Steroid Conversion Calculator
Convert between equivalent corticosteroid doses across 8 commonly used systemic glucocorticoids. Includes glucocorticoid and mineralocorticoid potency comparison, duration-of-action classification, and clinical guidance for switching, tapering, and special populations.
Convert Corticosteroid Dose
Select the corticosteroid the patient is currently taking and enter the dose. The calculator will display the equivalent dose for all other systemic corticosteroids based on relative glucocorticoid potency.
Dose equivalence is based on anti-inflammatory (glucocorticoid) potency only. It does not guarantee equivalent mineralocorticoid, immunosuppressive, or HPA-axis-suppressive effects. Clinical response may vary between agents due to differences in pharmacokinetics, tissue distribution, receptor affinity, and individual patient factors. Always verify converted doses against current prescribing information.
Understanding Corticosteroid Equivalence
Corticosteroid equivalence is founded on the principle that different glucocorticoids have different potencies per milligram, but at their respective equivalent doses they produce comparable anti-inflammatory effects. The reference standard is hydrocortisone (cortisol) — the body’s endogenous glucocorticoid — with all other agents expressed as multiples of its potency.
These equivalence ratios were established through a combination of in vitro receptor binding assays, in vivo anti-inflammatory bioassays (such as the granuloma pouch model and croton oil ear test), and clinical observation over decades of use. It is important to recognise that these ratios are approximations derived from population-level data and may not perfectly apply to every patient or clinical scenario.
Conversion Formula
Equivalent Dose = Source Dose × (Source Equiv ÷ Target Equiv)
Example: Prednisone 40 mg → Dexamethasone: 40 × (5 ÷ 0.75) inverted = 40 × (0.75 ÷ 5) = 6 mg
Physiological Replacement
Cortisol production ≈ 5–10 mg/m²/day
Equivalents: Hydrocortisone 15–25 mg/day ≈ Prednisone 3.75–6.25 mg/day ≈ Dexamethasone 0.5–0.75 mg/day. Doses above this range are pharmacological, not replacement.
Glucocorticoid vs mineralocorticoid potency: Equivalence tables address anti-inflammatory (glucocorticoid) potency. Mineralocorticoid activity — which governs sodium retention, potassium excretion, and blood pressure effects — varies independently. Hydrocortisone and cortisone have significant mineralocorticoid activity, whereas dexamethasone, betamethasone, and triamcinolone have essentially none. When switching from a steroid with mineralocorticoid effect to one without it, supplemental fludrocortisone may be required for adrenal insufficiency patients.
Potency & Pharmacology Comparison
The following table provides a comprehensive comparison of all eight systemic corticosteroids, including their equivalent dose, relative potencies, biological half-life, and duration of action classification.
| Corticosteroid | Equivalent Dose (mg) | GC Potency | MC Potency | Biological t½ | Duration |
|---|---|---|---|---|---|
| Hydrocortisone | 20 | 1 | 1 | 8–12 hr | Short |
| Cortisone | 25 | 0.8 | 0.8 | 8–12 hr | Short |
| Prednisone | 5 | 4 | 0.8 | 12–36 hr | Intermediate |
| Prednisolone | 5 | 4 | 0.8 | 12–36 hr | Intermediate |
| Methylprednisolone | 4 | 5 | 0.5 | 12–36 hr | Intermediate |
| Triamcinolone | 4 | 5 | 0 | 12–36 hr | Intermediate |
| Dexamethasone | 0.75 | 25–30 | 0 | 36–72 hr | Long |
| Betamethasone | 0.6 | 25–33 | 0 | 36–72 hr | Long |
GC = Glucocorticoid potency (relative to hydrocortisone = 1). MC = Mineralocorticoid potency (relative to hydrocortisone = 1). Biological t½ = biological (tissue) half-life, distinct from the shorter plasma half-life.
Prednisone vs prednisolone: Prednisone is a prodrug that must be hepatically converted to its active form, prednisolone. In patients with severe hepatic impairment (cirrhosis, acute liver failure), this conversion may be impaired, and prednisolone should be used preferentially. In most other patients, the two are clinically interchangeable at a 1:1 ratio.
Duration of Action — Clinical Implications
Clinical Considerations for Steroid Switching & Tapering
Converting between corticosteroids is not simply a mathematical exercise. Clinicians must account for the reason for the switch, the duration of prior therapy, the risk of adrenal suppression, and the clinical trajectory of the patient.
Common clinical scenarios requiring steroid conversion include transitioning from intravenous to oral therapy during hospital discharge (e.g., IV methylprednisolone to oral prednisone), switching from a short-acting agent used for replacement to an intermediate agent for anti-inflammatory purposes, changing from a steroid with mineralocorticoid effects to one without (or vice versa), and availability or formulary constraints requiring substitution with a different agent.
Less common but important indications include switching to dexamethasone when maximum glucocorticoid potency without mineralocorticoid activity is required (e.g., cerebral oedema, spinal cord compression), converting to hydrocortisone for physiological replacement when an inflammatory condition has resolved and the patient needs to taper to replacement doses, and converting when a patient develops adverse effects that may be mitigated by a different agent (e.g., methylprednisolone may cause fewer mood disturbances than prednisone in some patients, though evidence is limited).
Any corticosteroid given at pharmacological (supraphysiological) doses for more than 2–3 weeks can suppress the hypothalamic-pituitary-adrenal (HPA) axis, reducing endogenous cortisol production. The risk is dose- and duration-dependent, but significant HPA suppression has been documented even with doses as low as prednisone 5 mg/day given for several months. Long-acting agents (dexamethasone, betamethasone) suppress the HPA axis more readily per equivalent dose due to their prolonged biological half-life.
When tapering or discontinuing corticosteroids, the rate must be slow enough to allow the adrenal glands to recover their capacity for endogenous cortisol production. Abrupt discontinuation after prolonged therapy can precipitate adrenal crisis — a life-threatening emergency characterised by hypotension, hypoglycaemia, hyperkalaemia, and cardiovascular collapse. General tapering guidance suggests reducing by no more than 10–20% of the dose every 1–2 weeks once below the equivalent of prednisone 20 mg/day. Below prednisone 5 mg/day (approximate physiological replacement), the taper should be even more gradual, with monitoring for symptoms of adrenal insufficiency (fatigue, nausea, myalgia, postural hypotension).
- Duration > 3 weeks at any pharmacological dose: taper required
- Morning cortisol level can be used to assess HPA recovery
- ACTH stimulation test (Synacthen) for definitive assessment
- Stress-dose steroids may be needed during illness or surgery even after taper
When converting between steroids with different mineralocorticoid potencies, clinicians must consider the impact on sodium/water balance and potassium homeostasis. Hydrocortisone and cortisone have significant mineralocorticoid activity — at replacement doses, hydrocortisone often provides sufficient mineralocorticoid effect without supplemental fludrocortisone. However, switching an adrenal-insufficient patient from hydrocortisone to dexamethasone (which has zero mineralocorticoid activity) without adding fludrocortisone will result in mineralocorticoid deficiency, manifesting as hyperkalemia, hyponatremia, and postural hypotension.
Conversely, patients receiving high-dose hydrocortisone (e.g., stress dosing at 200–300 mg/day) will experience significant sodium and water retention, oedema, and hypokalaemia due to the mineralocorticoid load. In heart failure or renal patients, switching to methylprednisolone or dexamethasone at the equivalent anti-inflammatory dose may be preferable to minimise fluid retention, since these agents have minimal to no mineralocorticoid activity.
Standard equivalence ratios are best validated at low-to-moderate anti-inflammatory doses. At very high pharmacological doses — sometimes called “pulse” therapy (e.g., IV methylprednisolone 500–1000 mg/day for severe lupus nephritis or acute transplant rejection) — the linear equivalence relationship may not hold, and direct clinical evidence for the specific indication should guide dosing rather than simple mathematical conversion.
For example, pulse methylprednisolone 1000 mg/day is widely used for acute renal transplant rejection. The calculated equivalent of dexamethasone (~167 mg) or prednisone (~1250 mg) is not standard practice for the same indication. At pulse-dose ranges, pharmacokinetic saturation, receptor occupancy, and non-genomic steroid effects (which occur at high doses) mean that the clinical response is not proportional to the simple potency ratio. When converting from pulse IV therapy to oral maintenance, clinicians should step down to a conventional high dose (e.g., prednisone 1 mg/kg/day) rather than attempting an exact equivalence conversion of the pulse dose.
Most corticosteroids have excellent oral bioavailability. Prednisolone, methylprednisolone, and dexamethasone are nearly 100% bioavailable when given orally, meaning that the IV-to-oral conversion is approximately 1:1 for these agents. The transition from IV methylprednisolone to oral prednisone can be done at the standard potency ratio (4 mg IV methylprednisolone = 5 mg oral prednisone) without an additional bioavailability adjustment.
Exceptions to be aware of include patients with significant gastrointestinal pathology (vomiting, malabsorption, short-bowel syndrome, ileus) where oral absorption may be impaired, and situations where the clinical urgency requires the immediate peak levels achievable only with IV administration. Additionally, prednisone’s conversion to prednisolone may be impaired in severe liver disease, so IV methylprednisolone or IV hydrocortisone may be preferred when hepatic function is significantly compromised.
When switching between corticosteroids, ask three questions: (1) Is the anti-inflammatory dose correctly converted? (2) Does the mineralocorticoid activity change, and does the patient need fludrocortisone supplementation? (3) Does the duration of action change, and does the dosing frequency need to be adjusted?
Special Populations
Steroid equivalence ratios apply broadly, but certain patient populations require additional considerations beyond simple dose conversion when selecting and dosing corticosteroids.
Placental barrier matters for steroid selection in pregnancy: When the goal is to treat the mother (e.g., asthma, lupus, inflammatory bowel disease), use prednisone or prednisolone. When the goal is to treat the foetus (e.g., foetal lung maturation at 24–34 weeks’ gestation), use betamethasone or dexamethasone because they cross the placenta intact.
Common Pitfalls & Limitations
Equivalent anti-inflammatory dose does not mean equivalent clinical effect in all situations. The choice of corticosteroid depends on the clinical indication, required duration of action, mineralocorticoid profile, and route of administration. Substituting dexamethasone for hydrocortisone at the equivalent dose would provide the same anti-inflammatory potency but would eliminate mineralocorticoid coverage, dramatically extend the biological half-life, and suppress the HPA axis more profoundly.
How to avoid: Always consider why a particular steroid was chosen. If a patient is on hydrocortisone for adrenal insufficiency, do not convert to dexamethasone “for convenience” — the pharmacological profiles are fundamentally different. Equivalence tables guide dose conversion, but the choice of agent is a separate clinical decision.
When converting from hydrocortisone or cortisone (which have significant mineralocorticoid activity) to an agent with none (dexamethasone, triamcinolone, betamethasone), the patient loses mineralocorticoid coverage. In primary adrenal insufficiency, this will rapidly manifest as hyperkalemia, hyponatremia, postural hypotension, and salt craving. In patients without adrenal disease, the loss of mineralocorticoid effect may cause a modest decrease in blood pressure and sodium retention.
How to avoid: When switching to an agent with lower mineralocorticoid potency, specifically assess whether the patient needs fludrocortisone supplementation (typically 0.05–0.2 mg/day in adrenal insufficiency). When switching in the opposite direction (e.g., from dexamethasone to hydrocortisone), anticipate increased sodium and water retention, which may be clinically significant in patients with heart failure, hypertension, or renal disease.
Prednisone is an inactive prodrug that requires hepatic 11β-hydroxysteroid dehydrogenase conversion to its active form, prednisolone. In patients with severe hepatic impairment (decompensated cirrhosis, acute liver failure), this conversion may be significantly impaired, resulting in a subtherapeutic response despite apparently adequate dosing. Studies in cirrhotic patients have shown conversion rates reduced by 20–50% compared to healthy controls.
How to avoid: In patients with significant liver disease, use prednisolone (the active metabolite), methylprednisolone, or dexamethasone — all of which are already in their active form and do not depend on hepatic activation. This also applies to patients with acute hepatic injury. The equivalence conversion itself remains unchanged; only the drug selection needs modification.
The standard equivalence table applies to systemic oral or intravenous dosing only. It does not apply to inhaled, topical, intra-articular, or epidural corticosteroids, which have entirely different pharmacokinetics, tissue concentrations, and potency rankings. For example, budesonide (an inhaled corticosteroid) does not appear in the systemic equivalence table, and fluticasone topical potency ranking follows a different classification system from systemic glucocorticoid potency.
How to avoid: Never use this calculator for non-systemic preparations. Topical steroids have their own potency classification (Class I–VII in the US system), inhaled steroids are dosed in micrograms with their own equivalence tables, and intra-articular doses are procedure-specific. Use dedicated references for each route of administration.
When converting from a short-acting steroid (hydrocortisone, dosed 2–3 times daily) to a long-acting agent (dexamethasone, dosed once daily), the total daily equivalent dose should be given at the appropriate frequency for the new agent. If a patient on hydrocortisone 10 mg three times daily (total 30 mg/day) is switched to dexamethasone, the equivalent is approximately 1.1 mg of dexamethasone given once daily — not 0.37 mg three times daily. Conversely, switching from once-daily dexamethasone to hydrocortisone requires splitting the daily equivalent into divided doses.
How to avoid: After calculating the equivalent total daily dose, look up the standard dosing frequency for the target steroid. Short-acting agents (hydrocortisone, cortisone) are typically divided into 2–3 daily doses. Intermediate agents (prednisone, methylprednisolone) are often given once or twice daily. Long-acting agents (dexamethasone, betamethasone) are almost always once daily.
Quick Reference Summary
(Reference dose)
(= 5 mg prednisone)
(= 5 mg prednisone)
(= 5 mg prednisone)
| Clinical Scenario | Key Conversion Point |
|---|---|
| IV methylprednisolone → oral prednisone | 4 mg IV = 5 mg oral (1:1.25 ratio); bioavailability ~100% |
| Dexamethasone 6 mg → prednisone | ≈ 40 mg prednisone (common COVID-19 conversion) |
| Physiological replacement | Hydrocortisone 15–25 mg/day ≈ Prednisone 3.75–6.25 mg/day |
| Switching steroids in pregnancy (maternal) | Use prednisone/prednisolone (placenta-inactivated); avoid dexamethasone |
| Foetal lung maturation | Use betamethasone or dexamethasone (crosses placenta intact) |
| Liver failure patient | Use prednisolone (not prednisone); or methylprednisolone / dexamethasone |
The Golden Rule: Equivalence tables convert anti-inflammatory dose only. They do not guarantee equivalent mineralocorticoid, immunosuppressive, or HPA-suppressive effects. When switching agents, always consider the full pharmacological profile — not just the milligrams.
Disclaimer & References
For Educational Purposes Only. This calculator and the accompanying clinical information are intended as educational tools for healthcare professionals. They do not replace clinical judgement. Results should be interpreted in the full clinical context. Lab reference ranges vary by institution — verify with your own laboratory. Drug dosages should be confirmed against current prescribing information.
References
- Liu D, Ahmet A, Ward L, et al. A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy Asthma Clin Immunol. 2013;9(1):30. DOI: 10.1186/1710-1492-9-30
- Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clin Pharmacokinet. 2005;44(1):61-98. DOI: 10.2165/00003088-200544010-00003
- Becker DE. Basic and clinical pharmacology of glucocorticosteroids. Anesth Prog. 2013;60(1):25-32. DOI: 10.2344/0003-3006-60.1.25
- Hopkins RL, Leinung MC. Exogenous Cushing’s syndrome and glucocorticoid withdrawal. Endocrinol Metab Clin North Am. 2005;34(2):371-384. DOI: 10.1016/j.ecl.2005.01.013
- RECOVERY Collaborative Group. Dexamethasone in hospitalized patients with Covid-19. N Engl J Med. 2021;384(8):693-704. DOI: 10.1056/NEJMoa2021436
- Paragliola PE, Papi G, Pontecorvi A, Corsello SM. Treatment with synthetic glucocorticoids and the hypothalamus-pituitary-adrenal axis. Int J Mol Sci. 2017;18(10):2201. DOI: 10.3390/ijms18102201
- Johannesdottir SA, Horváth-Puhó E, Dekkers OM, et al. Use of glucocorticoids and risk of venous thromboembolism: a nationwide population-based case-control study. JAMA Intern Med. 2013;173(9):743-752. DOI: 10.1001/jamainternmed.2013.122
- Roberts D, Brown J, Medley N, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2017;3(3):CD004454. DOI: 10.1002/14651858.CD004454.pub3