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Mechanism of Action
US Drug Names
8 mg PO every 6 hours or 16 mg PO every 12 hours for 7 to 10 days. The World Health Organization strongly recommends the use of systemic corticosteroids in patients with severe or critical COVID-19. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend methylprednisolone as an alternative corticosteroid for hospitalized patients who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). The NIH recommends 32 mg PO once daily (or in 2 divided doses) for up to 10 days or until hospital discharge (whichever comes first). The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting methylprednisolone.
8 mg IV every 6 hours or 16 mg IV every 12 hours for 7 to 10 days. The World Health Organization strongly recommends the use of systemic corticosteroids in patients with severe or critical COVID-19. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend methylprednisolone as an alternative corticosteroid for hospitalized patients who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO). The NIH recommends 32 mg IV once daily (or in 2 divided doses) for up to 10 days or until hospital discharge (whichever comes first). The NIH advises clinicians to review the patient's medical history and assess the potential risks and benefits before starting methylprednisolone.
40 to 80 mg/day IV or IM in 1 to 2 divided doses until peak expiratory flow is 70% of predicted or personal best is recommended by the NAEPP.
2 mg/kg IV, IM, or IO load (Max: 60 mg/dose), then 0.5 mg/kg/dose IV every 6 hours or 1 mg/kg/dose IV every 12 hours (Max: 120 mg/day). Some experts recommend 0.5 to 1 mg/kg/dose IV every 4 to 6 hours.
Corticosteroid use in ARDS is controversial. If there are no signs of improvement 7 to 14 days after ARDS onset, 1.6 to 3.2 mg/kg/day IV in divided doses for 7 to 14 days has been recommended. Alternatively, a tapered dosage (2 mg/kg/day on days 1 to 14; 1 mg/kg/day on days 15 to 21; 0.5 mg/kg/day on days 22 to 28; 0.25 mg/kg/day on days 29 to 30; 0.125 mg/kg/day on days 31 to 32) is used. Initiate with the IV route, given in 4 divided doses; PO doses are administered as a single daily dose.
7.5 to 60 mg PO administered once daily in the morning or as alternate-day therapy as needed for symptom control; use lowest effective dose. Consider add-on low dose oral corticosteroids (CS) (7.5 mg/day or less of prednisone equivalent) only for those with poor symptom control and/or frequent exacerbation despite good inhaler technique and treatment adherence. Add CS only after exclusion of other contributory factors and consideration of other add-on treatments.
7.5 to 60 mg PO once daily in the morning or as alternate-day therapy as needed for symptom control; use lowest effective dose. In pediatric patients, the use of oral corticosteroids is usually limited to a few weeks until asthma control is improved and the patient can be stabilized on other, preferred treatments.
0.25 to 2 mg/kg/day PO administered once daily in the morning or as alternate-day therapy as needed for symptom control. Use lowest effective dose. Max: 60 mg/day. Usual age-based Max: 20 mg/day for children less than 2 years, 30 mg/day for children 3 to 5 years, and 40 mg/day for children 6 to 11 years. In pediatric patients, the use of oral corticosteroids is usually limited to a few weeks until asthma control is improved and the patient can be stabilized on other, preferred treatments.
High-dose (pulse doses) of 1 to 2 grams IV once weekly or every other week; however, there is no proven advantage over oral corticosteroids.
Initially, 24 to 32 mg PO per day. Alternatively, 40 to 48 mg PO every other day has also been used. Taper after several weeks to the lowest effective maintenance dose (often 8 to 12 mg PO every other day). Treatment with corticosteroids is usually indicated only if elevated calcium is present or if there is a decline in the function of a vital organ (lungs, kidneys, eyes, heart, or CNS).
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 all patients, however, 66% relapsed 1 year later. One patient without oral maintenance corticosteroids and 3 patients with oral maintenance corticosteroids showed persistent improvement. Treatment with corticosteroids is usually indicated only if elevated calcium is present or if there is a decline in the function of a vital organ (lungs, kidneys, eyes, heart, or CNS).
30 mg/kg IV given over 15 minutes, followed 45 minutes later by 5.4 mg/kg/hour IV infusion given for 23 hours. Although not widely employed or recommended, the continuous infusion has been repeated for an additional 23 hours in selected patients. Use has been controversial, as small benefits in mortality, motor function, or sensation have not translated to clinically relevant outcomes for long-term recovery, and treatment may result in an increased risk for adverse events such as embolus, hyperglycemia, or infection.   
0.75 to 1 mg/kg/day IV (Max: 60 to 80 mg/day IV). Maximum recommended duration at full dose is 2 weeks; switch to oral therapy once a response is achieved, then taper over 8 to 12 weeks. Systemic corticosteroids are helpful to induce remission.   Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible. 
1 to 1.5 mg/kg/day (Max: 60 mg/day) IV or IM in 1 to 2 divided doses for 2 to 4 weeks; transition to oral corticosteroids as soon as feasible and slowly taper over several weeks after response achieved.     Pulse methylprednisolone therapy (20 to 30 mg/kg/day [Max: 1 gram/day] IV for 3 days) has also been used successfully to induce remission in children with moderate to severe ulcerative colitis. Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible. 
4 to 48 mg PO per day, administered in 4 divided doses is the general FDA-approved dose range. A methylprednisolone dose of 48 mg/day PO in divided doses, once response is achieved with IV, is suggested. Maximum recommended duration at full dose is 2 weeks. Thereafter, tapering by 4 to 8 mg/week until complete discontinuation within 8 to 12 weeks is recommended. Systemic corticosteroids are helpful to induce remission.   Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible. 
1 to 1.5 mg/kg/day (Max: 60 mg/day) PO in 1 to 2 divided doses for 2 to 4 weeks, followed by a slow taper over several weeks after response achieved, has been suggested for inflammatory bowel disease in pediatrics.     Usual pediatric dose range: 0.5 to 1.7 mg/kg/day PO given in divided doses.  Because of the potential complications of steroid use, steroids should be used selectively and in the lowest dose possible for the shortest duration as possible. 
Daily doses of 200 mg PO of prednisolone for 1 week, followed by 80 mg PO every other day for 1 month, have been shown to be effective (Determine the equivalent dosage of methylprednisolone; each 4 mg of methylprednisolone is equivalent to 5 mg of prednisolone).
Initially, 12 to 20 mg PO per day. Increase, as needed, by 4 mg PO every 2 to 3 days until there is marked clinical improvement or to a maximum of 40 mg/day PO. Dose is usually continued for 1 to 3 months and then is gradually tapered to an alternate-day dosage. Some clinicians use initial dosages of 48 to 64 mg PO per day with gradual tapering. Although higher initial dosages may provide more rapid benefit, early exacerbations of myasthenic weakness may be more common than with lower initial dosages. The methylprednisolone dosage listed is based on a recommended prednisone dose converted to an equivalent methylprednisolone dose.
4 to 48 mg/day PO, administered in 4 divided doses. Adjust to response and severity of condition.
0.5 to 1.7 mg/kg/day PO, given in divided doses every 6 to 12 hours. 
10 to 80 mg at the appropriate site, depending upon degree of inflammation and size and location of affected area. Repeat doses are not usually required for 1 to 5 weeks. Dosage ranges for specific joints: large joints: 20 to 80 mg; medium joints: 10 to 40 mg; small joints: 4 to 10 mg. Suggested intralesional dosage range is 20 to 60 mg.
Initially, 10 to 40 mg IV or IM. Subsequent IV/IM doses are determined by response and condition.
In pediatric patients, the initial dose range is 0.11 to 1.6 mg/kg/day IV or IM in 3 or 4 divided doses (3.2 to 48 mg/m2/day). Adjust to patient condition and response.  
10 to 120 mg IM. Subsequent doses may be given determined by patient response and condition.
0.5 to 1.7 mg/kg/day IM (a single injection during each 24-hour period equal to the total daily oral dose is usually sufficient). Determine need for repeat IM doses based on condition and patient response.
4 to 48 mg/day PO, administered in 4 divided doses. Adjust to severity of condition and patient response.
Initially, 10 to 40 mg IV or IM. Subsequent IV/IM doses are determined by response and condition.
10 to 120 mg IM. Subsequent doses are determined by patient response and condition.
32 to 80 mg PO per day is usually effective for hypercalcemia due to hematologic cancers. 12 to 24 mg PO per day may be sufficient for other tumors (e.g., breast cancer). The dosage listed is based on a recommended prednisone dose converted to an equivalent methylprednisolone dose.
Initially, 10 to 40 mg IV or IM. Subsequent IV/IM doses are determined by response and condition. IM administration is contraindicated in patients with ITP.
In pediatric patients, the initial dose range is 0.11 to 1.6 mg/kg/day IV or IM in 3 or 4 divided doses (3.2 to 48 mg/m2/day). Adjust to patient condition and response. IM administration is contraindicated in ITP.  
4 to 48 mg/day PO, administered in 4 divided doses. Adjust depending on severity of the condition treated and patient response. Hydrocortisone and cortisone are the preferred drugs; methylprednisolone has little to no mineralocorticoid properties. For acute conditions, parenteral therapy is recommended. Dosing is highly variable.
0.5 to 1.7 mg/kg/day PO, given in divided doses every 6 to 12 hours.  Hydrocortisone and cortisone are the preferred drugs; methylprednisolone has little to no mineralocorticoid properties. For acute conditions, parenteral therapy is recommended. Dosing is highly variable.
Initially, 10 to 40 mg IV. Subsequent IV/IM doses are determined by response and condition. Hydrocortisone and cortisone are the preferred drugs; methylprednisolone has little to no mineralocorticoid properties. For acute conditions, parenteral therapy is recommended. Dosing is highly variable.
In pediatric patients, the initial dose range is 0.11 to 1.6 mg/kg/day IV or IM in 3 or 4 divided doses (3.2 to 48 mg/m2/day). Hydrocortisone and cortisone are the preferred drugs; methylprednisolone has little to no mineralocorticoid properties. For acute conditions, parenteral therapy is recommended. Dosing is highly variable.
FDA-approved initial dose is 4 to 48 mg/day PO in divided doses. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis.  Initial doses in clinical trials for tuberculosis in general use the following doses: 48 mg/day PO daily for 4 weeks or 20 mg/kg/day IV for weight of 50 kg or less or 1 gram/day IV for weight greater than 50 kg for 5 days; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids. A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis, which may be influenced by genetic variation at the LTA4H gene.
FDA-approved initial dose is 10 to 40 mg IM or IV, with subsequent doses and adjustments depending upon the disease being treated. When high-dose therapy is desired, the recommended dose is 30 mg/kg administered IV over at least 30 minutes. This dose may be repeated every 4 to 6 hours for 48 hours. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis.  Initial doses in clinical trials for tuberculosis in general use the following doses: 48 mg/day PO daily for 4 weeks or 20 mg/kg/day IV for weight of 50 kg or less or 1 gram/day IV for weight greater than 50 kg for 5 days; many trials were prior to the use of rifampin, which may decrease bioavailability and increase plasma clearance of corticosteroids. A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis, which may be influenced by genetic variation at the LTA4H gene.
The FDA-approved dose is 4 to 120 mg IM per day, depending upon the disease being treated. Adjunctive corticosteroid therapy has been shown to improve survival for patients with tuberculosis involving the CNS and pericardium, but has not been universally recommended by guidelines for all forms of tuberculosis.  Trials have mostly involved use of oral or intravenous dose forms, using oral dosing for 4 weeks or intravenous administration for 5 days. A meta-analysis suggests that steroid use may reduce mortality in all forms of tuberculosis, which may be influenced by genetic variation at the LTA4H gene.
The optimal dosage has not been established; critically-ill patients may require high doses (e.g., 48 mg PO or IV per day) for 2 or more weeks. The dosage listed is based on a recommended prednisone dose converted to an equivalent methylprednisolone dose.
30 to 45 mg IV 2 to 3 times daily; taper dose after 5 to 7 days over 1 to 2 weeks. A suggested taper is 30 mg IV twice daily on days 1 to 5; then 30 mg IV once daily on days 6 to 10; then 15 mg IV once daily on days 11 to 21. Start therapy as early as possible and within 72 hours after starting specific PCP therapy. Recommended for patients with moderate to severe infection, defined by a PaO2 less than 70 mmHg at room air or an alveolar-arterial DO2 gradient of 35 mmHg or more. The benefits of starting corticosteroids after 72 hours are unclear.     
1 mg/kg/dose IV every 6 hours on days 1 to 7; then 1 mg/kg/dose IV twice daily on days 8 to 9; then 0.5 mg/kg/dose twice daily on days 10 to 11; then 1 mg/kg/dose IV once daily on days 12 to 16. Start therapy as early as possible and within 72 hours after starting specific PCP therapy. Recommended for patients with moderate to severe infection, defined by a PaO2 less than 70 mmHg at room air or an alveolar-arterial DO2 gradient more than 35 mmHg.     
A treatment protocol based on the treatment of 31 patients with probable SARS (diagnosed according to WHO criteria) in Hong Kong, suggests methylprednisolone 1 mg/kg IV every 8 hours for 5 days, followed by 1 mg/kg IV every 12 hours for 5 days, in conjunction with ribavirin, and followed by prednisolone PO to complete a 21-day corticosteroid regimen. Another regimen used ribavirin IV with methylprednisolone 240 to 320 mg daily IV in divided doses or hydrocortisone IV (4 mg/kg every 8 hours, tapered to 200 mg every 8 hours). Other than supportive care, there is no established treatment for SARS. Due to lack of efficacy data, ribavirin and methylprednisolone combination therapy should be reserved for patients with the following: extensive or bilateral chest radiographic involvement; persistent chest radiographic involvement and persistent high fever for 2 days; clinical, chest radiographic, or laboratory findings suggestive of worsening; or oxygen saturation less than 95% on room air.
Glucocorticoids are reserved for severe cases. Although prednisone is commonly used, a methylprednisolone dosage of 16 to 32 mg/day PO has similar potency.
4 to 48 mg, depending on disease treated, PO per day administered in 4 divided doses.
10 to 120 mg IM. Frequency of dosing varies with the condition being treated and patient response.
There is variation in the literature with regard to dosage regimens. Methylprednisolone 125 mg IV every 6 hours for a few days, followed by prednisone or prednisolone tapered over 3 to 6 weeks is commonly reported. Following biopsy to confirm diagnosis, corticosteroids are usually instituted soon afterward. Corticosteroid use is an adjunctive measure; removal of the suspected offending agent /cause is the primary treatment. While many case reports suggest a possible net benefit to the use of corticosteroids for AIN, some experts advocate for more prospective study of their value.
There is variation in the literature with regard to dosage regimens. Methylprednisolone 1 mg/kg IV every 6 hours for a few days, followed by oral prednisone or prednisolone tapered over 3 to 6 weeks has been reported.
250 to 1,000 mg IV given once daily or on alternate days for 3 to 5 doses. Renal transplant guidelines recommend corticosteroids for the initial treatment of acute rejection. 
2 to 2.5 mg/kg/day IV, tapered slowly over 2 to 3 weeks. Initial doses of 10 mg/kg/day IV have also been used; although there is no definitive data that higher doses are more effective than lower doses. For GVHD limited to the skin, an initial dose of 1 mg/kg/day IV may be used. One study indicated that a cumulative methylprednisolone dose of 2,000 mg/m2 (or roughly 50 mg/kg) is required for complete resolution of acute graft-versus-host disease in most patients.
According to guidelines, 250 to 1,000 mg/day IV for 3 days is first line for symptomatic acute cellular rejection irrespective of ISHLT endomyocardial biopsy grade. The regimen should also be used for asymptomatic severe (ISHLT 3R) acute cellular rejection and can be used for for asymptomatic moderate acute cellular rejection (ISHLT 2R). Also consider for hyperacute rejection and for antibody-mediated rejection. A taper can be considered.
4 to 48 mg/day PO, administered in 4 divided doses. Adjust to condition severity and response.
10 to 120 mg IM. Subsequent doses are determined by response and condition.
40 to 80 mg as a single injection adjacent to the carpal tunnel. Reassess at 6 to 8 weeks. To avoid median-nerve injury, use specialized administration techniques. Use of 2 or more repeat injections is not advised; local tendon damage may occur. The definitive treatment for median-nerve entrapment is surgery. Corticosteroids are temporary measures; patients who have intermittent pain and paresthesias without any fixed motor-sensory deficits may respond to conservative therapy.
30 mg/kg/dose (Max: 1 gram/dose) IV or IM once daily for 1 to 3 days.     High-dose pulse steroids may be considered as an alternative to a second infusion of IVIG or for retreatment of patients who have had recurrent or recrudescent fever after additional IVIG, but should not be used as routine primary therapy with IVIG in patients with Kawasaki disease. Corticosteroid treatment has been shown to shorten the duration of fever in patients with IVIG-refractory Kawasaki disease or patients at high risk for IVIG-refractory disease.   A reduction in the frequency and severity of coronary artery lesions has also been reported with pulse dose methylprednisolone treatment.  
Dosage not established. 1 or 1.5 mg/kg IV every 8 hours for 6 doses or 30 mg/kg IV every 4 hours for 2 doses has been used.  
2 to 30 mg/kg/day IV for 3 days. Methylprednisolone is recommended to be given at the same time as intravenous immunoglobulin (IVIG) for high-risk children with Kawasaki disease-like phenotype (children younger than 12 months and those with coronary artery changes). Methylprednisolone is recommended as second-line therapy in patients who remain unwell 24 hours after infusion of IVIG, especially if they have ongoing pyrexia. 
4 to 48 mg/day PO, given in 4 divided doses; adjust dose to condition treated and patient response.
0.11 to 2 mg/kg/day PO in 1 to 4 divided doses is the general initial dose range for methylprednisolone.
16 mg PO every 8 hours for 3 days. Taper over 2 weeks to the lowest effective dose. If beneficial, limit total duration of use to 6 weeks. Considered by experts to be a last-line treatment option for patients who have failed other therapies.
16 mg IV every 8 hours for 3 days. Taper over 2 weeks to the lowest effective dose - may switch to oral therapy if feasible. If beneficial, limit total duration of use to 6 weeks. Considered by experts to be a last-line treatment option for patients who have failed other therapies.
Systemic dosage may need adjustment depending on the degree of hepatic insufficiency, but quantitative recommendations are not available.
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
Methylprednisolone and its derivatives, methylprednisolone sodium succinate and methylprednisolone acetate, are synthetic glucocorticoids used orally or parenterally as antiinflammatory or immunosuppressive agents. Methylprednisolone is used in many conditions in adult and pediatric patients, including many allergic, dermatologic, and inflammatory states when systemic treatment is medically necessary. The drug is commonly used parenterally when a patient cannot take oral prednisone. Methylprednisolone has very little mineralocorticoid activity and is therefore not used to manage adrenal insufficiency unless a more potent mineralocorticoid is administered concomitantly. Systemic corticosteroids may be added to other long-term maintenance medications in the management of uncontrolled severe persistent asthma. Once stabilization of asthma is achieved, regular attempts should be made to reduce or eliminate the use of systemic corticosteroids due to the side effects associated with chronic administration. Short courses of systemic corticosteroid treatment may be used in moderate to severe exacerbations of asthma or COPD. If long-term therapy with methylprednisolone is required for any indication, the lowest possible effective dose should be used.
Updates for coronavirus disease 2019 (COVID-19):
The World Health Organization strongly recommends the use of systemic corticosteroids, including methylprednisolone, in patients with severe or critical COVID-19; but suggests against use in patients with non-severe COVID-19. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend using another corticosteroid, dexamethasone, in hospitalized patients with COVID-19 who require supplemental oxygen, including those on high-flow oxygen, noninvasive ventilation, mechanical ventilation, or extracorporeal membrane oxygenation (ECMO); however, methylprednisolone may be used as an alternative corticosteroid if dexamethasone is unavailable. The NIH recommends against the use of corticosteroids in patients with mild to moderate COVID-19 (i.e., non-hospitalized patients or hospitalized patients that do not require supplemental oxygen).
NOTE: Dosage must be individualized and is very variable depending on the nature and severity of the disease, and on the patients response. If therapy is continued for more than a few days, withdrawal must be gradual.
For storage information, see the specific product information within the How Supplied section.
Direct intravenous injection:
Intermittent intravenous infusion:
Glucocorticoids are responsible for protein metabolism, and prolonged therapy can result in various musculoskeletal manifestations, including: myopathy (myalgia, muscle wasting, muscle weakness, quadriparesis), impaired wound healing, bone matrix atrophy (osteoporosis), bone fractures such as vertebral compression fractures or fractures of long bones, and avascular necrosis of femoral or humoral heads. These effects are more likely to occur in older or debilitated patients. Glucocorticoids interact with calcium metabolism at many sites, including: calcinosis, decreasing the synthesis by osteoblasts of the principle proteins of bone matrix, malabsorption of calcium in both the nephron and the gut, and reduction of sex hormone concentrations. Although all of these actions probably contribute to glucocorticoid-induced osteoporosis, the actions on osteoblasts is most important. Glucocorticoids do not modify vitamin D metabolism. Postmenopausal women, in particular, should be monitored for signs of osteoporosis during methylprednisolone therapy. Because of retardation of bone growth, children receiving prolonged corticosteroid therapy may have growth inhibition. Intra-articular injections of corticosteroids can cause Charcot-like arthropathy and postinjection flare. Atrophy at the site of injection has been reported following administration of soluble glucocorticoids. Tendon rupture has also been reported.  
Methylprednisolone can mask the symptoms of infection and should be avoided during an acute viral, fungal, or bacterial infection; as well, patients receiving corticosteroids are more susceptible to infections than are healthy individuals. Leukocytosis has been reported and is a common physiologic effect of systemic corticosteroid therapy and may need to be differentiated from the leukocytosis that occurs with inflammatory or infectious processes.   Immunosuppression is most likely to occur in patients receiving high-dose (e.g., equivalent to 1 mg/kg or more of prednisone daily), systemic corticosteroid therapy for any period of time, particularly in conjunction with corticosteroid-sparing drugs (e.g., troleandomycin) and/or concomitant immunosuppressant agents; however, patients receiving moderate dosages of systemic corticosteroids for short periods or low dosages for prolonged periods also may be at risk. Corticosteroids can reactivate tuberculosis and should not be used in patients with a history of active tuberculosis except when chemoprophylaxis is instituted concomitantly. Patients receiving immunosuppressive doses of corticosteroids should be advised to avoid exposure to measles or varicella (chickenpox) and, if exposed to these diseases, to seek medical advice immediately.  
Corticosteroids are divided into two classes: mineralocorticoids and glucocorticoids. Methylprednisolone is a glucocorticoid with minimal mineralocorticoid activity. Mineralocorticoids alter electrolyte and fluid balance by facilitating sodium retention and hydrogen and potassium excretion at the level of the distal renal tubule, resulting in increased plasma volume. Although the incidence of effects with this medication are not well elicited, mineralocorticoid properties can cause fluid retention; electrolyte disturbances (hypokalemia, hypokalemic metabolic alkalosis, hypernatremia, hypocalcemia); and edema. In a review of 93 studies of corticosteroid use, hypertension was found to develop approximately 4 times as often in steroid recipients compared to control groups. As a result of the steroid-induced edema and elevated blood pressure, congestive heart failure can occur in susceptible patients. Dietary salt restriction and potassium supplementation may be needed in persons receiving treatment with methylprednisolone.  
Cardiovascular adverse events have been reported during and/or after treatment with parenteral methylprednisolone. These adverse events include bradycardia, cardiac arrest, cardiac arrhythmia exacerbation, cardiac failure, cardiomegaly, fat (lipid) emboli, hypertrophic cardiomyopathy (in premature infants), pulmonary edema, sinus tachycardia, syncope, and vasculitis. Additionally, corticosteroid therapy has also been associated with ruptures of the left ventricular free wall in persons having recently experienced a myocardial infarction; thus, caution is advised when prescribing methylprednisolone to these patients. 
Although corticosteroids are used to treat Graves' ophthalmopathy, ocular effects, such as exophthalmos, posterior subcapsular cataracts, retinopathy, or ocular hypertension, can result from prolonged use of methylprednisolone and could result in glaucoma or ocular nerve damage including optic neuritis. Temporary or permanent visual impairment, including blindness, has been reported with glucocorticoid administration by several routes of administration including intranasal and ophthalmic administration. Secondary bacterial, fungal, and viral ocular infection can be exacerbated by corticosteroid therapy. Corneal perforation may occur if corticosteroids are administered to patients with ocular herpes simplex and, thus, should not be used during active ocular herpes simplex infection.  
Prolonged therapy of methylprednisolone can adversely affect the endocrine system, resulting in hypercorticism (Cushing's syndrome), menstrual irregularity including amenorrhea or dysmenorrhea, hyperglycemia, glycosuria, and aggravation of diabetes mellitus in susceptible patients.   In a published review of 93 studies of corticosteroid use, the development of diabetes mellitus was determined to occur 4 times more frequently in steroid recipients compared to control groups. Insulin or oral hypoglycemic dosages may require adjustment.
Adverse GI effects associated with long-term corticosteroid administration include nausea, vomiting, and anorexia. Appetite stimulation with weight gain, diarrhea, constipation, abdominal pain and distention, esophageal ulceration, gastritis, GI perforation, and pancreatitis also have been reported. A few patients receiving prolonged corticosteroid administration have experienced production, reactivation, perforation, or delayed healing of peptic ulcer disease. Although it was once believed that corticosteroids like methylprednisolone contributed to the development of peptic ulcer disease, in a published review of 93 studies of corticosteroid use, the incidence of peptic ulcer disease was not found to be higher in steroid recipients compared to control groups. Cases of hepatomegaly and elevated hepatic enzymes (reversible upon discontinuation) have been associated with the use of methylprednisolone.   Rarely, high doses of cyclically pulsed IV methylprednisolone can induce a toxic form of acute hepatitis. This may occur several weeks after exposure and resolution has been observed after treatment is discontinued. However, serious liver injury may occur, which could result in acute hepatic failure and death. Discontinue IV methylprednisolone if toxic hepatitis occurs. Avoid future use of high dose IV methylprednisolone in patients with toxic hepatitis caused by methylprednisolone.
Adverse neurologic effects have been reported during prolonged corticosteroid administration and include headache, insomnia, vertigo, restlessness, ischemic peripheral neuropathy, neuritis, seizures or convulsions, and EEG changes. Mental disturbances, including depression, anxiety, euphoria, personality changes, and psychosis, have also been reported; emotional lability and psychotic problems can be exacerbated by methylprednisolone therapy.  
Various adverse dermatologic effects reported during corticosteroid therapy include rash (unspecified), skin atrophy, dry skin or xerosis, acne vulgaris, alopecia or thinning scalp hair, diaphoresis, impaired wound healing, facial erythema, striae, petechiae, hirsutism or hypertrichosis, ecchymosis, and easy bruising. Hypersensitivity reactions may manifest as allergic dermatitis, urticaria, anaphylactoid reactions, and/or angioedema. Paresthesias (burning or tingling) in the perineal area may occur following IV injection of corticosteroids like methylprednisolone. Parenteral corticosteroid therapy has also produced skin hypopigmentation, skin hyperpigmentation, scarring, and other types of injection site reaction (e.g., induration, delayed pain or soreness, subcutaneous and cutaneous atrophy, and sterile abscesses); use via incorrect route of administration and/or excessive doses may increase risk of such effects. 
Pharmacologic doses of methylprednisolone administered for prolonged periods can result in physiological dependence due to hypothalamic-pituitary-adrenal (HPA) suppression. Exogenous corticosteroids exert negative feedback on the pituitary, inhibiting the secretion of adrenocorticotropin (ACTH). This inhibition decreases ACTH-mediated synthesis of endogenous corticosteroids and androgens by the adrenal cortex. The severity of glucocorticoid-induced secondary adrenocortical insufficiency varies among individuals and is dependent on the dose, frequency, time of administration, and duration of therapy. Administering the drug on alternate days may help to alleviate this adverse effect. Patients with HPA suppression will require increased doses of corticosteroids during periods of physiologic stress. Acute adrenal insufficiency and even death can occur if sudden withdrawal of the drugs is undertaken. Withdrawal from prolonged oral corticosteroid therapy should be gradual; HPA suppression can last for up to 12 months following cessation of therapy, and patients may need supplemental corticosteroid treatment during periods of physiologic stress such as surgery, acute blood loss, or infection, even after the drug has been discontinued. A non-HAP withdrawal syndrome can occur following abrupt discontinuance of corticosteroid therapy and is apparently unrelated to adrenocortical insufficiency. This syndrome includes symptoms such as anorexia, lethargy, nausea, vomiting, headache, fever, arthralgia, myalgia, exfoliative dermatitis, weight loss, and hypotension. These effects are believed to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels. Increased intracranial pressure with papilledema (i.e., pseudotumor cerebri) has also been reported with withdrawal of glucocorticoid therapy.  
Hypercholesterolemia, atherosclerosis, fat (lipid) emboli, thrombosis, thromboembolism, and phlebitis, specifically, thrombophlebitis have been associated with corticosteroid therapy. Other adverse events reported during treatment with corticosteroids include abnormal fat deposits (moon face), hiccups, malaise, and changes (increase or decrease) in the motility and number of spermatozoa. Palpitations, glossitis, stomatitis, urinary incontinence, and urinary urgency have been rarely reported. Corticosteroids like methylprednisolone may also decrease serum concentrations of vitamin C (ascorbic acid) and vitamin A which may rarely produce symptoms of vitamin A deficiency or vitamin C deficiency.  
The Solu-Medrol 40 mg presentation contains lactose monohydrate produced from cow's milk. In situations where allergic symptoms worsen or new allergic symptoms occur after administration of this preparation, consider the potential for hypersensitivity reactions to cow's milk ingredients. Additionally, lactose intolerance symptoms such as nausea/vomiting, bloating, abdominal pain (cramps), and flatulence may occur. Use appropriate precautions when administering to patients with a cow's milk sensitivity or lactose intolerance. If hypersensitivity reactions occur with the Solu-Medrol 40 mg presentation, consider discontinuing treatments and using alternative treatments, including corticosteroid formulations that do not contain ingredients produced from cow's milk.
An increased incidence of scleroderma renal crisis (SRC) has been observed in patients with systemic sclerosis (systemic scleroderma) treated with corticosteroids. SRC is characterized by malignant hypertension and acute renal failure (unspecified) that may be accompanied by oliguria or anuria.  
Increased dosages of rapid-acting corticosteroids may be necessary for patients undergoing physiologic stress such as major surgical procedure, acute infection, or blood loss. Methylprednisolone should be administered before, during, and after the stressful situation.
The Solu-Medrol 40 mg presentation contains lactose monohydrate produced from cow's milk and is contraindicated in patients with a known or suspected hypersensitivity to cow's milk or it's components or other dairy products.
Severe medical events have occurred following administration of parenteral methylprednisolone via an incorrect route; to minimize the incidence of adverse events, care must be taken to administer the drug as intended and to not exceed recommended doses in each injection. Use of methylprednisolone is contraindicated for intrathecal administration.  Do not give methylprednisolone acetate (e.g., Depo-Medrol) via intravenous administration. Do not administer any form of parenteral methylprednisolone into the deltoid muscle as subcutaneous atrophy occurs with high frequency following such use.  Epidural administration of corticosteroids should be used with great caution. Rare, but serious neurologic events, including cortical blindness, stroke, spinal cord infarction, paralysis, seizures, nerve injury, brain edema, and death have been associated with epidural administration of injectable corticosteroids. These events have been reported with and without the use of fluoroscopy. Many cases were temporally associated with the corticosteroid injection; reactions occurred within minutes to 48 hours after injection. Some cases were confirmed through magnetic resonance imaging (MRI) or computed tomography (CT) scan. Many patients did not recover from the reported adverse effects. Discuss the benefits and risks of epidural corticosteroid injections with the patient before treatment. If a decision is made to proceed with corticosteroid epidural administration, counsel patients to seek emergency medical attention if they experience symptoms after injection such as vision changes, tingling in the arms or legs, dizziness, severe headache, seizures, or sudden weakness or numbness of face, arm, or leg. 
Corticosteroid therapy can mask the symptoms of infection, reactivate latent infection, exacerbate concurrent infection, and result in the development of secondary infection. Regardless of the dosage formulation, use of methylprednisolone is contraindicated in patients with systemic fungal infection, except when the acetate parenteral suspension (e.g., Depo-Medrol) is administered as an intra-articular injection for a localized joint condition  or when the sodium succinate parenteral solution (e.g., Solu-Medrol) or oral formulations are used to control drug reactions. Further, use of any methylprednisolone formulation is not advised in cases of viral infection or bacterial infections that are not adequately controlled by antiinfective agents. The safety and efficacy of methylprednisolone sodium succinate in patients with sepsis syndrome and septic shock have not been established; study suggests that such use may increase the risk of mortality in patients with elevated serum creatinine levels and in those who develop secondary infections after methylprednisolone use. Do not administer parenteral methylprednisolone intra-articularly, intrabursally, or for intratendinous use for local effect in the presence of an acute infection  ; further, local administration of methylprednisolone acetate into a previously infected site is not usually recommended. Activation of latent disease or exacerbation of intercurrent infection due to pathogens such as Amoeba, Candida, Cryptococcus, Mycobacterium (mycobacterial infection), Nocardia, Pneumocystis, or Toxoplasma can occur in patients receiving systemic corticosteroids. Rule out infection with latent or active amebiasis before initiating methylprednisone therapy in patients who have spent time in the tropics or who have unexplained diarrhea. Use methylprednisone with caution in patients with known or suspected Strongyloides (threadworm) infestation as the immunosuppressive effects may lead to disseminated infection, severe enterocolitis, and sepsis. Cases of severe and disseminated strongyloidiasis have been reported following use of corticosteroids in combination with tocilizumab to treat patients with coronavirus disease 2019 (COVID-19). Before giving these drugs together to patients from strongyloidiasis endemic areas, consider administering ivermectin as prophylactic treatment. Reserve systemic corticosteroid therapy in active tuberculosis for patients with fulminating or disseminated disease and only in conjunction with appropriate antituberculosis therapy. Reactivation of tuberculosis may occur in patients with latent tuberculosis or tuberculin reactivity; close observation for disease reactivation is needed if methylprednisone is indicated in such patients. Furthermore, chemoprophylaxis is advised if prolonged methylprednisone therapy is needed. Advise patients receiving immunosuppressive doses of systemic corticosteroids to avoid exposure to persons with a viral infection (i.e., measles or varicella) because these diseases may be more serious or even fatal in immunosuppressed patients. Instruct patients to get immediate medical advice if exposure occurs.  
Patients should be instructed to notify their physician immediately if signs of infection or injury occur, both during treatment or up to 12 months following cessation of therapy with methylprednisolone. Dosages should be adjusted, or glucocorticoid therapy reintroduced, if required. If surgery is needed, patients should advise the attending physician of the corticosteroid they have received within the last 12 months and the disease for which they were being treated. Identification cards that include the name of the patient's disease, the currently administered type and dose of corticosteroid, and the patient's physician should be carried with the patient at all times.
Corticosteroid therapy has been associated with left ventricular free-wall rupture in patients with recent myocardial infarction and methylprednisolone should therefore be used cautiously in these patients.
Corticosteroids cause edema, which can exacerbate congestive heart failure or hypertension. Methylprednisolone should be used with caution in these patients.
Corticosteroids should be used cautiously in patients with glaucoma or other visual disturbance. Corticosteroids are well known to cause cataracts and increased intraocular pressure and can exacerbate glaucoma during long-term administration. Patients receiving methylprednisolone chronically should be periodically assessed for cataract formation.
Methylprednisolone should be used with extreme caution in patients with psychosis, emotional instability, herpes infection (especially ocular herpes simplex infections), osteoporosis, diabetes mellitus, renal disease or seizure disorder because corticosteroids can exacerbate these conditions. Caution should also be used when treating patients with systemic sclerosis (scleroderma); an increased incidence of scleroderma renal crisis has been observed with the use of corticosteroids, including methylprednisolone.  
Methylprednisolone should be used with caution in patients with myasthenia gravis who are being treated with anticholinesterase agents (see Interactions). Muscle weakness can be transiently increased during the initiation of glucocorticoid therapy in patients with myasthenia gravis, necessitating respiratory support.
Systemic corticosteroids should be used with caution in patients with active or latent peptic ulcer disease, diverticulitis, fresh intestinal anastomoses, and nonspecific ulcerative colitis, since steroids may increase the risk of a gastrointestinal (GI) perforation. Signs of peritoneal irritation following GI perforation in patients receiving corticosteroids may be minimal or absent. Corticosteroids should not be used in patients where there is a possibility of impending GI perforation, abscess, or pyogenic infection. There is an enhanced effect due to decreased metabolism of corticosteroids in patients with severe hepatic disease with cirrhosis.  
Glucocorticoids rarely can increase blood coagulability and cause intravascular thrombosis, thrombophlebitis, and thromboembolism. Therefore, methylprednisolone should be used with caution in patients with coagulopathy and/or thromboembolic disease. It is important to note that corticosteroid use via intramuscular administration for immune thrombocytopenic purpura (ITP) is contraindicated, though intravascular and oral administration of methylprednisolone are utilized for this condition. 
There are no adequate or well controlled studies of the use of methylprednisolone in pregnant women. Complications, including cleft palate, stillbirth, and premature abortion, have been reported when corticosteroids were administered during pregnancy in animals. If these drugs must be used during pregnancy, the potential risks should be discussed with the patient. Babies born to women receiving large doses of corticosteroids during pregnancy should be monitored for signs of adrenal insufficiency, and appropriate therapy should be initiated, if necessary. Corticosteroids have been shown to impair fertility in male rats.  Under certain circumstances, methylprednisolone may be considered for use in the pregnant patient (e.g., severe asthma exacerbation); poorly-controlled asthma and exacerbations generally present a greater risk to the mother and fetus than do needed asthma treatments. The American College of Obstetricians and Gynecologists (ACOG) include methylprednisolone as a last-line treatment option for nausea and vomiting of pregnancy in patients who have failed other therapies and suggest a limited duration of use for this purpose in responding patients.
Corticosteroids distribute into breast milk, and the manufacturer states that because of the potential for serious adverse reactions in nursing babies, a decision should be made whether to discontinue nursing or to discontinue the drug. However, there have been reports of breast-feeding in 3 babies who were breast-fed from birth during maternal use of methylprednisolone (6 to 8 mg PO daily) with no reported adverse effects up to 3 months.  In one of the reports, 2 babies had normal blood cell counts, no increase in infections, and above average growth rates. At higher daily methylprednisolone doses, avoidance of breast-feeding during times of peak milk concentrations (usually until 3 to 4 hours following a dose) can help limit infant exposure. While the American Academy of Pediatrics does not comment on the use of methylprednisolone during breast-feeding, it does consider other corticosteroids (prednisone and prednisolone) to be usually compatible with breast-feeding. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.
Pediatric-specific issues should be considered prior to treatment initiation with systemic corticosteroids, such as methylprednisolone. The potential for growth inhibition should be monitored during prolonged therapy in infants, children, and adolescents, and the potential for growth effects should be weighed against the clinical benefit obtained and the availability of other treatment alternatives. Administration of corticosteroids to pediatric patients should be limited to the least amount compatible with an effective therapeutic regimen. Pediatric patients may be more susceptible to developing systemic toxicity; adrenal suppression and increased intracranial pressure have been reported with the use and/or withdrawal of various corticosteroid formulations in young patients.  Further, children receiving corticosteroids are immunosuppressed and are therefore more susceptible to infection. Normally innocuous infections can become fatal in children receiving systemic corticosteroids, so care should be taken to avoid exposure to patients with infectious diseases, particularly those with chicken pox or measles.
Glucocorticoids can produce or aggravate Cushing's syndrome, thus methylprednisolone should be avoided in patients with Cushing's disease.
Pharmacologic doses of methylprednisolone administered for prolonged periods may result in hypothalamic-pituitary-adrenal (HPA) suppression. Acute adrenal insufficiency and even death may occur following abrupt discontinuation. Withdrawal from prolonged oral corticosteroid therapy should be gradual; HPA suppression can last for up to 12 months following cessation of therapy, and patients may need supplemental corticosteroid treatment during periods of physiologic stress, such as surgery, acute blood loss, or infection, even after the drug has been discontinued. Also, a non-HPA withdrawal syndrome may occur following abrupt discontinuation of corticosteroid therapy, and is apparently unrelated to adrenocortical insufficiency. These effects are thought to be due to the sudden change in glucocorticoid concentration rather than to low corticosteroid levels (see Adverse Reactions).
All forms of methylprednisolone should be used with caution in newborns due to potential for drug-induced growth inhibition and immunosuppression. Hypertrophic cardiomyopathy may develop after parenteral administration of methylprednisolone to premature neonates, therefore appropriate diagnostic evaluation and monitoring of cardiac function and structure should be performed. Several commercial formulations of parenteral methylprednisolone are contraindicated in premature neonates and should be avoided in neonates because these products contain benzyl alcohol. Administration of benzyl alcohol to neonates can result in 'gasping syndrome,' which is a potentially fatal condition characterized by metabolic acidosis and CNS, respiratory, circulatory, and renal dysfunction; it is also characterized by high concentrations of benzyl alcohol and its metabolites in the blood and urine. While the minimum amount of benzyl alcohol at which toxicity may occur is not known, 'gasping syndrome' has been associated with benzyl alcohol dosages greater than 99 mg/kg/day in neonates and low-birth-weight neonates. Additional symptoms may include gradual neurological deterioration, seizures, intracranial hemorrhage, hematologic abnormalities, skin breakdown, hepatic failure, renal failure, hypotension, bradycardia, and cardiovascular collapse. Rare cases of death, primarily in preterm infants, have been reported. Further, an increased incidence of kernicterus, especially in small, preterm infants has been reported. Practitioners administering this and other medications containing benzyl alcohol should consider the combined daily metabolic load of benzyl alcohol from all sources. Premature infants, infants with a low birth weight, and patients who receive a high dose may be more likely to develop toxicity.  
True corticosteroid hypersensitivity reactions are rare. The use of methylprednisolone products in a patient who has previously experienced a hypersensitivity reaction to that product is contraindicated. While a hypersensitivity reaction could be to a specific salt of the corticosteroid (i.e., methylprednisolone sodium succinate), patients who have demonstrated a prior hypersensitivity reaction to methylprednisolone should receive any form of methylprednisolone with extreme caution. It is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids; there have been reports that a cross-sensitivity between hydrocortisone and methylprednisolone may exist. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Such patients should be carefully monitored during and following the administration of any corticosteroid.
Additional monitoring and/or periodic methylprednisolone dosage adjustments may been needed in patients with thyroid disease, as corticosteroid metabolic clearance is affected by thyroid function. Patients with hyperthyroidism have an increased rate of methylprednisolone elimination and may have a less than expected drug-effect; while those with hypothyroidism have decreased corticosteroid clearance and can have an exaggerated drug response.  
Use systemic corticosteroids with caution in the geriatric patient; the risks and benefits of therapy should be considered for any individual patient. According to the Beers Criteria, systemic corticosteroids are considered potentially inappropriate medications (PIMs) for use in geriatric patients with delirium or at high risk for delirium and should be avoided in these patient populations due to the possibility of new-onset delirium or exacerbation of the current condition. The Beers expert panel notes that oral and parenteral corticosteroids may be required for conditions such as exacerbation of chronic obstructive pulmonary disease (COPD) but should be prescribed in the lowest effective dose and for the shortest possible duration. The federal Omnibus Budget Reconciliation Act (OBRA) regulates medication use in residents of long-term care facilities. According to the OBRA guidelines, the need for continued use of a glucocorticoid, with the exception of topical or inhaled formulations, should be documented, along with monitoring for and management of adverse consequences. Intermediate or longer-term use may cause hyperglycemia, psychosis, edema, insomnia, hypertension, osteoporosis, mood lability, or depression.
Patients receiving high-dose systemic corticosteroid therapy, such as methylprednisolone, for any period of time are at risk to develop immunosuppression; patients receiving moderate dosages of systemic corticosteroids for short periods or low doses for prolonged periods also may be at risk. When given in combination with other immunosuppressive agents, there is a risk of significant immunosuppression.
Corticosteroid therapy such as methylprednisolone usually does not contraindicate vaccination with live-virus vaccines when such therapy is of short-term (< 2 weeks); low to moderate dose; long-term alternate day treatment with short-acting preparations; maintenance physiologic doses (replacement therapy); or via topical administration (skin or eye), by aerosol, or by intra-articular, bursal or tendon injection. The immunosuppressive effects of steroid treatment differ, but many clinicians consider a dose equivalent to either 2 mg/kg/day or 20 mg/day of prednisone as sufficiently immunosuppressive to raise concern about the safety of immunization with live-virus vaccines. In general, patients with severe immunosuppression due to large doses of corticosteroids should not receive vaccination with live-virus vaccines. When cancer chemotherapy or immunosuppressive therapy is being considered (e.g., for patients with Hodgkin's disease or organ transplantation), vaccination should precede the initiation of chemotherapy or immunotherapy by >= 2 weeks. Patients vaccinated while on immunosuppressive therapy or in the 2 weeks prior to starting therapy should be considered unimmunized and should be revaccinated at least 3 months after discontinuation of therapy. In patients who have received high-dose, systemic corticosteroids for >= 2 weeks, it is recommended to wait at least 3 months after discontinuation of therapy before administering a live-virus vaccine.
Results from one multicenter, randomized, placebo-controlled study with methylprednisolone hemisuccinate, an IV corticosteroid, showed an increase in early (at 2 weeks) and late (at 6 months) mortality in patients with head trauma who were determined not to have other clear indications for corticosteroid treatment. High doses of systemic corticosteroids, including methylprednisolone, should not be used for the treatment of traumatic brain injury.
Glucocorticoids are naturally occurring hormones that prevent or suppress inflammation and immune responses when administered at pharmacological doses. At the molecular level, unbound glucocorticoids readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a response by modifying transcription and, ultimately, protein synthesis to achieve the steroid's intended action. Such actions can include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, and suppression of humoral immune responses. Some of the net effects include reduction in edema or scar tissue as well as a general suppression in immune response. The degree of clinical effect is normally related to the dose administered. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor molecule arachidonic acid. Likewise, the numerous adverse effects related to corticosteroid use are usually related to the dose administered and the duration of therapy.
Methylprednisolone is administered orally; methylprednisolone sodium succinate solution is administered by IM and IV injection, and by IV infusion; methylprednisolone acetate suspension is administered by IM, intra-articular, intralesional, or soft tissue injection. The onset and duration of action of parenteral methylprednisolone are dependent on the route of administration, the site of administration, and, if the drug is administered by intra-articular or IM injection, the extent of the local blood supply. As with other corticosteroids, once in systemic circulation, methylprednisolone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into breast milk and cross the placenta. Methylprednisolone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The biological half-life of methylprednisolone is 18 to 36 hours.
Affected cytochrome P450 isoenzymes and drug transporters: CYP3A4
Methylprednisolone is a substrate of both CYP3A4, and may exhibit drug interactions with CYP3A4 inducers or inhibitors.
Methylprednisolone is rapidly absorbed following an oral dose. Peak effects following oral administration occur within 1—2 hours.
Following IV administration of methylprednisolone sodium succinate, effects occur within 1 hour and excretion is almost complete within 12 hours. Repeat dosing is needed every 4 to 6 hours if continuously high plasma levels of methylprednisolone are required.
Systemic absorption is rapid following IM administration of methylprednisolone sodium succinate.
Absorption of methylprednisolone from an intra-articular injection site can be very slow, continuing over about 7 days.
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