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[Glucocorticoid-induced osteoporosis: recent findings]
A Angeli1, G Osella, G Reimondo
1Dipartimento di Scienze Cliniche e Biologiche, Università degli Studi di Torino. angeli@pasteur.sluigi.unito.it
Annali Italiani Di Medicina Interna : Organo Ufficiale Della Societa Italiana Di Medicina Interna
|June 8, 2000
Summary
Cushing's syndrome causes bone loss, particularly in trabecular bone, leading to fractures. Early treatment with calcium, vitamin D, or bisphosphonates is crucial to reduce fracture risk.
Area of Science:
- Endocrinology
- Bone Metabolism
- Pharmacology
Context:
- Cushing's syndrome, characterized by hypercortisolism, is linked to significant bone damage.
- Glucocorticoid-induced osteoporosis is well-documented with exogenous steroid use, but less so with endogenous hypercortisolism.
- Adrenal incidentalomas with silent hypercortisolism may also impact bone health.
Purpose:
- To review the clinical features, pathogenesis, and management of bone involvement in Cushing's syndrome.
- To report personal data on bone mineral density and turnover markers in Cushing's syndrome and adrenal incidentalomas.
- To discuss current and potential future therapeutic strategies for glucocorticoid-induced osteoporosis.
Summary:
- Bone loss in Cushing's syndrome primarily affects trabecular bone, increasing vertebral fracture risk.
- Both endogenous (Cushing's syndrome) and exogenous (glucocorticoid therapy) hypercortisolism lead to similar bone damage.
- Current treatments include supplementation, hormone therapy, and bisphosphonates; selective glucocorticoid receptor modulators offer future promise.
Impact:
- Highlights the critical need for prompt and effective management of bone loss in hypercortisolism to prevent fractures.
- Emphasizes the qualitative similarities in bone damage from endogenous and exogenous glucocorticoid excess.
- Suggests novel therapeutic avenues, such as selective glucocorticoid receptor modulators, for managing glucocorticoid-induced osteoporosis.