von Brackel Felix N, Grambeck Jonathan, Barvencik Florian, Amling Michael, Oheim Ralf
Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Lottestrasse 59, 22529 Hamburg, Germany.
JBMR Plus. 2024 Nov 9;8(12):ziae139. doi: 10.1093/jbmrpl/ziae139. eCollection 2024 Dec.
Iron deficiency anemia is treated by iron supplementation. Increasing evidence has shown that the carbohydrate components in iron infusions can cause hypophosphatemia and subsequent osteomalacia due to excess intact fibroblast growth factor 23 (iFGF23). We here undertook an in-depth characterization of 13 patients with iron infusion-induced osteomalacia (IIIO). Patients were characterized (monocentric institutional practice) by means of laboratory, bone density, HR-pQCT, and virtual osteoid volume estimation. We additionally report a patient who was treated with burosumab because iron infusions had to be continued despite osteomalacia. All 13 patients received ferric carboxymaltose (FCM) infusions and presented with low phosphate levels. Stopping the FCM infusions and supportive treatment by substitution of phosphate, calcium, native, and/or active Vitamin D was the chosen therapeutic approach. Pain, mobility, and biochemical data, such as serum phosphate levels, BMD, bone microstructure, and virtual osteoid volume, were the main outcome measures. Our results indicate biochemical normalization (eg, phosphate levels pre: 0.50 mmol/L ± 0.23 mmol/L, post: 0.93 mmol/L ± 0.32 mmol/L, <.001) after stopping the FCM infusion and establishing supportive treatment. Additionally, pain levels on the visual analog scale (VAS) decreased (VAS 7.31 ± 1.22, VAS 2.73 ± 1.27, <.0001) and areal BMD (expressed by T-score) improved significantly (T-score: -1.85 ± 1.84, T-score: -0.91 ± 2.13, <.05). One patient requiring ongoing FCM infusions experienced significant additional benefits from burosumab treatment. In conclusion, our results highlight the importance of monitoring phosphate in patients treated with FCM infusions. Stopping FCM infusions is effective in addressing the excess of iFGF23 and thereby phosphate wasting. Supportive therapy enables quick recovery of the musculoskeletal system and improves pain levels in these patients.
缺铁性贫血通过补充铁剂进行治疗。越来越多的证据表明，铁剂输注中的碳水化合物成分可因完整的成纤维细胞生长因子23（iFGF23）过量而导致低磷血症及随后的骨软化症。我们在此对13例铁剂输注所致骨软化症（IIIO）患者进行了深入研究。通过实验室检查、骨密度、高分辨率外周定量CT（HR-pQCT）和虚拟类骨质体积估计对患者进行特征分析（单中心机构实践）。我们还报告了1例患者，尽管患有骨软化症，但因必须继续进行铁剂输注而接受了布罗索尤单抗治疗。所有13例患者均接受了羧基麦芽糖铁（FCM）输注，且均出现低磷水平。停止FCM输注并通过补充磷酸盐、钙、天然和/或活性维生素D进行支持性治疗是所选择的治疗方法。疼痛、活动能力以及生化数据，如血清磷水平、骨密度、骨微结构和虚拟类骨质体积，是主要的结局指标。我们的结果表明，停止FCM输注并建立支持性治疗后，生化指标恢复正常（例如，磷水平：治疗前0.50 mmol/L±0.23 mmol/L，治疗后0.93 mmol/L±0.32 mmol/L，P<0.001）。此外，视觉模拟评分法（VAS）的疼痛水平降低（VAS：7.31±1.22，VAS：2.73±1.27，P<0.0001），且面积骨密度（以T值表示）显著改善（T值：-1.85±1.84，T值：-0.91±2.13，P<0.05）。1例需要持续进行FCM输注的患者从布罗索尤单抗治疗中获得了显著的额外益处。总之，我们的结果突出了在接受FCM输注治疗的患者中监测磷酸盐的重要性。停止FCM输注可有效解决iFGF23过量问题，从而减少磷酸盐流失。支持性治疗能够使这些患者的肌肉骨骼系统快速恢复并改善疼痛水平。
