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논문 기본 정보

자료유형
학술저널
저자정보
Jakob Starup-Linde (Aarhus University Hospital) Katrine Hygum (Aarhus University Hospital) Bente Lomholt Langdahl (Department of Endocrinology and Internal Medicine Aarhus University Hospital)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.33 No.3
발행연도
2018.1
수록면
339 - 351 (13page)

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초록· 키워드

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Type 2 diabetes (T2D) is associated with an increased risk of fracture, which has been reported in several epidemiological studies. However, bone mineral density in T2D is increased and underestimates the fracture risk. Common risk factors for fracture do notfully explain the increased fracture risk observed in patients with T2D. We propose that the pathogenesis of increased fracture risk inT2D is due to low bone turnover caused by osteocyte dysfunction resulting in bone microcracks and fractures. Increased levels ofsclerostin may mediate the low bone turnover and may be a novel marker of increased fracture risk, although further research isneeded. An impaired incretin response in T2D may also affect bone turnover. Accumulation of advanced glycosylation endproductsmay also impair bone strength. Concerning antidiabetic medication, the glitazones are detrimental to bone health and associated withincreased fracture risk, and the sulphonylureas may increase fracture risk by causing hypoglycemia. So far, the results on the effectof other antidiabetics are ambiguous. No specific guideline for the management of bone disease in T2D is available and current evidenceon the effects of antiosteoporotic medication in T2D is sparse. The aim of this review is to collate current evidence of thepathogenesis, detection and treatment of diabetic bone disease.

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