A 40-year-old man with autoimmune hepatitis on prednisolone for 8 months develops new-onset back pain. Imaging shows multiple vertebral compression fractures. The mechanism of corticosteroid-induced osteoporosis is best described as:
- A Direct activation of RANKL on osteoclasts causing excessive bone resorption
- B Suppression of intestinal calcium absorption, inhibition of osteoblast function and survival, stimulation of osteoclastogenesis via RANKL/OPG imbalance, and reduction of sex hormones ✓
- C Inhibition of 1-alpha-hydroxylase in the kidney, reducing 1,25-dihydroxyvitamin D3 synthesis
- D Competitive antagonism at vitamin D receptors in osteoblasts, preventing mineralisation of osteoid
Explanation
Glucocorticoid-induced osteoporosis is multifactorial: corticosteroids reduce intestinal calcium absorption (by inhibiting vitamin D-dependent calbindin), increase renal calcium excretion, suppress osteoblast proliferation and promote osteoblast/osteocyte apoptosis, shift the RANKL/OPG ratio favouring osteoclast activity, and suppress gonadal hormone production (reducing anabolic stimuli). This creates a dual defect of reduced bone formation and increased bone resorption. Prevention includes calcium, vitamin D, and bisphosphonate supplementation. Option C describes vitamin D deficiency, not a glucocorticoid-specific mechanism.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.