Corticosteroid Dose Converter

Glucocorticoid potency is determined by receptor binding affinity, bioavailability after oral administration, protein binding, metabolic half-life, and tissue distribution. Dexamethasone's fluorine substituent markedly increases its glucocorticoid receptor affinity and resistance to metabolic inactivation, making it much more potent per mg than hydrocortisone. Bioavailability also varies — methylprednisolone has near-complete oral bioavailability, while prednisone requires hepatic conversion to prednisolone.

Mineralocorticoid activity refers to the ability of a glucocorticoid to act on aldosterone receptors in the kidney, causing sodium and water retention and potassium excretion. Hydrocortisone has the highest mineralocorticoid activity among systemic glucocorticoids (about 1/500 that of aldosterone but still clinically relevant). Prednisolone has weak mineralocorticoid activity; dexamethasone and betamethasone have virtually none. Patients needing mineralocorticoid replacement (primary adrenal insufficiency) must receive fludrocortisone regardless of their glucocorticoid choice.

Prednisone is a prodrug that is converted in the liver to prednisolone (its active form). In patients with severe hepatic disease, this conversion is impaired, making prednisolone the preferred agent. For practical purposes, 5 mg prednisone equals 5 mg prednisolone in patients with normal hepatic function, as both are included in the standard equivalence table at equal potency.

Dexamethasone's high potency, long duration of action, negligible mineralocorticoid activity (reducing fluid retention risk), and excellent CNS penetration make it ideal for treating peritumoral cerebral oedema. Its prolonged anti-inflammatory effect with once or twice-daily dosing is also advantageous for PONV prophylaxis. A single dose of dexamethasone 4-8 mg reduces PONV incidence by 25-30% without significant immunosuppression risk.

Inhaled corticosteroid (ICS) doses cannot be directly converted using the systemic equivalence table because topical potency, inhalation device efficiency, particle size, and systemic bioavailability all differ dramatically from oral glucocorticoids. Approximate ICS to systemic equivalences exist (e.g., fluticasone propionate 1000 mcg/day inhaled is approximately equivalent to prednisolone 5-10 mg/day systemically in terms of HPA suppression), but these are estimates and vary between individuals.

The systemic equivalence table applies to systemically administered glucocorticoids (oral, IV, IM). Topical and intra-articular preparations have very different local and systemic exposure profiles. However, clinically significant systemic absorption from topical steroids (particularly high-potency agents on large skin areas or under occlusion) and intra-articular injections can suppress the HPA axis, and the systemic equivalent exposure should be estimated when managing patients at risk.

These ICS agents are not included in the standard systemic equivalence table because they are primarily designed for topical pulmonary or gastrointestinal use. Oral budesonide (for IBD) has approximately 9-fold lower systemic bioavailability than prednisolone due to extensive first-pass hepatic metabolism, which is why it causes less systemic side effects at equivalent local anti-inflammatory doses.

In septic shock or critical illness, physiological cortisol requirements can increase from a normal 15-25 mg/day equivalent to 200-400 mg hydrocortisone-equivalent per day. Stress-dose hydrocortisone (200 mg/day as continuous infusion or 50 mg 6-hourly) is recommended in refractory septic shock despite adequate volume resuscitation and vasopressors. The conversion table equivalences still apply for calculating stress-dose equivalents of other agents.