NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Methylprednisolone

; .

Author Information

Last Update: July 18, 2021.

Continuing Education Activity

Methylprednisolone is an FDA-approved medication for the management and treatment of allergic conditions, arthritis, asthma exacerbations, long-term asthma maintenance, acute exacerbation of multiple sclerosis, and as an anti-inflammatory and immunosuppressive agent. It is in the systemic corticosteroid class of medications. This activity outlines the indications, action, and contraindications for methylprednisolone as a valuable agent in treating many endocrine, inflammatory, immunologic, hematologic, and respiratory disorders.

Objectives:

  • Identify the mechanism of action of methylprednisolone.
  • Describe the potential adverse effects for patients taking methylprednisolone.
  • Review and select the appropriate monitoring for patients on methylprednisolone.
  • Outline the importance of improving care coordination and communication amongst the interprofessional team to enhance care delivery and improve outcomes for patients receiving methylprednisolone.
Access free multiple choice questions on this topic.

Indications

Methylprednisolone is a systemic synthetic corticosteroid, which, just as the naturally occurring glucocorticoids, exerts a wide range of physiologic effects. Clinical use of methylprednisolone is mainly due to its anti-inflammatory and immunosuppressive activity in the human body.

Labeled indications of methylprednisolone subcategorize by its use in different organ systems:

  • In dermatology, it has utility in managing atopic dermatitis, contact dermatitis, pemphigus vulgaris, and foliaceus, bullous pemphigus, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis.[1][2][3][4]
  • In endocrinology, it is used to manage congenital adrenal hyperplasia, hypercalcemia associated with cancer, and as a second-line treatment in conjunction with mineralocorticoids for primary or secondary adrenocortical insufficiency.
  • In gastroenterology, methylprednisolone's use is for acute exacerbations of inflammatory bowel disease.[5][6][5][7]
  • In hematology, it serves to treat autoimmune hemolytic anemia, congenital (erythroid) aplastic anemia, and immune thrombocytopenia.[8][9][10]
  • In neurology, it is the mainstay therapy in acute exacerbations of multiple sclerosis.[11]
  • In ophthalmology, it is a therapeutic choice in severe allergic and inflammatory processes of the eye and its adnexa, such as uveitis, scleritis, chorioretinitis, iritis and iridocyclitis, keratitis, optic neuritis, retinal vasculitis, and allergic conjunctivitis,
  • In nephrology, it is helpful in the management of nephrotic syndrome, idiopathic type, or secondary to lupus nephritis.[12][13][14]
  • In pulmonology, its indications include aspiration pneumonitis, asthma, chronic beryllium disease as an adjunct to antituberculous chemotherapy in disseminated pulmonary tuberculosis, eosinophilic pneumonia, and symptomatic sarcoidosis.[15][16][17][18]
  • In rheumatology, it has indications for the management of acute rheumatic carditis, acute gout, ankylosing spondylitis, dermatomyositis and polymyositis, psoriatic arthritis, and rheumatoid arthritis, including the juvenile type and systemic lupus erythematosus.[19][20][21][22][23][24][25]

Other miscellaneous labeled indications for methylprednisolone include:

  • Intraarticular and soft tissue administration in acute gouty arthritis, acute and subacute bursitis, acute tenosynovitis, epicondylitis, and synovitis of osteoarthritis.[26][27]
  • Intralesional administration in alopecia areata, discoid lupus erythematosus, keloid disease, and lichen planus.[28][29][30][31]

Off-label indications of methylprednisolone include:

  • Adjunct therapy for acute spinal cord injury
  • Moderate to severe acute distress respiratory syndrome and severe alcoholic hepatitis
  • As a preventive agent in bronchiolitis obliterans syndrome
  • Hormonal resuscitation in cadaveric organ recovery
  • Treatment of acute cellular and antibody-mediated rejection in cardiac transplant
  • Adjunct in the management of acute exacerbation of chronic obstructive pulmonary disease
  • Severe/refractory nausea and vomiting of pregnancy
  • Adjunct treatment of Pneumocystis pneumonia in HIV-infected patients
  • As palliation alternative in castration-resistant metastatic prostate cancer

Mechanism of Action

Methylprednisolone and its derivatives, methylprednisolone acetate succinate and methylprednisolone sodium, are intermediate-acting, synthetic glucocorticoids. They are used mainly as anti-inflammatory or immunosuppressive agents. Methylprednisolone is five times more potent in its anti-inflammatory properties relative to hydrocortisone (cortisol), with minimal mineralocorticoid activities compared to the latter.[32]

Methylprednisolone diffuses passively across the cellular membrane and binds to the intracellular glucocorticoid receptor. This complex translocates into the nucleus, where it interacts with specific DNA sequences, resulting in either enhancement or suppression of transcription of particular genes. The methylprednisolone-glucocorticoid receptor complex binds and blocks promoter sites of proinflammatory genes,[33] promotes expression of anti-inflammatory gene products,[34] and inhibits the synthesis of inflammatory cytokines, mainly by blocking the function of transcription factors, such as nuclear factor-kappa-B (NF-kB).[35]

Like the rest of the corticosteroids, methylprednisolone also suppresses the synthesis of cyclooxygenase (COX)-2, responsible for the production of prostaglandins in damaged tissue leading to the inflammation cascade.[36]

By reversing capillary permeability, suppressing the migration of fibroblasts and polymorphonuclear leukocytes, controlling the rate of protein synthesis, and stabilizing lysosomes at the cellular level, methylprednisolone may control or prevent inflammation through these actions as well.

Methylprednisolone inhibits cell-mediated immunologic functions, especially those dependent on lymphocytes. Glucocorticoid administration results in neutrophilic leukocytosis, smaller elevations in monocytes, dramatic reductions in circulating eosinophils, and lesser reductions in lymphocytes. The use of methylprednisolone and other glucocorticoids results in a reduced ability of leukocytes to adhere to vascular endothelium and exit from the circulation. Glucocorticoids impair a variety of T cell functions, and moderate-to-high doses induce T cell apoptosis while keeping B cell function and antibody production preserved.[37]

Tissue-specific responses to steroids can occur by the presence in each tissue of specific protein regulators controlling the interaction between the hormone-receptor complex and particular DNA response elements. This activity leads to a wide array of gene expression and physiological responses by corticosteroids.

Some of the most important effects of methylprednisolone and the rest of the corticosteroids are the result of homeostatic responses by insulin and glucagon. Glucocorticoids stimulate gluconeogenesis, which results in elevated blood glucose, catabolism of muscle protein, and stimulation of insulin secretion. Both lipolysis and lipogenesis become stimulated, with a net increase of fat deposition in certain areas (e.g., face, shoulders, and back).[38]

Methylprednisolone and the rest of the glucocorticoids cause muscle protein catabolism. Also, lymphoid and connective tissue, fat, and skin undergo wasting under the influence of high concentrations of these steroids. Catabolic effects on the bone can lead to osteoporosis. In children, growth inhibition takes place.

Administration

Methylprednisolone may be administered orally with food or milk to decrease gastrointestinal adverse effects. Administration may also be intramuscularly or intravenously. When administered intramuscularly (in the form of methylprednisolone acetate or succinate), the administration should not be into the deltoid muscle due to evidence of subcutaneous atrophy. Injections into the dermis should be avoided, and injection should not be into areas that have evidence of acute local infection.

Intravenous administration of methylprednisolone (in the form of methylprednisolone succinate) is rate dependent upon the dose and severity of the condition. Most commonly, with intermittent infusion, methylprednisolone is administered over 15 to 60 minutes. The administration of large doses should be over at least 30 to 60 minutes. 

There are reports of hypotension, cardiac arrhythmias, and sudden death when methylprednisolone administration occurs under 30 minutes in doses greater or equal than 250 mg.[39]

The onset of action of intravenous methylprednisolone succinate is within 1 hour, while intra-articular administration of IV acetate is of 1 week, with a duration of 1 to 5 weeks. Methylprednisolone has an oral bioavailability of 88% approximately. The half-life elimination of intravenous methylprednisolone is of 0.25 hours, with an oral half-life of 2-5 hours. It has hepatic metabolism and undergoes urinary excretion.[40][41]

Adverse Effects

The significant undesirable effects of glucocorticoids result from their hormonal actions, which lead to the clinical picture of iatrogenic Cushing syndrome. Facial rounding, puffiness, fat deposition, and plethora usually appear (moon facies). Fat tends to redistribute from the extremities to the trunk, the back of the neck, and the supraclavicular fossae. There is increased growth of fine hair on the face, thighs, and trunk. Steroid-induced punctate acne may appear, and insomnia and increased appetite are also effects.

With concurrent use of methylprednisolone, protein catabolism will continue, diverting amino acids to glucose production, thus increasing the need for insulin and over time resulting in weight gain. Myopathy and muscle wasting can occur, as well as thinning of the skin, with striae and bruising. Hyperglycemia and eventually osteoporosis can develop, as well as diabetes and aseptic necrosis of the hip.[42]

A more detailed way to review the adverse effects of methylprednisolone and other corticosteroids is by classifying them based on the different organ systems affected:

  • Dermatologic and side effects in appearance include skin thinning and ecchymoses, Cushingoid features, and weight gain.
  • Ophthalmologic side effects include the formation of cataracts, increased intraocular pressure, and the development of exophthalmos.
  • Cardiovascular side effects include fluid retention and hypertension, premature atherosclerotic disease, arrhythmias, and possible hyperlipidemia.
  • Gastrointestinal effects include the increased risk of gastritis, ulcer formation, and gastrointestinal bleeding. 
  • Bone and muscle effects include osteoporosis, osteonecrosis, and myopathy.
  • Neuropsychiatric side effects include mood disorders, psychosis, and memory impairment.
  • Metabolic and endocrine side effects consist of hyperglycemia and hypothalamic-pituitary-adrenal axis suppression.
  • Immune system effects include increased susceptibility to infections.
  • Hematologic side effects include leukocytosis and neutrophilia.

Contraindications

Methylprednisolone contraindications include patients with documented hypersensitivity to the drug or components, systemic fungal infection, intrathecal administration, live or attenuated virus vaccine, idiopathic thrombocytopenia purpura, or in premature infants.[43]

Like all other glucocorticoids, methylprednisolone must be used with great caution in patients with peptic ulcers, heart disease or hypertension with heart failure, certain infectious illnesses such as varicella and tuberculosis psychoses, diabetes, osteoporosis, or glaucoma.[44]

Monitoring

Blood pressure, blood glucose, electrolytes, weight, bone mineral density, HPA hypothalamic-pituitary-adrenal (HPA) axis suppression, and intraocular pressure all require monitoring in patients taking methylprednisolone. Growth and development monitoring should be in place for children.

Patients receiving methylprednisolone must be monitored carefully for the development of hyperglycemia, glycosuria, sodium retention with edema or hypertension, hypokalemia, peptic ulcers, osteoporosis, and hidden infections.

The dosage should be as low as possible. Even patients maintained on low doses of methylprednisolone may require supplementary therapy at times of stress, such as during surgery, intercurrent illness, or trauma occurs.

Toxicity

Most of the toxic effects of methylprednisolone and other glucocorticoids are predictable from their impact on the body's physiology. Some are life-threatening and include metabolic effects (growth inhibition, diabetes, muscle wasting, osteoporosis), salt retention (although less common with methylprednisolone), and psychosis.

Methods for minimizing these toxicities include local application, alternate-day therapy (to reduce pituitary suppression), and tapering the dose promptly after attaining a therapeutic response. Additional "stress doses" may be necessary during serious illness or before major surgery to prevent adrenal insufficiency in patients who have received long-term treatment with methylprednisolone.

Enhancing Healthcare Team Outcomes

Methylprednisolone is a widely-used drug in multiple fields of medicine, mainly due to its anti-inflammatory and immunosuppressive properties. Interprofessional healthcare team members, including nurses, pharmacists, mid-level practitioners, and clinicians, should be aware of its broad spectrum of clinical applications, both labeled and off-labeled indications while considering its contraindications and individualizing its use based on the patient's comorbidities and tolerance of side effects. Of particular importance, patients receiving methylprednisolone should undergo monitoring for the development of hyperglycemia, hypertension, peptic ulcer, osteoporosis, and hidden infections.

Clinicians (MDs, DOs, NPs, PAs) will be prescribing or ordering the medication. Nursing will administer if inpatient and can monitor for adverse effects in both inpatient and outpatient settings. Pharmacists should be involved to verify dosing and perform medication reconciliation. Both pharmacists and nurses need to alert the healthcare team if they encounter any issues of concern. All these interprofessional healthcare team members need to communicate and collaborate across interprofessional lines to ensure optimal therapeutic results. [Level 5]

As with all glucocorticoids, methylprednisolone's adverse effects are both dose- and duration-dependent and can range from non-serious displeasing appearance to those that are life-threatening. Interprofessional coordination and care between healthcare workers are needed to ensure that methylprednisolone dosage remains minimal and for the shortest period necessary to achieve the treatment goals. Preexisting comorbidities that may become exacerbated when treated with methylprednisolone require management, and that patients under treatment should be monitored by the pharmacist, nurse, and clinician for adverse effects, identifying who may benefit from additional intervention. An interprofessional team approach will lead to the best outcomes. [Level 5]

Review Questions

References

1.
Torrelo A. Methylprednisolone aceponate for atopic dermatitis. Int J Dermatol. 2017 Jun;56(6):691-697. [PubMed: 28258632]
2.
Lachapelle JM, Gimenez-Arnau A, Metz M, Peters J, Proksch E. Best practices, new perspectives and the perfect emollient: optimizing the management of contact dermatitis. J Dermatolog Treat. 2018 May;29(3):241-251. [PubMed: 28866951]
3.
Rose E, Wever S, Zilliken D, Linse R, Haustein UF, Bröcker EB. Intravenous dexamethasone-cyclophosphamide pulse therapy in comparison with oral methylprednisolone-azathioprine therapy in patients with pemphigus: results of a multicenter prospectively randomized study. J Dtsch Dermatol Ges. 2005 Mar;3(3):200-6. [PubMed: 16372814]
4.
Del Pozzo-Magana BR, Lazo-Langner A, Carleton B, Castro-Pastrana LI, Rieder MJ. A systematic review of treatment of drug-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in children. J Popul Ther Clin Pharmacol. 2011;18:e121-33. [PubMed: 21467603]
5.
Speiser PW, Arlt W, Auchus RJ, Baskin LS, Conway GS, Merke DP, Meyer-Bahlburg HFL, Miller WL, Murad MH, Oberfield SE, White PC. Congenital Adrenal Hyperplasia Due to Steroid 21-Hydroxylase Deficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018 Nov 01;103(11):4043-4088. [PMC free article: PMC6456929] [PubMed: 30272171]
6.
Unal S, Durmaz E, Erkoçoğlu M, Bayrakçi B, Bircan O, Alikaşifoğlu A, Cetin M. The rapid correction of hypercalcemia at presentation of acute lymphoblastic leukemia using high-dose methylprednisolone. Turk J Pediatr. 2008 Mar-Apr;50(2):171-5. [PubMed: 18664083]
7.
Rosenberg W, Ireland A, Jewell DP. High-dose methylprednisolone in the treatment of active ulcerative colitis. J Clin Gastroenterol. 1990 Feb;12(1):40-1. [PubMed: 2303687]
8.
Jaime-Pérez JC, Rodríguez-Martínez M, Gómez-de-León A, Tarín-Arzaga L, Gómez-Almaguer D. Current approaches for the treatment of autoimmune hemolytic anemia. Arch Immunol Ther Exp (Warsz). 2013 Oct;61(5):385-95. [PubMed: 23689532]
9.
Frickhofen N, Kaltwasser JP, Schrezenmeier H, Raghavachar A, Vogt HG, Herrmann F, Freund M, Meusers P, Salama A, Heimpel H. Treatment of aplastic anemia with antilymphocyte globulin and methylprednisolone with or without cyclosporine. The German Aplastic Anemia Study Group. N Engl J Med. 1991 May 09;324(19):1297-304. [PubMed: 2017225]
10.
Godeau B, Chevret S, Varet B, Lefrère F, Zini JM, Bassompierre F, Chèze S, Legouffe E, Hulin C, Grange MJ, Fain O, Bierling P., French ATIP Study Group. Intravenous immunoglobulin or high-dose methylprednisolone, with or without oral prednisone, for adults with untreated severe autoimmune thrombocytopenic purpura: a randomised, multicentre trial. Lancet. 2002 Jan 05;359(9300):23-9. [PubMed: 11809183]
11.
Murray TJ. Diagnosis and treatment of multiple sclerosis. BMJ. 2006 Mar 04;332(7540):525-7. [PMC free article: PMC1388131] [PubMed: 16513709]
12.
Charkoudian LD, Ying GS, Pujari SS, Gangaputra S, Thorne JE, Foster CS, Jabs DA, Levy-Clarke GA, Nussenblatt RB, Rosenbaum JT, Suhler EB, Kempen JH. High-dose intravenous corticosteroids for ocular inflammatory diseases. Ocul Immunol Inflamm. 2012 Apr;20(2):91-9. [PMC free article: PMC3306126] [PubMed: 22409561]
13.
Murnaghan K, Vasmant D, Bensman A. Pulse methylprednisolone therapy in severe idiopathic childhood nephrotic syndrome. Acta Paediatr Scand. 1984 Nov;73(6):733-9. [PubMed: 6524363]
14.
Illei GG, Austin HA, Crane M, Collins L, Gourley MF, Yarboro CH, Vaughan EM, Kuroiwa T, Danning CL, Steinberg AD, Klippel JH, Balow JE, Boumpas DT. Combination therapy with pulse cyclophosphamide plus pulse methylprednisolone improves long-term renal outcome without adding toxicity in patients with lupus nephritis. Ann Intern Med. 2001 Aug 21;135(4):248-57. [PubMed: 11511139]
15.
Zhao JN, Liu Y, Li HC. Corticosteroids in treatment of aspiration-related acute respiratory distress syndrome: results of a retrospective cohort study. BMC Pulm Med. 2016 Feb 10;16:29. [PMC free article: PMC4748555] [PubMed: 26864571]
16.
Alangari AA. Corticosteroids in the treatment of acute asthma. Ann Thorac Med. 2014 Oct;9(4):187-92. [PMC free article: PMC4166064] [PubMed: 25276236]
17.
Rhee CK, Min KH, Yim NY, Lee JE, Lee NR, Chung MP, Jeon K. Clinical characteristics and corticosteroid treatment of acute eosinophilic pneumonia. Eur Respir J. 2013 Feb;41(2):402-9. [PubMed: 22599359]
18.
Wallaert B, Ramon P, Fournier EC, Hatron PY, Muir JF, Tonnel AB, Voisin C. High-dose methylprednisolone pulse therapy in sarcoidosis. Eur J Respir Dis. 1986 Apr;68(4):256-62. [PubMed: 3732422]
19.
Herdy GV, Pinto CA, Olivaes MC, Carvalho EA, Tchou H, Cosendey R, Ribeiro R, Azeredo F, de Souza D, Herdy AH, Lopes VG. Rheumatic carditis treated with high doses of pulsetherapy methylprednisolone. Results in 70 children over 12 years. Arq Bras Cardiol. 1999 May;72(5):601-6. [PubMed: 10668230]
20.
Groff GD, Franck WA, Raddatz DA. Systemic steroid therapy for acute gout: a clinical trial and review of the literature. Semin Arthritis Rheum. 1990 Jun;19(6):329-36. [PubMed: 2196674]
21.
Peters ND, Ejstrup L. Intravenous methylprednisolone pulse therapy in ankylosing spondylitis. Scand J Rheumatol. 1992;21(3):134-8. [PubMed: 1604251]
22.
Matsubara S, Hirai S, Sawa Y. Pulsed intravenous methylprednisolone therapy for inflammatory myopathies: evaluation of the effect by comparing two consecutive biopsies from the same muscle. J Neuroimmunol. 1997 Jun;76(1-2):75-80. [PubMed: 9184635]
23.
Nash P. Therapies for axial disease in psoriatic arthritis. A systematic review. J Rheumatol. 2006 Jul;33(7):1431-4. [PubMed: 16724371]
24.
Smith MD, Ahern MJ, Roberts-Thomson PJ. Pulse methylprednisolone therapy in rheumatoid arthritis: unproved therapy, unjustified therapy, or effective adjunctive treatment? Ann Rheum Dis. 1990 Apr;49(4):265-7. [PMC free article: PMC1004053] [PubMed: 2187419]
25.
Badsha H, Edwards CJ. Intravenous pulses of methylprednisolone for systemic lupus erythematosus. Semin Arthritis Rheum. 2003 Jun;32(6):370-7. [PubMed: 12833245]
26.
Pyne D, Ioannou Y, Mootoo R, Bhanji A. Intra-articular steroids in knee osteoarthritis: a comparative study of triamcinolone hexacetonide and methylprednisolone acetate. Clin Rheumatol. 2004 Apr;23(2):116-20. [PubMed: 15045624]
27.
Garg N, Perry L, Deodhar A. Intra-articular and soft tissue injections, a systematic review of relative efficacy of various corticosteroids. Clin Rheumatol. 2014 Dec;33(12):1695-706. [PubMed: 24651914]
28.
Senila SC, Danescu SA, Ungureanu L, Candrea E, Cosgarea RM. Intravenous methylprednisolone pulse therapy in severe alopecia areata. Indian J Dermatol Venereol Leprol. 2015 Jan-Feb;81(1):95. [PubMed: 25566921]
29.
Fabbri P, Cardinali C, Giomi B, Caproni M. Cutaneous lupus erythematosus: diagnosis and management. Am J Clin Dermatol. 2003;4(7):449-65. [PubMed: 12814335]
30.
Syed F, Singh S, Bayat A. Superior effect of combination vs. single steroid therapy in keloid disease: a comparative in vitro analysis of glucocorticoids. Wound Repair Regen. 2013 Jan-Feb;21(1):88-102. [PubMed: 23126666]
31.
Snyder RA, Schwartz RA, Schneider JS, Elias PM. Intermittent megadose corticosteroid therapy for generalized lichen planus. J Am Acad Dermatol. 1982 Jun;6(6):1089-90. [PubMed: 7096672]
32.
Langhoff E, Ladefoged J. Relative immunosuppressive potency of various corticosteroids measured in vitro. Eur J Clin Pharmacol. 1983;25(4):459-62. [PubMed: 6653640]
33.
Zhang G, Zhang L, Duff GW. A negative regulatory region containing a glucocorticosteroid response element (nGRE) in the human interleukin-1beta gene. DNA Cell Biol. 1997 Feb;16(2):145-52. [PubMed: 9052735]
34.
Scheinman RI, Cogswell PC, Lofquist AK, Baldwin AS. Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids. Science. 1995 Oct 13;270(5234):283-6. [PubMed: 7569975]
35.
Auphan N, DiDonato JA, Rosette C, Helmberg A, Karin M. Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis. Science. 1995 Oct 13;270(5234):286-90. [PubMed: 7569976]
36.
Chen CC, Sun YT, Chen JJ, Chiu KT. TNF-alpha-induced cyclooxygenase-2 expression in human lung epithelial cells: involvement of the phospholipase C-gamma 2, protein kinase C-alpha, tyrosine kinase, NF-kappa B-inducing kinase, and I-kappa B kinase 1/2 pathway. J Immunol. 2000 Sep 01;165(5):2719-28. [PubMed: 10946303]
37.
Mathian A, Jouenne R, Chader D, Cohen-Aubart F, Haroche J, Fadlallah J, Claër L, Musset L, Gorochov G, Amoura Z, Miyara M. Regulatory T Cell Responses to High-Dose Methylprednisolone in Active Systemic Lupus Erythematosus. PLoS One. 2015;10(12):e0143689. [PMC free article: PMC4667921] [PubMed: 26629828]
38.
Shaw WA, Issekutz TB, Issekutz B. Gluconeogenesis from glycerol at rest and during exercise in normal, diabetic, and methylprednisolone-treated dogs. Metabolism. 1976 Mar;25(3):329-39. [PubMed: 1250166]
39.
Ditzian-Kadanoff R, Ellman MH. How safe is it? High dose intravenous methylprednisolone. IMJ Ill Med J. 1987 Dec;172(6):432-4. [PubMed: 2892818]
40.
Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clin Pharmacokinet. 2005;44(1):61-98. [PubMed: 15634032]
41.
Garg DC, Ng P, Weidler DJ, Sakmar E, Wagner JG. Preliminary in vitro and in vivo investigations on methylprednisolone and its acetate. Res Commun Chem Pathol Pharmacol. 1978 Oct;22(1):37-48. [PubMed: 725320]
42.
Stanbury RM, Graham EM. Systemic corticosteroid therapy--side effects and their management. Br J Ophthalmol. 1998 Jun;82(6):704-8. [PMC free article: PMC1722622] [PubMed: 9797677]
43.
Ferrell CL. Anaphylactic Reaction to Methylprednisolone. J Emerg Nurs. 2015 Nov;41(6):470-3. [PubMed: 26296715]
44.
Tseng CL, Chen YT, Huang CJ, Luo JC, Peng YL, Huang DF, Hou MC, Lin HC, Lee FY. Short-term use of glucocorticoids and risk of peptic ulcer bleeding: a nationwide population-based case-crossover study. Aliment Pharmacol Ther. 2015 Sep;42(5):599-606. [PubMed: 26096497]
Copyright © 2021, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated.

Bookshelf ID: NBK544340PMID: 31335060

Views

  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...