Continuing Education Activity

Prednisone is a synthetic glucocorticoid converted in the liver to the active metabolite prednisolone. This agent exerts anti-inflammatory and immunosuppressive effects by modulating immune activity and reducing inflammation. Indicated for various conditions—including endocrine, rheumatic, allergic, dermatologic, ophthalmic, respiratory, hematologic, neoplastic, and gastrointestinal disorders—prednisone remains a cornerstone in managing chronic and acute inflammatory diseases. Delayed-release formulations allow for timing flexibility in symptom control, particularly in conditions with circadian variation.

This educational activity provides an in-depth review of prednisone's mechanism of action, pharmacokinetics, dosing strategies, and clinical applications. Special attention is given to drug interactions, contraindications, and adverse effects, including risks such as immunosuppression, osteoporosis, and glucose intolerance. Emphasis is placed on tailoring prednisone therapy to patient-specific variables and disease severity to enhance therapeutic benefit while minimizing harm. This activity reinforces the importance of interprofessional collaboration in monitoring and managing therapy across care settings. Understanding prednisone's pharmacological properties and clinical implications supports evidence-based decision-making and improves patient outcomes.

Objectives:

• Evaluate the mechanism of action of prednisone.
• Identify the FDA-approved indications and off-label uses for prednisone.
• Screen patients for contraindications associated with prednisone.
• Implement effective collaboration and communication among interprofessional team members to improve outcomes and treatment efficacy for patients who might benefit from prednisone therapy.

Indications

Prednisone is a synthetic, anti-inflammatory glucocorticoid that is derived from cortisone. Prednisone is biologically inert and converted to prednisolone in the liver.

FDA-Approved Indications

Prednisone is an FDA-approved, delayed-release corticosteroid indicated as an anti-inflammatory or immunosuppressive agent to treat a broad range of diseases, including immunosuppressive/endocrine, rheumatic, collagen, dermatologic, allergic states, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, acute exacerbations of multiple sclerosis, and as an anti-inflammatory and an antineoplastic agent. Prednisone is a corticosteroid (cortisone-like medicine or steroid). This medication acts on the immune system to help relieve swelling, redness, itching, and allergic reactions and is available only by prescription.[1] According to the Endocrine Society's clinical practice guidelines for the perioperative evaluation and management of patients receiving glucocorticoid therapy, continuation of the patient's usual daily glucocorticoid regimen, supplemented with a brief perioperative course of intravenous glucocorticoids tailored to the expected degree of surgical stress, is considered sufficient.[2] Prednisone is also used as a treatment for urticaria.[3][4] The Global Initiative for Asthma guidelines suggest prednisone use in asthma exacerbations.[5] COPD exacerbations may also be treated with prednisone.[6]

Off-Label Uses

Prednisone is commonly prescribed for other indications or in a different dosage than described in the label information. These are called off-label uses or non-FDA-approved indications. Other countries may mention "approved" or "licensed" indications that do not apply in the United States.[7] Various corticosteroids have been used as part of treatment regimens during the COVID-19 pandemic. The Infectious Disease Society of America endorses dexamethasone for critically ill hospitalized patients. If dexamethasone is unavailable, equivalent total daily doses of alternative glucocorticoids (eg, methylprednisolone or prednisone) can be administered.[8] For patients with giant cell arteritis, the American College of Rheumatology endorses the use of prednisone. For patients with threatened or imminent vision loss, IV glucocorticoids followed by high-dose steroids such as prednisone are used.[9] As described in the KDIGO (Kidney Disease: Improving Global Outcomes) guidelines, for patients with proliferative lupus nephritis (LN), reduced-dose glucocorticoids following a short initial course of methylprednisolone pulses can be tried if kidney and extrarenal disease manifestations are adequately improving. Unless prescribed for extrarenal manifestations, maintenance phase doses of glucocorticoids should be tapered to the lowest effective dose and discontinued completely should complete clinical renal response be achieved for a minimum of 12 months. The tapering regimen typically begins with large doses (0.8 to 1.0 mg/kg, up to 80 mg) and tapers to <5 mg by week 24, depending on response.[10][11]

Mechanism of Action

Steroids like prednisone reduce inflammation by inhibiting phospholipase A2 (PLA2), an enzyme that releases arachidonic acid from cell membranes. This prevents the production of pro-inflammatory mediators like prostaglandins and leukotrienes.[12] Prednisone reduces inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Prednisone also suppresses the immune system by decreasing the activity and volume of the immune system. The antineoplastic effects may correlate with inhibiting glucose transport, phosphorylation, or induction of cell death in immature lymphocytes. Prednisone may also demonstrate antiemetic effects by blocking the emetic center's cerebral innervation via prostaglandin inhibition.

Prednisone is a prodrug to prednisolone, which mediates its glucocorticoid effects.[13] Prednisone is a synthetic glucocorticoid with anti-inflammatory and immunomodulating properties.

After cell surface receptor attachment and entry into the cell, prednisone enters the nucleus, binds, and activates specific nuclear receptors, resulting in altered gene expression and inhibiting pro-inflammatory cytokine production. This agent decreases the number of circulating lymphocytes, inducing cell differentiation, and stimulates apoptosis in sensitive tumor cell populations. The effects of glucocorticoids are subject to mediation by mechanisms that alter DNA replication within the nucleus.[14]

Pharmacokinetics

Absorption: Prednisone is rapidly absorbed and metabolized to its active metabolite, prednisolone. The IR formulations achieve peak concentrations in about 2 hours, while the sustained-release formulations are designed to take effect in about 6 hours.

Distribution: Prednisolone's distribution increases with dosage; a 0.15 mg/kg dose corresponds to a volume of distribution of 29.3 L, while a 0.30 mg/kg dose is associated with a volume of 44.2 L. Following IV administration, high concentrations are found in the kidneys, liver, spleen, lungs, small intestine, and bile.

Metabolism: Prednisone is primarily converted into prednisolone in the liver.[15] This drug is metabolized into other compounds, such as 6β-hydroxy-prednisone and 20α-dihydro-prednisone.

Elimination: Prednisone metabolites, conjugated with sulfates and glucuronides, are excreted via the kidneys.[16] Trace amounts of prednisone and its metabolites are excreted in bile.

Administration

Available Dosage Forms and Strengths

The oral concentrate is available in a 30 mL bottle at 5 mg/mL; the oral solution is 5 mg/5 mL. Oral tablets are available in various strengths: 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, and 50 mg. A delayed-release oral tablet comes in 1 mg, 2 mg, and 5 mg strengths. Prednisone is also available in oral therapy pack forms for tapering/customized regimens.

Adult Dosage

Prednisone may be administered orally with food or milk to decrease gastrointestinal upset. Maximal adrenal cortex activity occurs between 2:00 AM and 8:00 AM, and minimal between 4:00 PM and midnight. Exogenous corticosteroids suppress endogenous adrenocortical activity the least when administered during the period of maximal activity (early morning) for single-dose administration. Therefore, prednisone should be administered in the morning before 9:00 AM. When administering large doses, the patient should use antacids between meals to help prevent peptic ulcers. Multiple-dose therapy should involve an even dose distribution in evenly spaced daily intervals. Antacids may also be administered between meals to help prevent peptic ulcers.[17]

The delayed-release tablets should be swallowed whole without breaking, dividing, crushing, or chewing. The oral solution should be administered with the provided calibrated dropper only. Other forms of steroids may be available if the oral formulation is not well-tolerated, such as intramuscular (IM) or subcutaneous (SQ) administration. Depending on the disease process, topical steroids may also be an option. Best results occur when this medicine is taken with food. The medicine should be stored in a tightly closed container at room temperature, away from heat, moisture, and direct light. The oral liquid should not be frozen. Other routes of administration include liquid, solution, syrup, tablet, delayed-release tablets, nasal, rectal, injection, and intravenous. The dosage for individual conditions should be according to clinical condition and institutional protocol.

Specific Patient Populations

Hepatic impairment: Corticosteroid biotransformation is decreased in patients with cirrhosis; thus, half-life and bioavailability are increased.[18]

Renal impairment: In patients with renal dysfunction, specific dose adjustments are not outlined in the prescribing information. However, existing studies suggest that prednisolone may offer protective benefits for patients with IgA nephropathy.[19]

Pregnancy considerations: Fluorinated glucocorticoids, like dexamethasone and betamethasone, cross the placenta; however, prednisone and prednisolone are mostly metabolized before reaching the fetus.[20] Prednisone may be administered for antiphospholipid syndrome in pregnant women.[21] High-dose corticosteroids can increase the risk of hypertension and diabetes. However, when administered at lower doses (≤10 mg/kg daily), they are generally considered safe and are associated with minimal risk of adverse effects. In one study, researchers examined the risk of preterm birth in women with rheumatoid arthritis who were receiving prednisone. Higher doses (>10 mg/kg daily) correlated with an increased risk of preterm birth, while lower doses did not have the same risk.

The placenta helps break down non-fluorinated glucocorticoids, so only about 10% of the inactive metabolites pass into the fetal circulation when the maternal dose is <20 mg.[22] Patients with immune thrombocytopenia (ITP) should be initiated on prednisone at 20 mg/d, adjusting to the minimum effective dose. Post-delivery, clinicians should monitor platelet count and taper corticosteroids slowly to prevent rapid declines and protect the mother's mental health.[23] Corticosteroids are often necessary during pregnancy to manage conditions like rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel disease. Some evidence suggests a slight increase in risk of conditions involving a cleft lip or palate during the first trimester. However, the review found no strong evidence linking systemic corticosteroid use during pregnancy to increased risks of low birth weight, preterm birth, or preeclampsia.[24]

Breastfeeding considerations: Prednisone levels in breast milk are low, with no reported adverse effects on breastfed infants. Clinicians are advised to wait 4 hours after a dose before breastfeeding. Higher corticosteroid doses can cause a temporary reduction in lactation when administered systemically.[25]

Pediatric patients: According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, oral prednisone or pulsed intravenous methylprednisolone should be administered to children with mild or moderate immunoglobulin-A vasculitis–associated nephritis (IgAVN).[26]

Older patients: Clinicians should administer the lowest effective dose possible.

Adverse Effects

Adverse effects are common in patients receiving glucocorticoids in high doses or over a long period. Regimens involving prednisone administration of ≥40 mg daily are considered "high-dose." The primary adverse effects associated with prednisone therapy include hyperglycemia, insomnia, increased appetite, hypertension, osteoporosis, edema, adrenal suppression, cataracts, delayed wound healing, skin fragility, weight gain, increased risk of infections, and fractures. Potential cardiovascular and metabolic effects include hypertension, hyperglycemia, and dyslipidemia.[27]

Other adverse reactions include adrenal insufficiency, particularly for patients with sepsis or undergoing stressful procedures; this is typically diagnosable when the patient is hypotensive and not responsive to fluids, vasopressors, or cardiogenic medications. Once adrenal insufficiency is suspected, treatment should be initiated immediately with a dose of 100 mg of hydrocortisone every 8 hours. Osteonecrosis of the femoral head has also been reported.[28]

Drug-Drug Interactions

• Amphotericin B: Prednisone combined with amphotericin B or other potassium-lowering drugs may cause hypokalemia. Therefore, clinicians are advised to monitor electrolyte levels in patients receiving these medications.
• Macrolides: Some macrolide antibiotics (eg, clarithromycin) may slow the breakdown of prednisone, leading to increased steroid levels.
• Warfarin: When warfarin is taken with prednisone, the former's anticoagulant effects can become inconsistent. Frequent INR checks are recommended.
• Isoniazid: Isoniazid levels may drop when given with prednisone, which might lower its effectiveness.
• Bupropion: Combining prednisone with bupropion may increase seizure risk. If used together, doses should start low and increase slowly.
• Cholestyramine: Cholestyramine may reduce how long prednisone stays active by increasing its elimination rate.
• Cyclosporine: When prednisone and cyclosporine are used together, the risk of immunosuppression increases.
• Digoxin: Individuals receiving digoxin could be more prone to abnormal heart rhythms if potassium levels fall due to steroid therapy.
• Estrogens: Estrogens can slow prednisone metabolism, leading to prolonged steroid action.
• Fluoroquinolones: Tendon injuries, including ruptures, have been reported in patients receiving fluoroquinolones like ciprofloxacin together with prednisone, especially in older adults.
• CYP3A4 inducers/inhibitors: Drugs that increase CYP3A4 enzyme activity (eg, phenytoin or rifampin) can make prednisone less effective. On the flip side, CYP3A4 inhibitors (like ketoconazole) may increase steroid levels and the risk of adverse effects.
• Ketoconazole: Ketoconazole may also hinder natural steroid production, which can lead to problems if prednisone is stopped too quickly.
• NSAIDs: Taking NSAIDs (eg, aspirin) with prednisone increases the risk of stomach ulcers or bleeding.[29]

Contraindications

Prednisone is contraindicated for patients with documented hypersensitivity to the drug or formulation components and systemic fungal infections.[30][31] Administering live or live-attenuated vaccines is also contraindicated during immunosuppressive prednisone therapy.

Warnings and Precautions

• Fluid and electrolyte imbalance: Corticosteroids may contribute to fluid retention, hypertension, and hypokalemia, all of which can complicate management of cardiovascular or renal comorbidities.
• Adrenal suppression: Abrupt discontinuation after chronic use can precipitate adrenal insufficiency. Clinicians are advised to taper doses.
• Masked infections: Steroids cause immunosuppression and mask signs of active infection.
• Latent tuberculosis: Reactivation may occur during corticosteroid therapy, particularly at higher doses or with concurrent immunosuppressant administration.
• Varicella-zoster virus: Patients without prior exposure or vaccination may develop severe disseminated disease; post-exposure prophylaxis should be considered.
• Hepatitis B reactivation: This has been documented even in patients with resolved infections; pre-treatment screening is prudent.
• Fungal infections: Systemic corticosteroids can exacerbate fungal infections; caution is advised for patients with endemic mycoses or immunocompromised states.
• Strongyloidiasis: Hyperinfection syndrome may occur following corticosteroid use in chronically infected individuals; screening and empirical treatment may be warranted.
• Cerebral malaria: Corticosteroids are contraindicated, as they may worsen outcomes without clinical benefit.
• Ocular complications: Long-term corticosteroid therapy increases the risk of cataracts, glaucoma, and secondary infections.
• Kaposi sarcoma: This condition has been associated with corticosteroid use in patients with immunosuppression.[32]
• Dose minimization: To minimize adverse effects, the minimal effective dose should be administered, and treatment should be tapered whenever clinically feasible.
• GI perforation: Corticosteroids may obscure clinical signs, particularly in patients with diverticulitis or peptic ulcer disease.[33]
• Pediatric growth concerns: Long-term corticosteroids can interfere with normal bone development in children.[34]
• Psychiatric effects: Insomnia, mild irritability, and mood changes are possible. In rare cases, psychosis has been reported, especially in patients with a prior mental health history.[35][36]
• Myopathy: Muscle weakness may develop during treatment, especially in the thighs or shoulders. This typically occurs during high-dose or prolonged therapy. The risk of myopathy is increased in patients with underlying neuromuscular conditions. Recovery can take time after stopping the drug.[37]
• Glaucoma: Corticosteroid therapy lasting longer than a few weeks may raise ocular pressure. Patients receiving chronic treatment should get routine eye checks to catch changes early.[38]

Monitoring

Patients receiving prednisone are at an increased risk for allergic reactions (itching or hives, swelling in the face or hands, swelling or tingling in the mouth or throat, chest tightness, trouble breathing), dark freckles, skin color changes, coldness, weakness, tiredness, nausea, vomiting, weight loss, rapid weight gain, depression, unusual thoughts, feelings, or behaviors, difficulty sleeping, fever, chills, cough, sore throat, and body aches, muscle pain or weakness, severe stomach pain, red or black stools, skin changes or growths, vision changes, eye pain, or headache.

Clinicians must monitor patients with giant cell arteritis because increased cumulative glucocorticoid exposure is associated with an increased risk of glucocorticoid-related adverse effects.[39]

Doctors can also track serum glucose, blood pressure, electrolytes, weight, bone mineral density, hemoglobin, occult blood loss, growth in pediatric patients, and infections. The HPA axis suppression should also be assessed using the morning cortisol test, adrenocorticotropic hormone stimulation test, and the urinary free cortisol test.

When monitoring, it is essential to remember that the elimination half-life of prednisone is 3 to 4 hours in adults and 1 to 2 hours in children.

More common symptoms to monitor include aggression, agitation, blurred vision, a decrease in the amount of urine, dizziness, irregular heartbeat or pulse, headache, irritability, mood changes, irregular breathing, numbness or tingling in the arms or legs, pounding in the ears, shortness of breath, swelling of the fingers, hands, feet, or lower legs, trouble thinking, speaking, or walking, difficulty with breathing at rest, or weight gain.

Monitoring patients receiving glucocorticoid therapy involves measuring weight, height, body mass index (BMI), and blood pressure. The routine investigations are complete blood count (CBC), glucose levels, and lipid profiles. Bone health should be assessed annually with bone mineral density (BMD) checks, particularly 12 months after starting glucocorticoids. Lateral spine X-rays are recommended for adults older than 65, and FRAX can be used to estimate fracture risk. For children, baseline BMD and X-rays are advised after 3 months of glucocorticoid use, with follow-ups if risk factors persist. HPA-axis functioning and growth in children and adolescents should be closely monitored, with referrals to specialists made for any growth issues. Lipid levels and cardiovascular risk should be assessed at 1 month and then every 6 to 12 months, using the Framingham Risk Score to evaluate cardiovascular risk. Hyperglycemia and diabetes should be monitored through regular glucose screenings, with annual checks recommended for at-risk children. Annual ophthalmologic exams are recommended, with earlier referrals for those at risk of glaucoma or other eye conditions.[40]

Toxicity

Signs and Symptoms of Overdose

Like any anti-inflammatory agent, steroid toxicity is treated similarly to any non-steroidal anti-inflammatory drug overdose or toxicity. Although the frequency of life-threatening complications from steroids and NSAID overdose is low, the overdose response ranges from no symptoms to death despite intensive-care treatment. Most symptoms are due to the excessive pharmacological action of steroids and NSAIDs and include abdominal pain, nausea, vomiting, drowsiness, dizziness, headache, ear ringing, and nystagmus. A significant dose-response relationship occurs with the long-term use of systemic corticosteroids and the development of systemic corticosteroid-related complications for patients with severe asthma, resulting in an increased burden and costs on the healthcare system.[41]

Management of Overdose

Assessment of all organ systems can help identify problems. If necessary, hypertension and salt retention should be treated with salt restriction and diuretics.[42] Gastrointestinal perforation requires surgical intervention. Antibiotics and antifungals should be prescribed for infections. An iatrogenic crushing syndrome caused by a supplement containing dexamethasone has been reported.[43] Gradual tapering of corticosteroids is advisable to prevent adrenal insufficiency. Potent proton pump inhibitors should be prescribed for gastroprotection. Hypokalemia can be treated by replacement. Steroid-induced psychosis can be managed with antipsychotics.[44] Hyperglycemia should be treated with insulin in critically ill patients. After stabilization, patients should be prescribed vitamin D and calcium. Mitotane and ketoconazole decrease cortisol production and should be used only under the supervision of an endocrinologist.[45]

Enhancing Healthcare Team Outcomes

The management of adverse drug reactions induced by steroids requires an interprofessional team of healthcare professionals, including a nurse, laboratory technologists, pharmacists, and several physicians in different specialties. Without proper management, the adverse effects of prednisone overdose are high. Systemic corticosteroids have extensive use in the treatment of various autoimmune and inflammatory disorders. Prolonged use, especially at high doses of 40 mg daily, can cause serious adverse effects. The most common systems involved include the gastrointestinal (GI), musculoskeletal, endocrine, cardiovascular, and central nervous system (CNS). Prednisone's adverse effects can be minimized by monitoring the patient and putting preventative measures in place. Some of these preventive measures include using lower-potency dosages and starting patients on the lowest effective dosage, as per guidelines. The patient needs to be informed of the adverse effects so they may understand and be aware of making the proper lifestyle modifications to help reduce the risk of adverse effects. Patients should receive counsel to seek medical attention if they experience any of these known adverse effects. A steroid treatment card can be recommended to show to all healthcare professionals involved in their care and management. The differences in monitoring and care between adults and children should be noted, particularly regarding growth curve complications, adrenal suppression, and osteoporosis.[40]

To achieve this, interprofessional collaboration is essential. Clinicians prescribe the drug and need to inform the patients about the adverse event profile; this is often the task of the nursing staff. They can also assess patient compliance and inform the prescribing clinician about any potential issues. Pharmacists can counsel patients on proper administration and reinforce the importance of reporting adverse events. Pharmacists must also perform medication reconciliation and report any potential interactions to the prescribing office.[46] An interprofessional team approach with open communication among physicians, advanced practice providers, nurses, and pharmacists can enhance patient outcomes and mitigate the adverse reactions associated with prednisone therapy.

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Disclosure: Yana Puckett declares no relevant financial relationships with ineligible companies.

Disclosure: Preeti Patel declares no relevant financial relationships with ineligible companies.

Disclosure: Abdullah Bokhari declares no relevant financial relationships with ineligible companies.