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Methylprednisolone dose for asthma exacerbation


Detailed Methylprednisolone dosage information for adults and children. Includes dosages for Allergic Rhinitis, Osteoarthritis, Asthma - Maintenance and more; plus renal, liver and dialysis adjustments. SOLU-MEDROL Sterile Powder is an anti-inflammatory glucocorticoid, which contains methylprednisolone sodium succinate as the active ingredient. Methylprednisolone sodium succinate, USP, is the sodium succinate ester of methylprednisolone, and it occurs as . The best strategy for management of acute exacerbations of asthma is early recognition and intervention, before attacks become severe and potentially life-threa.
Epidemiology and background. Asthma is a common, chronic inflammatory disorder of the airways associated with airway hyper-responsiveness. Asthma exacerbations are the leading cause of hospitalization in children, and the lifetime prevalence of asthma in Canadian children has been estimated at 11% to 16%.. For this statement, asthma exacerbation is defined as an acute or . A dose of 30 mg/kg IV once a week for 6 weeks, with or without oral maintenance corticosteroid therapy, has been used. Therapy produced immediate improvement in . Methylprednisolone Acetate Injectable Suspension USP is an anti-inflammatory glucocorticoid for intramuscular, intra-articular, soft tissue, or intralesional injection.


Possible side effects of prednisone

Guidelines for the diagnosis and management of asthma. Prospective, placebo-controlled trial of 5 vs 10 days of oral prednisolone in acute adult asthma. Reprints are not available from the authors. Methylprednisolone dose for asthma exacerbation Management: Consider methylprednisolone dose increases in patients receiving strong CYP3A4 inducers and monitor closely for reduced steroid efficacy. Consider therapy modification. CYP3A4 Inhibitors (Strong): May increase the serum concentration of MethylPREDNISolone. Management: Consider methylprednisolone dose reduction in patients receiving strong CYP3A4 inhibitors and monitor for increased steroid related adverse effects.  Pregnant women with poorly controlled asthma or asthma exacerbations may have a greater fetal/maternal risk than what is associated with appropriately used medications. Uncontrolled asthma is associated with an increased risk of perinatal mortality, preeclampsia, preterm birth, and low birth weight infants. Asthma exacerbations can be classified as mild, moderate, severe, or life threatening. Criteria for exacerbation severity are based on symptoms and physical examination parameters, as well as lung function and oxygen saturation.  Multiple doses of inhaled anticholinergic medication combined with beta2 agonists improve lung function and decrease hospitalization in school-age children with severe asthma exacerbations. Intravenous magnesium sulfate has been shown to significantly increase lung function and decrease the necessity of hospitalization in children. The administration of systemic corticosteroids within one hour of emergency department presentation decreases the need for hospitalization, with the most pronounced effect in patients with severe exacerbations. Dosages of drugs for asthma exacerbations (continued). Medication. Child Dose*.  Randomized clinical trial of intramuscular vs oral methylprednisolone in the treatment of asthma exacerbations following discharge from an emergency department. Chest ;(2)–8. Lee DL, Hsu CW, Lee H, Chang HW, Huang YC.

Treatment at these doses should be limited to a 48 - 72 hour period until the patient's condition has stabilised, as prolonged high dose corticosteroid therapy can cause serious corticosteroid induced side effects see Undesirable effects and Special warnings and special precautions for use.

This dosage may be repeated for three pulses either daily or on alternate days. There is no information to suggest that a change in dosage is warranted in the elderly.

However, treatment of elderly patients should be planned bearing in mind the more serious consequences of the common side-effects of corticosteroids in old age and close clinical supervision is required see Special warnings and special precautions for use.

In anaphylactic reactions adrenaline or noradrenaline should be administered first for an immediate haemodynamic effect, followed by intravenous injection of methylprednisolone sodium succinate with other accepted procedures.

There is evidence that corticosteroids through their prolonged haemodynamic effect are of value in preventing recurrent attacks of acute anaphylactic reactions. In sensitivity reactions Methylprednisolone sodium succinate is capable of providing relief within one half to two hours. In patients with status asthmaticus Methylprednisolone sodium succinate may be given at a dose of 40 mg intravenously, repeated as dictated by patient response.

In some asthmatic patients it may be advantageous to administer by slow intravenous drip over a period of hours. In graft rejection reactions following transplantation doses of up to 1 g per day have been used to suppress rejection crises, with doses of mg to 1 g most commonly used for acute rejection. Treatment should be continued only until the patient's condition has stabilised; usually not beyond 48 - 72 hours. In cerebral oedema corticosteroids are used to reduce or prevent the cerebral oedema associated with brain tumours primary or metastatic.

In patients with oedema due to tumour, tapering the dose of corticosteroid appears to be important in order to avoid a rebound increase in intracranial pressure. If brain swelling does occur as the dose is reduced intracranial bleeding having been ruled out , restart larger and more frequent doses parenterally. Patients with certain malignancies may need to remain on oral corticosteroid therapy for months or even life. Similar or higher doses may be helpful to control oedema during radiation therapy.

In the treatment of acute exacerbations of multiple sclerosis in adults, the recommended dose is mg daily for 3 days. In other indications, initial dosage will vary from 10 to mg depending on the clinical problem being treated. Larger doses may be required for short term management of severe, acute conditions. The initial dose, up to mg, should be given intravenously over a period of at least 5 minutes, doses exceeding mg should be given intravenously over a period of at least 30 minutes.

Subsequent doses may be given intravenously or intramuscularly at intervals dictated by the patient's response and clinical condition. Corticosteroid therapy is an adjunct to, and not replacement for, conventional therapy.

Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Corticosteroids may increase susceptibility to infection, may mask some signs of infection, and new infections may appear during their use.

Suppression of the inflammatory response and immune function increases the susceptibility to fungal, viral and bacterial infections and their severity. The clinical presentations may often be atypical and may reach an advanced stage before being recognised. Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals.

Chickenpox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids. Chickenpox is of serious concern since this normally minor illness may be fatal in the immunosuppressed patients.

Patients or parents of children without a definite history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster and if exposed they should seek urgent medical attention. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased. Exposure to measles should be avoided. Medical advice should be sought immediately if exposure occurs.

Prophylaxis with normal intramuscular immuneglobulin may be needed. Similarly, corticosteroids should be used with great care in patients with known or suspected parasitic infections such as Strongyloides threadworm infestation, which may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram- negative septicaemia. Although Methylprednisolone is not approved for use in any shock indication, the following warning statement should be adhered to.

Data from clinical study conducted to establish the efficacy of methylprednisolone in septic shock, suggest that a higher mortality occurred in subsets of patients who entered the study with elevated serum creatinine levels or who developed a secondary infection after therapy began. Therefore this product should not be used in the treatment of septic syndromes or septic shock. The role of corticosteroids in septic shock has been controversial, with early studies reporting both beneficial and detrimental effects.

More recently, supplemental corticosteroids have been suggested to be beneficial in patients with established septic shock who exhibit 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 a review suggest that longer courses days of low-dose corticosteroids might reduce mortality. Live vaccines should not be given to individuals with impaired immune responsiveness. The antibody response to other vaccines may be diminished. The use of corticosteroids in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate anti-tuberculosis 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. Aspirin and nonsteroidal anti-inflammatory agents should be used cautiously in conjunction with corticosteroids.

Allergic reactions may occur. Physicians using the drug should be prepared to deal with such a possibility. Appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of drug allergy. Pharmacological doses of corticosteroids administered for prolonged periods may result in hypothalamic-pituitary-adrenal HPA suppression secondary adrenocortical insufficiency.

The degree and duration of adrenocortical insufficiency produced is variable among patients and depends on the dose, frequency, time of administration, and duration of glucocorticoid therapy. This effect may be minimized by use of an alternate-day therapy. In addition, acute adrenal insufficiency leading to a fatal outcome may occur if glucocorticoids are withdrawn abruptly.

In patients who have received more than physiological doses of systemic corticosteroids approximately 6 mg methylprednisolone for greater than 3 weeks, withdrawal should not be abrupt. Drug-induced secondary adrenocortical insufficiency may therefore be minimised by the gradual reduction of dosage. How dose reduction should be carried out depends largely on whether the disease is likely to relapse as the dose of systemic corticosteroids is reduced.

Clinical assessment of disease activity may be needed during withdrawal. If the disease is unlikely to relapse on withdrawal of systemic corticosteroids, but there is uncertainty about HPA suppression, the dose of systemic corticosteroids may be reduced rapidly to physiological doses.

Once a daily dose of 6 mg methylprednisolone is reached, dose reduction should be slower to allow the HPA-axis to recover. Abrupt withdrawal of systemic corticosteroid treatment, which has continued up to 3 weeks is appropriate if it considered that the disease is unlikely to relapse. Abrupt withdrawal of doses up to 32 mg daily of methylprednisolone for 3 weeks is unlikely to lead to clinically relevant HPA-axis suppression, in the majority of patients. In the following patient groups, gradual withdrawal of systemic corticosteroid therapy should be considered even after courses lasting 3 weeks or less:.

Patients should carry 'Steroid Treatment' cards which can give clear guidance on the precautions to be taken to minimise risk and which provide details of prescriber, drug, dosage and duration of treatment.

This type of relative insufficiency may persist for months after discontinuation of therapy, therefore, in any situations of stress occurring during that period, hormone therapy should be reinstituted. In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting corticosteroid before, during and after stress situation is indicated.

A steroid 'withdrawal syndrome', seemingly unrelated to adrenocortical insufficiency, may also occur following abrupt discontinuance of glucocorticoids. This syndrome includes symptoms such as: These effects are thought to be due to sudden change in glucocorticoid concentration rather than to low corticosteroid levels.

Because glucocorticoids can produce or aggravate Cushing's syndrome, glucocorticoids should be avoided in patients with Cushing's disease. There is an enhanced effect of corticosteroids on patients with hypothyroidism. Frequent patient monitoring is necessary in patients with hypothyroidism. Frequent patient monitoring is necessary in patients with diabetes mellitus or a family history of diabetes.

Corticosteroids including methylprednisolone can increase blood glucose, worsen pre-existing diabetes, and predispose those on long-term corticosteroid therapy to diabetes mellitus. Symptoms typically emerge within a few days or weeks of starting treatment. Most reactions recover after either dose reduction or withdrawal, although specific treatment may be necessary. Particular care is required when considering the use of systemic corticosteroids in patients with existing or previous history of severe affective disorders in themselves or in their first degree relatives.

These would include depressive or manic-depressive illness and previous steroid psychosis. Frequent patient monitoring is necessary in patients with existing or previous history of severe affective disorders especially previous steroid psychosis. Corticosteroids should be used with caution in patients with seizure disorders. Frequent patient monitoring is necessary in patients with epilepsy. Corticosteroids should be used with caution in patients with myasthenia gravis also see myopathy statement in Musculoskeletal Effects section below.

Frequent patient monitoring is necessary in patients with myasthenia gravis. Frequent patient monitoring is necessary in patients with glaucoma or a family history of glaucoma and in patients with ocular herpes simplex, for fear of corneal perforation.

Prolonged use of corticosteroids may produce 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 nerves. Establishment of secondary fungal and viral infections of the eye may also be enhanced in patients receiving glucocorticoids.

Adverse effects of glucocorticoids on the cardiovascular system, such as dyslipidemia and hypertension, may predispose treated patients with existing cardiovascular risk factors to additional cardiovascular effects, if high doses and prolonged courses are used.

Accordingly, corticosteroids should be employed judiciously in such patients and attention should be paid to risk modification and additional cardiac monitoring if needed. Low dose and alternated day therapy may reduce the incidence of complications in corticosteroid therapy.

Bradycardia has been reported during or after the administration of large doses of methylprednisolone sodium succinate, and may be unrelated to the speed and duration of infusion. Systemic corticosteroids should be used with caution, and only if strictly necessary, in cases of congestive heart failure.

Frequent patient monitoring is necessary in patients with congestive heart failure or recent myocardial infarction myocardial rupture has been reported.

Steroids should be used with caution in patients with hypertension. Frequent patient monitoring is necessary. Thrombosis including venous thromboembolism has been reported to occur with corticosteroids. As a result corticosteroids should be used with caution in patients who have or may be predisposed to thromboembolic disorders. There is no universal agreement on whether corticosteroids per se are responsible for peptic ulcers encountered during therapy, however, glucocorticoid therapy may mask the symptoms of peptic ulcer so that perforation or haemorrhage may occur without significant pain.

Particular pain is required when considering the use of systemic corticosteroids in patients with the following conditions and frequent patient monitoring is necessary:. Rare cases of hepatotoxicity have been reported.

The time to onset can be several weeks or longer. In the majority of case reports resolution of the adverse events has been observed after treatment was discontinued. Therefore, appropriate monitoring is required. Particular care is required when considering the use of systemic corticosteroids in patients with myasthenia gravis or osteoporosis post-menopausal females are particularly at risk and frequent patient monitoring is necessary.

Osteoporosis is a common but infrequently recognised adverse effect associated with long-term use of large doses of glucocorticoid.

Particular care is required when considering the use of systemic corticosteroids in patients with renal insufficiency and frequent patient monitoring is necessary. Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt and water retention, and increased excretion of potassium. These effects are less likely to occur with synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary.

All corticosteroids increase calcium excretion. Corticosteroids should not be used for the management of head injury or stroke because it is unlikely to be of benefit and may even be harmful. The lowest possible dose of corticosteroid should be used to control the condition under treatment and when reduction in dosage is possible, the reduction should be gradual. Growth and development of infants and children on prolonged corticosteroid therapy should be carefully observed.

Growth may be suppressed in children receiving long- term, daily divided-dose glucocorticoid therapy and use of such regimen should be restricted to the most urgent indications. Alternate-day glucocorticoid therapy usually avoids or minimizes this side effect. Infants and children on prolonged corticosteroid therapy are at special risk from raised intracranial pressure. The common adverse effects of systemic corticosteroids may be associated with more serious consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility to infection and thinning of the skin.

Caution is recommended with prolonged corticosteroid treatment in the elderly due to a potential increase risk for osteoporosis, as well as increased risk of fluid retention with possible resultant hypertension. Close clinical supervision is required to avoid life-threatening reactions. To be taken into consideration by patients on a controlled sodium diet. Many other compounds are also substrates of CYP3A4, some of which as well as other drugs have been shown to alter glucococorticoid metabolism by induction upregulation or inhibition of the CYP3A4 enzyme.

In the presence of a CYP3A4 inhibitor, the dose of methylprednisolone may need to be titrated to avoid steroid toxicity. Co-treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic side-effects.

The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side-effects, in which case patients should be monitored for systemic corticosteroid effects. Coadministration may require an increase in methylprednisolone dosage to achieve the desired result. It is possible that adverse events associated with the use of either drug alone may be more likely to occur with coadministration.

An increase in the plasma concentration of methylprednisolone may occur. The dose of methylprednisolone may need to be treated to avoid steroid toxicity. In addition, there is a potential effect of methylprednisolone on the acetylation rate and clearance of isoniazid. A decrease in the plasma concentration of methylprednisolone may occur. Co-administration may require an increase in methylprednisolone dosage to achieve the desired result. The hepatic clearance of methylprednisolone may be inhibited or induced, resulting in an increase or decrease in the plasma concentration of methylprednisolone.

A corresponding dosage adjustment may be required. T is possible that adverse events associated with the use of either drug alone may be more likely to occur with administration. Protease inhibitors , such as indinavir and ritonavir, may increase plasma concentration of corticosteroids. Therefore, it is possible that adverse events associated with the use of either drug alone may be more likely to occur upon coadministration.

It is possible that adverse events associated with the use of either drug alone may be more likely to occur with administration. The effect of methylprednisolone on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effects.

Corticosteroids may influence the effect of anticholinergics. This interaction may be expected with all competitive neuromuscular blockers. Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. Aminoglutethimide-induced adrenal suppression may impede endocrine changes caused by prolonged glucocorticoid treatment. This decrease in salicylate serum levels could lead to an increased risk of salicylate toxicity when methylprednisolone is withdrawn.

When corticosteroids are administered concomitantly with potassium depleting agents patients should be observed closely for development of hypokalemia. Corticosteroids antagonise the hypotensive effect of all antihypertensives. There is an increased risk of hypokalaemia when corticosteroids are given with cardiac glycosides. To avoid compatibility and stability problems, it is recommended that methylprednisolone sodium succinate be administered separately from other compounds that are administered via the IV route of administration.

There may be decreased resistance and inability to localise infection when corticosteroids are used. Infections with any pathogen including viral, bacterial, fungal, protozoan or helminthic organisms, in any location in the body, may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect cellular or humoral immunity, or neutrophil function.

These infections may be mild, but can be severe and at times fatal. With increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. Patients or parents of children without a definite history of chickenpox should be advised to avoid close personal contact with chickenpox or herpes zoster and if exposed they should seek urgent medical attention. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment.

Corticosteroids should not be stopped and the dose may need to be increased. Symptoms typically emerge within a few days or weeks of starting treatment.

Most reactions recover after either dose reduction or withdrawal, although specific treatment may be necessary. Particular care is required when considering the use of systemic corticosteroids in patients with existing or previous history of severe affective disorders in themselves or in their first degree relatives.

These would include depressive or manic-depressive illness and previous steroid psychosis. In such children or adults, particular care should be taken to avoid exposure to measles. If exposed, prophylaxis with intramuscular pooled immunoglobulin IVIG may be indicated.

Exposed patients should be advised to seek medical advice without delay. Killed or inactivated vaccines may be administered to patients receiving immunosuppressive doses of corticosteroids; however, the response to such vaccines may be diminished. Indicated immunization procedures may be undertaken in patients receiving non-immunosuppressive doses of corticosteroids.

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.

Bradycardia has been reported during or after the administration of large doses of methylprednisolone sodium succinate, Methylprednisolone and may be unrelated to the speed or duration of infusion. Frequent ophthalmic monitoring is necessary. Secondary fungal and viral infections of the eye may also be enhanced in patients receiving glucocorticoids. The study results revealed an increased mortality in the 2 weeks after injury in patients administered Methylprednisolone compared to placebo 1.

A causal association with methylprednisolone sodium succinate treatment has not been established. Rare cases of hepatotoxicity have been reported. The time to onset can be several weeks or longer. In the majority of case reports resolution of the adverse events has been observed after treatment was discontinued. Therefore, appropriate monitoring is required. Particular care is required when considering the use of systemic corticosteroids in patients with the following conditions and frequent patient monitoring is necessary.

Also existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. As a result corticosteroids should be used with caution in patients who have or may be predisposed to thromboembolic disorders. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis.

Elevations of creatine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years. Discontinuation of corticosteroids may result in clinical remission. Corticosteroids cause growth retardation in infancy, childhood and adolescence, which may be irreversible.

Treatment should be limited to the minimum dosage for the shortest possible time. In order to minimise suppression of the hypothalamo-pituitary-adrenal axis and growth retardation, treatment should be administered where possible as a single dose on alternate days. The common adverse effects of systemic corticosteroids may be associated with more serious consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility to infection and thinning of the skin.

Close clinical supervision is required to avoid life-threatening reactions. Convulsions have been reported with concurrent use of methylprednisolone and ciclosporin.

Since concurrent administration of these agents results in a mutual inhibition of metabolism, it is possible that convulsions and other adverse events associated with the individual use of either drug may be more apt to occur.

Immunosuppressants, as methotrexate, may have synergistic effect on disease state which may allow to reduce dose of corticosteroid. Drugs that induce hepatic enzymes, such as rifampicin, rifabutin, carbamazepine, phenobarbitone, phenytoin, primidone, and aminoglutethimide enhance the metabolism of corticosteroids and its therapeutic effects may be reduced. It may be necessary to increase the Methylprednisolone dose to achieve the desired response. Drugs that inhibit the cytochrome P enzymatic system particularly CYP3A4 , such as erythromycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance.

Therefore, the dose of methylprednisolone should be titrated to avoid steroid toxicity. Steroids may reduce the effects of anticholinesterases in myasthenia gravis. The desired effects of hypoglycaemic agents including insulin , anti-hypertensive and diuretic drugs are antagonised by corticosteroids, and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced. The efficacy of coumarin anticoagulants may be enhanced by concurrent corticosteroid therapy and close monitoring of the INR or prothrombin time is required to avoid spontaneous bleeding.

The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication. Salicylates and non-steroidal anti-inflammatory agents should be used cautiously in conjunction with corticosteroids in hypothrombinaemia. Steroids have been reported to interact with neuromuscular blocking agents such as pancuronium with partial reversal of the neuromuscular block.

Antipsychotics can cause recurrence or poor control of CNS symptoms, when used with methylprednisolone, which may require a dose adjustment. Sympathomimetic agents, as salbutamol, can increase the efficacy and potentially increase toxicity by increased response to sympathetic agents, when used with methylprednisolone.

Animal studies have shown that high corticosteroid doses to pregnant females may cause foetal malformations. However, corticosteroids do not appear to cause congenital malformations when given to pregnant women. Despite this, methylprednisolone sodium succinate should be used during pregnancy in critical cases only as studies in humans cannot establish the safety of the product during use in pregnancy. Some corticosteroids cross the placenta easily.

In a retrospective study, an increased frequency of low birth-weight was observed in children whose mothers had been using corticosteroids. Although adrenal insufficiency is rare in children who have been exposed to corticosteroids in utero, children exposed to high corticosteroid doses should be monitored carefully and examined for the risk of adrenal insufficiency.

Cataract has been observed in neonates whose mothers have received long-term corticosteroid treatment during pregnancy. Corticosteroids excreted in breast milk can suppress the growth of breast-fed infants and disturb endogenous production of glucocorticoids. As reproduction studies with corticosteroids in humans are inadequate, corticoids should be used in lactating mothers only if the benefit from the treatment is assessed greater than the possible risks to the child.

The possible benefits of corticosteroid medication must be weighed against possible adverse effects to the mother and embryo or foetus before giving this medicinal product to pregnant or lactating women, or to women of fertile age. The effect of Methylprednisolone on the ability to drive or use machinery has not been systematically evaluated. Undesirable effects, such as dizziness, vertigo, visual disturbances, and fatigue are possible after treatment with corticosteroids.

If affected, patients should not drive or operate machinery. Under normal circumstances Methylprednisolone therapy would be considered as short term.

However, the possibility of side effects attributable to corticosteroid therapy should be recognised, particularly when high dose therapy is being used see Section 4. Suppression of the hypothalamo-pituitary-adrenal axis, growth suppression in infancy, childhood and adolescence, menstrual irregularity and amenorrhoea. Reactions are common and may occur in both adults and children.

Psychological effects have been reported on withdrawal of corticosteroids. Increased intra-cranial pressure with papilloedema in children pseudotumour cerebri has been reported, usually after treatment withdrawal of methylprednisolone. Seizures, increase of intracranial pressure with oedema of optical papilla [intracranial benign hypertension] , amnesia, cognitive disturbances, dizziness, headache. Nausea, vomiting and bad taste in mouth may occur especially with rapid administration.

These changes are usually small, not associated with any clinical syndrome and are reversible upon discontinuation. Too rapid a reduction of corticosteroid dosage following prolonged treatment can lead to acute adrenal insufficiency, hypotension and death. Reporting suspected adverse reactions after authorisation of the medicinal product is important. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: Reports of acute toxicity and metabolic disturbances with glucocorticoids are rare but do occur.

There is no clinical syndrome of acute overdosage with Methylprednisolone. Acute overdose may possibly aggravate pre-existing disease states such as ulceration of the gastrointestinal tract, electrolyte disturbances, infections, diabetes and oedema. Repeated high doses of methylprednisolone have caused hepatic necrosis and an increase in amylase. Bradyarrhythmias, ventricular arrhythmias and cardiac arrest have been observed in cases of intravenous administration of high doses of methylprednisolone.

Repeated frequent doses daily or several times per week over a protracted period may result in a Cushingoid state. The possibility of adrenal suppression should be guarded against by gradual diminution of dose levels over a period of time. In the event of an overdose, no specific antidote is available; treatment is symptomatic and supportive, including respiratory and cardiovascular function.

In chronic toxicity, fluids and electrolytes should be monitored closely. Serum levels are not clinically useful. Methylprednisolone is a potent anti-inflammatory steroid. It has a greater anti-inflammatory potency than prednisolone and even less tendency than prednisolone to induce sodium and water retention.

Its anti-inflamatory activity is at least five times that of hydrocortisone. Methylprednisolone sodium succinate has the same metabolic and anti-inflammatory actions as methylprednisolone. When given parenterally and in equimolar quantities, the two compounds are equivalent in biologic activity. The relative potency of methylprednisolone sodium succinate and hydrocortisone sodium succinate, as indicated by depression of eosinophil count, following intravenous administration, is at least four to one.

This is in good agreement with the relative oral potency of methylprednisolone and hydrocortisone. An enhanced separation of glucocorticoid and mineralocorticoid effect results in a reduced incidence of sodium and water retention. Methylprednisolone is extensively bound to plasma proteins, mainly to globulin and less so to albumin. Only unbound corticosteroid has pharmacological effects or is metabolised. Metabolism occurs in the liver and to a lesser extent in the kidney. Metabolites are excreted in the urine.

Peak methylprednisolone plasma levels of Although with intramuscular IM injection lower peak levels are obtained than with intravenous IV injection, the plasma levels persist longer such that the extent of methylprednisolone absorption is equivalent with either route of administration. Methylprednisolone is widely distributed throughout the body and is described by a two-compartment model. Its apparent volume of distribution is approximately 1. Methylprednisolone, like many CYP3A4 substrates, may also be a substrate for the ATP-binding cassette ABC transport protein p-glycoprotein, influencing tissue distribution and interactions with other medicines.

Methylprednisolone peak CSF levels occurred within five minutes to one hour after IV administration of a mg dose to patients with lupus cerebritis. Methylprednisolone and its sodium succinate salt cross the placental barrier. Although there is no data regarding methylprednisolone passage into breast milk of humans, it is present in breast milk of animals. Methylprednisolone, the sodium succinate ester of methylprednisolone, is rapidly and extensively hydrolysed in vivo by cholinesterases to free methylprednisolone.

Metabolism in the liver occurs primarily via the CYP3A4. The mean elimination half-life ranges for total methylprednisolone is in the range of 1.

Methylprednisolone clearance is altered by concurrent administration of troleandomycin, erythromycin, rifampin, anti-convulsants, and theophylline. Twenty percent of the total dose was excreted in the bile, but the time course was not cited.

Non-clinical data reveal no unexpected hazards for mice, rats, rabbits and dogs based on conventional studies of safety pharmacology and repeated dose toxicity with intravenous, intraperitoneal, subcutaneous, intramuscular, and peroral administration. Methylprednisolone is a potent steroid the pharmacological effects of which are comparable to those of glucocorticoids, including the effects on carbohydrate metabolism, electrolyte and fluid balance, blood cells, lymphatic tissue and protein metabolism, which can lead to reduction or cessation of weight gain, lymphopenia, and atrophy of the spleen, thymus, lymph nodes, adrenal cortex and testes as well as fatty liver, and hyperplasia of pancreatic islet cells.

A 30 day study on reversibility in rats which had received methylprednisolone showed that the vital functions returned to normal after about 1 month from discontinuing the drug. Following a week-long administration of methylprednisolone suleptanate to rats, many parameters returned to normal after a 9 week period of reversibility.

Toxicities detected in studies with repeated dosage are those that can be expected after continuous exposure to exogenous adrenocortical steroids.

No long-term studies in animals have been done to assess carcinogenicity as the drug substance is meant for short-term use only, and no signs of a carcinogenic effect have been detected.

There is no evidence of carcinogenicity of corticosteroids. In DNA damage determination by the alkaline elution technique in V79 cells of the Chinese hamster, no evidence on genetic or chromosomal mutations was obtained. Methylprednisolone did not cause chromosomal damage without the hepatic activation system.

Methylprednisolone aseponate was teratogenic in rats when less than 1.

Dietary salt restriction and potassium supplementation may be necessary. The use of systemic corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes. Neoplasms benign, malignant and unspecified including cysts and polyps. Subscribe to free Drugs. Methylprednisolone dose for asthma exacerbation
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