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RISS 인기검색어
- 검색키워드
- 저자 : Bente Lomholt Langdahl (검색결과 2 건)
- 무료
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Treatment of Osteoporosis: Unmet Needs and Emerging Solutions
Bente Lomholt Langdahl,Jane Dahl Andersen 대한골대사학회 2018 대한골대사학회지 Vol.25 No.3
Efficient therapies are available for the treatment of osteoporosis, however, there are still unmet needs. Anti-resorptive therapies only increase bone mineral density to a certain extent and reduce the risk of non-vertebral fractures by 20%, only one anabolic option is available in most parts of the world –the effect of which levels off over time, and the evidence for combination therapy targeting both resorption and formation is limited. In addition, identification and treatment of patients with high and imminent fracture risk following a recent fracture and long-term adherence to treatment are 2 other very prominent challenges to the management of osteoporosis. The current review will focus on emerging osteoporosis treatments and optimized use of the existing treatments that may help overcome the currently unmet needs in the management of osteoporosis.
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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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