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RISS 인기검색어
- 검색키워드
- 저자 : Jakob Starup-Linde (검색결과 2 건)
- 무료
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Skeletal Fragility in Type 2 Diabetes Mellitus
Jakob Starup-Linde,Katrine Hygum,Bente Lomholt Langdahl 대한내분비학회 2018 Endocrinology and metabolism Vol.33 No.3
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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Katrine Hygum,Jakob Starup-Linde,Langdahl 대한골다공증학회 2019 Osteoporosis and Sarcopenia Vol.5 No.2
Bone disease is a serious complication to diabetes. Patients with type 1 diabetes (T1D) and type 2 diabetes (T2D) suffer from an increased risk of fracture, most notably at the hip, compared with patients without diabetes. Confounders such as patient sex, age, body mass index, blood glucose status, fall risk, and diabetes medications may influence the fracture risk. Different underlying mechanisms contribute to bone disease in patients with diabetes. Bone quality is affected by low bone turnover in T1D and T2D, and furthermore, incorporation of advanced glycation end-products, changes in the incretin hormone response, and microvascular complications contribute to impaired bone quality and increased fracture risk. Diagnosis of bone disease in patients with diabetes is a challenge as current methods for fracture prediction such as bone mineral density T-score and fracture risk assessment tools underestimate fracture risk for patients with T1D and T2D. This review focuses on bone disease and fracture risk in patients with diabetes regarding epidemiology, underlying disease mechanisms, and diagnostic methods, and we also provide considerations regarding the management of diabetes patients with bone disease in terms of an intervention threshold and different treatments.
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