Dexamethasone is preferred over hydrocortisone for suppression of adrenal androgen excess (e.g., CAH) and for fetal lung maturation. The pharmacological basis is:
- A Dexamethasone has higher mineralocorticoid potency, causing greater sodium retention and ACTH suppression
- B Dexamethasone has poor placental transfer and acts locally on the pituitary to suppress ACTH
- C Dexamethasone has 25–30× greater glucocorticoid potency than hydrocortisone, longer duration, no significant mineralocorticoid activity, and crosses the placenta because it is not metabolized by placental 11β-HSD2 ✓
- D Dexamethasone is the only glucocorticoid that upregulates surfactant protein B gene transcription directly
Explanation
Dexamethasone has 25–30 times the glucocorticoid potency of hydrocortisone with negligible mineralocorticoid activity, making it preferred for ACTH suppression without fluid retention. Crucially, dexamethasone (and betamethasone) are not inactivated by placental 11β-hydroxysteroid dehydrogenase type 2 (which converts cortisol/hydrocortisone to inactive cortisone), allowing intact drug to reach the fetus and stimulate surfactant production. Hydrocortisone is efficiently inactivated by placental 11β-HSD2.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.