Solu-medrol lyophilisate for injection 500mg vial №1 + solvent

Dosage form

Lyophilisate for solution for injection

Composition

1 fl. contains methylprednisolone (as sodium succinate) 500 mg,
Excipients: monobasic sodium phosphate monohydrate; Sodium phosphate

Packaging

In a pack of 1 bottle complete with solvent.

Mechanism of action

Solu-Medrol has a glucocorticoid effect. Slows down the release of interleukin1, interleukin2, gamma Interferon from lymphocytes and macrophages. It has anti-inflammatory, anti-allergic, desensitizing, anti-shock, anti-toxic and immunosuppressive effects. Suppresses the release of pituitary ACTH and beta-lipotropin, but does not reduce the concentration of circulating beta-endorphin. It inhibits the secretion of TSH and FSH. Increases the excitability of the central nervous system, reduces the number of lymphocytes and eosinophils, increases - red blood cells (stimulates the production of erythropoietin). It interacts with specific cytoplasmic receptors and forms a complex that penetrates into the cell nucleus, and stimulates the synthesis of mRNA; the latter induces the formation of proteins, incl.lipocortin mediating cellular effects. Lipocortin inhibits phospholipase A2, inhibits the release of arachidonic acid and inhibits the synthesis of endoperekisy, Pg, leukotrienes, promoting the processes of inflammation, allergies, etc. liver and kidney; enhances protein catabolism in muscle tissue. Lipid metabolism: increases the synthesis of higher fatty acids and TG, redistributes fat (fat accumulation mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia. Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase, leading to an increase in glucose uptake from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases leading to the activation of gluconeogenesis. Water and electrolyte metabolism: retains Na + and water in the body, stimulates the excretion of K + (MKS activity), reduces the absorption of Ca2 + from the gastrointestinal tract, "washes out" Ca2 + from the bones, increases the excretion of Ca2 + by the kidneys. Anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; induction of lipocortin formation and reduction in the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes and membranes of organelles (especially lysosomal).Antiallergic effect develops as a result of suppression of the synthesis and secretion of allergy mediators, inhibition of release from sensitized mast cells and histamine basophils and other biologically active substances, reduction in the number of circulating basophils, suppression of the development of lymphoid and connective tissue, reduction in the number of T- and B-lymphocytes, fat cells, reducing the sensitivity of effector cells to mediators of allergy, inhibition of antibody production, changes in the immune response of the body. Anti-shock and anti-toxic effects are associated with an increase in blood pressure (by increasing the concentration of circulating catecholamines and restoring sensitivity of adrenoreceptors to them, as well as vasoconstriction), reducing vascular permeability, membrane-protective properties, activation of liver enzymes involved in endo- and xenobiotic metabolism. The immunodepressive effect is due to the inhibition of the release of cytokines (interleukin1, interleukin2; interferon gamma) from lymphocytes and macrophages. Inhibits the synthesis and secretion of ACTH and secondary synthesis of endogenous corticosteroids. It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation. In COPD, it is mainly based on the inhibition of inflammatory processes, the suppression of the development or the prevention of edema of the mucous membranes, the inhibition of eosinophilic infiltration of the submucosal epithelium of the bronchi,deposition in the bronchial mucosa of circulating immune complexes, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of beta-adrenoreceptors of the bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus due to inhibition or reduction of its products. 5 times more active than Hydrocortisone for anti-inflammatory action. After i / m administration of 80 mg of the drug, its effect lasts for 12 hours, and the suppressive effect on the level of plasma Cortisone is observed for another 17 days.

Indications and usage

Shock (burn, traumatic, operative, toxic, cardiogenic) with the failure of other therapies. Allergic reactions (acute, severe), blood transfusion shock, anaphylactic shock, anaphylactoid reactions. Cerebral edema (including against the background of a brain tumor or associated with surgery, radiation therapy or head trauma). Bronchial asthma (severe), asthmatic status. Systemic diseases of connective tissue (SLE, rheumatoid arthritis). Acute adrenal insufficiency. Thyrotoxic crisis. Acute hepatitis, hepatic coma. Poisoning with cauterizing liquids (reducing inflammation and preventing cicatricial contractions).

Contraindications

For short-term use for "vital" indications, the only contraindication is hypersensitivity.For intraarticular administration: previous arthroplasty, abnormal bleeding (endogenous or caused by anticoagulants), intraarticular bone fracture, infectious (septic) inflammation in the joint and periarticular infections (including a history), as well as a common infectious disease, marked periarticular osteoporosis, the absence of signs of inflammation in the joint (the so-called "dry" joint, for example, in osteoarthritis without synovitis), severe bone destruction and deformity of the joint (sharp angling joint space, ankylosis), instability of the joint as a result of arthritis, aseptic necrosis of the epiphyses of the bones forming the joint.

Dosage and administration

Solu-Medrol is administered intravenously, intramuscularly, or as an intravenous infusion, but for emergency conditions, treatment is started with intravenous injection. Children should be given lower doses (but not less than 0.5 mg / kg / day), but when choosing a dose, first of all, take into account the severity of the condition and the patient's response to therapy, rather than age and body weight. As an additional therapy in life-threatening conditions - in / in, 30 mg / kg for at least 30 minutes. The administration can be repeated every 4-6 hours for no more than 48 hours. Oncological diseases in the terminal stage - to improve the quality of life - i / v 125 mg / day daily for up to 8 weeks. Prevention of nausea and vomiting associated with Chemotherapy for cancer.With chemotherapy, characterized by a slight or moderate emetic effect, i.v. / in 250 mg for at least 5 minutes 1 hour before the administration of chemotherapy, at the beginning and after the end of the administration. To enhance the effect with the first dose of the drug Solu-Medrol, you can enter drugs chlorphenothiazine. With chemotherapy, characterized by a pronounced emetic effect, it is in / in 250 mg for at least 5 minutes in combination with appropriate doses of Metoclopramide or butyrophenone 1 hour before the administration of chemotherapy drugs, then in / in 250 mg at the beginning and after the end of the administration. Acute traumatic injuries of the spinal cord. Treatment must begin in the first 8 hours after injury. It is recommended intravenous bolus administration at a dose of 30 mg / kg for 15 minutes, then after a 45-minute break, a continuous infusion at a dose of 5.4 mg / kg / h is carried out for 23 hours. The drug should be administered using an infusion pump into an isolated vein. For other indications, the initial dose of Solu-Medrol is 10-500 mg IV depending on the nature of the disease. For a short course in severe acute conditions, higher doses may be required. An initial dose not exceeding 250 mg should be administered IV for at least 5 minutes, a dose of more than 250 mg should be at least 30 minutes. Subsequent doses are administered intravenously or intramuscularly, and the duration of the intervals between injections depends on the patient's response to therapy and on his clinical condition.

The frequency of development and severity of side effects depend on the duration of use, the magnitude of the dose used and the ability to comply with the circadian rhythm of the appointment.From endocrine system: reduction of glucose tolerance, "steroid" diabetes or a manifestation of latent diabetes mellitus, adrenal suppression, Cushing's syndrome (moon face, obesity, pituitary type, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis, striae) , delayed sexual development in children. On the part of the digestive system: nausea, vomiting, pancreatitis, "steroid" gastric and duodenal ulcer, erosive esophagitis, bleeding and perforation of the gastrointestinal tract, increased or decreased appetite, flatulence, hiccups. In rare cases - increased activity of "liver" transaminases and alkaline phosphatase. From the side of the cardiovascular system: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or increased severity of HF, ECG changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread of necrosis, slowing the formation of scar tissue, which can lead to rupture of the heart muscle. Nervous system disorders: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, pseudotumor of the cerebellum, headache, convulsions. On the part of the senses: sudden loss of vision (when administered parenterally in the head, neck, nasal conchae,Scalping is possible in the eye vessels), posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, a tendency to develop secondary bacterial, fungal or viral infections of the eye, trophic changes of the cornea, exophthalmos. On the part of the metabolism: increased excretion of Ca2 +, hypocalcemia, increased body weight, negative nitrogen balance (increased protein breakdown), increased perspiration. Caused by ISS activity - fluid retention and Na + (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue). On the part of the musculoskeletal system: growth retardation and the process of ossification in children (premature closure of the epiphyseal growth zones), osteoporosis (very rarely - pathological bone fractures, aseptic necrosis of the head of the humerus and femur), muscle tendon rupture, "steroid" myopathy, reduction muscle mass (atrophy). On the part of the skin and mucous membranes: delayed wound healing, petechiae, ecchymosis, thinning of the skin, hyper- or hypopigmentation, steroid acne, stretch marks, a tendency to the development of pyoderma and candidiasis. Allergic reactions: generalized (skin rash, itching, anaphylactic shock), local allergic reactions. Others: the development or exacerbation of infections (jointly used immunosuppressants and vaccination contribute to the occurrence of this side effect), leukocyturia, "withdrawal" syndrome.Local with parenteral administration: burning, numbness, pain, paresthesia at the injection site, infection at the injection site, rarely - necrosis of surrounding tissues, scarring at the injection site; atrophy of the skin and subcutaneous tissue when i / m administration (especially the introduction into the deltoid muscle). With a / in the introduction: arrhythmias, "hot flashes" of blood to the face, convulsions. When administered intracranially - nosebleeds. With intra-articular injection - increased pain in the joint.

During treatment, vaccination should not be carried out because of a possible decrease in the immune response. With active tuberculous process it is possible to use only in combination with appropriate anti-tuberculosis therapy. Ineffective in septic shock (possibly increased mortality). During pregnancy or during the intended pregnancy, treatment should be carried out only under the strictest indications. The available clinical experience of using GCS in the first third of pregnancy indicates the absence of an increased risk for the fetus. When injecting a newborn and especially a premature baby, distilled water must be used as a solvent. Due to the weak ISS effect, methylprednisolone cannot be used for substitution therapy in Addison's disease. Special care must be taken when administering GCS to patients with severe arterial hypertension and CHF (ECG and BP control are necessary).In patients with diabetes mellitus, the concentration of glucose in the blood should be monitored and, if necessary, therapy should be adjusted. X-ray control of the osteo-articular system is shown (pictures of the spine, hand). It can cause leukocyturia, which may be of diagnostic importance for the detection of latent leukocyturia in diseases of the kidneys and urinary tract. The concentration of metabolites 11- and 17-hydroxykethocorticosteroids increases. In rare cases - increased activity of "liver" transaminases and alkaline phosphatase. Under stress during the treatment of GCS, an increase in the dose is indicated. Perhaps the development of the syndrome of "cancellation" (usually with non-compliance with chronopharmacology, as well as with the original hidden adrenal insufficiency). In / to the introduction should not be deep. Depot forms should not be entered by non-recommended means (including in / in). In children during the growth period, GCS should be used only if absolutely indicated and under the most careful supervision of the attending physician.

Methylprednisolone pharmaceutical is incompatible with other drugs (may form insoluble compounds). Methylprednisolone increases the toxicity of cardiac glycosides (due to the resulting hypokalemia increases the risk of arrhythmias). Accelerates the elimination of ASA, reduces its concentration in the blood (with the abolition of methylprednisolone, the concentration of salicylates in the blood increases and the risk of side effects increases).When applied simultaneously with live antiviral vaccines and against the background of other types of immunizations, it increases the risk of virus activation and the development of infections. Increases the metabolism of isoniazid, meksiletin (especially in "fast acetylators"), which leads to a decrease in their plasma concentrations. Increases the risk of hepatotoxic reactions of Paracetamol (induction of "liver" enzymes and the formation of a toxic metabolite of paracetamol). Increases (with long-term therapy) the concentration of folic acid. Hypokalemia caused by GCS can increase the severity and duration of muscle blockade on the background of muscle relaxants. In high doses, reduces the effect of somatropin. Antacids reduce the absorption of corticosteroids. Methylprednisolone reduces the effect of hypoglycemic drugs; enhances the anticoagulant action 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. Cyclosporine (inhibits metabolism) and Ketoconazole (decreases clearance) increase toxicity. Thiazide diuretics, carbonic anhydrase inhibitors, other GCS and amphotericin B increase the risk of hypokalemia, Na + -containing drugs - edema and increase blood pressure. NSAIDs and ethanol increase the risk of ulceration of the mucous membrane of the gastrointestinal tract and bleeding, in combination with NSAIDs for the treatment of arthritis may reduce the dose of corticosteroids due to the sum of the therapeutic effect.Indomethacin, displacing methylprednisolone from its association with albumin, increases the risk of its side effects. Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis. The therapeutic effect of corticosteroids is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin, and other inducers of "liver" microsomal enzymes (increased metabolic rate). Mitotan and other inhibitors of the function of the adrenal cortex may necessitate an increase in the dose of GCS. Clearance of GCS increases due to thyroid hormones. Immunosuppressants increase the risk of developing infections and lymphomas or other lymphoproliferative disorders associated with Epstein-Barr virus. Estrogens (including oral estrogen-containing contraceptives) reduce GC clearance, lengthen T1 / 2 and their therapeutic and toxic effects. The emergence of hirsutism and acne contributes to the simultaneous use of other steroid hormonal drugs - androgens, estrogens, anabolic steroids, oral contraceptives. Tricyclic antidepressants may increase the severity of GCS-induced depression (not indicated for the treatment of these side effects). The risk of developing cataracts is increased when applied against the background of other corticosteroids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine. The simultaneous appointment with m-anticholinergics (including antihistamine drugs, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.

In a dry, dark place at a temperature of no higher than 20 ° C.

5 years.