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-dehydrohydrocortisone(M=360). Synthetic corticosteroid with dominant glucocorticoid activity. Administered as watersoluble sodiumsuccinate ester.

Shock conditions. Antiallergic, antipruritic, immunosuppressive and antiinflammatory properties. Five times stronger antiinflammatory effect than hydrocortisone. The slower metabolism of synthetic corticosteroids with their lower plasma-protein binding affinity may account for their increased potency compared with the natural corticosteroid. Less potent pituitary suppressant activity than e.g. dexamethasone. Predominant glucocorticoid activity, after activating the nuclear glucocorticoid receptor increasing the expression of the genes for the key gluconeogenetic enzymes PEPCK and G6P, elevating blood glucose and initiating antiporphyrogenic insulin release.

Irrelevant.

Microsomal CYP-oxidation mainly in the liver. Biological half life 12-36 hours. Slower metabolism compared with the natural hormones. 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.

Skadberg, patient report (n=1): tolerated. Others, patient report (n=2): tolerated.

Uneventful use reported in 1 patient with acute porphyria.