METCORT Methylprednisolone 16mg Tablet 1's

Endocrine Disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the 1st choice; synthetic analogs eg, dexamethasone may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance); congenital adrenal hyperplasia; nonsuppurative thyroiditis; hypercalcemia associated with cancer.
Rheumatic Disorders: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in posttraumatic osteoarthritis (OA); synovitis of OA; rheumatoid arthritis (RA), including juvenile RA (selected cases may require low-dose maintenance therapy); ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; acute gouty arthritis; psoriatic arthritis; epicondylitis.
Collagen Diseases: During an exacerbation or as maintenance therapy in selected cases of systemic lupus erythematosus, polymyalgia rheumatica, systemic dermatomyositis (polymyositis), giant cell arteritis, acute rheumatic carditis.
Dermatologic Diseases: Pemphigus vulgaris, severe erythema multiforme (Stevens-Johnson syndrome), bullous dermatitis herpetiformis, exfoliative dermatitis, mycosis fungoides, severe seborrheic dermatitis, severe psoriasis.
Allergic States: Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment bronchial asthma, seasonal or perennial allergic rhinitis, allergic contact dermatitis, atopic dermatitis, serum sickness, drug hypersensitivity reactions.
Ophthalmic Diseases: Severe acute and chronic allergic and inflammatory processes involving the eye and its adnexa eg, herpes zoster ophthalmicus, anterior uveitis (iritis, iridocyclitis), diffuse posterior uveitis and choroiditis, chorioretinitis, optic neuritis, sympathetic ophthalmia, anterior segment inflammation, allergic conjunctivitis, keratitis, allergic corneal marginal ulcers.
Gastrointestinal Diseases: To tide the patient over a critical period of the disease in ulcerative colitis, regional enteritis, Crohn's disease.
Respiratory Diseases: Symptomatic sarcoidosis, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy, Loeffler's syndrome not manageable by other means, aspiration pneumonitis.
Hematologic Disorders: Idiopathic thrombocytopenic purpura in adults, erythroblastopenia (RBC anemia), secondary thrombocytopenia in adults, acquired (autoimmune) hemolytic anemia, congenital (erythroid) hypoplastic anemia.
Neoplastic Diseases: For palliative management of leukemias and lymphomas in adults, acute leukemia in children.
Edematous States: To induce diuresis or remission of proteinuria in nephrotic syndrome, without uremia, of the idiopathic type or that due to lupus erythematosus.
Nervous System Disorders: Acute exacerbations of multiple sclerosis and management of edema associated with brain tumor.
Organ Transplantations (Other Uses): Tuberculous meningitis with subarachnoid block or impending block when used concurrently with appropriate antituberculous chemotherapy, trichinosis with neurologic or myocardial involvement.

 

Complications of corticosteroid treatment are highly variable between patients as are durations of treatment. Dose, duration and mode (daily or intermittent) of treatment should be individually determined based on assessment of risk/benefit.
The lowest effective corticosteroid dose should be used to control the condition being treated. Gradual reduction of dosage is recommended whenever possible.
Dosage should be individualized based on the condition being treated and the patient's response. Maintain and/or adjust initial dosage until a satisfactory response is noted. Discontinue methylprednisolone and shift the patient to other appropriate therapy if clinical response is unsatisfactory after a reasonable period of time. Constant monitoring is needed as regard to dosage. Situations which make dosage adjustments necessary include changes in clinical status secondary to remissions or exacerbations in the disease process; the patient's individual drug responsiveness and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment; it may be necessary to increase the dosage of methylprednisolone for a period of time consistent with the patient's condition.
Recommended Dose: Usual Initial Dose: 4-48 mg/day given in 4 divided doses depending on the specific disease being treated. However, initial doses of up to ≥100 mg may be used in acute severe disease.
The initial suppressive dose level may vary depending on the condition being treated. This is continued until a satisfactory clinical response is obtained, a period usually of 3-7 days in the case of rheumatic disease (except for acute rheumatic carditis), allergic conditions affecting the skin or respiratory tract and ophthalmic diseases. Re-evaluate the case to confirm the original diagnosis if a satisfactory response is not achieved in 7 days. Upon obtaining a satisfactory response, decrease dose in small increments (not >2 mg at intervals of 7-10 days are suggested) either to terminate treatment in the case of acute conditions (ie, seasonal asthma, exfoliative dermatitis, acute ocular inflammations) or until the lowest level that maintains an adequate clinical response is reached in chronic conditions (ie, RA, systemic lupus erythematosus, bronchial asthma, atopic dermatitis).
Clinical situations which may require high dose therapy of corticosteroids eg, multiple sclerosis, cerebral edema and organ transplantation should maintain initial dosage or adjust until a satisfactory response is observed in the patient. Discontinue methylprednisolone and shift the patient to other appropriate therapy if clinical response is unsatisfactory after a reasonable period of time. If there is a lack of satisfactory clinical response after a reasonable period of time, discontinue methylprednisolone and transfer patient to other appropriate therapy. If after long-term therapy the drug is to be stopped, it is recommended that methylprednisolone be discontinued gradually rather than abruptly.
Suggested Initial Daily Methylprednisolone Dose (Given Either as Single Dose or in Divided Doses): Rheumatoid Arthritis: Severe: 12-16 mg; Moderately Severe: 8-12 mg; Moderate: 4-8 mg. Children: 4-8 mg.
Systemic Dermatomyositis: 48 mg.
Systemic Lupus Erythematosus: 20-100 mg.
Acute Rheumatic Fever: 48 mg until ESR normal for 1 week.
Allergic Diseases: 12-40 mg.
Bronchial Asthma: Up to 64 mg single dose/alternate day up to maximum of 100 mg.
Ophthalmic Diseases: 12-40 mg.
Hematological Disorders and Leukemias: 16-100 mg.
Malignant Lymphoma: 16-100 mg.
Ulcerative Colitis: 16-60 mg.
Crohn's Disease: Up to 48 mg/day in acute episodes.
Organ Transplantation: Up to 3.6 mg/kg/day.
Pulmonary Sarcoid: 32-42 mg on alternate days.
Giant Cell Arteritis/Polymyalgia Rheumatica: 64 mg.
Pemphigus Vulgaris: 80-360 mg.
Multiple Sclerosis: 200 mg/day.
Cerebral Edema: 200-1,000 mg/day.
Treatment of Acute Exacerbations of Multiple Sclerosis: 200 mg/day of prednisolone for 1 week followed by 80 mg every other day for 1 month have been shown to be effective (4 mg of methylprednisolone is equivalent to 5 mg of prednisolone).
Renal Impairment: There is no dosing adjustment recommended in patients with renal insufficiency.
Children: Methylprednisolone treatment should be based on severity of the condition and response of the patient more than by age, body weight or body surface area. Dosage should be decreased in small decrements to the lowest level that maintains an adequate clinical response after a satisfactory response is obtained. The range of initial doses is 0.117-1.66 mg/kg/day (3.3-50 mg/m² body surface area/day) given in 3 or 4 divided doses.
Alternate Day Therapy (ADT): Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of corticosteroid is administered every other morning. The rationale of this dosing regimen is for patients requiring long-term pharmacologic dose treatment to receive the beneficial effects of glucocorticoids while minimizing certain adverse effects (eg, pituitary-adrenal suppression, Cushingoid state, glucocorticoid withdrawal symptoms, growth suppression in children). This rationale is based on 2 major premises: The anti-inflammatory or therapeutic effect of glucocorticoids persists longer than their physical presence and metabolic effects, and administration of the corticosteroid every other morning allows for re-establishment of more nearly normal hypothalamic-pituitary-adrenal (HPA) activity on the off-corticosteroid day.
When considering ADT, the following should be kept in mind: Basic principles and indications for corticosteroid therapy should apply. The benefits of ADT should not encourage the indiscriminate use of corticosteroids.
This is usually recommended in patients who require long-term pharmacologic dose corticosteroid treatment.
It may be possible to initiate treatment with ADT in less severe cases in which corticosteroid therapy is indicated. More severe disease states will usually require daily divided high dose therapy for initial control of the disease. The initial suppressive dose level should be continued until satisfactory clinical response is obtained (usually 4-10 days in the case of many allergic and collagen diseases). It is important to keep the period of initial suppressive dose as brief as possible, particularly when subsequent use of ADT is intended. Once control has been established, either of these 2 regimens maybe utilized: Change to ADT and then gradually reduce the amount of corticosteroid given every other day or following control of the disease process, reduce the daily dose of corticosteroid to the lowest effective level as rapidly as possible and then change over to an ADT. Theoretically, the former regimen may be preferable.
Patients who have been on daily corticosteroids for long periods of time (eg, patients with RA) may already have suppressed HPA axis and establishing them on ADT may be difficult and not always successful. However, it is recommended that regular attempts be made to change them over to ADT. It may be helpful to triple or even quadruple the daily maintenance dose and administer this every other day rather than just doubling the daily dose. Once the patient is again controlled, an attempt should be made to reduce this dose to a minimum.
Certain corticosteroids (eg, dexamethasone and betamethasone) are not recommended for ADT because of their prolonged suppressive effect on adrenal activity.
The maximal activity of the adrenal cortex is between 2:00 am and 8:00 am and it is minimal between 4:00 pm and midnight. Exogenous corticosteroids suppress adrenocortical activity the least, when given at the time of maximal activity (am).
It is important to individualize and tailor the therapy to each patient when using ADT. Complete control of symptoms will not be possible in all patients. An explanation of the benefits of ADT will help the patient understand and tolerate the possible flare-up in symptoms which may occur in the latter part of the off-corticosteroid day. Other symptomatic therapy may be added or increased at this time if needed.
It may be necessary to return to a full suppressive daily divided corticosteroid dose for control in the event of an acute flare-up. ADT may be reinstituted once control is re-established.
Although many of the adverse effect of corticosteroids may be minimized by ADT, the physician must carefully weigh the benefit risk ratio for each patient in whom corticosteroid therapy is considered.

 

Overdosage

Should be taken with food.

Hypersensitivity to methylprednisolone or to any of the component of Metcort.
Systemic infections, unless specific anti-infective therapy is given and systemic fungal infections.
Administration of live or live attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids.

Immunosuppressive Effects/Increased Susceptibility to Infections: Glucocorticoids (especially in large doses) suppress the inflammatory response and immune function and may increase susceptibility to and/or mask symptoms of infection (viral, bacterial and fungal). It is not known how the dose, route and duration of corticosteroid administration affect the risk of developing a disseminated infection. The contribution of the underlying disease and/or prior corticosteroid treatment to the risk is also not known.
Corticosteroids may cause decreased resistance and inability to localize infection. Infections caused by any pathogen including viral, bacterial, fungal, protozoan or helminthic infections in any location of the body may be associated with corticosteroids alone or in combination with other immunosuppressive agents. These infections may be mild to severe (at times fatal) and occur more frequently with increasing doses of corticosteroids.
Viral Infections: Viral infections eg, chicken pox or measles can be more serious or even fatal in non-immunized children or adults on corticosteroids. Patients who have not had these diseases, should take particular care to avoid exposure. Prophylaxis with varicella zoster immune globulin (VZIG) may be indicated if exposed to chicken pox (given within 10 days upon exposure), while prophylaxis with immunoglobulin (IG) may be indicated if exposed to measles. If a diagnosis of chicken pox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased.
Special Pathogens: Corticosteroids may cause activation of latent diseases or exacerbation of intercurrent infections.
In patients with known or suspected Strongyloides (threadworm) infestation, corticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration which is often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia. Use corticosteroids with great care in these patients.
Tuberculosis: Use methylprednisolone in active tuberculosis only in fulminating or disseminated cases in which corticosteroids are used with appropriate antituberculous regimen.
Since reactivity to the disease may occur in patients with latent tuberculosis or tuberculin reactivity, observe these patients closely and administer chemoprophylaxis during prolonged corticosteroid therapy.
The role of corticosteroids in septic shock has been controversial with early studies reporting both beneficial and detrimental effects. Recent studies have shown that supplemental corticosteroids have been beneficial in patients with established septic shock who exhibit adrenal insufficiency. The routine use in septic shock however, is not recommended. A systematic review of short-course high-dose corticosteroids did not support their use. However, a meta-analyses and a review have suggested that longer courses (5-11 days) of low dose corticosteroids may reduce mortality especially in those with vasopressor-dependent septic shock.
Kaposi's sarcoma has been reported in patients receiving corticosteroids. Clinical improvement may be observed upon discontinuation of corticosteroids.
Vaccination: Do not administer live or live attenuated vaccines (including small pox vaccine) in patients receiving corticosteroids. This should be postponed until at least 3 months after stopping corticosteroid therapy. Although killed or inactivated vaccines may be administered in patients on corticosteroids, response to such vaccines cannot be predicted. Indicated immunization procedures may be undertaken in patients receiving non-immunosuppressive doses of corticosteroids.
Hypersensitivity Reactions: Allergic reactions eg, angioedema may occur.
Anaphylactoid reactions (eg, bronchospasm) have occurred rarely in patients receiving parenteral corticosteroid therapy. Prior to methylprednisolone administration, appropriate precautionary measures should be taken especially when the patient has a history of allergy to any drug.
Endocrine Effects: Pharmacologic dose of corticosteroids administered for prolonged periods may result in HPA suppression (secondary adrenocortical insufficiency). Symptoms of adrenal insufficiency include malaise, muscle weakness, mental changes, muscle and joint pain, desquamation of the skin, dyspnea, anorexia, nausea and vomiting, fever, hypoglycemia, hypotension and dehydration. This effect is variable among patients and is dependent on dose and duration of treatment and may be minimized by the use of ADT.
In some cases, withdrawal symptoms may stimulate a clinical relapse of the disease for which the patient has been under treatment and therefore, clinical assessment of disease activity may be important. If the disease is unlikely to relapse on withdrawal of systemic corticosteroids, but there is uncertainty of HPA suppression, the dose of systemic corticosteroids may be reduced rapidly to physiologic doses. Dose reduction should be slower once a daily dose of methylprednisolone 6 mg is reached to allow the HPA-axis to recover.
Acute adrenal insufficiency leading to a fatal outcome may also occur if corticosteroids are abruptly withdrawn. Although abrupt withdrawal of doses up to 32 mg/day methylprednisolone for 3 weeks is unlikely to lead to clinically relevant HPA-axis suppression in majority of patients, consider gradual withdrawal of systemic corticosteroid therapy in the following patient groups even after courses lasting ≤3 weeks: Those who have had repeated courses of systemic corticosteroids, particularly if taken for >3 weeks. When a short course has been prescribed within 1 year of discontinuation of long-term therapy (months or years). Those who may have reasons for adrenocortical insufficiency other than exogenous corticosteroid therapy. Moreover, acute adrenal insufficiency leading to a fatal outcome may occur if glucocorticoids are withdrawn abruptly. Those receiving systemic corticosteroid doses of >32 mg daily of methylprednisolone. Those taking doses in the evening repeatedly.
Metabolic clearance of corticosteroids may be altered in hypothyroid (decreased clearance) or hyperthyroid (increased clearance) patients. Patient monitoring based on thyroid status may be necessary for these patients.
Glucocorticoids should be avoided in patients with Cushing's disease since the drug can produce or aggravate Cushing's syndrome.
Cardiovascular-Renal Effects: Use corticosteroids with caution and only if strictly necessary, in cases of congestive heart failure.
Particular care with frequent monitoring is required when considering the use of systemic corticosteroids in the following patients: Patients who have experienced a recent myocardial infarction (myocardial rupture has been reported); with hypertension; predisposed to thrombophlebitis and with renal insufficiency.
Sodium retention resulting in edema, potassium loss, hypokalemic alkalosis and hypertension may occur in patients receiving glucocorticoids. Congestive heart failure may occur in susceptible patients. These effects may occur when synthetic corticosteroids are used in high dosage for prolonged periods. Dietary salt restriction and potassium supplementation may be advised when necessary. All corticosteroids increase calcium excretion which may result in hypocalcemia.
Metabolism and Nutrition Disorders: Use with caution in patients with or a family history of diabetes mellitus since corticosteroids may cause an increase in blood glucose (steroid-induced diabetes), worsen preexisting diabetes and predispose those on long-term corticosteroid therapy to diabetes.
Gastrointestinal Effects: An increased risk of perforation has been shown in active or latent peptic ulcers, diverticulitis, abscess or other pyogenic infections, fresh intestinal anastomoses and nonspecific ulcerative colitis and therefore, caution in the use of steroids is recommended.
Hepatobiliary Effects: The effect of corticosteroids is enhanced in patients with cirrhosis. Particular care and frequent monitoring may be required when considering the use of systemic corticosteroids in patients with liver failure or cirrhosis.
Musculoskeletal Effects: Acute myopathy which occurs most frequently in patients with disorders of neuromuscular transmission eg, myasthenia gravis or in patients receiving therapy with neuromuscular blocking agents eg, pancuronium, has been observed with use of high doses of corticosteroids. Acute myopathy, which may result in quadriparesis, is generalized and may involve ocular and respiratory muscles. Elevation of creatine kinase may also be observed. Clinical improvement or recovery after stopping corticosteroid therapy may need weeks to years.
Since postmenopausal women and geriatric or debilitated patients are especially prone to osteoporosis, special consideration must be given to these patients prior to initiation of corticosteroid therapy. Frequent patient monitoring is necessary.
Use corticosteroids with caution in patients with Duchenne's muscular dystrophy. Rhabdomyolysis and myoglobinuria have been reported after these patients have engaged in strenuous activity.
Patients with previous steroid myopathy must also use corticosteroids with caution.
Ophthalmic Effects: Prolonged use of corticosteroids may cause posterior subcapsular and nuclear cataracts (particularly in children), exophthalmos or increased intraocular pressure which may result in glaucoma or may occasionally damage the optic nerve. Development of secondary fungal and viral infections of the eye may be enhanced in patients receiving corticosteroids.
Use corticosteroids with caution in active ocular herpes simplex to avoid corneal scarring, loss of vision and corneal perforation.
Neuropsychiatric Effects: Corticosteroids should be used with caution in patients with seizure disorders or those with myasthenia gravis.
Although corticosteroids have been shown to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, data do not show that corticosteroids affect the ultimate outcome or natural history of the disease. Relatively high doses of corticosteroids are necessary to demonstrate a significant effect.
Corticosteroids may lead to mental disturbances including euphoria, insomnia, mood swings, anxiety, personality changes and depression to frank psychoses. Corticosteroids may also aggravate emotional instability or psychotic tendencies. Particular care is required when considering the use of corticosteroids in patients with existing or previous history of severe affective disorders. Symptoms of potentially severe psychiatric adverse reactions associated with corticosteroid use typically emerge within a few days or weeks of starting treatment. Psychological effects have also been reported upon corticosteroid withdrawal; frequency is unknown.
Injury: High doses of systemic corticosteroids should not be used for the treatment of traumatic brain injury.
Effects on the Ability to Drive or Operate Machinery: The effect of corticosteroids on the ability to drive or use machinery has not been established. There is no evidence to suggest that methylprednisolone may affect the ability to drive and use machines. No deleterious effect of corticosteroids on driving and operating machinery ability is expected.
Use in pregnancy: Corticosteroids may cause fetal damage (ie, cleft palate, intrauterine growth retardation and adverse effects on brain growth and development) and abortion when administered to pregnant animals. Although there is no evidence that the use of corticosteroids result in an increased incidence of congenital abnormalities eg, cleft palate in man, corticosteroids may increase the risk of intrauterine growth retardation when administered for long periods or repeatedly during pregnancy.
Women who are pregnant or planning on becoming pregnant while receiving corticosteroids should inform their physician. Methylprednisolone should only be used during pregnancy if the potential benefit justifies the potential risk to the fetus.
Methylprednisolone readily crosses the placenta. Carefully monitor infants born to women who received corticosteroids during pregnancy for symptoms of adrenal insufficiency.
There are no known effects of corticosteroids on labor and delivery.
Use in lactation: Corticosteroids are excreted in breast milk. Corticosteroid distributed into breast milk may suppress growth and interfere with endogenous glucocorticoid production in breastfeeding infants. Methylprednisolone should be administered to a breastfeeding mother only if the potential benefit outweighs the potential risk to the infant.
Use in children: The efficacy and safety of corticosteroids are considered to be similar in adults and children. Long-term administration of corticosteroids should be avoided in infancy, childhood and adolescence since this may cause growth retardation which may be irreversible.
Corticosteroid treatment should be administered where possible as a single dose on alternate days for the shortest possible duration in infants, children and adolescents.
Closely monitor growth and development of infants and children if prolonged therapy is necessary.
There are reports of increased intracranial pressure with papilledema in children (pseudomotor cerebri) usually after treatment withdrawal of methylprednisolone.
Use in the elderly: Methylprednisolone should be used with caution in the elderly especially in the long-term since the incidence of corticosteroid-induced side effects may be increased since these patients have a greater frequency of decreased hepatic, renal or cardiac function and of concomitant disease or other drug therapy.

 

Use In Pregnancy & Lactation

Gastrointestinal Effects: Dyspepsia, diarrhea, esophagitis, peptic ulcer with possible perforation and hemorrhage, abdominal distention, abdominal pain, esophageal ulceration, esophageal candidiasis, pancreatitis, perforation of bowel, gastric hemorrhage, nausea.
Musculoskeletal Effects: Arthralgia, muscle atrophy, muscular weakness, myalgia, steroid myopathy, neuropathic arthropathy, avascular osteonecrosis, osteoporosis, pathological fracture, long bone and spinal compression fractures and tendon rupture (particularly of the Achilles tendon).
Skin and Subcutaneous Tissue Disorders: Impaired wound healing, petechiae, ecchymosis, thin fragile skin, erythema, skin atrophy, striae, hyperhidrosis, hirsutism, telangiectasia, acne, urticaria, rash and pruritus. Reports of Kaposi's sarcoma occurrence in patients receiving corticosteroid therapy; discontinuation of corticosteroids may result in clinical remission.
Endocrine-Metabolic Effects: Suppression of HPA axis; growth suppression in infants, children and adolescents; development of cushingoid state, increased appetite which may result in weight gain, impaired glucose tolerance, increased requirements for insulin or oral hypoglycemic agents in diabetes, increased appetite, manifestations of latent diabetes mellitus, pituitary unresponsiveness, negative nitrogen and calcium balance.
Psychiatric Effects: Abnormal behavior, affective disorder (including affect lability, depressed and euphoric mood, psychological dependence, suicidal ideation), behavioral disturbances (including anxiety, confusional state, insomnia, irritability), mental disorder, mood swings, personality change, psychotic behavior and disorders (including mania, delusion, hallucination and aggravation of schizophrenia).
Nervous System Effects: Amnesia, cognitive disorder, convulsions, dizziness, headache, increased intracranial pressure with papilledema (benign intracranial hypertension).
Ophthalmic Effects: Glaucoma, increased intraocular pressure, posterior subcapsular cataracts, exophthalmos, corneal or scleral thinning, exacerbation of ophthalmic viral or fungal disease.
Cardiovascular Effects: Myocardial rupture following recent myocardial infarction, hypertension, hypotension, circulatory collapse.
Immune System Effects: Increased susceptibility to and severity of infections with suppression of clinical symptoms and signs, latent infections becoming active, including reactivation of tuberculosis and opportunistic infections, allergic reactions including anaphylactoid reactions, anaphylaxis and angioedema; may suppress reactions to skin tests.
Fluid and Electrolyte Disturbances: Congestive heart failure in susceptible patients, hypokalemic alkalosis, metabolic acidosis, fluid retention, potassium loss, sodium retention and increased calcium excretion.
Investigations: Elevation of serum liver enzyme levels (alanine transaminase, aspartate transaminase and alkaline phosphatase), hypokalemia, increased calcium excretion/urine calcium.
Reproductive System and Breast Disorders: Menstrual irregularities and amenorrhea.
Ear and Labyrinth Disorders: Vertigo, impaired hearing.
Others: Hiccups, leukocytosis, malaise, withdrawal symptoms and moon face.

 

CYP3A4 Inducers eg, Barbiturates, Phenytoin, Primidone, Rifampicin, Rifabutin, Aminoglutethamide, Carbamazepine and Other Drugs that Stimulate Hepatic Metabolism: These drugs may enhance methylprednisolone metabolism, shorten its plasma t_½ and lead to decreased plasma concentrations of methylprednisolone. Increased methylprednisolone dosage may be required.
CYP3A4 Inhibitors eg, Antifungals (Itraconazole, Ketoconazole), Antiemetics (Aprepitant, Fosaprepitant), Immunosuppressants (Ciclosporin, Cyclophosphamide, Tacrolimus), Macrolide Antibiotics (Clarithromycin, Erythromycin, Troleandomycin), HIV-Protease Inhibitors, Diltiazem, Grapefruit Juice: These may decrease methylprednisolone metabolism thereby increasing plasma concentrations of corticosteroids.
Increased activity of both ciclosporin and corticosteroids may occur when the 2 are used concomitantly. Convulsions have been reported with concomitant use.
Ketoconazole decreases the metabolism of certain corticosteroids by up to 60% leading to an increased risk of corticosteroid adverse effects.
CYP3A4 Substrates eg, Calcium Antagonists (Mibefradil), Histamine₂-Receptor Antagonists (Cimetidine), Contraceptives (Ethinylestradiol/Norethindrone) and Calcium Channel Blockers (Nifedipine, Felodipine): The hepatic clearance of methylprednisolone may be inhibited or induced in the presence of another CYP3A4 substrate. It is possible that the adverse events associated with the use of either drug alone may be more likely to occur when used concomitantly.
Sympathomimetics (eg, Salbutamol, Salmeterol, Terbutaline, Formoterol): Co-administration with high doses of corticosteroids may result in an increased risk of hypokalemia.
Antivirals: Protease inhibitors (ie, indinavir and ritonavir) may increase plasma concentrations of corticosteroids. On the other hand, corticosteroids may induce the metabolism of HIV-protease inhibitors resulting in reduced plasma concentrations.
Antacids: Antacids may decrease the absorption of corticosteroids when given concomitantly. Dose adjustments may be required in patients receiving small doses of corticosteroids.
Oral Contraceptives and Estrogen: These can cause alterations in plasma protein binding and metabolism of corticosteroids which can result in exposure of women to increased levels of the unbound corticosteroid for long periods of time. Dose adjustments may be warranted when commencing or stopping oral contraceptive therapy. There have also been isolated reports of contraceptive failure in women receiving corticosteroid therapy.
Aspirin or Other Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Concomitant use results in increased risk of gastrointestinal adverse effects eg, gastrointestinal bleeding and ulceration.
Use aspirin cautiously in conjunction with corticosteroids. The clearance of salicylates may be increased with concomitant use which could lead to increased salicylate toxicity when methylprednisolone is withdrawn.
Oral Anticoagulants (Warfarin): There is conflicting data on the effect of methylprednisolone and anticoagulants. There are reports of enhanced as well as diminished effects of anticoagulants when given concomitantly. Monitor coagulation indices [eg, international normalized ratio (INR) and prothrombin time] frequently to maintain the desired anticoagulant effect.
Diuretics (eg, Potassium-Depleting Diuretics eg, Furosemide and Thiazide or Carbonic Anhydrase Inhibitors eg, Acetazolamide): Observe patients closely for the development of hypokalemia.
Mifepristone: The effect of corticosteroids may be reduced for 3-4 days after taking mifepristone.
Amphotericin-B: Concomitant use may increase the risk of hypokalemia.
Anticholinergic Agents: Acute myopathy has been reported with concomitant use of high doses of corticosteroids and anticholinergics eg, neuromuscular blocking agents.
In patients taking corticosteroids, antagonism of the neuromuscular blocking effects of pancuronium and vecuronium may occur. This interaction may be expected with all competitive neuromuscular blockers.
Insulin and Oral Antidiabetic Agents: Corticosteroids eg, methylprednisolone may increase blood glucose concentrations and may cause impaired glucose tolerance. Dosage adjustment of antidiabetic agents may be required when these 2 drugs are used concomitantly.
Digitalis Glycosides: Patients may be at increased risk of arrhythmias due to hypokalemia.
Toxoids and Live or Inactivated Vaccines: Patients on prolonged corticosteroid therapy may exhibit diminished response to toxoids and live or inactivated vaccines due to inhibition of antibody response.

Storage

Action

Corticosteroid Hormones