Bone mineral density gains with a second 12-month course of romosozumab therapy following placebo or denosumab.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: DLK has been an investigator for Amgen, Astellas, AstraZeneca, and Eli Lilly; a speaker and consultant for Amgen, Pfizer, and Eli Lilly; and a member of a drug safety advisory board for Merck. HGB has been an investigator for Amgen, Merck, and Shire; a consultant for Amgen, Merck, Radius Health, and Shire; a speaker for Amgen, Radius Health, and Shire; and a member of a data/safety monitoring board for Grünenthal. FM has no disclosures. EG has been a speaker for Amgen and Takeda, and an advisory board member for UCB and Alexion. SP has been an investigator for Pfizer, Amgen, Gedeon Richter, and Exeltis; a speaker for Bayer Schering, Novo Nordisk, Servier, Pfizer, MSD, Gedeon Richter, ProCare Health, Shionogi, and Teva; and an advisory board member for Novo Nordisk, Gedeon Richter, ProCare Health, and Shionogi. JM and RVD are employees of and hold stock in Amgen. CY was an employee of Amgen at the time of the study and may hold stock in Amgen, and is currently an employee of Cambridge Statistics Ltd. and holds stock in Cambridge Statistics Ltd. SY was an employee of Amgen at the time of the study and may hold stock in Amgen, and is currently an employee of Atara Biotherapeutics and holds stock in Atara Biotherapeutics. CL is an employee of and holds stock in UCB Pharma. AG was an employee of Amgen at the time of the study and may hold stock in Amgen, and is currently an employee of Corcept Therapeutics and holds stock options in Corcept Therapeutics. 19. Curr Opin Endocrinol Diabetes Obes. 2007 Dec;14(6):446-50. doi: 10.1097/MED.0b013e3282f15407. Glucocorticoid-induced osteoporosis. Berris KK(1), Repp AL, Kleerekoper M. Author information: (1)Department of Internal Medicine, Wayne State University, Detroit, Michigan, USA. PURPOSE OF REVIEW: To present an overview of the peer-reviewed literature relating to glucocorticoid-induced osteoporosis that has been published since January 2006. RECENT FINDINGS: Understanding the pathophysiology of bone loss resulting from glucocorticoid use has become clearer. The role of the receptor-activated nuclear factor kappaB-ligand-osteoprotogerin system has been clarified and will likely lead to better targeted therapies. Minimal trauma fractures occur in patients treated with glucocorticoids at higher bone mineral density than is seen with other primary or secondary causes of osteoporosis. Uncertainty still remains about the lowest dose of glucocorticoids that is not associated with bone loss. Bisphosphonates remain the treatment of choice for glucocorticoid-induced osteoporosis, but despite this effective therapy the disease remains under recognized and undertreated. SUMMARY: Glucocorticoid-induced osteoporosis is a leading cause of secondary osteoporosis, one of the more devastating consequences of glucocorticoid therapy. Bone mineral density underestimates the risk of fragility fractures in glucocorticoid-induced osteoporosis, which may account for the underrecognition and undertreatment of the disease prior to fracture. DOI: 10.1097/MED.0b013e3282f15407