Prednisone is a biologically inert corticosteroid that is converted in the liver to the mainly glucocorticoid corticosteroid prednisolone. It has the same chemical relationship to prednisolone as cortisone has to hydrocortisone. Conclusive pharmacokinetic evidence not compatible with CYP-inducing capacity in clinical use. Being ligand to glucocorticoid nuclear receptor giving rise to endogenous protective glucose production. Feedback inhibition of adrenal androgen production will add to a protective effect. No reports of porphyrogenic side effects in clinical use, but well documented evidence of tolerance in acute porphyria.

1,2-Dehydrocortisone (M= 358.4). It is a synthetic glucocorticoid analog.

The indications and dosage of prednisone for oral use are exactly the same as those for prednisolone. Shock conditions. Antiallergic, antipruritic, immunosuppressive and antiinflammatory properties. Prednisone has four times stronger antiinflammatory effect than hydrocortisone. In the UK prednisolone has historically been preferred to prednisone, on the grounds that it does not require conversion to the active substance, but in practice this is rarely significant, and in some countries, such as the USA, prednisone is the drug of choice for many of the conditions in which routine systemic corticosteroid therapy is indicated.

Irrelevant.

Prednisolone and prednisone are both readily absorbed from the gastrointestinal tract, but whereas prednisolone already exists in a metabolically active form, prednisone must be converted in the liver to its active metabolite, prednisolone. In general, this conversion is rapid so this difference is of little consequence when seen in the light of intersubject variation in the pharmacokinetics of prednisolone itself; bioavailability also depends on the dissolution rates of the tablet formulations. As a ligand to glucocorticoid nuclear receptor, prednisolon may participate in PXR activation and subsequent ALAS1 induction. Inducer of gluconeogenetic enzymes. Substrate of CYP3A4, the metabolism affected by CYP-inducers as well as by CYP3A4 inhibitors. No effects on the elimination rate of other CYP-metabolized drugs. Systemic effects in rectal administration.

Uneventful use reported in 1 patient with acute porphyria.