What is Depo-Medrol used for?

INTRAMUSCULAR ADMINISTRATION When oral therapy is not feasible, intramuscular administration of DEPO-MEDROL is indicated in the following conditions: Endocrine disorders Primary or secondary adrenocortical insufficiency Note: hydrocortisone or cortisone is the drug of choice; synthetic analogues may be used in conjunction with mineralocorticoids where appropriate, and mineralocorticoid supplementation is essential in infants. Acute adrenocortical insufficiency Note: hydrocortisone or cortisone i

What pharmaceutical form is Depo-Medrol available in?

Depo-Medrol: Zawiesina do wstrzykiwań 40 mg/ml

What are the side effects of Depo-Medrol?

Adverse reactions are listed in the table below, organised by system organ class and frequency. Frequencies are defined as: very common (≥ 1/10), common (≥ 1/100 to < 1/10), uncommon (≥ 1/1,000 to < 1/100), rare (≥ 1/10,000 to < 1/1,000), very rare (< 1/10,000), and not known (cannot be estimated from the available data). The following adverse reactions have been reported with the following contraindicated routes of administration: intrathecal/epidural — arachnoiditis, functional gastrointestina

Who should NOT take Depo-Medrol?

Methylprednisolone acetate is contraindicated: in patients with systemic fungal infections, in patients with known hypersensitivity to methylprednisolone or to any of the excipients listed in section 6.1, for intrathecal administration, for intravenous administration, for epidural administration. Vaccination with live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.

Can Depo-Medrol be used during pregnancy?

Fertility Animal studies have shown that corticosteroids adversely affect fertility (see section 5.3 Preclinical safety data). However, the data from these studies are inadequate. Pregnancy Some animal studies have shown that corticosteroids administered during pregnancy may cause foetal malformation. Although the administration of corticosteroids to pregnant women does not appear to give rise to congenital abnormalities, the results of studies in pregnant women do not entirely exclude the possi

What ATC class does Depo-Medrol belong to?

Depo-Medrol: ATC H02AB04. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Depo-Medrol

This information is for educational purposes only. It is not intended as medical advice. Always consult a qualified healthcare professional.

Depo-Medrol — Description, Dosage, Side Effects | PillsCard

Methylprednisolone is a potent anti-inflammatory steroid. It exhibits greater anti-inflammatory activity than prednisolone and a lesser tendency to retain sodium and water. In general, methylprednisolone acetate shares the glucocorticoid properties of methylprednisolone, but it is less soluble and more slowly biotransformed, which accounts for its prolonged duration of action. Glucocorticoids diffuse across cell membranes and form complexes with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of mRNA and subsequent synthesis of various enzymatic proteins, which are thought to underlie the many effects observed following systemic administration. Glucocorticoids exert profound effects on inflammatory and immune processes and also influence carbohydrate, protein, and lipid metabolism. They likewise act on the cardiovascular system, skeletal muscle, and the central nervous system. Effects on inflammatory and immune processes: Most therapeutic applications are based on the anti-inflammatory, immunosuppressive, and antiallergic properties of glucocorticoids. These properties produce the following effects: reduced numbers of immunoactive cells in the vicinity of the inflammatory focus, diminished vasodilation, stabilisation of lysosomal membranes, inhibition of phagocytosis, decreased production of prostaglandins and related substances. A dose of 4.4 mg of methylprednisolone acetate (4 mg of methylprednisolone) produces the same glucocorticoid (anti-inflammatory) effect as 20 mg of hydrocortisone. Methylprednisolone has only minimal mineralocorticoid activity (200 mg of methylprednisolone is equivalent to 1 mg of deoxycorticosterone). Effects on carbohydrate and protein metabolism: Glucocorticoids exert a catabolic effect on protein. The released amino acids are converted in the liver, via gluconeogenesis, to glucose and glycogen. Peripheral tissue uptake of glucose is reduced, which can result in hyperglycaemia and glucosuria, particularly in patients predisposed to diabetes. Effects on lipid metabolism: Glucocorticoids exert a lipolytic effect, which is most pronounced in the limbs. They also have a lipogenic effect, most evident in the chest, neck, and head. The net result is a redistribution of body fat. The peak pharmacological activity of glucocorticoids lags behind peak blood levels, indicating that most of the drug's effects result from modification of enzymatic activity rather than from a direct action of the drug itself.

⚠️ Warnings

MGPC formulation (myristyl-gamma-picolinium chloride) This product is intended for single use only. Any unused suspension remaining after the required dose has been administered must be discarded. Although crystals of adrenocortical steroids in the skin suppress inflammatory reactions, their presence may lead to disintegration of cellular elements and to physicochemical changes in the underlying connective tissue. The occasional resulting dermal and/or subdermal changes may produce depressions in the skin at the injection site. The extent of this reaction varies with the amount of adrenocortical steroid injected. Complete regeneration usually occurs within several months or once all crystals of the adrenocortical steroid have been absorbed. To minimise the incidence of cutaneous and subcutaneous atrophy, care must be taken not to exceed the recommended injection doses. Whenever feasible, multiple small injections into the lesion should be made. The technique of intrasynovial and intramuscular injection also calls for caution to avoid injection into or leakage of the suspension into the skin. Because of the high incidence of subcutaneous atrophy, injection into the deltoid muscle must be avoided. DEPO-MEDROL must not be administered by any route other than those listed in section 4.1. It is essential to use the correct injection technique for DEPO-MEDROL in order for the drug to act properly in the body. Serious adverse events have been reported in association with the intrathecal/epidural route of administration (see section 4.8 Undesirable effects). Appropriate steps must be taken to avoid intravascular injection. Special warnings and precautions Intrasynovial injection of a corticosteroid may produce systemic as well as local effects. To rule out an infectious process, examination of any synovial fluid for the presence of organisms is necessary. Marked joint pain accompanied by swelling, restricted motion, fever, and malaise is suggestive of septic arthritis. If these symptoms persist and the diagnosis of sepsis is confirmed, appropriate antibiotic therapy should be instituted. Local injection of a steroid into an infected joint is to be avoided, as is injection of a steroid into an unstable joint. Strict aseptic technique must be used to prevent contamination. It should be borne in mind that the active substance is absorbed more slowly after intramuscular administration. Immunosuppressive effects/increased susceptibility to infections Corticosteroids may increase susceptibility to infection, may mask some signs of infection, may exacerbate existing infections, may increase the risk of reactivation or exacerbation of latent infections, and new infections may appear during their use. Reduced resistance and impaired ability to localise infection may be observed during corticosteroid therapy. Patients treated with corticosteroids alone or in combination with other immunosuppressants that affect cellular or humoral immunity or neutrophil function may develop viral, bacterial, fungal, or parasitic infections in any anatomical site. These infections may be mild, but they may also be severe and at times fatal. The rate of infectious complications increases with increasing corticosteroid doses. Monitor for development of infection, and consider corticosteroid withdrawal or dose reduction as appropriate. For local effect in acute infection, administration into the synovia, bursae, or tendons is not recommended. Persons receiving drugs that suppress the immune system are more susceptible to infections than healthy individuals. For example, chickenpox and measles can have a more serious or even fatal course in immunocompromised children or in adults taking corticosteroids. Administration of live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to such vaccines may be diminished. Indicated immunisation procedures may be undertaken in patients receiving non-immunosuppressive doses of corticosteroids. The use of corticosteroids in active tuberculosis should be restricted to cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for management of the disease in conjunction with an appropriate antituberculous regimen. If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged corticosteroid therapy these patients should receive chemoprophylaxis. Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy. Discontinuation of corticosteroids may result in clinical remission. The role of corticosteroids in septic shock has been controversial, with early studies reporting both beneficial and harmful effects. More recently, supplemental corticosteroids have been suggested to be beneficial in patients with persistent septic shock who have evidence of adrenal insufficiency. However, their routine use in septic shock is not recommended. A systematic review of short-course, high-dose corticosteroids did not support their use. However, meta-analyses and reviews suggest that longer courses (5–11 days) of low-dose corticosteroids may reduce mortality, especially in patients with vasopressor-dependent septic shock. Effects on the immune system Allergic reactions may occur. Because rare instances of skin reactions and anaphylactic/anaphylactoid reactions have been reported in patients receiving corticosteroid therapy, appropriate precautions should be taken prior to administration, especially when the patient has a history of allergy to any drug. Effects on the endocrine system In patients receiving corticosteroid therapy and exposed to unusual stress, increased doses of rapidly acting corticosteroids are indicated before, during, and after the stressful situation. Pharmacological doses of corticosteroids administered for prolonged periods may result in suppression of the hypothalamic–pituitary–adrenal (HPA) axis (secondary adrenocortical insufficiency). The degree and duration of the resulting adrenocortical insufficiency vary among patients and depend on the dose, frequency, time of administration, and duration of glucocorticoid therapy. This effect may be minimised by alternate-day dosing. Abrupt withdrawal of glucocorticoids may precipitate acute adrenal insufficiency, which can be fatal. Drug-induced secondary adrenocortical insufficiency may therefore be minimised by gradual dose reduction. This type of relative insufficiency may persist for months after cessation of therapy; therefore, in any stressful situation occurring during this period, hormone therapy should be reinstituted. A steroid "withdrawal syndrome", probably unrelated to adrenocortical insufficiency, may occur following abrupt discontinuation of corticosteroids. This syndrome includes symptoms such as anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, desquamation, myalgia, weight loss, and/or hypotension. These effects are thought to result from the sudden change in glucocorticoid concentration rather than from low concentrations. Because glucocorticoids may worsen the condition of patients with Cushing's syndrome, their administration to such patients is not recommended. The effect of corticosteroids is enhanced in patients with hypothyroidism. Metabolism and nutrition disorders Corticosteroids, including methylprednisolone, may raise blood glucose, worsen pre-existing diabetes mellitus, and predispose patients on long-term corticosteroid therapy to the development of diabetes mellitus. Psychiatric effects A range of psychiatric disturbances may occur during corticosteroid therapy, including euphoria, insomnia, mood swings, personality changes, and severe depression and frank psychotic manifestations. Pre-existing emotional instability or psychotic tendencies may also be aggravated. Potentially serious psychiatric adverse effects may occur with systemic steroids. Symptoms typically emerge within a few days or weeks of starting treatment. Most reactions resolve after either dose reduction or withdrawal, although specific treatment may be necessary. Psychological effects have been reported on corticosteroid withdrawal; the frequency is unknown. Patients/caregivers should be advised to seek medical attention if psychological symptoms develop, particularly if depressed mood or suicidal ideation is suspected. Patients/caregivers should be alert to possible psychiatric disturbances that may occur either during or immediately after tapering/withdrawal of systemic steroids. Effects on the nervous system Corticosteroids should be used with caution in patients with seizure disorders. Corticosteroids should be used with caution in patients with myasthenia gravis. (See also myopathy under Musculoskeletal effects.) Cases of epidural lipomatosis have been reported in patients taking corticosteroids, typically with long-term use at high doses. Effects on the eyes Visual disturbances may be reported with systemic and topical corticosteroid use. If a patient presents with symptoms such as blurred vision or other visual disturbances, the patient should be considered for referral to an ophthalmologist for evaluation of possible causes, which may include cataract, glaucoma, or rare diseases such as central serous chorioretinopathy (CSCR), which has been reported after the use of systemic and topical corticosteroids. Central serous chorioretinopathy may lead to retinal detachment. Long-term use of corticosteroids may cause posterior subcapsular cataracts and nuclear cataracts (particularly in children), exophthalmos, or increased intraocular pressure, which may result in glaucoma with possible damage to the optic nerve. The development of secondary fungal and viral infections of the eye may also be increased in patients receiving glucocorticoids. Corticosteroids should be used with caution in patients with ocular herpes simplex infection because of the risk of corneal perforation. Effects on the cardiovascular system Adverse effects of glucocorticoids on the cardiovascular system, such as dyslipidaemia and hypertension, may further predispose treated patients with existing cardiovascular risk factors to additional cardiovascular events if high doses are given over prolonged periods. Accordingly, corticosteroids should be used judiciously in such patients, and attention should be paid to risk modification and to additional cardiac monitoring as required. Systemic corticosteroids should be used with caution, and only when strictly necessary, in patients with congestive heart failure. Effects on the vascular system Thrombosis, including venous thromboembolism, has been reported with corticosteroid use. As a result, corticosteroids should be used with caution in patients who have or may be predisposed to thromboembolic disorders. Corticosteroids should be used with caution in patients with hypertension. Effects on the gastrointestinal system High doses of corticosteroids may induce acute pancreatitis. There is no universal agreement as to whether corticosteroids per se are responsible for gastric ulcers encountered during therapy. Glucocorticoid therapy may mask the symptoms of a gastric ulcer, so that perforation or haemorrhage may occur without significant pain. Glucocorticoid therapy may mask peritonitis or other signs and symptoms associated with gastrointestinal disorders such as perforation, obstruction, or pancreatitis. In combination with non-steroidal anti-inflammatory drugs (NSAIDs), there is an increased risk of developing gastrointestinal ulcers. In patients with non-specific ulcerative colitis, corticosteroids should be used with caution if there is the probability of impending perforation, abscess, or other pyogenic infection; corticosteroids should likewise be used with caution in patients with diverticulitis, fresh intestinal anastomoses, or active or latent peptic ulcer. Hepatobiliary effects Hepatobiliary disorders have been reported, which in most cases were reversible on discontinuation of therapy. Appropriate monitoring is therefore required. Effects on the musculoskeletal system Acute myopathy has been reported with the use of high doses of corticosteroids, most often in patients with disorders of neuromuscular transmission (e.g. myasthenia gravis) or in patients concomitantly receiving anticholinergic therapy such as neuromuscular blocking agents (e.g. pancuronium). This acute myopathy is generalised, may involve ocular and respiratory muscles, and may result in quadriparesis. Elevation of creatine kinase may occur. Following discontinuation of corticosteroids, clinical improvement and recovery may take weeks to months. Osteoporosis is a common but infrequently recognised adverse effect associated with long-term high-dose glucocorticoid therapy. Effects on the liver and biliary tract Drug-induced liver injury, including acute hepatitis or elevated liver enzymes, may result from cyclic pulse intravenous administration of methylprednisolone (usually at an initial dose ≥ 1 g/day). Rare cases of hepatotoxicity have been reported. The time to onset may be several weeks or longer. In most reported cases, the adverse reactions resolved after treatment was withdrawn. Patients should therefore be monitored appropriately. Renal and urinary disorders Caution is required in patients with systemic sclerosis because of an increased incidence of scleroderma renal crisis observed with corticosteroids, including methylprednisolone. Corticosteroids should be used with caution in patients with renal insufficiency. No dose adjustment is required in renal failure. Methylprednisolone is dialysable. Investigations Moderate to high doses of hydrocortisone or cortisone may cause elevation of blood pressure, sodium and water retention, and increased excretion of potassium. These effects are less likely to occur with synthetic derivatives of glucocorticoids except when used at high doses. Dietary salt restriction and potassium supplementation may be necessary in patients so treated. All corticosteroids increase calcium excretion. Injury, poisoning, and procedural complications Systemic corticosteroids are not indicated for and should not be used routinely for the treatment of traumatic brain injury. Results from a multicentre study demonstrated increased mortality at 2 weeks and 6 months after injury in patients given methylprednisolone sodium succinate compared with placebo. A causal relationship with methylprednisolone sodium succinate therapy has not been established. Other Because complications of glucocorticoid therapy depend on the dose and duration of treatment, a risk/benefit assessment must be made in each individual case as to dose and duration of treatment and whether daily or intermittent therapy should be used. Concomitant treatment with CYP3A inhibitors, including products containing cobicistat, is expected to increase the risk of systemic adverse effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid adverse effects, in which case patients should be monitored for systemic corticosteroid adverse effects (see section 4.5). Acetylsalicylic acid and non-steroidal anti-inflammatory drugs should be used cautiously in conjunction with corticosteroids. Concomitant use of oral anticoagulants and methylprednisolone may increase the risk of bleeding. Decreased effects of oral anticoagulants have also been reported. Frequent monitoring of prothrombin time (INR) is recommended in patients receiving vitamin K antagonists, particularly when initiating or adjusting methylprednisolone therapy (see section 4.5). Phaeochromocytoma crisis, which can be fatal, has been reported following the administration of systemic corticosteroids. Corticosteroids should only be administered to patients with suspected or identified phaeochromocytoma after an appropriate benefit/risk evaluation. Tumour lysis syndrome (TLS) has been reported in the postmarketing setting in patients with malignancies, including haematological malignancies and solid tumours, following the use of systemic corticosteroids alone or in combination with other chemotherapeutic agents. Patients at high risk of TLS — for example, those with malignancies with a high proliferative rate, high tumour burden, and high sensitivity to cytotoxic agents — should be monitored closely and appropriate measures taken. Thyrotoxic periodic paralysis (TPP) may occur in patients with hyperthyroidism and methylprednisolone-induced hypokalaemia. TPP should be suspected in patients receiving methylprednisolone who present with signs or symptoms of muscle weakness, particularly in those with hyperthyroidism. If TPP is suspected, blood potassium levels should be monitored immediately and corrected appropriately to ensure restoration of normal blood potassium levels. Use in children Growth and development of children receiving long-term corticosteroid therapy should be carefully monitored. Growth may be suppressed in children receiving long-term, daily, divided-dose glucocorticoid therapy, and use of such a regimen should be restricted to the most urgent indications. Alternate-day glucocorticoid therapy usually avoids or minimises this adverse effect. Infants and children on prolonged corticosteroid therapy are at increased risk of raised intracranial pressure. High doses of corticosteroids may induce pancreatitis in children. Depo-Medrol contains less than 1 mmol (23 mg) of sodium per millilitre of suspension, that is, essentially "sodium-free".

Depo-Medrol

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