We describe a unique case of hyperphosphatemia associated with a very high bone turnover rate in a 51-year-old postmenopausal woman with undiagnosed anorexia nervosa (AN) who presented with a low-trauma hip fracture. In view of her severely malnourished state, she was not fit for surgery. She was treated according to a refeeding protocol that mandated bed rest. Contrary to expectation, she developed sustained hyperphosphatemia and borderline hypercalcemia. Bone remodelling markers, both resorption and formation, were markedly elevated. Parathyroid hormone (PTH) was low-normal at 1.7 pmol/L, C-terminal fibroblast growth factor 23 (FGF23) was high at 293 RU/ml, but tubular maximum reabsorption of phosphate (TmPO4/GFR) was elevated at 1.93 mmol/L. Denosumab 60 mg was administered that was followed by: rapid normalisation of serum phosphate; normalisation of resorption markers, transient hypocalcaemia with secondary hyperparathyroidism, and normalisation of both TmPO4/GFR and C-terminal FGF23. We speculate that prolonged immobilization as part of AN management led to a high remodelling state followed by hyperphosphatemia and high-normal calcium with appropriate suppression of PTH and that marked hyperphosphatemia and high TmP/GFR despite high FGF23 indicates the necessity of PTH adequacy for excess FGF23 to lower TmP/GFR.

我们描述了一名患有未确诊的神经性厌食症 (AN) 的 51 岁绝经后女性，她因低创伤性髋部骨折就诊时发生高磷血症并伴有非常高的骨转换率。鉴于她严重的营养不良状况，她不适合进行手术。根据要求卧床休息的再喂养方案对她进行治疗。出乎意料的是，她出现了持续的高磷血症和临界性高钙血症。骨重塑标志物，包括再吸收和形成，均显着升高。甲状旁腺激素 (PTH) 低于正常水平，为 1.7 pmol/L，C 末端成纤维细胞生长因子 23 (FGF23) 高至 293 RU/ml，但肾小管最大磷酸盐重吸收 (TmPO4/GFR) 升高至 1.93 mmol/ L. 给予地诺单抗 60 mg，随后：血清磷酸盐快速正常化；再吸收标志物的正常化、继发性甲状旁腺功能亢进的短暂性低钙血症以及 TmPO4/GFR 和 C 末端 FGF23 的正常化。我们推测，作为 AN 管理的一部分，长期固定会导致高度重塑状态，然后是高磷血症和高正常钙，同时适当抑制 PTH，尽管 FGF23 高，但显着的高磷血症和高 TmP/GFR 表明 PTH 对过量 FGF23 的必要性降低 TmP/GFR。