Nomoto Hiroshi, Miyoshi Hideaki, Nakamura Akinobu, Nagai So, Kitao Naoyuki, Shimizu Chikara, Atsumi Tatsuya
Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University Division of Laboratory and Transfusion Medicine, Hokkaido University Hospital, Sapporo, Japan.
Medicine (Baltimore). 2017 Sep;96(39):e8147. doi: 10.1097/MD.0000000000008147.
Saccharated ferric oxide has been shown to lead to elevation of fibroblast growth factor 23, hypophosphatemia, and, consequently, osteomalacia. Moreover, mineral imbalance is often observed in patients with short-bowel syndrome to some degree.
A 62-year-old woman with short-bowel syndrome related with multiple resections of small intestines due to Crohn disease received regular intravenous administration of saccharated ferric oxide. Over the course of treatment, she was diagnosed with tetany, which was attributed to hypocalcemia. Additional assessments of the patient revealed not only hypocalcemia, but also hypophosphatemia, hypomagnesemia, osteomalacia, and a high concentration of fibroblast growth factor 23 (314 pg/mL).
We diagnosed her with mineral imbalance-induced osteomalacia due to saccharated ferric oxide and short-bowel syndrome.
Magnesium replacement therapy and discontinuation of saccharated ferric oxide alone.
These treatments were able to normalize her serum mineral levels and increase her bone mineral density.
This case suggests that adequate evaluation of serum minerals, including phosphate and magnesium, during saccharated ferric oxide administration may be necessary, especially in patients with short-bowel syndrome.
已证实含糖氧化铁可导致成纤维细胞生长因子23升高、低磷血症,进而引起骨软化症。此外,短肠综合征患者在一定程度上常出现矿物质失衡。
一名62岁女性,因克罗恩病接受多次小肠切除术后患有短肠综合征,定期静脉注射含糖氧化铁。在治疗过程中,她被诊断为手足搐搦症,归因于低钙血症。对该患者的进一步评估发现,不仅存在低钙血症,还伴有低磷血症、低镁血症、骨软化症以及高浓度的成纤维细胞生长因子23(314 pg/mL)。
我们诊断她为因含糖氧化铁和短肠综合征导致的矿物质失衡性骨软化症。
单独进行镁替代治疗并停用含糖氧化铁。
这些治疗使她的血清矿物质水平恢复正常,并提高了她的骨密度。
该病例表明,在使用含糖氧化铁期间,尤其是对于短肠综合征患者,可能有必要对包括磷酸盐和镁在内的血清矿物质进行充分评估。