神経性やせ症と骨・カルシウム代謝

Body weight and bone/calcium metabolism. Bone and calcium metabolism in anorexia nervosa.

　骨密度の低下や骨粗鬆症は神経性やせ症の主要な合併症であり，後遺症になる。カルシウム摂取量は低下し，84％がビタミンD不足・欠乏している。骨代謝は体重依存性の骨形成の低下と骨吸収の亢進で，30％がビタミンK不足で骨質も劣化している。腰椎骨密度低下の最大の危険因子は低体重期間であり，有効な予防と治療は体重増加である。しかし，患者は容易に体重増加を受け入れないので，薬物療法が必要になる。0.5μg/日の活性型ビタミンD3や30～45 mg/日のビタミンK2製剤（メナテトレノン）が超低体重患者の骨密度の低下を阻止し，エルデカルシトール0.5μg/日は初年度約５％の腰椎骨密度の増加作用を示す。ビスホスホネートや抗RANKL阻害剤デノスマブは若年者や妊娠を希望する患者には使用しない。

　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.