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Glucocorticoid-induced osteoporosis: pathogenesis and management
1Department of Clinical Immunology, Medical Institute of Bioregulation, Kyushu University, Beppu, Japan.
Journal of Bone and Mineral Metabolism
|October 29, 2000
Summary
Long-term glucocorticoid (GC) therapy can cause osteoporosis and fractures. Guidelines recommend bone density measurement and preventive therapies like calcium, vitamin D, and exercise for patients on GC therapy.
Area of Science:
- Endocrinology
- Bone Biology
- Rheumatology
Background:
- Long-term glucocorticoid (GC) therapy is associated with significant risks of osteoporosis and fractures.
- Conditions requiring GC therapy include rheumatoid arthritis, autoimmune diseases, inflammatory bowel diseases, asthma, and chronic lung diseases.
- GCs impact bone metabolism by affecting both bone formation and resorption.
Purpose of the Study:
- To summarize the pathogenesis of glucocorticoid-induced osteoporosis (GIOP).
- To outline current prevention and treatment strategies for GIOP.
Main Methods:
- Review of existing literature and guidelines on GIOP.
- Synthesis of information regarding GC effects on bone.
- Analysis of recommended preventive and therapeutic interventions.
Main Results:
- GCs disrupt bone remodeling, leading to reduced bone mineral density and increased fracture risk.
- Established guidelines recommend bone mineral density monitoring for patients on GC therapy (≥7.5 mg/day prednisolone for ≥6 months).
- First-line preventive therapies include calcium, vitamin D, sex hormone replacement, and weight-bearing exercise.
Conclusions:
- Glucocorticoid-induced osteoporosis is a serious complication of long-term GC treatment.
- Adherence to guidelines for monitoring and early intervention is crucial.
- Bisphosphonates are a recommended alternative for patients unable to undergo sex hormone replacement therapy.