Abstract
Postmenopausal women are at greatest risk of rapid bone loss and fracture with glucocorticoids and should be actively considered for prophylactic measures. In men and premenopausal women receiving glucocorticoids, the decision to use anti-osteoporosis prophylaxis is less clear and depends upon baseline bone mineral density [BMD], anticipated dose and duration of glucocorticoids. Based upon evidence the order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or hormone replacement therapy [HRT]. Calcium alone appears unable to prevent rapid bone loss in patients starting glucocorticoids. HRT should clearly be considered if hypogonadism is present. In patients receiving chronic low dose glucocorticoids, treatment with calcium and vitamin D may be sufficient to prevent further bone loss. However since fracture risk is a function of multiple factors including the degree of reduction in BMD as well as the duration of exposure, treatment with therapy to increase BMD will reduce fracture risk even in patients receiving chronic low dose glucocorticoids.
Keywords: osteoporosis, postmenopausal, bone mineral density, glucocorticoid therapy, histomorphometric picture, morphometric approach, cushings syndrome, alfacalcidol, mild hypercalcemia
Current Pharmaceutical Design
Title: Glucocorticoid Osteoporosis
Volume: 8 Issue: 21
Author(s): Philip N. Sambrook
Affiliation:
Keywords: osteoporosis, postmenopausal, bone mineral density, glucocorticoid therapy, histomorphometric picture, morphometric approach, cushings syndrome, alfacalcidol, mild hypercalcemia
Abstract: Postmenopausal women are at greatest risk of rapid bone loss and fracture with glucocorticoids and should be actively considered for prophylactic measures. In men and premenopausal women receiving glucocorticoids, the decision to use anti-osteoporosis prophylaxis is less clear and depends upon baseline bone mineral density [BMD], anticipated dose and duration of glucocorticoids. Based upon evidence the order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or hormone replacement therapy [HRT]. Calcium alone appears unable to prevent rapid bone loss in patients starting glucocorticoids. HRT should clearly be considered if hypogonadism is present. In patients receiving chronic low dose glucocorticoids, treatment with calcium and vitamin D may be sufficient to prevent further bone loss. However since fracture risk is a function of multiple factors including the degree of reduction in BMD as well as the duration of exposure, treatment with therapy to increase BMD will reduce fracture risk even in patients receiving chronic low dose glucocorticoids.
Export Options
About this article
Cite this article as:
Sambrook N. Philip, Glucocorticoid Osteoporosis, Current Pharmaceutical Design 2002; 8 (21) . https://dx.doi.org/10.2174/1381612023393648
DOI https://dx.doi.org/10.2174/1381612023393648 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Adverse Drug Reactions in the Oral Cavity
Current Pharmaceutical Design Transplantation of Adipose Derived Stem Cells for Peripheral Nerve Regeneration in Sciatic Nerve Defects of the Rat
Current Stem Cell Research & Therapy Kidney Diseases and Chemokines
Current Drug Targets Fe-S Proteins Acting as Redox Switch: New Key Actors of Cellular Adaptive Responses
Current Chemical Biology Angiotensin II, Cell Proliferation and Angiogenesis Regulator: Biologic and Therapeutic Implications in Cancer
Current Vascular Pharmacology Some Highlights on Epileptic EEG Processing
Recent Patents on Biomedical Engineering (Discontinued) Interleukin-7: a key Mediator in T Cell-driven Autoimmunity, Inflammation, and Tissue Destruction
Current Pharmaceutical Design Functional Neuroimaging of Sleep Disorders
Current Pharmaceutical Design Conference Report:
CNS & Neurological Disorders - Drug Targets Nephrotoxicity Associated with Antiretroviral Therapy in HIV-Infected Patients
Current Drug Safety Biochemical, Molecular and Epigenetic Mechanisms of Valproic Acid Neuroprotection
Current Molecular Pharmacology Disrupted Structural Brain Network in AD and aMCI: A Finding of Long Fiber Degeneration
Current Alzheimer Research Drug-Related Decrease in Neuropsychological Functions of Abstinent Drug Users
Current Drug Abuse Reviews Patents on Potential Drugs to Treat Alzheimer’s Disease: Special Emphasis on Small Peptides
Recent Patents on CNS Drug Discovery (Discontinued) COVID-19 Invades Several Important Organs other than the Lungs: Organs Crosstalk
Coronaviruses A Review on Cellular and Molecular Mechanisms Linked to the Development of Diabetes Complications
Current Diabetes Reviews Twenty Years of HIV-1 Non-Nucleoside Reverse Transcriptase Inhibitors: Time to Reevaluate their Toxicity
Current Medicinal Chemistry Relevant Modulation by Ferrous Ions of N-Methyl-D-Aspartate Receptors in Ischemic Brain Injuries
Current Neurovascular Research Nummular Eczema: An Updated Review
Recent Patents on Inflammation & Allergy Drug Discovery Sirtuins: Common Targets in Aging and in Neurodegeneration
Current Drug Targets