Solu-Medrol

Solu-Medrol

methylprednisolone

Manufacturer:

Pfizer

Distributor:

Zuellig Pharma
Full Prescribing Info
Contents
Methylprednisolone sodium succinate.
Description
Each vial contains the following excipients: Powder Compartment: Lactose, sodium biphosphate monohydrate and dibasic sodium phosphate. Diluent Compartment: Benzyl alcohol and water for injection.
Action
Pharmacology: Pharmacodynamics: Methylprednisolone is a potent anti-inflammatory steroid. It has greater anti-inflammatory potency than prednisolone and less tendency than prednisolone to induce sodium and water retention.
Methylprednisolone sodium succinate has the same metabolic and anti-inflammatory actions as methylprednisolone. When given parenterally and in equimolar quantities, the 2 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 IV administration, is at least 4-1. This is in good agreement with the relative oral potency of methylprednisolone and hydrocortisone.
Pharmacokinetics: Methylprednisolone pharmacokinetics is linear, independent of route of administration.
Absorption: After a methylprednisolone sodium succinate 40 mg IM dose to 14 healthy adult male volunteers, the average peak concentration of 454 ng/mL was achieved at 1 hr. At 12 hrs, the methylprednisolone plasma concentration has declined to 31.9 ng/mL. No methylprednisolone was detected 18 hrs after dosing. Based on area under the concentration-time curve (AUC), an indication of total drug absorbed, methylprednisolone IM sodium succinate was found to be equivalent to the same dose administered IV.
Results of a study demonstrated that the sodium succinate ester of methylprednisolone is rapidly and extensively converted to the active methylprednisolone moiety after all routes of administration. Extent of absorption of free methylprednisolone following IV and IM administrations were found to be equivalent and significantly greater than those following administration of the oral solution and oral methylprednisolone tablets. Since the extent of methylprednisolone absorbed following the IV and IM treatment was equivalent in spite of the greater amount of the hemisuccinate ester reaching the general circulation after IV administration, it appears that the ester is converted in the tissue after IM injection with subsequent absorption as free methylprednisolone.
Distribution: Methylprednisolone is widely distributed into the tissues, crosses the blood-brain barrier and is secreted in breastmilk. Its apparent volume of distribution is approximately 1.4 L/kg. The plasma protein-binding of methylprednisolone in humans is approximately 77%.
Metabolism: In humans, methylprednisolone is metabolized in the liver to inactive metabolites; the major ones are 20α-hydroxymethylprednisolone and 20β-hydroxymethylprednisolone. Metabolism in the liver occurs primarily via the CYP3A4 (see Interactions).
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.
Elimination: The mean elimination half-life (t½) for total methylprednisolone is in the range of 1.8-5.2 hrs. Total clearance is approximately 5-6 mL/min/kg.
Toxicology: Preclinical Safety Data: Based on conventional studies of safety pharmacology, repeated-dose toxicity, no unexpected hazards were identified. The toxicities seen in the repeated-dose studies are those expected to occur with continued exposure to exogenous adrenocortical steroids.
Carcinogenesis: Long-term studies in animals have not been performed to evaluate carcinogenic potential.
Mutagenesis: There was no evidence of a potential for genetic and chromosome mutations when tested in limited studies performed in bacterial and mammalian cells.
Reproductive Toxicity: Corticosteroids have been shown to reduce fertility when administered to rats.
Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. In animal reproduction studies, glucocorticoids eg, methylprednisolone have been shown to induce malformations (cleft palate, skeletal malformations) and intra-uterine growth retardation.
Indications/Uses
Endocrine Disorders: Primary or secondary adrenocortical insufficiency (in conjunction with mineralocorticoids where applicable); acute adrenocortical insufficiency (mineralocorticoid supplementation may be necessary); shock secondary to adrenocortical insufficiency or shock unresponsive to conventional therapy when adrenal cortical insufficiency may be present (when mineralocorticoid activity is undesirable); preoperatively or in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful; congenital adrenal hyperplasia; nonsuppurative thyroiditis; hypercalcemia associated with cancer.
Rheumatic Disorders (As Adjunctive Therapy for Short-Term Administration in the Management of an Acute Episode or Exacerbation): Posttraumatic osteoarthritis; synovitis of osteoarthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis; acute and subacute bursitis; epicondylitis; acute nonspecific tenosynovitis; acute gouty arthritis; psoriatic arthritis; ankylosing spondylitis.
Collagen Diseases and Immune Complex Diseases (During an Exacerbation or as Maintenance Therapy in Selected Cases): Systemic lupus erythematosus (and lupus nephritis); acute rheumatic carditis; systemic dermatomyositis (polymyositis); polyarteritis nodosa; Goodpasture's syndrome.
Dermatologic Diseases: Pemphigus; severe erythema multiforme (Stevens-Johnson syndrome); exfoliative dermatitis; severe psoriasis; bullous dermatitis herpetiformis; severe seborrheic dermatitis; mycosis fungoides.
Allergic States (To Control Severe or Incapacitating Allergic Conditions Intractable to Adequate Trials of Conventional Treatment): Bronchial asthma; contact dermatitis; atopic dermatitis; serum sickness; seasonal or perennial allergic rhinitis; drug hypersensitivity reactions; urticarial transfusion reactions; acute noninfectious laryngeal edema.
Ophthalmic Diseases (Severe Acute and Chronic Allergic and Inflammatory Processes Involving the Eye): Herpes zoster ophthalmicus; iritis, iridocyclitis; chorioretinitis; diffuse posterior uveitis and choroiditis; optic neuritis; sympathetic ophthalmia; anterior segment inflammation; allergic conjunctivitis; allergic corneal marginal ulcers; keratitis.
Gastrointestinal Diseases (To Manage Critical Periods of the Disease): Ulcerative colitis; regional enteritis.
Respiratory Diseases: Symptomatic sarcoidosis; berylliosis; fulminating or disseminated tuberculosis (when used concurrently with appropriate antituberculous chemotherapy); Loeffler's syndrome not manageable by other means; aspiration pneumonitis; moderate to severe Pneumocystis jiroveci pneumonia in acquired immune deficiency syndrome (AIDS) patients (as adjunctive therapy when given within the first 72 hrs of initial anti-pneumocystis treatment); exacerbations of chronic obstructive pulmonary disease (COPD).
Hematologic Disorders: Acquired (autoimmune) hemolytic anemia; idiopathic thrombocytopenic purpura in adults; secondary thrombocytopenia in adults; erythroblastopenia (RBC anemia); congenital (erythroid) hypoplastic anemia.
Neoplastic Diseases (Palliative Management): Leukemias and lymphomas in adults; acute leukemia of childhood. To improve quality of life in patients with terminal cancer.
Edematous States: To induce diuresis or remission of proteinuria in the nephrotic syndrome without uremia.
Nervous System: Cerebral edema from primary or metastatic tumors or surgical or radiation therapy; acute exacerbations of multiple sclerosis; acute spinal cord injury. The treatment should begin within 8 hrs of injury.
Other Indications: Tuberculous meningitis with subarachnoid block or impending block (when used concurrently with appropriate antituberculous chemotherapy); trichinosis with neurologic or myocardial involvement; organ transplantation; prevention of nausea and vomiting associated with cancer chemotherapy.
Dosage/Direction for Use

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To avoid compatibility and stability problems, it is recommended that methylprednisolone sodium succinate be administered separately from other drugs whenever possible, as either IV push through an IV medication chamber, or as an IV "piggy-back" solution (see Cautions for Usage).
Note: Some of the methylprednisolone sodium succinate formulations contain benzyl alcohol (see Precautions).
Administration: Methylprednisolone sodium succinate may be administered by IV injection or infusion or by IM injection. The preferred method for initial emergency use is IV injection. See Table 1 for recommended dosages. Dosage may be reduced for infants and children but should be selected base on the severity of the condition and the response of the patient rather than on the age or weight of the patient. The pediatric dose should not be <0.5 mg/kg every 24 hrs. (See Table 1.)
Overdosage
There is no clinical syndrome of acute overdosage with corticosteroids. Reports of acute toxicity and/or death following overdosage of corticosteroids are rare. In the event of overdosage, no specific antidote is available; treatment is supportive and symptomatic. Methylprednisolone is dialyzable.
Contraindications
Hypersensitivity to methylprednisolone or to any of the excipients of Solu-Medrol. Patients who have systemic fungal infections; for use by the intrathecal and epidural route of administration.
Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.
Warnings
Do not use Solu-Medrol in patients with peptic or intestinal ulcer, diabetics, tuberculosis, viral infection.
Do not use Solu-Medrol in patients with peptic or intestinal ulcer, diabetics, tuberculosis, viral infection.
Do not use in children <2 years.
Special Precautions
Immunosuppressant Effects/Increased Susceptibility to Infections: Corticosteroids may increase susceptibility to infection, may mask some signs of infection, and new infections may appear during their use. There may be decreased resistance and inability to localize 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.
Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. Chicken pox and measles eg, can have a more serious or even fatal course in non-immune children or adults on 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 immunization procedures may be undertaken in patients receiving non-immunosuppressive doses of corticosteroids.
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 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.
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 (5-11 days) of low-dose corticosteroids might reduce mortality, especially in patients with vasopressor-dependent septic shock.
Immune System Effects: Allergic reactions may occur. Because rare instances of skin reactions and anaphylactic/anaphylactoid reactions have occurred in patients receiving corticosteroid therapy, appropriate precautionary measures should be taken prior to administration, especially when the patient has a history of allergy to any drug.
Endocrine Effects: In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting corticosteroids before, during and after the stressful situation is indicated.
Pharmacologic 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 alternate-day therapy.
In addition, acute adrenal insufficiency leading to a fatal outcome may occur if glucocorticoids are withdrawn abruptly.
Drug-induced secondary adrenocortical insufficiency may therefore, be minimized by gradual reduction of dosage. This type of relative insufficiency may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted.
A steroid "withdrawal syndrome" seemingly unrelated to adrenocortical insufficiency, may also occur following abrupt discontinuance of glucocorticoids. This syndrome includes symptoms eg, anorexia, nausea, vomiting, lethargy, headache, fever, joint pain, desquamation, myalgia, weight loss, and/or hypotension. These effects are thought to be due to the 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.
Metabolism and Nutrition: Corticosteroids, including methylprednisolone, can increase blood glucose, worsen preexisting diabetes and predispose those on long-term corticosteroid therapy to diabetes mellitus.
Psychiatric Effects: Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression to frank psychotic manifestations. Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids.
Potentially severe psychiatric adverse reactions may occur with systemic steroids. 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. Psychological effects have been reported upon withdrawal of corticosteroids; the frequency is unknown. Patients/caregivers should be encouraged to seek medical attention if psychological symptoms develop in the patient, especially 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 dose tapering/withdrawal of systemic steroids.
Nervous System Effects: Corticosteroids should be used with caution in patients with seizure disorders.
Corticosteroids should be used with caution in patients with myasthenia gravis (see Musculoskeletal Effects as follows).
Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that corticosteroids affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect.
Severe medical events have been reported in association with the intrathecal/epidural routes of administration (see Adverse Reactions).
There have been reports of epidural lipomatosis in patients taking corticosteroids, typically with long-term use at high doses.
Ocular Effects: Corticosteroids should be used cautiously in patients with ocular herpes simplex because of possible corneal perforation.
Prolonged use of corticosteroids may produce posterior subcapsular cataracts and nuclear cataracts (particularly in children), exophthalmos or increased intraocular pressure (IOP), 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.
Corticosteroid therapy has been associated with central serous chorioretinopathy, which may lead to retinal detachment.
Cardiac Effects: Adverse effects of glucocorticoids on the cardiovascular system eg, 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 alternate day therapy may reduce the incidence of complications in corticosteroid therapy.
There are reports of cardiac arrhythmias, and/or circulatory collapse and/or cardiac arrest following the rapid administration of large IV doses of methylprednisolone sodium succinate (>0.5 g administered over a period of <10 min). Bradycardia has been reported during or after the administration of large doses of methylprednisolone sodium succinate and may be unrelated to the speed or duration of infusion.
Systemic corticosteroids should be used with caution and only if strictly necessary, in cases of congestive heart failure.
Vascular Effects: 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.
Steroids should be used with caution in patients with hypertension.
Gastrointestinal Effects: 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 hemorrhage may occur without significant pain. In combination with nonsteroidal anti-inflammatory drugs (NSAIDs), the risk of developing gastrointestinal ulcers is increased.
Corticosteroids should be used with caution in patients with nonspecific ulcerative colitis if there is a probability of impending perforation, abscess, or other pyogenic infection, diverticulitis, fresh intestinal anastomoses or active or latent peptic ulcer.
Hepatobiliary Effects: High doses of corticosteroids may produce acute pancreatitis.
Drug induced liver injury eg, acute hepatitis can result from cyclical pulsed IV methylprednisolone (usually at doses of 1 g/day). The time to onset of acute hepatitis can be several weeks or longer. Resolution of the adverse event has been observed after treatment was discontinued.
Musculoskeletal Effects: An acute myopathy has been reported with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission (eg, myasthenia gravis), or in patients receiving concomitant therapy with anticholinergics eg, neuromuscular blocking drugs (eg, pancuronium). 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.
Osteoporosis is a common but infrequently recognized adverse effect associated with a long-term use of large doses of glucocorticoid.
Renal and Urinary Disorders: Corticosteroids should be used with caution in patients with renal insufficiency.
Investigations: 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 the synthetic derivatives except when used in large doses. Dietary salt restriction and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.
Injury, Poisoning and Procedural Complications: Systemic corticosteroids are not indicated for and therefore, should not be used to treat, traumatic brain injury; a multicenter study revealed an increased mortality at 2 weeks and 6 months, after injury in patients administered Solu-Medrol compared to placebo. A causal association with methylprednisolone sodium succinate treatment has not been established.
Other Adverse Events: Since complications of treatment with glucocorticoids are dependent on the size of the dose and the duration of treatment, a risk or benefit decision must be made in each individual case as to dose and duration of treatment as to whether daily or intermittent therapy should be used.
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.
Aspirin and nonsteroidal anti-inflammatory agents should be used cautiously in conjunction with corticosteroids.
Pheochromocytoma crisis, which can be fatal, has been reported after administration of systemic corticosteroids. Corticosteroids should only be administered to patients with suspected or identified pheochromocytoma after an appropriate risk/benefit evaluation.
Effects on the Ability to Drive or Operate Machinery: The effect of corticosteroids on the ability to drive or use machinery has not been systematically evaluated. Adverse effects eg, dizziness, vertigo, visual disturbances and fatigue are possible after treatment with corticosteroids. If affected, patients should not drive or operate machinery.
Impairment of Fertility: Corticosteroids have been shown to impair fertility in animal studies (see Pharmacology: Toxicology under Actions).
Use in Pregnancy: Animal studies have shown that corticosteroids, when administered to the mother at high doses, may cause fetal malformations. However, corticosteroids do not appear to cause congenital anomalies when given to pregnant women. Nevertheless, because the studies in humans cannot rule out the possibility of harm, methylprednisolone sodium succinate should be used during pregnancy only if clearly needed.
Some corticosteroids readily cross the placenta. One retrospective study found an increased incidence of low-birth weights in infants born of mothers receiving corticosteroids. Infants born to mothers, who have received substantial doses of corticosteroids during pregnancy must be carefully observed and evaluated for signs of adrenal insufficiency, although neonatal adrenal insufficiency appears to be rare in infants who were exposed in utero to corticosteroids.
There are no known effects of corticosteroids on labor and delivery.
Cataracts have been observed in infants born to mothers treated with long-term corticosteroids during pregnancy.
Benzyl alcohol can cross the placenta (see Precautions).
Use in Lactation: Corticosteroids are excreted in breast milk.
Corticosteroids distributed into breast milk may suppress growth and interfere with endogenous glucocorticoid production in nursing infants. Since adequate reproductive studies have not been performed in humans with glucocorticoids, these drugs should be administered to nursing mothers the benefits of therapy are judged to outweigh the potential risks to the infant.
Use in Children: The preservative benzyl alcohol has been associated with serious adverse events, including the "gasping syndrome" and death in pediatric patients. Although normal therapeutic doses of Solu-Medrol ordinarily deliver amounts of benzyl alcohol that are substantially lower than those reported in association with the "gasping syndrome", the minimum amount of benzyl alcohol at which toxicity may occur is not known. The risk of benzyl alcohol toxicity depends on the quantity administered and the hepatic capacity to detoxify the chemical. Premature and low-birth weight infants may be more likely to develop toxicity.
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.
High doses of corticosteroids may produce pancreatitis in children.
Use In Pregnancy & Lactation
Use in Pregnancy: Animal studies have shown that corticosteroids, when administered to the mother at high doses, may cause fetal malformations. However, corticosteroids do not appear to cause congenital anomalies when given to pregnant women. Nevertheless, because the studies in humans cannot rule out the possibility of harm, methylprednisolone sodium succinate should be used during pregnancy only if clearly needed.
Some corticosteroids readily cross the placenta. One retrospective study found an increased incidence of low-birth weights in infants born of mothers receiving corticosteroids. Infants born to mothers, who have received substantial doses of corticosteroids during pregnancy must be carefully observed and evaluated for signs of adrenal insufficiency, although neonatal adrenal insufficiency appears to be rare in infants who were exposed in utero to corticosteroids.
There are no known effects of corticosteroids on labor and delivery.
Cataracts have been observed in infants born to mothers treated with long-term corticosteroids during pregnancy.
Benzyl alcohol can cross the placenta (see Precautions).
Use in Lactation: Corticosteroids are excreted in breast milk.
Corticosteroids distributed into breast milk may suppress growth and interfere with endogenous glucocorticoid production in nursing infants. Since adequate reproductive studies have not been performed in humans with glucocorticoids, these drugs should be administered to nursing mothers the benefits of therapy are judged to outweigh the potential risks to the infant.
Adverse Reactions
The following adverse reactions have been reported with the following contraindicated routes of administration: Intrathecal/Epidural: Arachnoiditis, functional gastrointestinal disorder/bladder dysfunction, headache, meningitis, parapareisis/paraplegia, convulsions, sensory disturbances. The frequency of these adverse reactions is not known (see Table 2).

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Drug Interactions
Methylprednisolone is a cytochrome P-450 enzyme (CYP) substrate and is mainly metabolized by the CYP3A4 enzyme. CYP3A4 is the dominant enzyme of the most abundant CYP subfamily in the liver of adult humans. It catalyzes 6β-hydroxylation of steroids, the essential phase I metabolic step for both endogenous and synthetic corticosteroids. Many other compounds are also substrates of CYP3A4, some of which (as well as other drugs) have been shown to alter glucocorticoid metabolism by induction (upregulation) or inhibition of the CYP3A4 enzyme.
CYP3A4 Inhibitors: Drugs that inhibit CYP3A4 activity generally decreased hepatic clearance and increased plasma concentration of CYP3A4 substrate medications eg, methylprednisolone. In the presence of a CYP3A4 inhibitor, the dose of methylprednisolone may need to be titrated to avoid steroid toxicity.
CYP3A4 Inducers: Drugs that induce CYP3A4 activity generally increase hepatic clearance, resulting in decreased plasma concentration of medications that are substrates for CYP3A4. Co-administration may require an increase in methylprednisolone dosage to achieve the desired result.
CYP3A4 Substrates: In the presence of another CYP3A4 substrate, the hepatic clearance of methylprednisolone may be affected, with corresponding dosage adjustments required. It is possible that adverse events associated with the use of either drug alone may be more likely to occur with co-administration.
Non-CYP3A4-Mediated Effects: Other interactions and effects that occur with methylprednisolone (see Table 3).
Table 3 provides a list and descriptions of the most common and/or clinically important drug interactions or effects with methylprednisolone.

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Incompatibilities: 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. Drugs that are physically incompatible in solution with methylprednisolone sodium succinate include but are not limited to: Allopurinol sodium, doxapram hydrochloride, tigecycline, diltiazem hydrochloride, calcium gluconate, vecuronium bromide, rocuronium bromide, cisatracurium besylate, glycopyrrolate, propofol.
The IV compatibility and stability of methylprednisolone sodium succinate solutions and with other drugs in IV admixtures is dependent on admixture pH, concentration, time, temperature and the ability of methylprednisolone to solubilize itself. Thus, to avoid compatibility and stability problems, whenever possible it is recommended that methylprednisolone sodium succinate be administered separately from other drugs and as either IV push, through an IV medication chamber, or as an IV "piggy-back" solution.
Caution For Usage
Instructions for Use and Handling: Preparation of Solutions: To prepare solutions for IV infusion, 1st reconstitute Solu-Medrol as directed. Therapy may be initiated by administering Solu-Medrol IV over a period of at least 5 min (eg, doses up to 250 mg) to at least 30 min (eg, doses of ≥250 mg). Subsequent doses may be withdrawn and administered similarly. If desired, the medication may be administered in dilute solutions by admixing the reconstituted product with dextrose 5% in water, normal saline, dextrose 5% in 0.45% or 0.9% sodium chloride; the resulting solutions are physically and chemically stable for 48 hrs.
Directions for using Act-O-Vial 2-Compartment Vial: Press down on plastic activator to force diluent into the lower compartment. Gently agitate to effect solution. Use solution within 48 hrs. Remove plastic tab covering center of stopper. Sterilize top of plunger-stopper with a suitable germicide. Insert needle through center of plunger-stopper until tip is just visible. Invert vial and withdraw dose.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration whenever solution and container permit.
Storage
Store solution below 25°C. Use solution within 48 hrs after mixing.
ATC Classification
H02AB04 - methylprednisolone ; Belongs to the class of glucocorticoids. Used in systemic corticosteroid preparations.
Presentation/Packing
Infusion (vial) 500 mg (sterile powd) x 1's. 1,000 mg x 1's. 2 g x 1's. Act-O-Vial 40 mg (sterile powd, single-dose) x 1's. 125 mg x 1's.
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