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Update on Glucocorticoid Induced Osteoporosis

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dc.contributor.authorCho, Soo-Kyung-
dc.contributor.authorSung, Yoon-Kyoung-
dc.date.accessioned2022-07-06T17:16:58Z-
dc.date.available2022-07-06T17:16:58Z-
dc.date.created2021-08-25-
dc.date.issued2021-06-
dc.identifier.issn2093-596X-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/141720-
dc.description.abstractGlucocorticoids are used to treat many autoimmune and inflammatory diseases. However, an adverse systemic effect is a deleterious effect on bone, which may lead to glucocorticoid-induced osteoporosis, characterized by a rapid and transient increase in bone resorption and fracture risk, which may increase rapidly within 3 months of commencing oral glucocorticoids. Therefore, early risk assessment and intervention are crucial for preventing fractures in patients receiving glucocorticoids. Recent practice guidelines recommend an assessment for fracture risk in patients beginning or receiving glucocorticoids for more than 3 months, and they have suggested fracture risk assessment tool values for identifying patients who need preventive treatment. Bisphosphonates are currently the recommended first-line therapy for the prevention and treatment of glucocorticoid-induced osteoporosis. These have been shown to increase the bone mineral density in the spine and hip and to decrease the incidence of vertebral fractures. Recently, a more potent antiresorptive agent, denosumab, has been shown to increase the bone density in patients receiving glucocorticoids. Teriparatide has been shown to have a preventive effect on vertebral fractures, but not on nonvertebral fractures. In this article we aimed to providean update on glucocorticoid-induced osteoporosis by focusing on the assessment of its risk and treatment options.-
dc.language영어-
dc.language.isoen-
dc.publisher대한내분비학회-
dc.titleUpdate on Glucocorticoid Induced Osteoporosis-
dc.typeArticle-
dc.contributor.affiliatedAuthorCho, Soo-Kyung-
dc.contributor.affiliatedAuthorSung, Yoon-Kyoung-
dc.identifier.doi10.3803/EnM.2021.1021-
dc.identifier.scopusid2-s2.0-85109671726-
dc.identifier.wosid000668158300007-
dc.identifier.bibliographicCitationEndocrinology and Metabolism, v.36, no.3, pp.536 - 543-
dc.relation.isPartOfEndocrinology and Metabolism-
dc.citation.titleEndocrinology and Metabolism-
dc.citation.volume36-
dc.citation.number3-
dc.citation.startPage536-
dc.citation.endPage543-
dc.type.rimsART-
dc.identifier.kciidART002728697-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaEndocrinology & Metabolism-
dc.relation.journalWebOfScienceCategoryEndocrinology & Metabolism-
dc.subject.keywordPlusCLINICAL-PRACTICE GUIDELINES-
dc.subject.keywordPlusFRACTURE RISK-
dc.subject.keywordPlusPOSTMENOPAUSAL WOMEN-
dc.subject.keywordPlusDOUBLE-BLIND-
dc.subject.keywordPlusRHEUMATOID-ARTHRITIS-
dc.subject.keywordPlusORAL CORTICOSTEROIDS-
dc.subject.keywordPlusVERTEBRAL FRACTURES-
dc.subject.keywordPlusBONE LOSS-
dc.subject.keywordPlusPREVENTION-
dc.subject.keywordPlusMANAGEMENT-
dc.subject.keywordAuthorGlucocorticoids-
dc.subject.keywordAuthorOsteoporosis-
dc.subject.keywordAuthorTherapeutics-
dc.identifier.urlhttps://www.e-enm.org/journal/view.php?doi=10.3803/EnM.2021.1021-
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