontinued, clinical remission may occur).
— The effectiveness of MEDROL® in septic shock is questionable. The results of a systematic review of the use of the drug in short courses at high doses do not support its use in this regimen. However, it is assumed that the use of MEDROL® in long courses (5-11 days) in low doses may reduce mortality.
— When using the drug MEDROL® in therapeutic doses for a long period, suppression of the hypothalamic-pituitary-adrenal system (secondary adrenocortical insufficiency) may develop. The degree and duration of adrenocortical insufficiency are individual for each patient and depend 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 (see section “Method of administration and dosage”),
— In addition, the development of acute adrenal insufficiency, leading to death, is possible with abrupt discontinuation of the drug MEDROL®. Caution is warranted in patients with systemic scleroderma as an increased incidence of acute scleroderma nephropathy has been observed when taking corticosteroids, including methylprednisolone.
- Since methylprednisolone may enhance the clinical manifestations of Cushing's syndrome, the use of methylprednisolone should be avoided in patients with Cushing's disease.
— Acute myopathy most often develops with the use of high doses of methylprednisolone in patients with impaired neuromuscular transmission (for example, with myasthenia gravis), or in patients simultaneously receiving anticholinergic drugs, such as peripheral muscle relaxants (for example, pancuronium bromide). Such acute myopathy is generalized in nature, can affect the muscles of the eye and respiratory system, and lead to the development of tetraparesis. Creatine kinase levels may be elevated. However, improvement or recovery after discontinuation of methylprednisolone may occur only after many weeks or even several years.
- Withdrawal syndrome, apparently not related to adrenal insufficiency, can also occur due to abrupt discontinuation of the drug MEDROL®. This syndrome includes symptoms such as anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, skin peeling, myalgia, weight loss and/or decreased blood pressure. It is assumed that these effects occur due to sharp fluctuations in the concentration of methylprednisolone in the blood plasma, and not due to a decrease in the concentration of methylprednisolone in the blood plasma.
— The carcinogenic and mutagenic effects of the drug, as well as its adverse effects on reproductive functions, have not been established.
Medrol 4mg No. 30 tablets
Medrol 4mg No. 30 tablets
Active ingredient Methylprednisolone
Composition 1 tablet contains: Active ingredient: methylprednisolone 4 mg; Excipients: calcium stearate; corn starch; lactose; sucrose.
Pharmacological action Synthetic glucocorticoid with anti-inflammatory, antiallergic, immunosuppressive activity. Under the influence of Medrol, there is a decrease in the number of immunoactive cells around the inflammatory focus, a decrease in vasodilation, stabilization of lysosomal membranes, inhibition of phagocytosis, and a decrease in the production of prostaglandins and related substances. Medrol at a dose of 4 mg has the same anti-inflammatory effect as hydrocortisone at a dose of 20 mg. The drug has minimal mineralocorticoid effect (200 mg of the drug is equivalent to 1 mg of deoxycorticosterone). The drug has a catabolic effect. Reduces the absorption of glucose by peripheral tissues, which can lead to hyperglycemia and glucosuria, especially in patients predisposed to diabetes. Medrol has a lipolytic effect, mainly in the extremities, also a lipogenic effect, most pronounced on the chest, neck and head, leading to the redistribution of fat deposits. May cause osteoporosis.
Indications: systemic lupus erythematosus, rheumatoid arthritis, severe psoriasis, neurodermatitis, severe allergic diseases, bronchial asthma, glomerulonephritis.
Use during pregnancy and breastfeeding The use of Medrol during pregnancy is possible if the expected effect of therapy exceeds the potential risk to the fetus (adequate and strictly controlled safety studies have not been conducted). Women of childbearing age should be warned of the potential risk to the fetus (corticosteroids cross the placenta). Breastfeeding women are advised to stop either breastfeeding or the use of drugs, especially in high doses (corticosteroids pass into breast milk and can inhibit the production of endogenous corticosteroids, suppress growth and cause undesirable effects in offspring).
Contraindications: severe arterial hypertension, severe heart failure, diabetes mellitus, gastric and duodenal ulcers, mental illness, glaucoma, viral infections, fungal infections, increased sensitivity to the drug Medrol.
effects : sodium retention, chronic heart failure in patients with a corresponding predisposition, increased blood pressure, fluid retention in the body, potassium loss and hypokalemic alkalosis, negative nitrogen balance due to protein catabolism. From the musculoskeletal system: steroid myopathy, muscle weakness, osteoporosis, pathological fractures, vertebral compression fractures, aseptic necrosis of the epiphyses of tubular bones, tendon ruptures, especially the Achilles tendon. From the digestive system: peptic ulcer with possible perforation and bleeding, gastric bleeding, pancreatitis, esophagitis, intestinal perforation. After treatment with GCS, an increase in the activity of ALT, AST and alkaline phosphatase in the blood serum was observed. Usually these changes are minor, not associated with any clinical syndromes and are reversible after cessation of treatment. Dermatological reactions: slow wound healing, petechiae and ecchymosis, thinning and decreased strength of the skin. From the nervous system: increased intracranial pressure, pseudotumor cerebri, mental disorders, convulsions. From the endocrine system: menstrual irregularities, hirsutism, development of Cushing's syndrome, suppression of the pituitary-adrenal system, decreased tolerance to carbohydrates, manifestation of latent diabetes mellitus, increased need for insulin or oral hypoglycemic agents in patients with diabetes, growth retardation in children. From the organ of vision: posterior subcapsular cataract, increased intraocular pressure with the risk of damage to the optic nerve, exophthalmos. Allergic reactions: hypersensitivity reactions, including allergic systemic reactions, suppression of reactions during skin testing is possible. Other: blurred clinical picture in infectious diseases, activation of latent infections, the occurrence of infections caused by opportunistic pathogens, GCS withdrawal syndrome.
Interaction Increases the toxicity of cardiac glycosides (due to the resulting hypokalemia, the risk of developing arrhythmias increases). Accelerates the elimination of ASA, reduces its concentration in the blood (when methylprednisolone is discontinued, the concentration of salicylates in the blood increases and the risk of side effects increases). 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. Increases the metabolism of isoniazid, mexiletine (especially in “fast” acetylators), which leads to a decrease in their plasma concentrations. Increases the risk of developing hepatotoxic reactions of paracetamol (induction of “liver” enzymes and the formation of a toxic metabolite of paracetamol). Increases (with long-term therapy) the content of folic acid. Hypokalemia caused by GCS can increase the severity and duration of muscle blockade due to muscle relaxants. In high doses, it reduces the effect of somatropin. Antacids reduce the absorption of corticosteroids. Reduces the effect of hypoglycemic drugs; enhances the anticoagulant effect of coumarin derivatives. Weakens the effect of vitamin D on the absorption of Ca2+ in the intestinal lumen. Ergocalciferol and parathyroid hormone prevent the development of osteopathy caused by GCS. Reduces the concentration of praziquantel in the blood. Ketoconazole reduces the clearance and increases the toxicity of methylprednisolone. Combined use with cyclosporine causes mutual inhibition of metabolism - the risk of developing side effects of both drugs (cases of seizures have been reported when used together). Thiazide diuretics, carbonic anhydrase inhibitors, other corticosteroids and amphotericin B increase the risk of hypokalemia, while Na+-containing drugs increase the risk of edema and increased blood pressure. NSAIDs and ethanol increase the risk of developing ulceration of the gastrointestinal mucosa and bleeding; in combination with NSAIDs for the treatment of arthritis, it is possible to reduce the dose of GCS due to the summation of the therapeutic effect. Indomethacin, displacing methylprednisolone from its association with albumin, increases the risk of developing its side effects. Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis. The therapeutic effect of GCS is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of “liver” microsomal enzymes (increased metabolic rate). Mitotane and other inhibitors of adrenal cortex function may necessitate an increase in the dose of GCS. The clearance of GCS increases against the background of thyroid hormones. Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders associated with the Epstein-Barr virus. Estrogens (including oral estrogen-containing contraceptives) reduce the clearance of GCS, prolong T1/2 and their therapeutic and toxic effects. The appearance of hirsutism and acne is facilitated by the simultaneous use of other steroid hormonal drugs - androgens, estrogens, anabolic steroids, oral contraceptives. Tricyclic antidepressants may increase the severity of depression caused by taking corticosteroids (not indicated for the treatment of these side effects). The risk of developing cataracts increases when used in conjunction with other corticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine. Simultaneous administration with m-anticholinergics (including antihistamines, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.
How to take, course of administration and dosage Orally. The dose may vary and should be individualized depending on the nature of the disease and the patient's response to therapy. The initial dose is from 4 to 48 mg/day, depending on the nature of the disease. For less severe illnesses, lower doses are usually sufficient, although individual patients may require higher doses. High doses may be required for 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 clinical effect is not obtained after a sufficient period of time, the drug should be discontinued and the patient should be prescribed another type of therapy. For children, the dose is determined by the doctor taking into account the weight or surface area of the body. For adrenal insufficiency - 0.18 mg/kg or 3.33 mg/m2/day in 3 doses, for other indications - 0.42–1.67 mg/kg or 12.5–50 mg/m2/day in 3 receptions. It is recommended to discontinue the drug after long-term therapy gradually. If a good effect is obtained during treatment, 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 allows maintaining the achieved clinical effect. It should be remembered that constant monitoring of the drug dosage regimen is necessary. Situations may arise in which dose adjustment is required, for example, changes in the clinical condition caused by the onset of remission or exacerbation of the disease, the patient’s individual reaction to the drug, as well as the impact on the patient of stressful situations that are not directly related to the underlying disease for which the therapy is aimed; 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. Alternative therapy. Alternating therapy is a dosage regimen in which a double daily dose of glucocorticosteroids is administered every other day in the morning. The goal of such therapy is to achieve maximum clinical effect in a patient taking the drug for a long time while minimizing some undesirable effects, such as suppression of the pituitary-adrenal axis, glucocorticosteroid withdrawal syndrome and growth retardation in children.
Overdose The clinical syndrome of acute overdose of the drug has not been described. Reports of cases of acute toxicity following an overdose of GCS are extremely rare. Symptoms: frequent repeated use (daily or several times a week) for a long time can lead to the development of Cushing's syndrome and other complications characteristic of long-term GCS therapy. Treatment: symptomatic therapy. Methylprednisolone is eliminated by dialysis. There is no specific antidote.
Special instructions Before starting treatment, the patient should be examined to identify possible contraindications. Clinical examination should include a study of the cardiovascular system, x-ray examination of the lungs, examination of the stomach and duodenum; urinary system, visual organs. Before and during steroid therapy, it is necessary to monitor a general blood count, the concentration of glucose in the blood and urine, and electrolytes in the plasma. For intercurrent infections, septic conditions and tuberculosis, simultaneous antibiotic therapy is necessary. Immunizations should not be performed during treatment. With sudden withdrawal, especially in the case of previous use of high doses, GCS “withdrawal” syndrome occurs: decreased appetite, nausea, lethargy, generalized musculoskeletal pain, asthenia. After discontinuation, relative insufficiency of the adrenal cortex persists for several months. If stressful situations arise during this period, GCS is prescribed (according to indications) for the duration, if necessary - in combination with MCS. Children who during the treatment period were in contact with patients with measles or chickenpox are prescribed specific Ig prophylactically. To reduce side effects, it is justified to prescribe anabolic steroids and increase the intake of K+ from food. In Addison's disease, simultaneous administration of barbiturates should be avoided - there is a risk of developing acute adrenal insufficiency (Addisonian crisis). Use during pregnancy in the first trimester and during lactation: prescribed taking into account the expected therapeutic effect and negative effect on the fetus and child. With long-term therapy during pregnancy, fetal growth is impaired. In the third trimester of pregnancy, there is a risk of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in the newborn. 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.
Release form Tablets
Storage conditions At a temperature of 20–25 °C
Shelf life 5 years
