Methylprednisolone

Earn CME/CE in your profession:


Continuing Education Activity

Methylprednisolone is an FDA-approved medication used for managing and treating various conditions, including allergic reactions, arthritis, asthma exacerbations, long-term asthma maintenance, and acute exacerbations of multiple sclerosis. As a systemic corticosteroid, methylprednisolone exhibits anti-inflammatory and immunosuppressive properties, effectively treating endocrine, inflammatory, immunologic, hematologic, and respiratory disorders. This activity focuses on the medication's indications, mechanisms, and contraindications, emphasizing the importance of understanding its role in different organ systems. Additionally, methylprednisolone's adverse event profiles, pharmacokinetics, clinical toxicology, monitoring, and drug interactions will also be discussed.

Understanding the intricate pharmacology of this synthetic corticosteroid helps healthcare professionals tailor treatment plans to meet individual patient needs. This initiative enhances clinician proficiency regarding methylprednisolone therapy to ensure patient-centered care. The goal is to minimize adverse effects while maximizing therapeutic efficacy, thus improving patient outcomes and elevating standards of care. By optimizing methylprednisolone therapy, healthcare providers can deliver personalized and safe management for conditions requiring this medication, promoting optimal patient outcomes and enhancing the overall quality of care.

Objectives:

  • Identify the mechanism of action of methylprednisolone.

  • Assess the potential adverse drug reactions of methylprednisolone.

  • Select the appropriate monitoring parameters for patients on methylprednisolone.

  • Implement effective collaboration and communication among interprofessional team members to improve outcomes and treatment efficacy for patients who might benefit from methylprednisolone therapy.

Indications

Methylprednisolone is a systemic synthetic corticosteroid that exerts a wide range of physiologic effects similar to naturally occurring glucocorticoids. Methylprednisolone is typically prescribed due to its anti-inflammatory and immunosuppressive activity in the human body. The FDA-approved indications and off-label uses for methylprednisolone therapy are listed below.

FDA-Approved Indications

The following indications for methylprednisolone administration approved by the U.S. Food and Drug Administration are categorized below by organ system.

Dermatology:

  • Atopic dermatitis
  • Contact dermatitis
  • Pemphigus vulgaris
  • Pemphigus foliaceous
  • Bullous pemphigus
  • Erythema multiforme
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis [1][2][3][4] 

Endocrinology: 

  • Congenital adrenal hyperplasia associated with cancer
  • Hypercalcemia associated with cancer
  • Primary or secondary adrenocortical insufficiency (as a second-line treatment in conjunction with mineralocorticoids)

Gastroenterology:

  • Inflammatory bowel disease (acute exacerbations) [5][6][7]

Hematology:

  • Autoimmune hemolytic anemia
  • Congenital (erythroid) aplastic anemia
  • Immune thrombocytopenia [8][9][10]

Neurology:

  • Multiple sclerosis (acute exacerbations) [11]

Ophthalmology:

  • Uveitis
  • Scleritis
  • Chorioretinitis
  • Iritis and iridocyclitis
  • Keratitis
  • Optic neuritis
  • Retinal vasculitis
  • Allergic conjunctivitis

Nephrology:

  • Nephrotic syndrome (idiopathic or secondary to lupus nephritis) [12][13][14]

Pulmonology:

  • Aspiration pneumonitis
  • Asthma
  • Chronic beryllium disease
  • Disseminated pulmonary tuberculosis (as an adjunct to antituberculous chemotherapy)
  • Eosinophilic pneumonia
  • Symptomatic sarcoidosis [15][16][17][18]

Rheumatology:

  • Acute rheumatic carditis
  • Acute gout
  • Ankylosing spondylitis
  • Dermatomyositis and polymyositis
  • Psoriatic arthritis
  • Rheumatoid arthritis (including juvenile type)
  • Systemic lupus erythematosus [19][20][21][22][23][24][25]

The FDA-approved indications and methods for the administration of methylprednisolone acetate formulation specifically are listed below.[26][27][28][29][30][31]

Intra-articular and soft tissue administration:

  • Acute gouty arthritis
  • Acute and subacute bursitis
  • Acute tenosynovitis
  • Epicondylitis
  • Synovitis of osteoarthritis

Intralesional administration:

  • Alopecia areata
  • Discoid lupus erythematosus
  • Keloid disease
  • Lichen planus

Off-Label Uses

Methylprednisolone may be administered for the following conditions or scenarios. The U.S. Food and Drug Administration has not approved these indications.

  • As adjunct therapy for patients with acute spinal cord injury.[32] The administration of methylprednisolone within 8 hours following a spinal cord injury requires careful individual consideration due to potential complications.[33]
  • Myasthenia gravis [34]
  • Severe urticaria [35]
  • Sjögren's syndrome [36]
  • Severe/refractory nausea and vomiting during pregnancy [37]
  • COVID-19 requiring oxygen or ventilatory support [38]
  • Amiodarone-induced thyrotoxicosis (drug-resistant) [39]
  • Moderate to severe acute distress respiratory syndrome (ARDS)
  • Severe alcoholic hepatitis
  • As a preventive agent in bronchiolitis obliterans syndrome
  • Hormonal resuscitation in cadaveric organ recovery
  • Acute cellular or antibody-mediated rejection in cardiac transplant
  • As adjunct therapy for patients with acute exacerbation of chronic obstructive pulmonary disease (COPD)
  • As adjunct treatment of Pneumocystis pneumonia in patients with HIV
  • As a palliative option for patients with 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 typically prescribed as anti-inflammatory or immunosuppressive agents. As an anti-inflammatory, methylprednisolone is 5 times as potent as hydrocortisone (cortisol) while demonstrating minimal mineralocorticoid activity.[40] Methylprednisolone diffuses passively across the cellular membrane and binds to the intracellular glucocorticoid receptor. This complex translocates into the nucleus to interact with specific DNA sequences and enhance or suppress the transcription of particular genes. The methylprednisolone-glucocorticoid receptor complex blocks the promoter sites of proinflammatory genes, promotes the expression of anti-inflammatory gene products, and inhibits the synthesis of inflammatory cytokines; these actions are accomplished primarily by blocking the function of transcription factors, such as nuclear factor-kappa-B (NF-kB).[41][42][43] 

As a corticosteroid, methylprednisolone also suppresses the synthesis of cyclooxygenase (COX)-2, an enzyme that produces prostaglandins in damaged tissue and contributes to the inflammation cascade.[44] Through these actions, methylprednisolone can reduce or prevent inflammation 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 inhibits cell-mediated immunologic functions, especially those dependent on lymphocytes. Glucocorticoid administration results in neutrophilic leukocytosis, reduced monocyte elevations, dramatic reductions in circulating eosinophils, and milder reductions in lymphocytes. Methylprednisolone and other glucocorticoids reduce leukocytes' ability to adhere to vascular endothelium and exit the circulation. Glucocorticoids impair various T-cell functions; moderate and high doses induce T-cell apoptosis while preserving B-cell functions, including antibody production.[45] Tissue-specific responses to steroids can occur due to specific protein regulators in each tissue 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 critical effects of methylprednisolone and other corticosteroids result from homeostatic responses by insulin and glucagon. Glucocorticoids stimulate gluconeogenesis, which elevates blood glucose levels, increases muscle protein and bone catabolism, and stimulates insulin secretion. Glucocorticoids stimulate lipolysis and lipogenesis, causing a net increase of fat deposition in some body areas (ie, face, shoulders, and back).[46] Glucocorticoids also cause wasting of lymphoid and connective tissue, fat, and skin at high doses. Catabolic effects on the bone can lead to osteoporosis in adults and growth inhibition in children.

Pharmacokinetics

Absorption: Depending on the administration route and dose, a 2-compartment (for high IV doses) or 1-compartment model (for lower IV and oral doses) is appropriate for describing methylprednisolone's pharmacokinetics. Methylprednisolone exhibits rapid and linear absorption, with peak concentrations achieved 48 minutes after administration. The onset of action of intravenous methylprednisolone succinate occurs within 1 hour. For intra-articular methylprednisone acetate, the onset of action occurs at 1 week and lasts 1 to 5 weeks. Methylprednisolone has an oral bioavailability of approximately 88%.

Distribution: Methylprednisolone succinate has a volume of distribution (Vd) of 24 ± 6 L and a steady-state volume of distribution (Vss) of 27 ± 8.2 L. This drug primarily binds to albumin in plasma.

Metabolism:  Methylprednisolone undergoes hepatic metabolism to produce metabolites such as 20-carboxymethylprednisolone and 6β-hydroxy-20α-hydroxymethylprednisolone.

Elimination: Methylprednisolone is primarily excreted in urine, following a bi-exponential pattern.[47] The half-life elimination of intravenous methylprednisolone is 0.25 hours, with an oral half-life of 2-5 hours.[48][49]

Administration

Available Dosage Forms and Strengths

Methylprednisolone is available in tablet formulations of 2 mg, 4 mg, 8 mg, 16 mg, and 32 mg, injectable suspension formulations at concentrations of 20 mg/mL, 40 mg/mL, and 80 mg/mL, and as a powder for injection in doses of 40 mg, 125 mg, 500 mg, 1000 mg, and 2000 mg.

Adult Dosage

Methylprednisolone may be administered orally with food or milk to reduce gastrointestinal adverse effects. Methylprednisolone may also be administered intramuscularly or intravenously. When administered intramuscularly (methylprednisolone acetate or succinate), it should not be injected into the deltoid muscle, which may cause subcutaneous atrophy. Injections into the dermis or areas with evidence of acute local infection should be avoided. Intravenous administration (methylprednisolone succinate) is rate-dependent upon the dose and severity of the condition. Methylprednisolone is most commonly administered over 15 to 60 minutes with intermittent infusion. Large doses should be administered over a minimum of 30 minutes. Hypotension, arrhythmia, and sudden death have been reported when methylprednisolone doses of 250 mg or greater are administered in less than 30 minutes.[50]

COVID-19: For most patients with COVID-19 requiring supplemental oxygen, the National Institutes of Health (NIH) advises dexamethasone plus remdesivir; if dexamethasone is unavailable, clinicians can consider methylprednisolone, prednisone or hydrocortisone.[78]

A recent cohort study investigated the impact of intravenous (IV) methylprednisolone pulse therapy on in-hospital mortality risk in patients with acute COVID-19. Among patients receiving invasive mechanical ventilation, IV methylprednisolone pulse therapy at doses of 500 to 1000 mg daily reduced the risk of in-hospital mortality compared to those not receiving steroid pulse therapy or intermediate steroid doses.[51]

Anaphylaxis: The American Academy of Allergy, Asthma, and Immunology guidelines recommend that 1.0 to 2.0 mg/kg per dose of methylprednisolone be administered for adjunct treatment of anaphylaxis. Antihistamines and corticosteroids are adjunctive therapies for patients with anaphylaxis; epinephrine remains the primary treatment.[52]

Ulcerative colitis: The American College of Gastroenterology (ACG) recommends methylprednisolone 60 mg daily for remission in patients with severe ulcerative colitis.[53]

Lupus nephritis: According to the KDGIO 2024 guidelines, methylprednisolone pulses may be followed by a regimen of glucocorticoids during the initial treatment of active lupus nephritis upon satisfactory improvement in renal and extrarenal disease manifestations. Initial treatment typically involves IV methylprednisolone at a dose of 0.25 to 0.5 g/day for up to 3 days.[54] The study investigated the effects of high-dose methylprednisolone (above 100 mg) during cardiac arrest, revealing improved rates of sustained return of spontaneous circulation (ROSC) and overall survival at hospital discharge.[55]

Asthma exacerbation: According to the Global Initiative for Asthma (GINA) guidelines, methylprednisolone should be administered to patients 5 years or younger at 1 mg/kg, followed by oral steroids based upon clinical response.[79]

Juvenile idiopathic arthritis: Methylprednisolone can be used to treat juvenile idiopathic arthritis. However, intra-articular glucocorticoids such as triamcinolone are recommended as part of the initial therapy for active oligoarthritis.[56]

Steroid-resistant nephrotic syndrome: According to the International Pediatric Nephrology Association, pulse therapy with intravenous methylprednisolone (500 mg/m2 or 15 mg/kg) may be considered for patients with steroid-resistant nephrotic syndrome.[57]

Specific Patient Populations

Hepatic impairment: No dosage adjustments are provided in the product labeling. Caution is advised.

Renal impairment: No dose adjustment is required; caution is advised as high corticosteroid doses are associated with scleroderma renal crisis.[58]

Pregnancy considerations: The American College of Obstetricians and Gynecologists (ACOG) recommends steroids such as prednisone or methylprednisolone during pregnancy due to their conversion to less active forms facilitated by 11β-hydroxysteroid dehydrogenase in the human placenta.[59]

Breastfeeding considerations: Methylprednisolone levels in breast milk are very low, with no reported adverse effects on breastfed infants even after intravenous doses of 1 g. These infants are exposed to doses lower than their daily cortisol production, well below therapeutic neonatal doses. There is no accumulation of methylprednisolone in breast milk with consecutive daily doses. To minimize infant exposure, breastfeeding should be avoided during and for 2 hours after a 1 g intravenous dose. Smaller oral doses and local injections (eg, for tendinitis) do not require special precautions. However, systemic or joint injections, especially with medium to large corticosteroid doses, may temporarily reduce lactation.[60]

Pediatric patients: Weight-based dosing is preferred for pediatric patients.

Older patients: According to the American College of Rheumatology (ACR), intravenous glucocorticoid pulse doses are recommended for patients with giant cell arteritis (GCA), with methylprednisolone at a dosage range of 500 to 1000 mg per day for 5 days in adults.[61] Doses typically start at the lower end of the range due to the higher prevalence of reduced renal or cardiac function, concurrent diseases, and other medications.

Adverse Effects

The significant adverse effects of glucocorticoids stem from their hormonal actions, which can result in iatrogenic Cushing syndrome. Facial rounding, puffiness, fat deposition, and plethora (moon facies) are usually apparent. Fat redistributes from the extremities to the trunk, the back of the neck, and the supraclavicular fossae. Fine hair grows more quickly on the face, thighs, and trunk. Steroid-induced punctate acne may appear, and insomnia and increased appetite may be observed. With concurrent use of methylprednisolone, protein catabolism continues, diverting amino acids to glucose production, thus increasing the need for insulin and resulting in weight gain. Myopathy and muscle wasting can occur, as well as skin thinning, with striae and bruising. Hyperglycemia and osteoporosis can develop, as well as diabetes and aseptic necrosis of the hip.[62] 

The adverse reactions associated with methylprednisolone and other corticosteroids are classified based on the different organ systems affected below.

Dermatology:

  • Skin thinning
  • Ecchymoses
  • Cushingoid features
  • Weight gain[63]

Ophthalmology:

  • Cataracts
  • Increased intraocular pressure
  • Exophthalmos

Cardiovascular:

  • Fluid retention
  • Hypertension
  • Premature atherosclerotic disease
  • Arrhythmias
  • Hyperlipidemia

Gastrointestinal:

  • Gastritis
  • Ulcer formation
  • Gastrointestinal bleeding 

Musculoskeletal: 

  • Osteoporosis
  • Osteonecrosis
  • Myopathy

Neuropsychiatric: 

  • Mood disorders
  • Psychosis
  • Memory impairment

Metabolic and endocrine:[64]

  • Hyperglycemia
  • Hypothalamic-pituitary-adrenal axis suppression [64]

Immune:

  • Increased susceptibility to infections

Hematologic:

  • Leukocytosis
  • Neutrophilia (due to peripheral demargination) [65]

Drug-Drug Interactions

Chimeric antigen receptor T-cell therapy (CAR T-cell therapy): There is concern regarding the use of prophylactic corticosteroids due to the potential risk of diminishing CAR T-cell activity in the context of CAR T-cell therapy. Despite these concerns, existing evidence suggests that administering corticosteroids to manage adverse effects such as cytokine release syndrome (CRS) does not significantly impact the therapeutic outcomes of CAR T-cell therapy. Nonetheless, it is prudent to use corticosteroids with caution.[66]

Hepatic enzyme inducers: Co-administration with enzyme inducers such as phenobarbital, phenytoin, and rifampin may increase the metabolic clearance of methylprednisolone, necessitating potential dose adjustments to maintain therapeutic efficacy.

Hepatic enzyme inhibitors: Co-administration with enzyme inhibitors like ketoconazole/itraconazole may reduce the clearance of methylprednisolone, potentially increasing the risk of toxicity; dose titration may be required.[67]

Oral anticoagulants: The effect of methylprednisolone on oral anticoagulants can be variable, with reported cases of both enhanced and diminished anticoagulant activity. Regular monitoring of coagulation parameters is essential to ensure the desired anticoagulant effect is achieved.[68][69]

Live vaccines: The Advisory Committee on Immunization Practices (ACIP) recommends that live-virus vaccines should be avoided during and shortly after high-dose corticosteroid therapy (≥2 mg/kg or ≥20 mg/day of prednisone for ≥14 days) due to potential immunosuppression. Live virus vaccination is generally deferred for at least 1 month after discontinuing.[80]

Contraindications

Contraindications to methylprednisolone administration include documented hypersensitivity to the drug or components, systemic fungal infection, intrathecal administration, live or attenuated virus vaccine, and idiopathic thrombocytopenic purpura.[70] 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.[71]

Warning and Precautions

  • Certain formulations of methylprednisolone contain benzyl alcohol, which is known to cause gasping syndrome in infants; these formulations should be avoided in premature infants. The label should be consulted for excipients before use.
  • Certain formulations of methylprednisolone contain lactose, which is contraindicated in individuals with hypersensitivity to dairy products.[72]

Monitoring

Blood pressure, blood glucose, electrolytes, weight, bone mineral density, hypothalamic-pituitary-adrenal 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, and osteoporosis. Corticosteroid use raises the risk of reactivation of latent tuberculosis infection (LTBI).[73][74] The dosage should be as low as possible. Even patients maintained on low doses of methylprednisolone may require supplementary therapy during times of stress, such as during surgery, intercurrent illness, or trauma.[75]

Toxicity

Signs and Symptoms of Overdose

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 (eg, growth inhibition, diabetes, muscle wasting, osteoporosis), salt retention (although less common with methylprednisolone), and psychosis.[76]

Management of Overdose

Treatment of acute overdose involves supportive and symptomatic care. 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.[77] Additional "stress doses" may be necessary during severe illness or before major surgery to prevent adrenal insufficiency in patients who have received long-term treatment with methylprednisolone. Treatment of acute overdose involves supportive and symptomatic care.

Enhancing Healthcare Team Outcomes

Methylprednisolone is widely used in multiple fields due to its anti-inflammatory and immunosuppressive properties. Interprofessional healthcare team members, including nurses, pharmacists, advanced practice providers, and physicians, should be aware of its broad spectrum of clinical applications, both labeled and off-label 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. The healthcare team should monitor for adverse effects in inpatient and outpatient settings. Pharmacists should be involved in verifying dosing and performing medication reconciliation. Both pharmacists and nurses need to alert other members of the healthcare team if they encounter any issues of concern. All these interprofessional healthcare team members must communicate and collaborate across interprofessional lines to ensure optimal therapeutic results.

As with all glucocorticoids, methylprednisolone's adverse effects are both dose- and duration-dependent and can range from nonserious displeasing appearances to those that are life-threatening. Interprofessional coordination and care between healthcare professionals are needed to ensure that methylprednisolone dosage remains minimal and that the treatment goals are achieved in the shortest period. Preexisting comorbidities that may become exacerbated when treated with methylprednisolone require management, and 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 leads to the best outcomes. An interprofessional team approach and communication among clinicians, pharmacists, specialists, and nurses are crucial to decreasing potential adverse effects, improving disease course and quality of life, and improving patient outcomes related to methylprednisolone therapy.


Details

Author

Antonio Ocejo

Editor:

Ricardo Correa

Updated:

8/11/2024 10:50:56 AM

References


[1]

Torrelo A. Methylprednisolone aceponate for atopic dermatitis. International journal of dermatology. 2017 Jun:56(6):691-697. doi: 10.1111/ijd.13485. Epub 2017 Mar 4     [PubMed PMID: 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. The Journal of dermatological treatment. 2018 May:29(3):241-251. doi: 10.1080/09546634.2017.1370074. Epub 2017 Sep 19     [PubMed PMID: 28866951]

Level 3 (low-level) evidence

[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. Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG. 2005 Mar:3(3):200-6     [PubMed PMID: 16372814]

Level 1 (high-level) evidence

[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. Journal of population therapeutics and clinical pharmacology = Journal de la therapeutique des populations et de la pharmacologie clinique. 2011:18():e121-33     [PubMed PMID: 21467603]

Level 1 (high-level) evidence

[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. The Journal of clinical endocrinology and metabolism. 2018 Nov 1:103(11):4043-4088. doi: 10.1210/jc.2018-01865. Epub     [PubMed PMID: 30272171]

Level 1 (high-level) evidence

[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. The Turkish journal of pediatrics. 2008 Mar-Apr:50(2):171-5     [PubMed PMID: 18664083]


[7]

Rosenberg W, Ireland A, Jewell DP. High-dose methylprednisolone in the treatment of active ulcerative colitis. Journal of clinical gastroenterology. 1990 Feb:12(1):40-1     [PubMed PMID: 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. Archivum immunologiae et therapiae experimentalis. 2013 Oct:61(5):385-95. doi: 10.1007/s00005-013-0232-3. Epub 2013 May 21     [PubMed PMID: 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. The New England journal of medicine. 1991 May 9:324(19):1297-304     [PubMed PMID: 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 (London, England). 2002 Jan 5:359(9300):23-9     [PubMed PMID: 11809183]

Level 1 (high-level) evidence

[11]

Murray TJ. Diagnosis and treatment of multiple sclerosis. BMJ (Clinical research ed.). 2006 Mar 4:332(7540):525-7     [PubMed PMID: 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. Ocular immunology and inflammation. 2012 Apr:20(2):91-9. doi: 10.3109/09273948.2011.646382. Epub     [PubMed PMID: 22409561]


[13]

Murnaghan K, Vasmant D, Bensman A. Pulse methylprednisolone therapy in severe idiopathic childhood nephrotic syndrome. Acta paediatrica Scandinavica. 1984 Nov:73(6):733-9     [PubMed PMID: 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. Annals of internal medicine. 2001 Aug 21:135(4):248-57     [PubMed PMID: 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 pulmonary medicine. 2016 Feb 10:16():29. doi: 10.1186/s12890-016-0194-4. Epub 2016 Feb 10     [PubMed PMID: 26864571]

Level 2 (mid-level) evidence

[16]

Alangari AA. Corticosteroids in the treatment of acute asthma. Annals of thoracic medicine. 2014 Oct:9(4):187-92. doi: 10.4103/1817-1737.140120. Epub     [PubMed PMID: 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. The European respiratory journal. 2013 Feb:41(2):402-9. doi: 10.1183/09031936.00221811. Epub 2012 May 17     [PubMed PMID: 22599359]


[18]

Wallaert B, Ramon P, Fournier EC, Hatron PY, Muir JF, Tonnel AB, Voisin C. High-dose methylprednisolone pulse therapy in sarcoidosis. European journal of respiratory diseases. 1986 Apr:68(4):256-62     [PubMed PMID: 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. Arquivos brasileiros de cardiologia. 1999 May:72(5):601-6     [PubMed PMID: 10668230]


[20]

Groff GD, Franck WA, Raddatz DA. Systemic steroid therapy for acute gout: a clinical trial and review of the literature. Seminars in arthritis and rheumatism. 1990 Jun:19(6):329-36     [PubMed PMID: 2196674]


[21]

Peters ND, Ejstrup L. Intravenous methylprednisolone pulse therapy in ankylosing spondylitis. Scandinavian journal of rheumatology. 1992:21(3):134-8     [PubMed PMID: 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. Journal of neuroimmunology. 1997 Jun:76(1-2):75-80     [PubMed PMID: 9184635]


[23]

Nash P. Therapies for axial disease in psoriatic arthritis. A systematic review. The Journal of rheumatology. 2006 Jul:33(7):1431-4     [PubMed PMID: 16724371]

Level 1 (high-level) evidence

[24]

Smith MD, Ahern MJ, Roberts-Thomson PJ. Pulse methylprednisolone therapy in rheumatoid arthritis: unproved therapy, unjustified therapy, or effective adjunctive treatment? Annals of the rheumatic diseases. 1990 Apr:49(4):265-7     [PubMed PMID: 2187419]


[25]

Badsha H, Edwards CJ. Intravenous pulses of methylprednisolone for systemic lupus erythematosus. Seminars in arthritis and rheumatism. 2003 Jun:32(6):370-7     [PubMed PMID: 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. Clinical rheumatology. 2004 Apr:23(2):116-20     [PubMed PMID: 15045624]

Level 2 (mid-level) evidence

[27]

Garg N, Perry L, Deodhar A. Intra-articular and soft tissue injections, a systematic review of relative efficacy of various corticosteroids. Clinical rheumatology. 2014 Dec:33(12):1695-706. doi: 10.1007/s10067-014-2572-8. Epub 2014 Mar 21     [PubMed PMID: 24651914]

Level 1 (high-level) evidence

[28]

Senila SC, Danescu SA, Ungureanu L, Candrea E, Cosgarea RM. Intravenous methylprednisolone pulse therapy in severe alopecia areata. Indian journal of dermatology, venereology and leprology. 2015 Jan-Feb:81(1):95. doi: 10.4103/0378-6323.148608. Epub     [PubMed PMID: 25566921]


[29]

Fabbri P, Cardinali C, Giomi B, Caproni M. Cutaneous lupus erythematosus: diagnosis and management. American journal of clinical dermatology. 2003:4(7):449-65     [PubMed PMID: 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 and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. 2013 Jan-Feb:21(1):88-102. doi: 10.1111/j.1524-475X.2012.00862.x. Epub 2012 Nov 5     [PubMed PMID: 23126666]

Level 2 (mid-level) evidence

[31]

Snyder RA, Schwartz RA, Schneider JS, Elias PM. Intermittent megadose corticosteroid therapy for generalized lichen planus. Journal of the American Academy of Dermatology. 1982 Jun:6(6):1089-90     [PubMed PMID: 7096672]


[32]

Fehlings MG, Wilson JR, Tetreault LA, Aarabi B, Anderson P, Arnold PM, Brodke DS, Burns AS, Chiba K, Dettori JR, Furlan JC, Hawryluk G, Holly LT, Howley S, Jeji T, Kalsi-Ryan S, Kotter M, Kurpad S, Kwon BK, Marino RJ, Martin AR, Massicotte E, Merli G, Middleton JW, Nakashima H, Nagoshi N, Palmieri K, Skelly AC, Singh A, Tsai EC, Vaccaro A, Yee A, Harrop JS. A Clinical Practice Guideline for the Management of Patients With Acute Spinal Cord Injury: Recommendations on the Use of Methylprednisolone Sodium Succinate. Global spine journal. 2017 Sep:7(3 Suppl):203S-211S. doi: 10.1177/2192568217703085. Epub 2017 Sep 5     [PubMed PMID: 29164025]

Level 1 (high-level) evidence

[33]

Liu LJW, Rosner J, Cragg JJ. Journal Club: High-dose methylprednisolone for acute traumatic spinal cord injury: A meta-analysis. Neurology. 2020 Aug 11:95(6):272-274. doi: 10.1212/WNL.0000000000009263. Epub 2020 Apr 8     [PubMed PMID: 32269114]

Level 1 (high-level) evidence

[34]

Ozawa Y, Uzawa A, Kanai T, Oda F, Yasuda M, Kawaguchi N, Himuro K, Kuwabara S. Efficacy of high-dose intravenous methylprednisolone therapy for ocular myasthenia gravis. Journal of the neurological sciences. 2019 Jul 15:402():12-15. doi: 10.1016/j.jns.2019.05.003. Epub 2019 May 7     [PubMed PMID: 31100651]


[35]

Chu X, Wang J, Ologundudu L, Brignardello-Petersen R, Guyatt GH, Oykhman P, Bernstein JA, Saini SS, Beck LA, Waserman S, Moellman J, Khan DA, Ben-Shoshan M, Baker DR, Oliver ET, Sheikh J, Lang D, Mathur SK, Winders T, Eftekhari S, Gardner DD, Runyon L, Asiniwasis RN, Cole EF, Chan J, Wheeler KE, Trayes KP, Tran P, Chu DK. Efficacy and Safety of Systemic Corticosteroids for Urticaria: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. The journal of allergy and clinical immunology. In practice. 2024 Jul:12(7):1879-1889.e8. doi: 10.1016/j.jaip.2024.04.016. Epub 2024 Apr 18     [PubMed PMID: 38642709]

Level 1 (high-level) evidence

[36]

Hu G, Yu YF, Yin S, Yang XY, Xu Q, You H. Efficacy and safety of iguratimod combined with methylprednisolone for primary Sjögren's syndrome: a meta-analysis and trial sequential analysis. European review for medical and pharmacological sciences. 2023 Aug:27(16):7544-7556. doi: 10.26355/eurrev_202308_33406. Epub     [PubMed PMID: 37667931]

Level 1 (high-level) evidence

[37]

Committee on Practice Bulletins-Obstetrics. ACOG Practice Bulletin No. 189: Nausea And Vomiting Of Pregnancy. Obstetrics and gynecology. 2018 Jan:131(1):e15-e30. doi: 10.1097/AOG.0000000000002456. Epub     [PubMed PMID: 29266076]


[38]

Hong S, Wang H, Li S, Liu J, Qiao L. A systematic review and meta-analysis of glucocorticoids treatment in severe COVID-19: methylprednisolone versus dexamethasone. BMC infectious diseases. 2023 May 5:23(1):290. doi: 10.1186/s12879-023-08280-2. Epub 2023 May 5     [PubMed PMID: 37147596]

Level 1 (high-level) evidence

[39]

Lewandowski KC, Kawalec J, Kusiński M, Dąbrowska K, Matusiak AE, Dudek I, Lewiński A. The Utility of Intravenous Methylprednisolone as an Adjunct Treatment for Drug-Resistant Amiodarone-Induced Thyrotoxicosis. Journal of clinical medicine. 2024 Jan 6:13(2):. doi: 10.3390/jcm13020324. Epub 2024 Jan 6     [PubMed PMID: 38256458]


[40]

Langhoff E, Ladefoged J. Relative immunosuppressive potency of various corticosteroids measured in vitro. European journal of clinical pharmacology. 1983:25(4):459-62     [PubMed PMID: 6653640]


[41]

Zhang G, Zhang L, Duff GW. A negative regulatory region containing a glucocorticosteroid response element (nGRE) in the human interleukin-1beta gene. DNA and cell biology. 1997 Feb:16(2):145-52     [PubMed PMID: 9052735]


[42]

Scheinman RI, Cogswell PC, Lofquist AK, Baldwin AS Jr. Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids. Science (New York, N.Y.). 1995 Oct 13:270(5234):283-6     [PubMed PMID: 7569975]


[43]

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 (New York, N.Y.). 1995 Oct 13:270(5234):286-90     [PubMed PMID: 7569976]


[44]

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. Journal of immunology (Baltimore, Md. : 1950). 2000 Sep 1:165(5):2719-28     [PubMed PMID: 10946303]


[45]

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. doi: 10.1371/journal.pone.0143689. Epub 2015 Dec 2     [PubMed PMID: 26629828]


[46]

Shaw WA, Issekutz TB, Issekutz B Jr. Gluconeogenesis from glycerol at rest and during exercise in normal, diabetic, and methylprednisolone-treated dogs. Metabolism: clinical and experimental. 1976 Mar:25(3):329-39     [PubMed PMID: 1250166]


[47]

Upadhyay AK, Dubey S, Ahi S, Beotra A, Bhardwaj A, Shukla S, Jain S. A preliminary study on urinary excretion patterns of methylprednisolone after oral and intra-articular administration and effect on endogenous glucocorticosteroids profile. Indian journal of pharmacology. 2021 Nov-Dec:53(6):480-483. doi: 10.4103/ijp.ijp_946_20. Epub     [PubMed PMID: 34975136]


[48]

Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clinical pharmacokinetics. 2005:44(1):61-98     [PubMed PMID: 15634032]


[49]

Garg DC, Ng P, Weidler DJ, Sakmar E, Wagner JG. Preliminary in vitro and in vivo investigations on methylprednisolone and its acetate. Research communications in chemical pathology and pharmacology. 1978 Oct:22(1):37-48     [PubMed PMID: 725320]


[50]

Ditzian-Kadanoff R, Ellman MH. How safe is it? High dose intravenous methylprednisolone. IMJ. Illinois medical journal. 1987 Dec:172(6):432-4     [PubMed PMID: 2892818]


[51]

Moromizato T, Sakaniwa R, Tokuda Y, Taniguchi K, Shibuya K. Intravenous methylprednisolone pulse therapy and the risk of in-hospital mortality among acute COVID-19 patients: Nationwide clinical cohort study. Critical care (London, England). 2023 Feb 8:27(1):53. doi: 10.1186/s13054-023-04337-5. Epub 2023 Feb 8     [PubMed PMID: 36755340]


[52]

Campbell RL, Li JT, Nicklas RA, Sadosty AT, Members of the Joint Task Force, Practice Parameter Workgroup. Emergency department diagnosis and treatment of anaphylaxis: a practice parameter. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology. 2014 Dec:113(6):599-608. doi: 10.1016/j.anai.2014.10.007. Epub     [PubMed PMID: 25466802]


[53]

Rubin DT, Ananthakrishnan AN, Siegel CA, Sauer BG, Long MD. ACG Clinical Guideline: Ulcerative Colitis in Adults. The American journal of gastroenterology. 2019 Mar:114(3):384-413. doi: 10.14309/ajg.0000000000000152. Epub     [PubMed PMID: 30840605]


[54]

Kidney Disease: Improving Global Outcomes (KDIGO) Lupus Nephritis Work Group. KDIGO 2024 Clinical Practice Guideline for the management of LUPUS NEPHRITIS. Kidney international. 2024 Jan:105(1S):S1-S69. doi: 10.1016/j.kint.2023.09.002. Epub     [PubMed PMID: 38182286]

Level 1 (high-level) evidence

[55]

Zhou FW, Liu C, Li DZ, Zhang Y, Zhou FC. Efficacy and safety of corticosteroid therapy in patients with cardiac arrest: A meta-analysis of randomized controlled trials. The American journal of emergency medicine. 2024 Jan:75():111-118. doi: 10.1016/j.ajem.2023.10.031. Epub 2023 Oct 30     [PubMed PMID: 37939521]

Level 1 (high-level) evidence

[56]

Onel KB, Horton DB, Lovell DJ, Shenoi S, Cuello CA, Angeles-Han ST, Becker ML, Cron RQ, Feldman BM, Ferguson PJ, Gewanter H, Guzman J, Kimura Y, Lee T, Murphy K, Nigrovic PA, Ombrello MJ, Rabinovich CE, Tesher M, Twilt M, Klein-Gitelman M, Barbar-Smiley F, Cooper AM, Edelheit B, Gillispie-Taylor M, Hays K, Mannion ML, Peterson R, Flanagan E, Saad N, Sullivan N, Szymanski AM, Trachtman R, Turgunbaev M, Veiga K, Turner AS, Reston JT. 2021 American College of Rheumatology Guideline for the Treatment of Juvenile Idiopathic Arthritis: Therapeutic Approaches for Oligoarthritis, Temporomandibular Joint Arthritis, and Systemic Juvenile Idiopathic Arthritis. Arthritis & rheumatology (Hoboken, N.J.). 2022 Apr:74(4):553-569. doi: 10.1002/art.42037. Epub 2022 Mar 1     [PubMed PMID: 35233993]


[57]

Trautmann A, Vivarelli M, Samuel S, Gipson D, Sinha A, Schaefer F, Hui NK, Boyer O, Saleem MA, Feltran L, Müller-Deile J, Becker JU, Cano F, Xu H, Lim YN, Smoyer W, Anochie I, Nakanishi K, Hodson E, Haffner D, International Pediatric Nephrology Association. IPNA clinical practice recommendations for the diagnosis and management of children with steroid-resistant nephrotic syndrome. Pediatric nephrology (Berlin, Germany). 2020 Aug:35(8):1529-1561. doi: 10.1007/s00467-020-04519-1. Epub 2020 May 7     [PubMed PMID: 32382828]


[58]

Blagojevic J, Legendre P, Matucci-Cerinic M, Mouthon L. Is there today a place for corticosteroids in the treatment of scleroderma? Autoimmunity reviews. 2019 Dec:18(12):102403. doi: 10.1016/j.autrev.2019.102403. Epub 2019 Oct 19     [PubMed PMID: 31639515]


[59]

. ACOG Committee Opinion No. 776: Immune Modulating Therapies in Pregnancy and Lactation. Obstetrics and gynecology. 2019 Apr:133(4):e287-e295. doi: 10.1097/AOG.0000000000003176. Epub     [PubMed PMID: 30913201]

Level 3 (low-level) evidence

[60]

. Methylprednisolone. Drugs and Lactation Database (LactMed®). 2006:():     [PubMed PMID: 30000087]


[61]

Maz M, Chung SA, Abril A, Langford CA, Gorelik M, Guyatt G, Archer AM, Conn DL, Full KA, Grayson PC, Ibarra MF, Imundo LF, Kim S, Merkel PA, Rhee RL, Seo P, Stone JH, Sule S, Sundel RP, Vitobaldi OI, Warner A, Byram K, Dua AB, Husainat N, James KE, Kalot MA, Lin YC, Springer JM, Turgunbaev M, Villa-Forte A, Turner AS, Mustafa RA. 2021 American College of Rheumatology/Vasculitis Foundation Guideline for the Management of Giant Cell Arteritis and Takayasu Arteritis. Arthritis & rheumatology (Hoboken, N.J.). 2021 Aug:73(8):1349-1365. doi: 10.1002/art.41774. Epub 2021 Jul 8     [PubMed PMID: 34235884]


[62]

Stanbury RM, Graham EM. Systemic corticosteroid therapy--side effects and their management. The British journal of ophthalmology. 1998 Jun:82(6):704-8     [PubMed PMID: 9797677]


[63]

Al-Jabr KH, Alhumaidan LS, Alghamdi AA, Almutairi MSL, Alsubaihi AA, Alrasheedi SM, Alkhdairi A, Alzweihary AM, Alrasheedi MS, Alrasheedi KAM, Alrashdi MN. Awareness of Side Effects of Corticosteroids among Users and Nonusers in Saudi Arabia. Journal of pharmacy & bioallied sciences. 2024 Apr:16(Suppl 2):S1612-S1618. doi: 10.4103/jpbs.jpbs_925_23. Epub 2024 Apr 16     [PubMed PMID: 38882861]


[64]

Torpy DJ, Lim WT. Glucocorticoid-induced adrenal suppression: physiological basis and strategies for glucocorticoid weaning. The Medical journal of Australia. 2023 Nov 20:219(10):444-447. doi: 10.5694/mja2.52140. Epub 2023 Oct 26     [PubMed PMID: 37884339]


[65]

Hampe L, Daumoine S, Limagne E, Roussot N, Borsotti F, Vincent J, Ilie S, Truntzer C, Ghiringhelli F, Thibaudin M. Effect of radiochemotherapy on peripheral immune response in glioblastoma. Cancer immunology, immunotherapy : CII. 2024 May 16:73(7):133. doi: 10.1007/s00262-024-03722-5. Epub 2024 May 16     [PubMed PMID: 38753169]


[66]

Lakomy T, Akhoundova D, Nilius H, Kronig MN, Novak U, Daskalakis M, Bacher U, Pabst T. Early Use of Corticosteroids following CAR T-Cell Therapy Correlates with Reduced Risk of High-Grade CRS without Negative Impact on Neurotoxicity or Treatment Outcome. Biomolecules. 2023 Feb 17:13(2):. doi: 10.3390/biom13020382. Epub 2023 Feb 17     [PubMed PMID: 36830750]


[67]

Lebrun-Vignes B, Archer VC, Diquet B, Levron JC, Chosidow O, Puech AJ, Warot D. Effect of itraconazole on the pharmacokinetics of prednisolone and methylprednisolone and cortisol secretion in healthy subjects. British journal of clinical pharmacology. 2001 May:51(5):443-50     [PubMed PMID: 11422002]


[68]

Peng TR, Lee LL, Wu TW. Interactions Between Warfarin and Prednisolone: A Case Report. American journal of therapeutics. 2017 Jul/Aug:24(4):e494. doi: 10.1097/MJT.0000000000000530. Epub     [PubMed PMID: 27849633]

Level 3 (low-level) evidence

[69]

Hazlewood KA, Fugate SE, Harrison DL. Effect of oral corticosteroids on chronic warfarin therapy. The Annals of pharmacotherapy. 2006 Dec:40(12):2101-6     [PubMed PMID: 17119104]


[70]

Ferrell CL. Anaphylactic Reaction to Methylprednisolone. Journal of emergency nursing. 2015 Nov:41(6):470-3. doi: 10.1016/j.jen.2015.06.010. Epub 2015 Aug 18     [PubMed PMID: 26296715]


[71]

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. Alimentary pharmacology & therapeutics. 2015 Sep:42(5):599-606. doi: 10.1111/apt.13298. Epub 2015 Jun 22     [PubMed PMID: 26096497]

Level 3 (low-level) evidence

[72]

Porcaro F, Paglietti MG, Diamanti A, Petreschi F, Schiavino A, Negro V, Pecora V, Fiocchi A, Cutrera R. Anaphylactic shock with methylprednisolone sodium succinate in a child with short bowel syndrome and cow's milk allergy. Italian journal of pediatrics. 2017 Nov 17:43(1):104. doi: 10.1186/s13052-017-0422-4. Epub 2017 Nov 17     [PubMed PMID: 29149860]


[73]

Patil S, Jadhav A. Short Course of High-dose Steroids for Anaphylaxis Caused Flare Up of Tuberculosis: A Case Report. Journal of translational internal medicine. 2019 Mar:7(1):39-42. doi: 10.2478/jtim-2019-0008. Epub 2019 Mar 29     [PubMed PMID: 30997356]

Level 3 (low-level) evidence

[74]

Fehily SR, Al-Ani AH, Abdelmalak J, Rentch C, Zhang E, Denholm JT, Johnson D, Ng SC, Sharma V, Rubin DT, Gibson PR, Christensen B. Review article: latent tuberculosis in patients with inflammatory bowel diseases receiving immunosuppression-risks, screening, diagnosis and management. Alimentary pharmacology & therapeutics. 2022 Jul:56(1):6-27. doi: 10.1111/apt.16952. Epub 2022 May 20     [PubMed PMID: 35596242]


[75]

Pitre T, Drover K, Chaudhuri D, Zeraaktkar D, Menon K, Gershengorn HB, Jayaprakash N, Spencer-Segal JL, Pastores SM, Nei AM, Annane D, Rochwerg B. Corticosteroids in Sepsis and Septic Shock: A Systematic Review, Pairwise, and Dose-Response Meta-Analysis. Critical care explorations. 2024 Jan:6(1):e1000. doi: 10.1097/CCE.0000000000001000. Epub 2024 Jan 19     [PubMed PMID: 38250247]

Level 1 (high-level) evidence

[76]

Bachu AK, Davis V, Abdulrahim M, Harbaugh L, Prasad S, Kotapati VP, Srinivas S. Corticosteroid-Induced Psychosis: A Report of Three Cases. Cureus. 2023 May:15(5):e39221. doi: 10.7759/cureus.39221. Epub 2023 May 19     [PubMed PMID: 37337486]

Level 3 (low-level) evidence

[77]

Mandell BF. Balancing the myths of corticosteroid therapy. Cleveland Clinic journal of medicine. 2022 Sep 1:89(9):480-481. doi: 10.3949/ccjm.89b.09022. Epub 2022 Sep 1     [PubMed PMID: 37907445]