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Class: Adrenals
Note: This monograph also contains information on Methylprednisolone Acetate, Methylprednisolone Sodium Succinate
ATC Class: H02AB04
VA Class: HS051
CAS Number: 83-43-2
Brands: A-methaPred, Depo-Medrol, Medrol, Medrol Dosepak, Meprolone Unipak, Solu-Medrol


Synthetic glucocorticoid; minimal mineralocorticoid activity.b c d

Uses for Methylprednisolone

Treatment of a wide variety of diseases and conditions principally for glucocorticoid effects as an anti-inflammatory and immunosuppressant agent and for its effects on blood and lymphatic systems in the palliative treatment of various diseases.c d

Usually, inadequate alone for adrenocortical insufficiency because of minimal mineralocorticoid activity.c

Adrenocortical Insufficiency

Corticosteroids are administered in physiologic dosages to replace deficient endogenous hormones in patients with adrenocortical insufficiency.a c

Because production of both mineralocorticoids and glucocorticoids is deficient in adrenocortical insufficiency, hydrocortisone or cortisone (in conjunction with liberal salt intake) usually is the corticosteroid of choice for replacement therapy.a c d m

If methylprednisolone is used, must also administer a mineralocorticoid (fludrocortisone), particularly in infants.a c d

In suspected or known adrenal insufficiency, parenteral therapy may be used preoperatively or during serious trauma, illness, or shock unresponsive to conventional therapy.d e m

In shock unresponsive to conventional therapy, IV therapy in conjunction with other therapy for shock is essential; hydrocortisone is preferred, but a synthetic glucocorticoid like methylprednisolone can be substituted.c e

Adrenogenital Syndrome

Lifelong glucocorticoid treatment of congenital adrenogenital syndrome.a c

In salt-losing forms, cortisone or hydrocortisone is preferred in conjunction with liberal salt intake; a mineralocorticoid may be necessary in conjunction through at least 5–7 years of age.c

A glucocorticoid, usually alone, for long-term therapy after early childhood.c

In hypertensive forms, a “short-acting” glucocorticoid with minimal mineralocorticoid activity (e.g., methylprednisolone, prednisone) is preferred;c avoid long-acting glucocorticoids (e.g., dexamethasone) because of tendency toward overdosage and growth retardation.c


Treatment of hypercalcemia associated with malignancy.a c d m

Usually ameliorates hypercalcemia associated with bone involvement in multiple myeloma.c

Most effective long-term treatment for hypercalcemia associated with breast cancer in postmenopausal women.c

Efficacy varies in other malignancies.c

Treatment of hypercalcemia associated with sarcoidosis.c

Treatment of hypercalcemia associated with vitamin D intoxication.c

Not effective for hypercalcemia caused by hyperparathyroidism.c


Treatment of granulomatous (subacute, nonsuppurative) thyroiditis.a c d m

Anti-inflammatory actions relieves fever, acute thyroid pain, and swelling.c

May reduce orbital edema in endocrine exophthalmos (thyroid ophthalmopathy).c

Usually reserved for palliative therapy in severely ill patients unresponsive to salicylates and thyroid hormones.c

Rheumatic Disorders and Collagen Diseases

Short-term palliative treatment of acute episodes or exacerbations and systemic complications of rheumatic disorders (e.g., rheumatoid arthritis, juvenile arthritis, psoriatic arthritis, acute gouty arthritis, posttraumatic osteoarthritis, synovitis of osteoarthritis, epicondylitis, acute nonspecific tenosynovitis, ankylosing spondylitis, Reiter syndrome, rheumatic fever [especially with carditis]) and collagen diseases (e.g., acute rheumatic carditis, systemic lupus erythematosus, dermatomyositis [polymyositis], polyarteritis nodosa, vasculitis) refractory to more conservative measures.a c d l m

Relieves inflammation and suppresses symptoms but not disease progression.c

Rarely indicated as maintenance therapy.c

May be used as maintenance therapy (e.g., in rheumatoid arthritis, acute gouty arthritis, systemic lupus erythematosus, acute rheumatic carditis) as part of a total treatment program in selected patients when more conservative therapies have proven ineffective.a b c d

Glucocorticoid withdrawal is extremely difficult if used for maintenance; relapse and recurrence usually occur with drug discontinuance.c

Local injection can provide dramatic relief initially for articular manifestations of rheumatic disorders (e.g., rheumatoid arthritis) that involve only a few persistently inflamed joints or for inflammation of tendons or bursae;c inflammation tends to recur and sometimes is more intense after drug cessation.c

Local injection used for the management of cystic tumors of an aponeurosis or tendon (ganglia).d

Local injection can prevent invalidism by facilitating movement of joints that might otherwise become immobile.c

Controls acute manifestations of rheumatic carditis more rapidly than salicylates and may be life-saving; cannot prevent valvular damage and no better than salicylates for long-term treatment.c

Adjunctively for severe systemic complications of Wegener’s granulomatosis, but cytotoxic therapy is the treatment of choice.c

Primary treatment to control symptoms and prevent severe, often life-threatening complications in patients with dermatomyositis and polymyositis, polyarteritis nodosa, relapsing polychondritis, polymyalgia rheumatica and giant-cell (temporal) arteritis, or mixed connective tissue disease syndrome.a c High dosage may be required for acute situations; after a response has been obtained, drug must often be continued for long periods at low dosage.c

Polymyositis associated with malignancy and childhood dermatomyositis may not respond well.c

Rarely indicated in psoriatic arthritis, diffuse scleroderma (progressive systemic sclerosis), acute and subacute bursitis, or osteoarthritis; risks outweigh benefits.a c d m

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In osteoarthritis, intra-articular injections may be beneficial but should be limited in number as joint damage may occur.c d

Dermatologic Diseases

Treatment of pemphigus and pemphigoid, bullous dermatitis herpetiformis, severe erythema multiforme (Stevens-Johnson syndrome), exfoliative dermatitis, uncontrollable eczema, cutaneous sarcoidosis, mycosis fungoides, lichen planus, lichen simplex chronicus (neurodermatitis), severe psoriasis, and severe seborrheic dermatitis.a c d e

Usually reserved for acute exacerbations unresponsive to conservative therapy.c

Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris and pemphigoid, and high or massive doses may be required.c

For control of severe or incapacitating allergic conditions (e.g., contact dermatitis, atopic dermatitis) intractable to adequate trials of conventional treatment.a d e f m

Chronic skin disorders seldom an indication for systemic glucocorticoids.c

Intralesional or sublesional injections occasionally indicated for localized chronic skin disorders, keloids, psoriatic plaques, alopecia areata, discoid lupus erythematosus, necrobiosis lipoidica diabeticorum, granuloma annulared m unresponsive to topical therapy.c

Rarely indicated for psoriasis;c if used, exacerbation may occur when the drug is withdrawn or dosage is decreased.c

Rarely indicated systemically for alopecia (areata, totalis, or universalis).c May stimulate hair growth, but hair loss returns when the drug is discontinued.c

Allergic Conditions

For control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment and control of acute manifestations, including anaphylactic and anaphylactoid reactions, angioedema, acute noninfectious laryngeal edema, serum sickness, allergic symptoms of trichinosis, asthma, urticarial transfusion reactions, drug hypersensitivity reactions, and severe seasonal or perennial rhinitis.a c d e f m

Systemic therapy usually reserved for acute conditions and severe exacerbations.c

For acute conditions, usually used in high dosage and with other therapies (e.g., antihistamines, sympathomimetics).c

Reserve prolonged treatment of chronic allergic conditions for disabling conditions unresponsive to more conservative therapy and when risks of long-term glucocorticoid therapy are justified.c

Ocular Disorders

To suppress a variety of allergic and nonpyogenic ocular inflammations.c

To reduce scarring in ocular injuries.c

For the treatment of severe acute and chronic allergic and inflammatory processes involving the eye and adnexa (e.g., allergic conjunctivitis, keratitis, allergic corneal marginal ulcers, herpes zoster ophthalmicus, iritis and iridocyclitis, chorioretinitis, diffuse posterior uveitis and choroiditis, anterior segment inflammation, optic neuritis, sympathetic ophthalmia, temporal arteritis).a c d e f m

Acute optic neuritis optimally treated with initial high-dose IV therapy followed by chronic oral therapy. Assists in recovery of vision and slows progression to clinically definite multiple sclerosis.

Less severe allergic and inflammatory allergic conditions of the eye are treated with topical (to the eye) corticosteroids.g

Topically applied glucocorticoids appear to be as effective as systemic steroids for the treatment of most anterior ocular inflammations.c

Systemically in stubborn cases of anterior segment eye disease and when deeper ocular structures are involved.c


Adjunctively for moderate to severe exacerbations of asthma and for maintenance in persistent asthma.c g

Systemically (oral or IV) for treatment of moderate to severe acute exacerbations of asthma (oral prednisone usually preferred); speeds resolution of airflow obstruction and reduces rate of relapse.g

Because onset of effects is delayed, do not use alone for emergency treatment.c

Early systemic glucocorticoid therapy particularly important for asthma exacerbations in infants and children.g

In hospital management of an acute asthma exacerbation, may give systemic adjunctive glucocorticoids if response to oral inhalation therapy is not immediate, if oral corticosteroids were used as self-medication prior to hospitalization, or if the episode is severe.c

For severe persistent asthma once initial control is achieved, high dosages of inhaled corticosteroids are preferable to oral glucocorticoids for maintenance because inhaled corticosteroids have fewer systemic effects.

Maintenance therapy with low doses of an orally inhaled corticosteroid is preferred treatment for adults and children with mild persistent asthmac (i.e., patients with daytime symptoms of asthma more than twice weekly but less than once daily, and nocturnal symptoms of asthma more than twice per month).b

Orally as an adjunct to other therapy to speed resolution of all but the mildest exacerbations of asthma when response to a short-acting inhaled β2-agonist is not prompt or sustained after 1 hour or in those who have a history of severe exacerbations.c

Oral glucocorticoids with minimal mineralocorticoid activity and relatively short half-life (e.g., prednisone, prednisolone, methylprednisolone) are preferred.


For severe exacerbations of COPD, a short (e.g., 1–2 weeks) course of oral glucocorticoids can be added to existing therapy.

Effects in stable COPD are much less dramatic than in asthma, and role of glucocorticoids in the management of stable COPD is limited to very specific indications.


Adjunctive treatment of croup in pediatric patients.g

Decreases edema in laryngeal mucosa.g

Reduces need for hospitalization, shorter duration of hospitalization, and reduces need for subsequent interventions (e.g., epinephrine).g


Management of symptomatic sarcoidosis.a c d e f m

Systemic glucocorticoids are indicated for hypercalcemia; ocular, CNS, glandular, myocardial, or severe pulmonary involvement; or severe skin lesions unresponsive to intralesional injections of glucocorticoids.c

Advanced Pulmonary and Extrapulmonary Tuberculosis

Systemically as adjunctive therapy with effective antimycobacterial agents (e.g., streptomycin, isoniazid) to suppress manifestations related to the host’s inflammatory response to the bacillus (Mycobacterium tuberculosis) and ameliorate complications in severe pulmonary or extrapulmonary tuberculosis.a m

Adjunctive glucocorticoid therapy may enhance short-term resolution of disease manifestations (e.g., clinical and radiographic abnormalities) in advanced pulmonary tuberculosis and also may reduce mortality associated with certain forms of extrapulmonary disease (e.g., meningitis, pericarditis).

Systemic adjunctive glucocorticoids may reduce sequelae (e.g., intellectual impairment) and/or improve survival in moderate to severe tuberculous meningitis; used in the treatment of tuberculous meningitis with subarachnoid block or impending block concurrently with appropriate antituberculous chemotherapy.a d e f m

Systemic adjunctive glucocorticoid therapy rapidly reduces the size of pericardial effusions and the need for drainage procedures and decreases mortality (probably through control of hemodynamically threatening effusion) in acute tuberculous pericarditis.

Hastens the resolution of pain, dyspnea, and fever associated with tuberculous pleurisy.c

Lipid Pneumonitis

Promotes the breakdown or dissolution of pulmonary lesions and eliminates sputum lipids in lipid pneumonitis.c

Pneumocystis jiroveci Pneumonia

Systemic adjunctive glucocorticoids decrease the likelihood of deterioration of oxygenation, respiratory failure, and/or death in moderate to severe Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia in AIDS.

Prevents early deterioration in oxygenation associated with antipneumocystis therapy; initiate adjunctive glucocorticoid therapy as early as possible in moderate to severe pneumocystis pneumonia.

Not known whether patients with mild pneumocystis pneumonia (arterial oxygen pressure >70 mm Hg or arterial-alveolar gradient <35 mm Hg on room air) will have clinically important benefit with adjunctive glucocorticoid therapy.

Oral prednisone or parenteral methylprednisolone generally is preferred.

Loeffler’s Syndrome

Symptomatic relief of acute manifestations of symptomatic Loeffler’s syndrome not manageable by other means.a f


Symptomatic relief of acute manifestations of berylliosis.a d f m

Aspiration Pneumonitis

Symptomatic relief of acute manifestations of aspiration pneumonitis.a d f


Adjunct to anti-infective therapy in the treatment of anthrax in an attempt to ameliorate toxin-mediated effects associated with Bacillus anthracis infections.

For cutaneous anthrax if there are signs of systemic involvement or extensive edema involving the neck and thoracic region, anthrax meningitis, and inhalational anthrax that occurs as the result of exposure to anthrax spores in the context of biologic warfare or bioterrorism if extensive edema, respiratory compromise, or meningitis is present.

Hematologic Disorders

Management of acquired (autoimmune) hemolytic anemia, pure red cell aplasia, idiopathic thrombocytopenic purpura (ITP), secondary thrombocytopenia, erythroblastopenia, or congenital (erythroid) hypoplastic anemia.a d e f m

High or even massive dosages decrease bleeding tendencies and normalize blood counts; does not affect the course or duration of hematologic disorders.c

Glucocorticoids, immune globulin IV (IGIV), or splenectomy are first-line therapies for moderate to severe ITP, depending on the extent of bleeding involved.

May not affect or prevent renal complications in Henoch-Schoenlein purpura.c

Insufficient evidence of effectiveness in aplastic anemia in children, but widely used.c


Although IV glucocorticoids may be life-saving in shock secondary to adrenocortical insufficiency (see Adrenocortical Insufficiency under Uses), the value of the drugs in the treatment of shock resulting from other causes is controversial.c

Management of shock should be based on specific treatment of the primary cause and secondary abnormalities, and glucocorticoids, if used, should be regarded only as adjunctive supportive treatment.c

Value in adjunctive treatment of septic shock is particularly controversial. Conflicting evidence regarding effects of high-dose regimens on morbidity and mortality in septic shock. In a clinical study, methylprednisolone was ineffective in the treatment of sepsis syndrome and septic shock, and may increase the risk of mortality in certain patients (i.e., patients with increased Scr or those who develop secondary infections after treatment).e


To reduce the pain, fever, and inflammation of pericarditis, including that associated with MI.c

Glucocorticoids can provide effective symptomatic relief, but aspirin considered the treatment of choice for post-MI pericarditis because of greater evidence establishing benefit.

Important to distinguish between pain caused by pericarditis and that caused by ischemia since management will differ.

Consider possibility that cardiac rupture may account for recurrent pain since use of glucocorticoids may be a risk factor in its development.

Glucocorticoids may cause thinning of developing scar and myocardial rupture.

Management of tuberculous pericarditis. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.)

GI Diseases

Short-term palliative therapy for acute exacerbations and systemic complications of ulcerative colitis, regional enteritis (Crohn’s disease), and celiac disease.a c d e f m

Do not use if a probability of impending perforation, abscess, or other pyogenic infection.e

Rarely indicated for maintenance therapy in chronic GI diseases (e.g., ulcerative colitis, celiac disease) since does not prevent relapses and may produce severe adverse reactions with long-term administration.c

Occasionally, low dosages, in conjunction with other supportive therapy, may be useful for disease unresponsive to the usual therapy indicated for chronic conditions.c

Management of mildly to moderately active and moderately to severely active Crohn’s disease .

Parenteral glucocorticoids recommended for patients with severe fulminant Crohn’s disease. Once patients respond to parenteral therapy, they should gradually be switched to an equivalent regimen of an oral glucocorticoid.

Some experts state that glucocorticoids should not be used for the management of mildly to moderately active Crohn’s disease because of the high incidence of adverse effects and their use should be reserved for patients with moderately to severely active disease.

Glucocorticoids should not be used for maintenance therapy of chronic GI diseases (e.g., ulcerative colitis, Crohn’s disease) because they usually do not prevent relapses and the drugs may produce severe adverse effects with long-term administration.a c

Glucocorticoids have been used in the management of moderately to severely active Crohn’s disease and in mild esophageal or gastroduodenal Crohn’s disease in pediatric patients.

Neoplastic Diseases

Alone or as a component of various chemotherapeutic regimens in the palliative treatment of neoplastic diseases of the lymphatic system (e.g., leukemias and lymphomas in adults and acute leukemias in children).a d e f m

Treatment of breast cancer; glucocorticoids alone not as effective as other agents (e.g., cytotoxic agents, hormones, antiestrogens) and should be reserved for unresponsive disease.c

Glucocorticoids alone or as a component of various combination chemotherapeutic regimens for palliative treatment of advanced, symptomatic (i.e., painful) hormone-refractory prostate cancer.

Cancer Chemotherapy-induced Nausea and Vomiting

Prevention of nausea and vomiting associated with emetogenic cancer chemotherapy.

Cerebral Edema

To decrease cerebral edema associated with brain tumors and neurosurgery.c d m

Cerebral edema associated with pseudotumor cerebri may also benefit, but efficacy of glucocorticoids is controversial and remains to be established.c

Edema resulting from brain abscesses is less responsive than that resulting from brain tumors.c

Pharmacologic management of cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy.c d f

Head Injury

Efficacy of glucocorticoid therapy is not established in patients with head injury; such therapy can be detrimental and is associated with a substantial increase in risk of death. Use to improve outcome or reduce intracranial pressure not recommended in patients with head injury.

Cerebral Malaria

Glucocorticoids are not effective and can have detrimental effects in the management of cerebral malaria caused by Plasmodium falciparum; no longer recommended for this condition.c

Acute Spinal Cord Injury

Some evidence indicates that large IV doses of glucocorticoids (i.e., methylprednisolone) can improve motor and sensory function in patients with acute spinal cord injury when treatment is initiated promptly following injury (within 8 hours). It is not known whether improvement in neurologic function with such therapy will routinely lead to specific improvements in disability.

Low Back Pain

Has been used epidurally (alone or combined with a local anesthetic and/or an opiate analgesic) for symptomatic relief of low back pain; although use remains controversial and convincing evidence of efficacy is lacking, most experts consider such therapy an option for short-term relief of acute, subacute, or chronic radicular pain in patients with low back pain and radiculopathy associated with disk disease or herniation or spinal stenosis when more conservative therapies (e.g., rest, analgesics, physical therapy) fail and as a means of potentially avoiding surgery.

Limited evidence suggests that therapeutic facet joint and intradiscal glucocorticoid injections are minimally effective or ineffective in the treatment of low back pain, although facet joint injections may be useful in some patients with facet arthropathy. Inclusion of a glucocorticoid in trigger point injections does not appear to be beneficial.

Sacroiliac joint injections performed using fluoroscopic guidance may provide temporary pain relief in some patients when the principal source of spinal pain is the sacroiliac joint.

Oral glucocorticoids have been used; however, they do not appear to be effective and evidence supporting such use is lacking.

Bacterial Meningitis

Limited data in animals suggest that dexamethasone may be superior to methylprednisolone in reversing certain CSF abnormalities (e.g., intracranial hypertension, elevated lactate concentrations) associated with bacterial meningitis, and experience is insufficient to allow recommendation of glucocorticoids other than dexamethasone for adjunctive therapy in bacterial meningitis.

Short-term IV adjunctive therapy with dexamethasone is preferred.

Multiple Sclerosis

Glucocorticoids are drugs of choice for the management of acute relapses of multiple sclerosisa d m and have replaced corticotropin as the therapy of choice because of a more rapid onset of action, more consistent effects, and fewer adverse effects.

Anti-inflammatory and immunomodulating effects accelerate neurologic recovery by restoring the blood-brain barrier, reducing edema, and possibly improving axonal conduction.

Shortens the duration of relapse and accelerates recovery; remains to be established whether the overall degree of recovery improves or the long-term course is altered.

Myasthenia Gravis

Management of myasthenia gravis, usually when there is an inadequate response to anticholinesterase therapy.

Parenterally for the treatment of myasthenic crisis.

Organ Transplants

In massive dosage, used concomitantly with other immunosuppressive drugs to prevent rejection of transplanted organs.c

Incidence of secondary infections is high with immunosuppressive drugs; limit to clinicians experienced in their use.c


Treatment of trichinosis with neurologic or myocardial involvement.a d e f

Nephrotic Syndrome and Lupus Nephritis

Treatment of idiopathic nephrotic syndrome without uremia.a d e f

Can induce diuresis and remission of proteinuria in nephrotic syndromea c d e f m secondary to lupus erythematosus or primary renal disease, especially when there is minimal renal histologic change.b d m

Treatment of lupus nephritis.a d e

Carpal Tunnel Syndrome

Local injection of glucocorticoids (e.g., methylprednisolone, betamethasone) into the tissue near the carpal tunnel has been used in a limited number of patients to relieve symptoms (e.g., pain, edema, sensory deficit) of carpal tunnel syndrome.

Methylprednisolone Dosage and Administration


  • Route of administration and dosage depend on the condition being treated and the patient response.a

Alternate-day Therapy

  • Alternate-day therapy in which a single dose (twice the usual daily dosage) is administered every other morning is the dosage regimen of choice for long-term oral glucocorticoid treatment of most conditions.a c This regimen provides relief of symptoms while minimizing adrenal suppression, protein catabolism, and other adverse effects.a c

  • If alternate-day therapy is preferred, only use a “short-acting” glucocorticoid that suppresses the HPA axis <1.5 days after a single oral dose (e.g., methylprednisolone, prednisone, prednisolone).c

  • Some conditions (e.g., rheumatoid arthritis, ulcerative colitis) require daily glucocorticoid therapy because symptoms of the underlying disease cannot be controlled by alternate-day therapy.c

Discontinuance of Therapy

  • A steroid withdrawal syndrome consisting of lethargy, fever, and myalgia can develop following abrupt discontinuance.c Symptoms often occur without evidence of adrenal insufficiency (while plasma glucocorticoid concentrations were still high but were falling rapidly).c

  • If used for only brief periods (a few days) in emergency situations, may reduce and discontinue dosage quite rapidly.c

  • Very gradually withdraw systemic glucocorticoids until recovery of HPA-axis function occurs following long-term therapy with pharmacologic dosages.c d e m (See Adrenocortical Insufficiency under Warnings.)

  • Exercise caution when transferring from systemic glucocorticoid to oral or nasal inhalation corticosteroid therapy.c

  • Many methods of slow withdrawal or “tapering” have been described.c

  • In one suggested regimen, decrease by 2–4 mg every 3–7 days of until the physiologic dose (4 mg) is reached.c

  • Other recommendations state that decrements usually should not exceed 2 mg every 1–2 weeks.c

  • When a physiologic dosage has been reached, single 20-mg oral morning doses of hydrocortisone can be substituted for whatever glucocorticoid the patient has been receiving.c After 2–4 weeks, may decrease hydrocortisone dosage by 2.5 mg every week until a single morning dosage of 10 mg daily is reached.c

  • For certain acute allergic conditions (e.g., contact dermatitis such as poison ivy) or acute exacerbations of chronic allergic conditions, glucocorticoids may be administered short term (e.g., for 6 days).c Administer an initially high dose on the first day of therapy, and then withdraw therapy by tapering the dose over several days.c


Administer orally, by IV injection or infusion, or IM injection.a d e f m

Administer for local effect by intra-articular, intralesional, intrasynovial, soft-tissue, or epidural injection.c d m

Generally reserve IM or IV therapy for patients who are not able to take the drug orally or for use in an emergency situation.d e After the initial emergency period, a longer-acting injectable corticosteroid preparation or oral administration of a corticosteroid should be considered.b

Methylprednisolone acetate injections (in multiple-dose vials) contain benzyl alcohol; do not administer intrathecally because of reports of severe adverse events with such use.m

Oral Administration


Administer orally as tablets.a

IV Administration

For solution and drug compatibility information, see Compatibility under Stability.

Methylprednisolone Sodium Succinate

Administer by IV injection or infusion.e

Reconstitution of Methylprednisolone Sodium Succinate

Reconstitute by pressing on a plastic activator to force the diluent provided from the manufacturer from an upper compartment of a 2-compartment vial to a lower compartment containing sterile powder.e Alternately, use bacteriostatic water for injection with benzyl alcohol for reconstitution.e

Dilution of Methylprednisolone Sodium Succinate

When administered by IV infusion, the drug can be added to 5% dextrose, or 0.9% sodium chloride, or 5% dextrose in sodium chloride injection.e

Rate of Administration of Methylprednisolone Sodium Succinate

Direct IV injection: Administer over a period of several minutes.e

IM Administration

Do not administer IM for conditions prone to bleeding (e.g., idiopathic thrombocytopenic purpura [ITP]).e

Methylprednisolone Acetate

Administer by IM injection.d m

Because it is slowly absorbed, IM administration is not indicated when an immediate effect of short duration is required.d

Commercially available single-dose vials are for single use only.d m Although initially sterile, multiple use of a single-dose vial may result in contamination, unless strict aseptic technique is observed.m

Methylprednisolone Sodium Succinate

Administer by IM injection.e

Absorption from IM injection sites is rapid.b

Intra-articular, Intralesional, and Soft Tissue Administration

Methylprednisolone Acetate

Administer by intra-articular, intralesional, intrasynovial, or soft tissue injection.b d m (See Dermatologic Effects under Cautions.)

May infiltrate the tissue surrounding the joint with a local anesthetic (e.g., procaine hydrochloride) before administration of methylprednisolone acetate.b d

Examine joint fluid to exclude sepsis and avoid injection into an infected site; if joint sepsis is evident, institute appropriate antibacterial therapy.c d m Symptoms of septic arthritis include local swelling, further restriction of joint motion, fever, or malaise.c d m Do not inject glucocorticoids into unstable joints and caution patients not to overuse joints in which the inflammatory process still is active despite symptomatic improvement.c

Epidural Administration

Long-acting injectable suspension has been administered by epidural injection, although safety of epidural injections using preserved formulations is controversial and epidural administration of these formulations is not recommended by the manufacturer.c Limited evidence suggests that large particles in glucocorticoid suspensions may cause embolic vascular occlusion following inadvertent intra-arterial injection.

Inject into the epidural space near the site where the nerve roots pass before entering the intervertebral foramen.

Epidural injections may be performed by caudal, interlaminar, or transforaminal approaches; the transforaminal approach requires the smallest injection volume and appears to be the most specific and possibly most effective route.

Because of the potential for complications related to improper needle placement or drug administration, many experts state that epidural injections should be performed by an experienced clinician using fluoroscopic guidance and contrast control to ensure that the needle is correctly positioned and that the injection is not performed intravascularly, intrathecally, or into tissues other than the epidural space.

Optimal technique, dosage, timing of initial injection, injection frequency, and maximum number of injections remain to be established.


Available as methylprednisolone, methylprednisolone acetate, and methylprednisolone sodium succinate.a b d e m Dosage of methylprednisolone sodium succinate or methylprednisolone acetate is expressed in terms of methylprednisolone or methylprednisolone acetate, respectively.d e m

After a satisfactory response is obtained, decrease dosage in small decrements to the lowest level that maintains an adequate clinical response, and discontinue the drug as soon as possible.a b e

Monitor patients continually for signs that indicate dosage adjustment is necessary, such as remissions or exacerbations of the disease and stress (surgery, infection, trauma).b

High dosages may be required for acute situations of certain rheumatic disorders and collagen diseases; after a response has been obtained, drug often must be continued for long periods at low dosage.c

High or massive dosages may be required in the treatment of pemphigus, exfoliative dermatitis, bullous dermatitis herpetiformis, severe erythema multiforme, or mycosis fungoides.c Early initiation of systemic glucocorticoid therapy may be life-saving in pemphigus vulgaris.c Reduce dosage gradually to the lowest effective level, but discontinuance may not be possible.c d m

Massive dosages may be required for treatment of shock.b

Increase dosage of rapidly acting corticosteroids in patients subjected to any unusual stress before, during, and after the stressful situation.a d e m

Pediatric Patients

Base pediatric dosage on severity of the disease and patient response rather than on strict adherence to dosage indicated by age, body weight, or body surface area.b e

Usual Dosage

0.117–1.66 mg/kg daily or 3.3–50 mg/m2 daily, administered in 3 or 4 divided doses.b


Methylprednisolone sodium succinate: 0.03–0.2 mg/kg or 1–6.25 mg/m2 IM 1–2 times daily has been used.b


To gain prompt control of asthma in infants and children ≤4 years of age with very poorly controlled, moderate-to-severe asthma (i.e., >3 exacerbations per year requiring oral corticosteroids) and in children 5–11 years of age with asthma of comparable control and severity (i.e., ≥2 exacerbations per year requiring oral corticosteroids): Methylprednisolone 1–2 mg/kg daily (maximum 60 mg daily) may be added to existing asthma therapy.

In children ≤11 years of age undergoing emergency department treatment for moderate-to-severe acute asthma exacerbations not controlled with an inhaled β2-adrenergic agonist: May add methylprednisolone 1–2 mg/kg daily in 2 divided doses (maximum 60 mg daily). Continue treatment until patient achieves a PEF of 70% of predicted or personal best.

Allergic Conditions

Methylprednisolone acetate: For control of severe or incapacitating allergic conditions (e.g., bronchial asthma, seasonal or perennial allergic rhinitis) intractable to adequate trials of conventional therapy, initially, 1–2 mg/kg.

To gain prompt control of asthma in infants and children ≤4 years of age or children ≥5 years of age with very poorly-controlled, moderate-to-severe asthma (as an alternative to a short course of an oral corticosteroid) who are vomiting or noncompliant with oral corticosteroid therapy: 7.5 mg/kg or 240 mg as a single dose of methylprednisolone acetate, respectively. Relief of asthma symptoms should occur within 6–48 hours and persist for several days to 2 weeks.d

Relief of coryzal symptoms of allergic rhinitis should occur within 6 hours and persist for several days to 3 weeks.d


Methylprednisolone sodium succinate: For control of severe or incapacitating allergic conditions (e.g., bronchial asthma) intractable to adequate trials of conventional therapy, initially, 1–2 mg/kg.


Methylprednisolone sodium succinate: Initially, 1–2 mg/kg.

Pneumocystis jiroveci Pneumonia

Methylprednisolone sodium succinate in children >13 years of age with AIDS and moderate to severe Pneumocystis jiroveci pneumonia: 30 mg twice daily for 5 days, followed by 30 mg once daily for 5 days, and then 15 mg once daily for 11 days (or until completion of the anti-infective regimen). Initiate within 24–72 hours of initial antipneumocystis therapy.

Acute Spinal Cord Injury

Methylprednisolone sodium succinate: 30 mg/kg IV (administered over 15 minutes), followed after 45 minutes by a continuous IV infusion of 5.4 mg/kg per hour for 23 hours.

Lupus Nephritis

Methylprednisolone sodium succinate: 30 mg/kg IV every other day for 6 doses.b


Usual Dosage

Initially, 2–60 mg daily, depending on disease being treated, and is usually divided into 4 doses.b

IV or IM

Methylprednisolone sodium succinate: Usually, 10–250 mg; may repeat up to 6 times daily.b

IV then IV or IM

Methylprednisolone sodium succinate: For high-dose therapy, administer 30 mg/kg over at least 30 minutes.e May repeat every 4–6 hours for 48 hours.e Continue high-dose therapy only until the condition stabilizes, usually ≤48–72 hours.e

For other conditions, 10–40 mg over several minutes.e Administer subsequent doses IV or IM depending on response and clinical condition.e


Methylprednisolone acetate: 10–80 mg.b

Methylprednisolone acetate for maintenance of patients with rheumatoid arthritis: 40–120 mg weekly.

When methylprednisolone acetate suspension is given as a temporary substitute for oral therapy, dose of the suspension should be equal to the total daily oral dose of methylprednisolone; administer IM once daily.d m If a prolonged effect is desired, may administer an IM dose of methylprednisolone acetate equal to 7 times the daily oral dose of methylprednisolone once weekly.d m

Intraarticular, Intrasynovial, Intralesional, or Soft-tissue Injection

Varies depending on location, size, and degree of inflammation.b d m In chronic cases, repeat injections at intervals ranging from 1–5 weeks or more, depending on degree of relief resulting from initial injection.d m

Large Joints (e.g., knee): 20–80 mg of methylprednisolone acetate.d m

Smaller Joints: 4–40 mg of methylprednisolone acetate repeated.d m

Bursae, Ganglia, Tendinitis, Epicondylitis: 4–30 mg of methylprednisolone acetate; repeat if necessary for recurrent or chronic conditions.d m

Soft Tissue: 4–30 mg of methylprednisolone acetate for soft tissue infiltration; repeat if necessary for recurrent or chronic conditions.d .


In adults and adolescents with very poorly controlled, moderate-to-severe asthma (i.e., ≥2 exacerbations per year requiring oral corticosteroids): May add methylprednisolone 40–60 mg daily as a single dose or in 2 divided doses to low-to-high maintenance dosages of the inhaled corticosteroid and a long-acting inhaled β2-agonist bronchodilator. Continue with a short course (usually 3–10 days) of oral corticosteroid therapy until patient achieves a PEF of 80% of his or her personal best and until symptoms resolve. May need a longer duration of treatment in some patients. There is no evidence that tapering the dosage after improvement will prevent a relapse.

In adults and adolescents with severe asthma who are inadequately controlled with a high-dose inhaled corticosteroid, intermittent oral corticosteroid therapy, and a long-acting inhaled β2-agonist bronchodilator (based on consensus and clinical experience): May use methylprednisolone 7.5–60 mg daily in the morning or every other day. May consider a short course (2 weeks) of oral corticosteroids to confirm clinical response prior to implementing long-term therapy with these agents. Once long-term oral corticosteroid therapy is initiated, use the lowest possible effective dosage (i.e., alternate-day or once-daily administration); monitor the patient carefully for adverse effects. Once asthma is well controlled, make repeated attempts to reduce the oral corticosteroid dosage.

In adults and adolescents undergoing emergency department treatment for moderate-to-severe acute asthma exacerbations not controlled with an inhaled β2-adrenergic agonist: May add methylprednisolone 40–80 mg daily as a single dose or in 2 divided doses to an inhaled β2-adrenergic agonist. Continue treatment until patient achieves a PEF of 70% of predicted or personal best.

Dermatologic Diseases
Intralesional Injection

Methylprednisolone acetate: 20–60 mg into the lesion.d For large lesions, it may be necessary to administer 20–40 mg doses by repeated local injections spaced across the affected area.d Usually, 1–4 injections are employed, with interval between injections varying with the type of lesion treated and the duration of improvement observed with each injection.d


Methylprednisolone acetate: In patients with dermatologic lesions, usually, 40–120 mg of methylprednisolone acetate once weekly for 1–4 weeks.d

Methylprednisolone acetate: In seborrheic dermatitis, 80 mg weekly may be adequate to control the condition.d m

Adrenogenital Syndrome

Methylprednisolone acetate: 40 mg every 2 weeks.d m

Allergic Conditions

For certain conditions (e.g., contact dermatitis, including poison ivy), 24 mg (6 tablets) for the first day, which is then tapered by 4 mg daily until 21 tablets have been administered. (See Tapered Dosage Schedule table.)b

Tapered Dosage Schedule

Day 1

Administer 8 mg (2 tablets) twice daily (before breakfast and at bedtime)b and 4 mg (1 tablet) twice daily (after lunch and dinner).

Day 2

Administer 4 mg (1 tablet) 3 times daily (before breakfast, after lunch, and after dinner) and 8 mg (2 tablets) at bedtime.b

Day 3

Administer 4 mg (1 tablet) 4 times daily (before breakfast, after lunch, after dinner, and at bedtime).b

Day 4

Administer 4 mg (1 tablet) 3 times daily (before breakfast, after lunch, and at bedtime).b

Day 5

Administer 4 mg (1 tablet) twice daily (before breakfast and at bedtime).b

Day 6

Administer 4 mg (1 tablet) before breakfast.b

Some clinicians suggest tapering the dosage of the drug over 12 days may be associated with a lower incidence of flare-up of the dermatitis than that associated with 6-day therapy.b


Methylprednisolone acetate: In acute severe dermatitis due to poison ivy, 80–120 mg as a single dose.d m In chronic contact dermatitis, repeated injections at 5- to 10-day intervals may be necessary.d

Methylprednisolone acetate: For control of severe or incapacitating allergic conditions (e.g., bronchial asthma, seasonal or perennial allergic rhinitis) intractable to adequate trials of conventional therapy, 80–120 mg.d m Relief of coryzal symptoms of allergic rhinitis should occur within 6 hours and persist for several days to 3 weeks.

To gain prompt control of asthma in patients with very poorly controlled, moderate-to-severe asthma (as an alternative to a short course of an oral corticosteroid) who are vomiting or noncompliant with oral corticosteroid therapy: 240 mg of methylprednisolone acetate as a single dose. Relief of asthma symptoms should occur within 6–48 hours and persist for several days to 2 weeks.d m

Acute Exacerbations of Multiple Sclerosis

For moderate to severe relapses, 1 g daily for 3–5 days, followed by 60 mg of oral prednisone daily, tapering the dosage over 12 days.

Alternatively, 1 g or 15 mg/kg of IV methylprednisolone tapered over 15 days to 1 mg/kg, followed by oral prednisone or prednisolone in gradually decreasing dosages over several weeks to months.c


160 mg daily for 1 week, followed by 64 mg every other day for a month.a d e f

Pneumocystis jiroveci Pneumonia

In adults with AIDS and moderate to severe Pneumocystis jiroveci pneumonia, 30 mg twice daily for 5 days, followed by 30 mg once daily for 5 days, and then 15 mg once daily for 11 days (or until completion of the anti-infective regimen). Initiate within 24–72 hours of initial antipneumocystis therapy.


Life-threatening shock: massive doses of methylprednisolone as the sodium succinate such as 30 mg/kg by direct IV injection (over 3–15 minutes) initially and repeated every 4–6 hours if needed or 100–250 mg by direct IV injection (over 3–15 minutes) initially and repeated at 2- to 6-hour intervals as required.b

Alternatively, following the initial dose by direct IV injection, additional doses of 30 mg/kg may be administered by slow continuous IV infusion every 12 hours for 24–48 hours.b

Continue high-dose therapy only until the patient’s condition has stabilized and usually not beyond 48–72 hours.b

Acute Spinal Cord Injury

Methylprednisolone sodium succinate: Initially, 30 mg/kg of methylprednisolone by rapid IV injection over 15 minutes, followed in 45 minutes by IV infusion of 5.4 mg/kg per hour for 23 hours (total dose administered over 24 hours), has been recommended.

Lupus Nephritis

Methylprednisolone sodium succinate: 1 g IV (over a 1-hour period) daily for 3 consecutive days (“pulse” therapy).b

“Pulse” therapy has been followed by long-term oral prednisone or prednisolone therapy (0.5–1 mg/kg per day).

Optic Neuritis

1 g daily for 3 days followed by oral prednisone 1 mg/kg daily for 11 days has been used.

Cautions for Methylprednisolone


  • Known hypersensitivity to methylprednisolone, any ingredient in the respective formulation, or any other corticosteroid.d m

  • IM administration in patients with idiopathic thrombocytopenic purpura.m

  • Systemic fungal infections,a d m except when administered as an intra-articular injection for localized joint conditions.d m

  • Concurrent administration of live or live, attenuated vaccines in patients receiving immunosuppressive doses of corticosteroids.a d e m (See Specific Drugs under Interactions.)

  • Intrathecal administration of methylprednisolone acetate.d m

  • Methylprednisolone sodium succinate injection preparations containing benzyl alcohol in premature neonates.e m

  • Methylprednisolone acetate injection preparations (in multiple-dose vials) containing benzyl alcohol in premature infants.m

  • Epidural administration in patients with local or systemic infection; individuals with bleeding disorders or receiving concurrent anticoagulant therapy (e.g., warfarin, heparin, antiplatelet agents); patients with known hypersensitivity to local anesthetic agents, contrast agents, or glucocorticoids; and patients who experienced complications with prior glucocorticoid injections.



Adrenocortical Insufficiency

When given in supraphysiologic doses for prolonged periods, glucocorticoids may cause decreased secretion of endogenous corticosteroids by suppressing pituitary release of corticotropin (secondary adrenocortical insufficiency).c

The degree and duration of adrenocortical insufficiency is highly variable among patients and depends on the dose, frequency and time of administration, and duration of glucocorticoid therapy.c

Acute adrenal insufficiency (even death) may occur if the drugs are withdrawn abruptly or if patients are transferred from systemic glucocorticoid therapy to local (e.g., inhalation) therapy.c

Withdraw methylprednisolone very gradually following long-term therapy with pharmacologic dosages.c d e m (See Discontinuance of Therapy under Dosage and Administration.)

Adrenal suppression may persist up to 12 months in patients who receive large dosages for prolonged periods.c

Until recovery occurs, signs and symptoms of adrenal insufficiency may develop if subjected to stress (e.g., infection, surgery, trauma) and replacement therapy may be required.c d e f m Since mineralocorticoid secretion may be impaired, sodium chloride and/or a mineralocorticoid should also be administered.c e f m

If the disease flares up during withdrawal, dosage may need to be increased and followed by a more gradual withdrawal.c


Increased susceptibility to infections secondary to glucocorticoid-induced immunosuppression.d e m Certain infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome in such patients.d e m (See Increased Susceptibility to Infection under Warnings.)

Administration of live virus vaccines, including smallpox, is contraindicated in patients receiving immunosuppressive dosages of glucocorticoids.a d e m If inactivated viral or bacterial vaccines are administered to such patients, the expected serum antibody response may not be obtained.e May undertake indicated immunization procedures in patients receiving glucocorticoids as replacement therapy (e.g., Addison’s disease).a d e f m

Increased Susceptibility to Infection

Glucocorticoids, especially in large doses, increase susceptibility to and mask symptoms of infection.a d e f m f

Infections with any pathogen, including viral, bacterial, fungal, protozoan, or helminthic infections in any organ system, may be associated with glucocorticoids alone or in combination with other immunosuppressive agents.a d e m

Infections may be mild, but they can be severe or fatal, and localized infections may disseminate.a d e m

Do not inject methylprednisolone acetate intra-articularly, bursally, or into a tendon for local effect in patients with acute infection.d m

Do not use, except in life-threatening situations, in patients with viral infections or bacterial infections not controlled by anti-infectives.c

Some infections (e.g., varicella [chickenpox], measles) can have a more serious or even fatal outcome, particularly in children.d m

Children and any adult who are not likely to have been exposed to varicella or measles should avoid exposure to these infections while receiving glucocorticoids.d m

If exposure to varicella or measles occurs in susceptible patients, treat appropriately (e.g., VZIG, IG, acyclovir).a d e m

Fatal outcome (e.g., in those developing hemorrhagic varicella) may not always be avoided even if appropriate therapy is initiated aggressively.

Immunosuppression may result in activation of latent infection or exacerbation of intercurrent infections (e.g., those caused by Candida, Mycobacterium, Toxoplasma, Strongyloides, Pneumocystis, Cryptococcus, Nocardia, Ameba).m

Use with great care in patients with known or suspected Strongyloides (threadworm) infection.e Immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.a d e m

Corticosteroids may exacerbate fungal infections and should not be used in the presence of such infections,a d e f m unless they are needed to control drug reactions.d m

Not effective and can have detrimental effects in the management of cerebral malaria.c d m Do not use corticosteroids in cerebral malaria.d m

Can reactivate tuberculosis.a d e f m Include chemoprophylaxis in patients with a history of active tuberculosis undergoing prolonged glucocorticoid therapy.a c d m Observe closely for evidence of reactivation.d Restrict use in active tuberculosis to those with fulminating or disseminated tuberculosis in which glucocorticoids are used in conjunction with appropriate chemoprophylaxis.a d e m c d m

Can reactivate latent amebiasis.c Exclude possible amebiasis in any patient who has been in the tropics or who has unexplained diarrhea prior to initiating therapy.c d m

Rarely, epidural abscess reported following epidural glucocorticoid injection; infectious complications (e.g., bacterial meningitis) also reported.

Musculoskeletal Effects

Muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones are manifestations of protein catabolism that may occur during prolonged therapy with glucocorticoids.c These adverse effects may be especially serious in geriatric or debilitated patients.c A high protein diet may help to prevent adverse effects associated with protein catabolism.c

An acute, generalized myopathy can occur with the use of high doses of glucocorticoids, particularly in patients with disorders of neuromuscular transmission (e.g., myasthenia gravis) or in patients receiving concomitant therapy with neuromuscular blocking agents (e.g., pancuronium).d e m

Tendon rupture, particularly of the Achilles tendon.

Osteoporosis and related fractures are one of the most serious adverse effects of long-term glucocorticoid therapy.

To minimize the risk of glucocorticoid-induced bone loss, the smallest possible effective dosage and duration should be used. Topical and inhaled preparations should be used whenever possible.

Before initiating glucocorticoid therapy in postmenopausal women, consider that they are especially prone to osteoporosis.c

Withdraw glucocorticoids if osteoporosis develops, unless their use is life-saving.c

Glucocorticoid-induced bone loss can be both prevented and treated. Baseline measurement of bone mass density (BMD) at the lumbar spine and/or hip should be obtained when initiating long-term (e.g., exceeding 6 months) glucocorticoid therapy and appropriate preventive therapy should be initiated. Longitudinal measurements may be repeated as often as every 6 months to detect possible bone loss. Less frequent (e.g., annually) follow-up probably is sufficient in patients who are receiving therapy to prevent bone loss.

Skeletal wasting is most rapid during the initial 6 months of therapy, and trabecular bone is affected to a greater degree than is cortical bone.

Calcium and vitamin D supplementation, bisphosphonate (e.g., alendronate, risedronate), and a weight-bearing exercise program that maintains muscle mass are suitable first-line therapies aimed at reducing the risk of adverse bone effects.

Calcitonin may be considered as second-line therapy for patients who refuse or do not tolerate bisphosphonate therapy or in whom the drugs are contraindicated.

Fluid and Electrolyte Disturbances

Sodium retention with resultant edema, potassium loss, hypokalemic alkalosis, and elevation of BP may occur with average and large doses of corticosteroids.a d e m These effects are less frequent with synthetic glucocorticoids than with hydrocortisone or cortisone, but may occur, especially when synthetic glucocorticoids are given in high dosage for prolonged periods.a c d e m Edema and CHF (in susceptible patients) may occur.c

Dietary salt restriction is advisable and potassium supplementation may be necessary.a c e m

Increased calcium excretion and possible hypocalcemia.a c e

Ocular Effects

Prolonged use may result in posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos, and/or increased IOP which may result in glaucoma or may occasionally damage the optic nerve.a c d e m

May enhance the establishment of secondary bacterial, fungal and viral infections of the eye.d e

Use with caution in patients with active ocular herpes simplex infections for fear of corneal perforation.c m

Transient blindness, amblyopia, acute retinal necrosis syndrome, and intraocular hemorrhage have occurred following epidural glucocorticoid injection.

Endocrine and Metabolic Effects

Administration over a prolonged period may produce various endocrine disorders including hypercorticism (cushingoid state) and amenorrhea or other menstrual difficulties.c

Increased or decreased motility and number of sperm in some men.c

May decrease glucose tolerance, produce hyperglycemia, and aggravate or precipitate diabetes mellitus, especially in patients predisposed to diabetes mellitus.c If glucocorticoid therapy is required in patients with diabetes mellitus, changes in insulin or oral antidiabetic agent dosage or diet may be necessary.c

Administer by epidural injection with caution in patients with diabetes mellitus.

Exaggerated response to the glucocorticoids in hypothyroidism; use with caution.a c d e m Changes in thyroid status may require dosage adjustment.d m

Cardiovascular Effects

Use with extreme caution in recent MI since an association between use of glucocorticoids and left ventricular free-wall rupture has been suggested.c d m

Use with caution in patients with CHF and hypertension.a d m

Bradycardia has occurred during or after IV administration of large doses of methylprednisolone sodium succinate; may be unrelated to rate or duration of infusion.c e

Cardiac arrhythmias, circulatory collapse, and/or cardiac arrest reported following rapid (<10 minutes) administration of large IV doses of methylprednisolone sodium succinate.e

Administer by epidural injection with caution in patients with CHF.

Dermatologic Effects

Dermal and/or subdermal changes forming depressions in the skin at the injection site reported with methylprednisolone acetate injectable suspension (Depo-Medrol).m Exercise care to minimize the incidence of dermal and subdermal atrophy; do not exceed recommended doses of the injections.m

For intralesional use, administer multiple small injections into the area of the lesion, whenever possible.d m

Avoid injection or leakage into the dermis; avoid injection into the deltoid muscle, because of high incidence of sub-Q atrophy.d m

Kaposi’s sarcoma has been reported in patients receiving glucocorticoid therapy; discontinuance of such therapy may result in clinical improvement of the disease.a d m

Sensitivity Reactions

Anaphylactic or anaphylactoid reactions with or without circulatory collapse, cardiac arrest, or bronchospasm.c d e m Take appropriate precautionary measures prior to administration, especially in patients with a history of allergy to any drug.d e

Urticaria and other allergic or hypersensitivity reactions reported.a d e f m

General Precautions


Prior to initiation of long-term glucocorticoid therapy, perform baseline ECGs, blood pressures, chest and spinal radiographs, glucose tolerance tests, and evaluations of HPA-axis function in all patients.c d e

Perform upper GI radiographs in patients predisposed to GI disorders, including those with known or suspected peptic ulcer disease.c d

During long-term therapy, perform periodic height, weight, chest and spinal radiographs, hematopoietic, electrolyte, glucose tolerance, and ocular and blood pressure evaluations.

Genitourinary Effects

Increased or decreased motility and number of sperm in some men.c

Nervous System Effects

May precipitate mental disturbances ranging from euphoria, insomnia, mood swings, depression and anxiety, and personality changes to frank psychoses.a d e m Use may aggravate emotional instability or psychotic tendencies.a d e m

Use with caution in patients with myasthenia gravis.a

Aseptic meningitis, arachnoiditis, exacerbation of pain, spinal cord trauma, subdural injection, intracranial air injection, increased intracranial pressure, nerve injury, seizures, bladder or bowel dysfunction, paraparesis or paralysis, sensory disturbances, and brain damage reported following epidural and/or intrathecal glucocorticoid injection. Unclear whether these effects involved improper needle placement or were related to administration of the drug and/or preservatives.

Results from a 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 cranial trauma who were determined not to have other clear indications for corticosteroid treatment.d m Do not use high doses of systemic corticosteroids, including methylprednisolone acetate (Depo-Medrol), for treatment of traumatic brain injury.d m

GI Effects

Corticosteroids should be used with caution in patients with diverticulitis, nonspecific ulcerative colitis (if there is a probability of impending perforation, abscess, or other pyogenic infection), or those with recent intestinal anastomoses.a d m

Use with caution in patients with active or latent peptic ulcer.a d m Manifestations of peritoneal irritation following GI perforation may be minimal or absent in patients receiving corticosteroids.c d m Suggest concurrent administration of antacids between meals to prevent peptic ulcer formation in patients receiving high dosages of corticosteroids.c d e

Specific Populations


Category C.d f m

If substantial dosage received during pregnancy, carefully observe infant for signs of hypoadrenalism.a

Fluoroscopy (recommended for ensuring proper needle placement for epidural injections) is contraindicated in pregnant women.


Glucocorticoids are distributed into milk and could suppress growth, interfere with endogenous glucocorticoid production, or cause other adverse effects in nursing infants.c d m Discontinue nursing or the drug.m

Pediatric Use

The effects of glucocorticoids on the pathophysiology and course of diseases are considered to be similar in adults and children.c d m Evidence of safety and efficacy of corticosteroids in pediatric patients is based on treatment of nephrotic syndrome (in patients >2 years of age) and aggressive leukemias and lymphomas (in patients >1 month of age).c d m Evidence of safety and efficacy in other pediatric indications (e.g., severe asthma and wheezing) is based on controlled trials in adults.c d

Adverse effects in pediatric patients are similar to those in adults.c d m As in adults, perform periodic evaluations of height, weight, IOP, and BP.c d Children, like adults, also should undergo clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis.c d m

With long-term use, may delay growth and maturation in children and adolescents.c d m Monitor carefully the growth and development of pediatric patients receiving prolonged corticosteroid therapy.a c d m Titrate dosage to the lowest effective level.c Alternate-day therapy with glucocorticoids that cause shorter HPA-axis suppression than does dexamethasone (e.g., prednisone, prednisolone, methylprednisolone) may minimize growth suppression and should be instituted if growth suppression occurs.c

Glucocorticoid-induced osteoporosis and associated fractures are common in children and adolescents receiving long-term systemic therapy. In addition, may prevent achievement of peak bone mass during adolescence by inhibiting bone formation. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DEXA]) in children and adolescents are similar to those in adults.

Ensure children and adolescents consistently ingest either through diet or supplementation adequate calcium and vitamin D.

Methylprednisolone sodium succinate (in single-dose vials) and methylprednisolone acetate (in multiple-dose vials) injection preparations containing benzyl alcohol are contraindicated in premature infants.e m Administration of injections preserved with benzyl alcohol has been associated with toxicity in neonates (gasping syndrome).c d e m (See Contraindications under Cautions.)

Geriatric Use

Insufficient experience in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults; select dosage with caution.d m Other clinical experience to date has not identified any differences in responses between geriatric and younger patients.d m

With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur.c May be especially serious in geriatric or debilitated patients.c

Select dosage with caution, usually initiating therapy at the low end of the dosing range, because of age-related decreases in hepatic, renal, and/or cardiac function and potential for concomitant disease and drug therapy.d m

Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.c

Use with caution in patients with osteoporosis.e

Hepatic Impairment

Patients with cirrhosis show an exaggerated response to glucocorticoids.a c d e m

Renal Impairment

Use with caution.a d e m

Common Adverse Effects

Associated with long-term therapy: Bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.i j

Interactions for Methylprednisolone

Metabolized by CYP3A4.c

Drugs Affecting Hepatic Microsomal Enzymes

Inhibitors of CYP3A4 (e.g., ketoconazole, macrolide antibiotics): Potential pharmacokinetic interaction (increased plasma concentrations and decreased corticosteroid clearance); may require decrease of corticosteroid dosage to avoid potential adverse effects).c d e m

Inducers of CYP3A4 (e.g., barbiturates, carbamazepine, ephedrine, phenytoin, rifampin): Potential pharmacokinetic interaction (increased metabolism of corticosteroids); may require increase of corticosteroid dosage).a c d m

Specific Drugs and Skin Tests





May result in a loss of corticoid-induced adrenal suppressiond m

Analgesics, opiate

Epidural injection: Potential for serious injuries (e.g., brain damage, death) when glucocorticoids are combined with local anesthetics and/or opiate analgesics

Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of local anesthetics and/or opiate analgesics from epidural glucocorticoid injections

Anesthetics, local

Epidural injection: Potential for serious injuries (e.g., brain damage, death) when glucocorticoids are combined with local anesthetics and/or opiate analgesics

Improve patient safety by excluding typical epidural doses (volumes in excess of intrathecal test doses) of local anesthetics and/or opiate analgesics from epidural glucocorticoid injections

Anticoagulants, oral

Conflicting reports of alterations in the anticoagulant responsea c d e m

Monitor coagulation indices to maintain desired anticoagulant effecta c d e


Concomitant use with corticosteroids may produce severe weakness in patients with myasthenia gravisd m

Withdraw anticholinesterases at least 24 hours before initiating corticosteroid therapyd m

Antidiabetic therapy

Increased blood glucose concentrations in diabetes mellitusm

May require dosage adjustment of concurrent insulin and/or oral hypoglycemic agentsm


May enhance metabolism of corticosteroidsm

Increase the clearance of methylprednisolonea c e

Increase dosage of methylprednisolonea c d m


May enhance metabolism of corticosteroidsm

Increase dosage of corticosteroidsd m


Increased clearance of oral corticosteroidsm

Contraceptives (oral; including estrogens)

May decrease hepatic metabolism of some corticosteroids, thus increasing their effectsd m


Plasma concentrations of cyclosporine may be increased during concomitant therapy with methylprednisolone.c Mutual inhibition of metabolism with concomitant usea e

Consider possibility of exacerbated toxicity (convulsions), as well as need for dosage adjustment with concomitant usea c e

Digitalis glycosides

Increased risk of arrhythmias associated with hypokalemiad m


Serum isoniazid concentration may be decreasedd m


Decreased metabolism of certain corticosteroids c d m

Titrate dosage of methylprednisolone to avoid potential adverse effectsc d e

Macrolide antibiotics (e.g., erythromycin, troleandomycin)

Increased plasma concentrations of corticosteroidsc d m

Decreased clearance of methylprednisolonea c d e

Titrate dosage of methylprednisolone to avoid potential adverse effectsa d e


Increases the risk of adverse GI effectsa c d m

Decreased serum salicylate concentrations;c d when corticosteroids are discontinued, serum salicylate concentration may increase, possibly resulting in salicylate intoxicationa c d e m

Use concurrently with cautiona c d m

Observe patients receiving both drugs closely for adverse effects of either drugc

May be necessary to increase salicylate dosage when corticosteroids are administered concurrently or decrease salicylate dosage when corticosteroids are discontinuedc

Use aspirin and corticosteroids with caution in hypoprothrombinemiad


May enhance metabolism of corticosteroidsc d m

Increase dosage of methylprednisolonec d e m

Potassium-depleting drugs (diuretics, amphotericin B)

Enhance the potassium-wasting effects of glucocorticoidsc

Use of hydrocortisone with amphotericin B may result bin cardiac enlargement and CHFd m

Monitor for development of hypokalemiac d m


May enhance metabolism of corticosteroidsc d m

Increase dosage of methylprednisolonec d e

Skin tests

May suppress reaction to skin testsd m

Vaccines and toxoids

May cause a diminished response to toxoids and live or inactivated vaccinesc d m

May potentiate replication of some organisms contained in live, attenuated vaccinesc d m

Can aggravate neurologic reactions to some vaccines (supraphysiologic dosages) c

Defer generally routine administration of vaccines or toxoids until corticosteroid therapy is discontinuedc d m

May need serologic testing to ensure adequate antibody response for immunizationb Additional doses of the vaccine or toxoid may be necessaryb

May undertake immunization procedures in patients receiving nonimmunosuppressive doses of glucocorticoidsc

Methylprednisolone Pharmacokinetics



Absorption from IM injection of methylprednisolone sodium succinate is rapid.b

Systemic absorption of methylprednisolone acetate occurs slowly following intra-articular, intrabursal, intrasynovial, intradermal, or soft tissue injection; c d m Absorption from intra-articular injection sites is usually very slow and continues for about 7 days.b


Following IM administration (80–120 mg) in patients with severe poison ivy, relief onset within 8–12 hours.d

Following oral administration in patients with asthma, effects may not be evident for several hours.


The duration of anti-inflammatory activity of methylprednisolone approximately equals the duration of HPA-axis suppression, about 1.25–1.5 days for a single 40-mg oral dose.c



Most glucocorticoids are removed rapidly from the blood and distributed to muscles, liver, skin, intestines, and kidneys.c

Glucocorticoids appear in breast milk and the placenta.c



Metabolized in most tissues, but mainly in the liver, to inactive compounds.c


Approximately 2.5–3.5 hours following oral administration of methylprednisolone or IV or IM administration of methylprednisolone sodium succinate.h

Special Populations

The metabolic clearance of corticosteroids may be decreased in patients with hypothyroidism and increased in those with hyperthyroidism.d m






Tight, light-resistant containers at 15–30°C (methylprednisolone tablets).f


Powder for Injection

Store unreconstituted at 20–25°C.e Store reconstituted solution at 20–25°C; use reconstituted solution within 48 hourse

Suspension for Injection

20–25°C.d m

Single-dose vials of methylprednisolone acetate injectable suspension (Depo-Medrol) are not intended for multiple-dose withdrawal; discard any remaining suspension.d

Avoid contamination of multiple-dose vials of methylprednisolone acetate injectable suspension by using strict aseptic technique.m Use povidone-iodine solution or similar product to cleanse the vial top prior to aspiration of contents.m Although initially sterile, such vials may become contaminated; use of disposable sterile syringes and needles is necessary.m

Similar to other corticosteroids, methylprednisolone acetate suspension is heat labile; do not autoclave when it is desirable to sterilize the outside of the vial.d m


For information on systemic interactions resulting from concomitant use, see Interactions.


Methylprednisolone Acetate

The manufacturer states that methylprednisolone acetate should not be diluted or mixed with other solutions because of possible physical incompatibilities.d

Methylprednisolone Sodium Succinate

Must reconstitute only with diluent provided by the manufacturer or bacteriostatic water for injection with benzyl alcohol.e The manufacturers state that reconstituted solution may be diluted with 5% dextrose, or 0.9% sodium chloride, or 5% dextrose in sodium chloride injection.e

Solution Compatibility (Methylprednisolone Sodium Succinate)HID


Amino acids 4.25%, dextrose 25%

Dextrose 5% in sodium chloride 0.45 or 0.9%

Ringer’s injection, lactated

Sodium chloride 0.9%


Dextrose 5% in water (compatibility concentration dependent)

Drug Compatibility (Methylprednisolone Sodium Succinate)
Admixture CompatibilityHID


Chloramphenicol sodium succinate

Clindamycin phosphate

Dopamine HCl

Granisetron HCl

Heparin sodium

Norepinephrine bitartrate

Penicillin G potassium

Ranitidine HCl


Verapamil HCl


Calcium gluconate


Nafcillin sodium

Penicillin G sodium




Y-Site CompatibilityHID


Acyclovir sodium


Amiodarone HCl

Amphotericin B cholesteryl sulfate complex




Cefepime HCl

Ceftaroline fosamil




Dexmedetomidine HCl

Dopamine HCl


Doxorubicin HCl liposome injection



Fludarabine phosphate

Granisetron HCl

Heparin sodium

Hetastarch in lactated electrolyte injection (Hextend)

Hydroxyethyl starch 130/0.4 in sodium chloride 0.9%


Melphalan HCl

Meperidine HCl

Methotrexate sodium


Midazolam HCl

Milrinone lactate

Morphine sulfate

Nicardipine HCl


Pemetrexed disodium

Piperacillin sodium–tazobactam sodium

Remifentanil HCl

Sodium bicarbonate





Topotecan HCl


Allopurinol sodium

Caspofungin acetate



Etoposide phosphate

Fenoldopam mesylate


Gemcitabine HCl

Ondansetron HCl


Palonosetron HCl




Vinorelbine tartrate


Cisatracurium besylate

Diltiazem HCl

Potassium chloride

Telavancin HCl


  • Principally an anti-inflammatory or immunosuppressant agent.d

  • Exhibits potent anti-inflammatory activity and minimal mineralocorticoid properties.c

  • Decreases inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes; or reducing leukocyte adhesion to capillary endothelium.c

  • Inhibits macrophage accumulation in inflamed areas.c

  • Reduces capillary wall permeability and edema formation.c

  • Antagonizes histamine activity and release of kinin from substrates.c

  • Reduces fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.c

  • Stimulates erythroid cells of bone marrow, prolongs survival time of erythrocytes and platelets, and produces neutrophilia and eosinopenia.c

  • Promotes gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance.c

  • Reduces intestinal absorption and increase renal excretion of calcium.c e

  • Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia.c

  • Decreases immunoglobulin and complement concentrations and passage of immune complexes through basement membranes.c

  • Depresses reactivity of tissue to antigen-antibody interactions.c

Advice to Patients

  • In patients receiving long-term therapy, importance of not discontinuing the drug abruptly or without supervision of a clinician.b d m

  • Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.c d m

  • Importance of carrying identification cards listing the diseases being treated, the glucocorticoid regimen, and the name and telephone number of the clinician.c

  • When surgery is required, importance of informing the attending physician, dentist, or anesthesiologist of recent (within 12 months) glucocorticoid therapy.c

  • In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs.a d e m

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.a c

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.a

  • Importance of informing patients of other important precautionary information.a c (See Cautions.)


Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name



Dosage Forms


Brand Names




2 mg

Medrol (scored)


4 mg*

Medrol (scored)


Medrol Dosepak


Meprolone Unipak


Methylprednisolone Tablets

8 mg

Medrol (scored)


Methylprednisolone Tablets

16 mg

Medrol (scored)


32 mg

Medrol (scored)


* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Methylprednisolone Acetate


Dosage Forms


Brand Names



Injectable suspension

20 mg/mL*



40 mg/mL*



Methylprednisolone Acetate Injectable Suspension

80 mg/mL*



Methylprednisolone Acetate Injectable Suspension

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Methylprednisolone Sodium Succinate


Dosage Forms


Brand Names



For injection

40 mg (of methylprednisolone)*



Methylprednisolone Sodium Succinate Injection



125 mg (of methylprednisolone)*



Methylprednisolone Sodium Succinate Injection



500 mg (of methylprednisolone)*



A-methaPred ADD-Vantage


Methylprednisolone Sodium Succinate Injection



1 g (of methylprednisolone)



A-methaPred ADD-Vantage


Methylprednisolone Sodium Succinate Injection



2 g (of methylprednisolone)



Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 02/2014. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Depo-Medrol 20MG/ML Suspension (PFIZER U.S.): 5/$28.64 or 10/$46.26

Medrol 16MG Tablets (PFIZER U.S.): 30/$102.99 or 90/$299.96

Medrol 32MG Tablets (PFIZER U.S.): 25/$127.99 or 75/$367.97

Medrol 4MG Tablets (PFIZER U.S.): 25/$44.70 or 75/$122.64

Medrol 8MG Tablets (PFIZER U.S.): 30/$65.99 or 90/$185.96

MethylPREDNISolone 16MG Tablets (CADISTA): 50/$147.00 or 150/$419.98

MethylPREDNISolone 8MG Tablets (CADISTA): 25/$51.99 or 75/$139.97

Solu-MEDROL 40MG Solution (PFIZER U.S.): 1/$12.99 or 3/$19.97

AHFS DI Essentials. © Copyright, 2004-2016, Selected Revisions July 10, 2013. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.


HID. Trissel LA. Handbook on injectable drugs. 17th ed. Bethesda, MD: American Society of Health-System Pharmacists; 2013:766-74.

a. Pfizer. Medrol (methylprednisolone) tablets prescribing information. New York, NY; 2006 Nov.

b. AHFS drug information 2004. McEvoy GK, ed. Methylprednisolone. Bethesda, MD: American Society of Health-System Pharmacists; 2004:2914-5.

c. AHFS drug information 2005. McEvoy GK, ed. Corticosteroids general statement. Bethesda, MD: American Society of Health-System Pharmacists; 2005:2908-21.

d. Pfizer. Depo-Medrol (methylprednisolone acetate) injectable suspension (single-dose vials) prescribing information. New York, NY; 2009 Apr.

e. Pfizer. Solu-Medrol (methylprednisolone sodium succinate) sterile powder for injection prescribing information. New York, NY; 2009 May.

f. BarrLaboratories. Methylprednisolone tablets prescribing information. Pomona, NY; 2001 Nov.

g. Behrman RE, Kliegman RM, Jenson HB, eds. Nelson textbook of pediatrics. 17th ed. Philadelphia: Saunders; 2004:1407-8.

h. Woodward HM. Upjohn Company unpublished data (personal communication), 1976.

i. Walsh LJ, Wong CA, Oborne J et al. Adverse effects of oral corticosteroids in relation to dose in patients with lung disease. Thorax. 2001; 56:279-84. [PubMed 11254818]

j. Bello CE, Garrett SD. Therapeutic issues in oral glucocorticoid use. Lippincotts Prim Care Pract. 1999; 3:333-41. [PubMed 10711134]

l. USP DI: drug information for the health care provider. 24th ed. Greenwood Village, CO: Thomson Micromedex; 2004;1:940-6.

m. Pfizer. Depo-Medrol (methylprednisolone acetate) injectable suspension (multiple-dose vials) prescribing information. New York, NY; 2009 May.