Sola-Medrol Methylprednisolone powd+sol 40mg/ml fl Act-O-Vial

Sola-Medrol Methylprednisolone powd+sol 40mg/ml fl Act-O-Vial

Product Code: 12439
Availability: In Stock

Ask a question about this product

Composition active substance: methylprednisolone; 1 vial contains methylprednisolone as methylprednisolone succinate 40 mg or 125 mg, or 500 mg, abo1000 mg excipients: for a dosage of 125 mg or 500 mg, or 1000 mg of dihydrogen phosphate monohydrate, phosphate anhydrous excipients: for a dosage of 40 mg of dihydrogen phosphate monohydrate, phosphate anhydrous lactose monohydrate, solvent: benzyl alcohol (9 mg/ml), water for injection. Dosage form Powder and solvent for preparation of solution for injection. Basic physico-chemical properties: powder from white to almost white lyophilizate; the solvent for dosing of 40 mg and 125 mg clear, colourless solution the solvent for dosing of 500 mg and 1000 mg: clear, colorless liquid with a slight odor of benzyl alcohol. Pharmacological group Corticosteroids for systemic use. Code ATH N02A B04.

Pharmacological properties This drug is an injectable form of methylprednisolone (synthetic GCS) for intramuscular and intravenous administration. This highly concentrated solution is suitable, in particular, for the treatment of pathological conditions in which the effective and rapid action of the hormone is necessary. Methylprednisolone has a strong anti-inflammatory, immunosuppressive and anti-allergic effect. Pharmacodynamics. Glucocorticoids penetrate the cell membrane through diffusion and form complexes with specific receptors in the cytoplasm. Further, these complexes enter the cell nucleus, bind to DNA (chromatin) and stimulate the transcription of mRNA and further synthesis of proteins by various enzymes, which, in turn, are responsible for the numerous effects of glucocorticoids after systemic application. Glucocorticoids not only detect a significant effect on inflammatory and immune processes, but also affect the metabolism of carbohydrates, proteins and fats. They also act on the cardiovascular system, skeletal muscles and the Central nervous system. Influence on inflammatory and immune processes Anti-inflammatory, immunosuppressive and anti-allergic properties of glucocorticoids are used in most therapeutic indications. The presence of these properties leads to such results: reducing the number of immunoactive cells around the inflammation focus; the reduction of vasodilation; stabilization of lysosomal membranes; oppression of phagocytosis; reducing the formation of prostaglandins and related substances. The dose of methylprednisolone 4 mg is showing the same GLUCOCORTICOSTEROID (anti-inflammatory) effect, 20 mg of hydrocortisone.

Methylprednisolone demonstrates only a minimal mineralocorticoid effect (200 mg methylprednisolone is equivalent to 1 mg desoxycorticosterone). Effect on the metabolism of carbohydrates and proteins Glucocorticoids have a catabolic effect on protein metabolism. The released amino acids in the liver are transformed by gluconeogenesis into glucose and glycogen. Thus, glucose absorption by peripheral tissues decreases, which can lead to hyperglycemia and glucosuria, especially in patients with a predisposition to diabetes. The effect on fat metabolism Glucocorticoids have a lipolytic action that is subject to mainly on the limbs. They also have a lipogenetic effect, most manifested in the chest, neck and head. All this leads to a redistribution of body fat. The maximum pharmacological effect of corticosteroids lags behind the achievement of their maximum concentration in the blood, which indicates that most of the effects of these drugs is the result of modification of the enzyme activity, rather than the direct action of these drugs. Pharmacokinetics. In vivo cholinesterase rapidly convert methylprednisolone succinate into free methylprednisolone by hydrolysis. In men, methylprednisolone forms a weak dissociated bond with albumin and transcortin. About 40-90% of the drug is bound. Infusion at a dose of 30 mg/kg of body weight when administered in 20 minutes or in a dose of 1 g when administered in 30-60 minutes results in about 15 minutes to a peak concentration of methylprednisolone in plasma, which is about 20 mg/ml After approximately 25 min after bolus injection at a dose of 40 mg peak indicator of methylprednisolone in plasma is 42 to 47 mg/100 ml After about 120 minutes after injection of the drug at a dose of 40 mg, the maximum concentration of methylprednisolone in plasma is 34 mg/100 ml. During injection, the peak rate is lower than for intravenous injection. During the injection, the concentration in the blood plasma remains for a long period, which leads to the fact that in both ways of administration the equivalent amount of methylprednisolone arrives. The clinical significance of these small differences is likely to be minimal, if we consider the mechanism of action of glucocorticoids. Clinical response is usually seen after 4 to 6 hours after drug administration. At treatment of bronchial asthma the first favorable results can already be noted in 1-2 hours. The half-life of methylprednisolone succinate from blood plasma is 2.3-4 hours and probably does not depend on the route of administration. Methylprednisolone is a corticosteroids average duration. Its half-life is 12-36 hours. Intracellular activity of glucocorticoids is displayed by a clear difference between the half-life of plasma and the pharmacological half-life period. Pharmacological activity persists after the drug level in blood plasma is not determined. The duration of anti-inflammatory activity of the GCS is approximately equal to the duration of oppression of the hypothalamic-pituitary-adrenal (HGA) system. Metabolism of methylprednisolone is carried out in the liver by the same processes as for cortisol. The major metabolites are 20 beta-hydroxymethylimidazole and 20-beta-hydroxy-6-alpha-methylprednisolone.

Metabolites are primarily excreted in the urine in the form of glucuronides, sulfates and non-conjugated compounds. After administration of methylprednisolone, labeled with C14, 75% of the total radioactivity observed in the urine within 96 hours, 9% - in 5 days in the feces of human and 20% - in the bile. Indications The use of glucocorticoids should be considered only as a symptomatic treatment, except for certain endocrine disorders, when they are used as substitution therapy. anti-inflammatory treatment rheumatic disease As auxiliary therapy for short-term use (to help the patient survive an acute episode or exacerbation) in such diseases: post-traumatic osteoarthritis; synovitis with osteoarthritis; rheumatoid arthritis, in particular juvenile rheumatoid arthritis (in some cases, may require maintenance therapy with a low dose) acute and subacute bursitis, epicondylitis; acute non-specific tendosynovit; acute gouty arthritis psoriatic arthritis ankylosing spondylitis; ; Collagenoses (systemic diseases of connective tissue) During an exacerbation or as maintenance therapy in selected cases, when such diseases as: systemic lupus erythematosus (and lupus nephritis); acute rheumatic carditis; systemic dermatomyositis (polymyositis) nodular periarteritis; goodpasture. ; dermatological diseases Pemphigus. Severe erythema multiforme (Stevens-Johnson syndrome). Exfoliative dermatitis. Bullous dermatitis herpetiformis. Severe seborrheic dermatitis. Severe psoriasis. Mycosis fungoides. Urticaria. ; allergic condition Control of severe or disabled allergic conditions that do not lend themselves to proper traditional treatment, in diseases such as: bronchial asthma; contact dermatitis atopic dermatitis serum sickness; seasonal or year-round allergic rhinitis hypersensitivity reactions to medicines; urticaria acute non-infectious oedema of the larynx (the first choice drug is epinephrine). ; ophthalmologic diseases Severe acute and chronic allergic and inflammatory processes in the eye area, in particular: full-time form of Herpes zoster; iritis, iridocyclitis; chorioretinitis, diffuse posterior uveitis and choroidal; optic neuritis; sympathetic ophthalmia; inflammation of the middle segment of the eye; allergic conjunctivitis; allergic corneal ulcer keratitis. ; Diseases of the gastrointestinal tract Critical periods in the following diseases: ulcerative colitis (systemic therapy); regional enteritis (systemic therapy). ; respiratory disease Sarcoidosis of the lungs. Berylliosis. Fulminant or disseminated tuberculosis of the lungs, while the use of appropriate anti-TB chemotherapy. Leffler syndrome, not treatable by other means. Aspiration pneumonitis. Medium to severe pneumonia caused by Pneumocystis carinii in AIDS Patients (as an adjuvant therapy during the first 72 hours of Pro-Pneumocystis therapy). Exacerbation of chronic obstructive pulmonary disease. ; State, accompanied by edema To induce diuresis or remission of proteinuria in nephrotic syndrome, proteinuria and without uremia. immunosuppressive treatment ; organ transplantation Treatment of hematological and oncological diseases ; haematological diseases Acquired (autoimmune) hemolytic anemia. Idiopathic thrombocytopenic purpura in adults (intravenous only; intramuscular use is contraindicated). Secondary thrombocytopenia adults. Erythroblastopenia (erythrocytic anemia). Congenital (erythroid) hypoplastic anemia. ; oncological disease Palliative care for diseases such as: leukemia and lymphoma in adults; acute leukemia in children to improve the quality of life of patients with terminal stage of cancer. other nervous system Brain edema caused by primary or metastatic tumor, and/or adjuvant treatment with surgery or radiotherapy. Exacerbation of multiple sclerosis. Acute spinal cord injury. Treatment should begin at the first 8:00 after injury. Tuberculous meningitis with subarachnoid space siege or threat of siege, while the use of appropriate anti-TB chemotherapy. Trichinellosis with damage to the nervous system or myocardium. Prevention of nausea and vomiting associated with chemotherapy for malignant neoplasm. endocrine disorders Primary or secondary adrenal cortex insufficiency. Acute adrenal cortex insufficiency. In these indications, the drugs of choice are hydrocortisone or cortisone.

Under certain circumstances it is possible to apply synthetic analogs in combination with a mineralocorticoid. Treatment of shock conditions: shock due to adrenal cortex insufficiency or shock, which does not correspond to traditional treatment, in the case of confirmed or suspected adrenal cortex insufficiency (total drug of choice is hydrocortisone). If the mineralocorticoid effects are undesirable, methylprednisolone may take precedence. Before surgery and in case of severe injury or disease in patients with established adrenal insufficiency or in case of doubt in the adrenal cortex reserve. Congenital adrenal hyperplasia. Purulent thyroiditis. Hypercalcemia associated with malignant neoplasm. Contraindications Methylprednisolone succinate is contraindicated: patients with systemic fungal infections; patients with hypersensitivity to methylprednisolone or any component of this drug; for use by intratecal administration; for use by epidural administration. The introduction of live or live Atanasova vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. The conspicuity of contraindications. Special risk groups. Patients who belong to the following special risk groups, careful medical supervision and treatment they should receive for a short period (see Also "precautions" and "Adverse reactions"): children, patients with diabetes, hypertension , psychiatric symptoms a history of individual infectious diseases, in particular tuberculosis or certain viral diseases such as herpes or herpes zoster, accompanied by symptoms in the eye area. Interaction with other medicinal products and other forms of interaction. Methylprednisolone is a substrate of cytochrome P450 enzymes (CYP), which is mainly metabolized by the enzyme CYP3A4. CYP3A4 is the main enzyme common to the subfamily of CYP enzymes in the liver of an adult. It catalyzes 6?-hydroxylation of steroids is an essential stage of the metabolism phase of endogenous and synthetic corticosteroids. Many other compounds are also substrates of the CYP3A4 enzyme, for some of them (as for other drugs) it has been shown that they can affect the metabolism of glucocorticoids by inducing (increasing regulation) or inhibiting the CYP3A4 enzyme. INHIBITORS OF CYP3A4. Drugs that inhibit CYP3A4 activity, usually reduces hepatic clearance and increase plasma concentrations of drugs - substrates of the enzyme CYP3A4 such as methylprednisolone. In the presence of CYP3A4 inhibitor, dose titration of methylprednisolone may be required to avoid the development of GCS toxicity. CYP3A4 inducer. Drugs that induce CYP3A4 activity usually increase hepatic clearance, which leads to a decrease in the plasma concentration of drugs that are substrates . Simultaneous use may require an increase in the dose of methylprednisolone to achieve the desired result. In the presence of another CYP3A4 substrate, the hepatic clearance of methylprednisolone may vary, which requires an appropriate adjustment of the dose. It is likely that adverse reactions associated with the use of each drug separately, may occur more often in their joint application. The effect is NOT due to CYP3A4. Other interactions and effects arising from the use of methylprednisolone are described in table 1 below. Table 1 provides a list and description of common and/or clinically significant interactions between drugs or the effects that are observed in the application of methylprednisolone. Table 1. Class or type of medicinal product/drug or substance Interaction/type of interaction antibacterial isoniazidresistant CYP3A4 (methylprednisolone has the potential to increase the acetylation rate and clearance of isoniazid).

Antibiotics, TB drugs rifampicinum CYP3A4 Anticoagulants (oral) The effect of methylprednisolone oral anticoagulants is variable. It is reported to increase, as well as the weakening of anticoagulants in the joint application with corticosteroids. Therefore, it is necessary to monitor blood clotting to maintain the desired effect of anticoagulants. anticonvulsant CARBAMAZEPINUM CYP3A4 (SUBSTRATE and) anticonvulsant phenobarbital phenytoin CYP3A4 inducer anticholinergics BLOCKERS neuromuscular predicitability can influence the effect of anticholinergics: with the simultaneous use of high doses of corticosteroids and anticholinergics, such as neuromuscular transmission blockers, it was reported the development of acute myopathy (see section " Features of application, the impact on the musculoskeletal system»); patients receiving corticosteroids, have reported antagonism of the action pankuronia and vecuronium in the blockade of neuromuscular transmission. This interaction can be expected in the application of all competitive blockers neuromuscular transmission. anticholinesterase redstarcosplay can weaken the effect of the anticholinesterase means in myasthenia gravis. crestapol antidiabetics corticosteroids may increase the concentration of glucose in the blood, may require dose adjustment of antidiabetic agents. antiemetic agents Aprepitant FOSAPREPITANT CYP3A4 antifungal agent itraconazole ketoconazole  antiviral agents INHIBITORS HIV proteaseinhibitor CYP3A4 (and SUBSTRATES) Protease inhibitors such as indinavir and ritonavir, may increase plasma concentrations of corticosteroids. Corticosteroids can induce the metabolism of HIV protease inhibitors, leading to a decrease in plasma concentrations. aromatase inhibitor aminoglutethimide adrenal induced by aminoglutethimide, may exacerbate endocrine changes caused by prolonged glucocorticoid treatment. Calcium channel CYP3A4 INHIBITOR (and SUBSTRATE) Contraceptives (oral) ethinyl estradiol/ norethindrone CYP3A4 INHIBITOR (and SUBSTRATE) grapefruit CYP3A4 caringinfo immunosuppressants cyclosporineinduced CYP3A4 (SUBSTRATE and)

With the simultaneous use of cyclosporine and methylprednisolone, mutual suppression of metabolism is observed, can increase the plasma concentrations of one or both drugs. Therefore, it is likely that adverse reactions associated with the use of each drug separately, may occur more often in their joint application. With simultaneous use of methylprednisolone and cyclosporine seizures were recorded. immunosuppressants  high-dose ASPIRIN (Acetylsalicylic acid)With the use of corticosteroids with NSAIDs may increase the incidence of gastrointestinal bleeding and ulcers. Methylprednisolone can increase clearance of high-dose aspirin, which can lead to a decrease in serum salicylate levels. Discontinuation of treatment with methylprednisolone may result in increased serum salicylate levels, which may increase the risk of salicylate toxicity. Means that output calisle corticosteroids are applied simultaneously with the means that remove potassium (e.g., diuretics), patients should be carefully observed for the development of hypokalemia. There is also an increased risk of hypokalemia with simultaneous use of corticosteroids with amphotericin B, Xanthen or beta2 agonists. The main cases of incompatibility In order to avoid compatibility and stability problems, methylprednisolone succinate is recommended to be administered separately from other intravenously administered compounds. To drugs that are characterized by physical incompatibility with methylprednisolone succinate in solution , calcium gluconate, vecuronium bromide, rocuronium bromide, cisatracurium besylate, glycopyrrolate are, propofol. Interaction with positive results. Prevention of nausea and vomiting associated with chemotherapy for malignant neoplasm. Chemotherapy, which causes mild or moderate emetogenic effect. To enhance the effect with the first dose of methylprednisolone chlorinated can be used phenothiazine (an hour before chemotherapy). Chemotherapy, which causes a pronounced emetogenic effect. To enhance the effect with the first dose of methylprednisolone can be used metoclopramide or butyrophenone (an hour before chemotherapy). Treatment with methylprednisolone of fulminant or disseminated pulmonary tuberculosis and tuberculosis meningitis with blockage of subarachnoid space or threat of blockade is carried out simultaneously with the use of appropriate anti-tuberculosis chemotherapy. Treatment with methylprednisolone neoplastic diseases, such as leukemia and lymphoma, is usually carried out in combination with alkylating agent, antimetabolite and barvinka alkaloid. Application features Immunosuppressive effects/increased susceptibility to infections GCS can increase susceptibility to infections, may mask some signs of infection, and their use may result in new infections. When using corticosteroids, the body's resistance and its ability to localize the infection may decrease. The use of corticosteroids in the form of monotherapy or in combination with other immunosuppressive agents that affect cellular, humoral immunity or neutrophil function can be accompanied by the development of infections caused by any pathogen, in particular viruses, bacteria, fungi, protozoa and helminths, in any part of the body. These infections may be mild but can be severe and sometimes fatal. With increasing doses of corticosteroids, the incidence of infectious complications increases. People taking medicines that suppress the immune system are more susceptible to infections than healthy individuals. For example, chickenpox and measles can have a more severe and even lead to death in non-immune children or adults who use corticosteroids. The introduction of live or live Atanasova vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines can be administered to patients who receive immunosuppressive doses of corticosteroids; however, the response to such vaccines may be reduced. These procedures immunization can be performed in patients who receive reimmunoprecipitation doses of corticosteroids. The use of corticosteroids in active tuberculosis should be limited to cases of fulminant or disseminated tuberculosis, in which corticosteroids are used to treat the disease in combination with the appropriate regimen of TB therapy. If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity for a, should be closely monitored, as it can occur reactivation of the disease. During long-term therapy with corticosteroids, these patients should receive chemoprophylaxis. In patients receiving corticosteroid therapy, was observed for Kaposi's sarcoma. Discontinuation of treatment with corticosteroids can lead to clinical remission. There is no consensus on the role of corticosteroids in the treatment of patients with septic shock. Early studies have reported both positive and negative effects of corticosteroids in this clinical setting.

The results of later studies showed that corticosteroids as an additional therapy had a beneficial effect in patients with septic shock, in which adrenal insufficiency was noted. However, patients with septic shock use of these drugs in the planned order is not recommended. As a result of a systematic review of data after short courses of high doses of corticosteroids, such patients were concluded that there was no evidence in favor of such use of these drugs. However, according to meta-analysis and one review it was shown that longer (5-11 days) courses of treatment with corticosteroids in low doses can cause a decrease in mortality, especially in patients with septic shock, dependent on vasopressor therapy. The effect on the immune system Allergic reactions may occur. Since skin reactions and anaphylactic/anaphylactoid reactions were rarely recorded in patients receiving corticosteroid therapy, appropriate measures should be taken before use, especially if the patient has a history of allergies to any drug. Effect on endocrine system Patients treated with corticosteroids and exposed to stress are shown to increase the dose of fast-acting corticosteroids before, during and after a stressful situation. Prolonged use of corticosteroids in pharmacological doses can lead to depression hypothalamic-pituitary-adrenal (HGA) system (secondary adrenal cortex insufficiency). The degree and duration of caused adrenal cortex insufficiency vary in patients and depend on the dose, frequency, time of use and duration of therapy GCS. This effect can be minimized through the use of alternating therapy. In addition, in the case of a sudden discontinuation of glucocorticoids can develop acute adrenal insufficiency, which leads to death. The development of secondary adrenal cortex insufficiency induced by the drug can be minimized by a gradual dose reduction.

This type of relative insufficiency can be observed within months after withdrawal of therapy; therefore, in the event of a stressful situation during this period, hormonal therapy must be restored. Since the secretion of mineralocorticoids may be disturbed, salt and/or mineralocorticoid should be used simultaneously. After a sudden discontinuation of glucocorticoids can also develop "withdrawal syndrome" corticosteroids, which, at first glance, is not associated with the insufficiency of the adrenal cortex. This syndrome includes the following symptoms: anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, skin peeling, myalgia, weight loss and/or arterial hypotension. It is believed that these effects are the result of sudden changes in the concentration of glucocorticoids, rather than low levels of corticosteroids. Because corticosteroids can cause or aggravate Cushing's syndrome, patients with Cushing's disease should avoid the use of glucocorticoids. In patients with hypothyroidism, the effect of corticosteroids increases. Metabolism, metabolism Corticosteroids, in particular methylprednisolone, can increase blood glucose levels, worsen the course of existing diabetes mellitus and promote the development of diabetes in patients receiving long-term therapy with GCS. mental disorder With the use of corticosteroids, may experience a mental disorder from euphoria, insomnia, mood swings, personality changes and severe depression to overt manifestations of psychosis.

Also, the use of corticosteroids can exacerbate existing emotional instability or a tendency to develop psychosis. When using systemic corticosteroids may develop a potentially severe psychiatric adverse reactions. Usually, symptoms appear within a few days or weeks from the start of treatment. Most reactions disappear after dose reduction or discontinuation of treatment, although specific treatment may be needed. The development of mental disorders after the withdrawal of corticosteroids has been reported; their frequency is unknown. Patients/care givers of the patient should be informed about the need to seek medical help if the patient has the mental symptoms, especially if you suspect a depressive mood or suicidal thinking. Patients/care givers of the patient should be warned about possible mental disorders that may occur during or immediately after gradual dose reduction/cancellation of systemic corticosteroids. Effect on the nervous system Corticosteroids should be used with caution in patients with convulsions. Corticosteroids should be used with caution in patients with gravis myasthenia gravis (see information about myopathy in the section "Influence on the musculoskeletal system"). Although controlled clinical studies have shown the efficacy of corticosteroids in reducing severe symptoms of multiple sclerosis exacerbations, they have not demonstrated the effect of corticosteroids on the end result or the natural course of the disease. According to the results of these studies, relatively high doses of corticosteroids should be used to demonstrate a significant effect. The use of the drug intratecal/epidural route was associated with the development of severe medical reactions (see section "Adverse reactions"). It was reported that the development of epidural lipomatosis in patients taking GCS, usually with prolonged use in high doses. Effects on the eyes Corticosteroids should be used with caution in patients with an internal form of herpes simplex due to the possibility of corneal perforation. Prolonged use of corticosteroids can cause the development of posterior subcapsular cataract and nuclear cataract (in particular in children), exophthalmos or increased intraocular pressure, which can lead to the development of glaucoma with possible damage to the optic nerves. In patients who receive glucocorticoids, may also accelerate the development of secondary fungal and viral infections of the eye.

The use of corticosteroids is associated with the development of Central serous homeopatie, which can lead to retinal detachment. Influence on the heart Undesirable effects of glucocorticoids on the cardiovascular system, as the development of dyslipidemia and hypertension in patients with pre-existing risk factors for complications from the cardiovascular system may increase the risk of additional cardiovascular effects, if used GCS in high doses and long courses. Accordingly, corticosteroids should be used wisely in such patients, as well as attention to risk modification and, if necessary, additional monitoring of cardiac activity. The use of low doses and alternating therapy can reduce the incidence of complications of corticosteroids. Systemic corticosteroids should be used with caution in congestive heart failure, and only when necessary. Effect on blood vessels Corticosteroids should be used with caution in patients with hypertension. The effect on the gastrointestinal tract There is no evidence that corticosteroids in themselves are the cause of peptic ulcers developing in therapy; however, GCS therapy can mask the symptoms of peptic ulcer disease in such a way that perforation or bleeding can occur in the absence of significant pain. In combination with NSAIDs the risk of developing gastrointestinal ulcers is increased. Corticosteroids should be used with caution by patients with ulcerative colitis, if there is a risk of perforation, abscess or other pyogenic infection, diverticulitis, recent intestinal anastomoses, active or latent peptic ulcers.

Effect on the hepatobiliary system High doses of corticosteroids can cause the development of acute pancreatitis. Influence on musculoskeletal system With the use of high doses of corticosteroids reported the development of acute myopathy, most often in patients with disorders of neuromuscular transmission (e.g. myasthenia gravis) or in patients receiving concomitant therapy with anticholinergic agents such as drugs that block neuromuscular transmission (e.g. pancuronium). This acute myopathy is generalized, may involve ocular and respiratory muscles and can lead to quadriparesis. May increase the level of CPK. Before the onset of clinical improvement or recovery after corticosteroid withdrawal can take place from a few weeks to several years. Osteoporosis is a frequent adverse reaction associated with prolonged use of high doses of corticosteroids, which, however, is rarely recognized. From the urinary system Corticosteroids should be used with caution in patients with renal insufficiency. research Medium and high doses of hydrocortisone or cortisone can cause an increase in blood pressure, salt and water retention in the body and increase potassium excretion. When using synthetic derivatives, except for high doses, the probability of these effects is less. There may be a need to limit the use of salt and additional potassium. All cortico.

Write a review

Note: HTML is not translated!
    Bad           Good

Recently viewed © 2019