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Corticosteroid-induced osteoporosis: an update for dermatologists
1Mayo Clinic School of Medicine, Rochester, MN, USA. Clarke.Bart@Mayo.edu
American Journal of Clinical Dermatology
|March 8, 2012
Summary
Long-term corticosteroid use commonly causes bone loss, leading to osteopenia, osteoporosis, and fractures. Early bone resorption and later suppressed bone formation occur, necessitating risk assessment and treatment with bisphosphonates or teriparatide.
Area of Science:
- Endocrinology
- Bone Metabolism
- Pharmacology
Background:
- Long-term corticosteroid therapy is a leading cause of secondary bone loss.
- Patients may develop osteopenia, osteoporosis, and fractures.
- Predicting skeletal complications is challenging due to disease variability and dosage fluctuations.
Purpose of the Study:
- To provide an updated overview of corticosteroid-induced osteoporosis.
- To cover pathophysiology, clinical presentation, evaluation, and management.
- To inform clinicians on current recommendations for prevention and treatment.
Main Methods:
- Review of current knowledge on corticosteroid-induced osteoporosis.
- Discussion of the mechanisms of bone loss, including OPG/RANKL pathway.
- Integration of recent recommendations for patient management.
Main Results:
- Corticosteroid therapy alters the OPG/RANKL ratio, increasing early bone resorption and suppressing bone formation long-term.
- Fracture risk assessment using bone mineral density is crucial.
- Bisphosphonates or teriparatide are recommended for high-risk patients.
Conclusions:
- Corticosteroid-induced osteoporosis is a significant clinical problem.
- Understanding the pathophysiology guides prevention and treatment strategies.
- Personalized management based on fracture risk is essential for patients on long-term corticosteroid therapy.
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