Abstract
Glucocorticoid administration is the most common cause of secondary osteoporosis and the leading cause of nontraumatic osteonecrosis. In patients receiving long-term therapy, glucocorticoids induce fractures in 30% to 50% and osteonecrosis in 9% to 40%. This article reviews glucocorticoid-induced osteoporosis and osteonecrosis, addressing the risk factors, pathogenesis, evaluation, treatment, and uncertainties in the clinical management of these disorders.
Published by Elsevier Inc.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Antibodies, Monoclonal, Humanized / pharmacology
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Antibodies, Monoclonal, Humanized / therapeutic use
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Apoptosis / drug effects
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Bone Density Conservation Agents / pharmacology
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Bone Density Conservation Agents / therapeutic use
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Bone and Bones / drug effects*
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Bone and Bones / metabolism
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Denosumab
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Diphosphonates / pharmacology
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Diphosphonates / therapeutic use
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Drug Monitoring
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Female
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Glucocorticoids / adverse effects*
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Humans
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Male
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Osteoblasts / drug effects
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Osteoblasts / metabolism
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Osteocytes / drug effects
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Osteocytes / metabolism
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Osteonecrosis / chemically induced*
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Osteonecrosis / drug therapy
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Osteonecrosis / physiopathology
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Osteoporosis / chemically induced*
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Osteoporosis / drug therapy
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Osteoporosis / physiopathology
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Osteoporotic Fractures / etiology
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Osteoporotic Fractures / prevention & control
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Teriparatide / pharmacology
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Teriparatide / therapeutic use
Substances
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Antibodies, Monoclonal, Humanized
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Bone Density Conservation Agents
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Diphosphonates
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Glucocorticoids
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Teriparatide
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Denosumab