体重和骨/钙代谢。神经性厌食症的骨钙代谢[j]。

Clinical calcium Pub Date : 2018-01-01 DOI:CliCa1807979986
Mari Hotta
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摘要

骨质疏松症是神经性厌食症的主要并发症之一。他们的钙摄入量减少,84%的人缺乏维生素d。严重消瘦的神经性厌食症患者的骨代谢异常包括骨形成减少和骨吸收增加。腰椎骨密度(BMD)的年变化与入组时的身体质量指数(BMI)有显著相关。BMD阳性增加的临界BMI为16.4±0.3 kg/m2。由于30%的患者缺乏维生素K,他们的骨骼质量恶化。当血清中胰岛素样生长因子Ⅰ(一种强效成骨因子)和雌二醇(一种强效骨吸收抑制剂)水平下降时,腰椎骨密度下降的危险因素是持续的消瘦。因此,预防和治疗是体重增加。然而,患者并不能轻易接受体重增加。活性形式的维生素D3 0.5μg/天或30-45 mg/天的维生素K2制剂防止骨密度进一步下降。依地骨糖醇0.5μg/d,第一年腰椎骨密度增加约5%。双膦酸盐和RANK配体抑制剂,denosumab不应用于年轻患者和希望怀孕的妇女。
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[Body weight and bone/calcium metabolism. Bone and calcium metabolism in anorexia nervosa.]

Osteoporosis is one of chief complications of anorexia nervosa. Their calcium intake decreases and 84%are lack of vitamin D. The abnormal bone metabolism in severely emaciated patients with anorexia nervosa involves both a reduction in bone formation and an increase in bone resorption. The annual change in lumbar bone mineral density(BMD)is significantly correlated with body mass index(BMI)at the entry. The critical BMI for a positive increase in BMD was 16.4±0.3 kg/m2. Since 30%of patients are lack of vitamin K, their bone quality deteriorates. The risk factors of a decrease in lumbar vertebrae BMD is a duration of emaciation when both serum levels of insulin-like growth factor-Ⅰ as a potent osteogenic factor and estradiol as a powerful bone resorption inhibitor decrease. Therefore, the prevention and the treatment are weight gain. However, the patient does not accept weight gain easily. Active form vitamin D3 of 0.5μg/day or 30-45 mg/day of vitamin K2 preparation prevents the further decrease in bone mineral density. Eldecalcitol of 0.5μg/day shows about 5%increase in lumbar vertebrae BMD in first year. Bisphosphonate and a RANK ligand inhibitors, denosumab should not be used for young patients and women in hope of the pregnancy.

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