SUN-727 Tumor-Induced Osteomalacia Complicated with Post-operative Hungry-Bone Syndrome and Delay Reduction of Fibroblast Growth Factor 23

Abstract Disclosure: H. Yeh: None. H. Nge: None. A. Ghimire: None. C.C. Gordner: None. Introduction: Tumor-induced osteomalacia (TIO), a rare paraneoplastic syndrome, develops when a tumor excessively produces fibroblast growth factor 23 (FGF23). Hypophosphatemia and low 1,25 (OH)2 vitamin D are the hallmark findings, along with bone pain, loss of bone mineral density, and debilitating myopathy. We present here a case of TIO complicated with hungry-bone syndrome (HBS) and delayed reduction of FGF23 following resection of the phosphaturic mesenchymal tumor (PMT). Case description: A 46-year-old male, with a history of cervical myelopathy, presented for metabolic bone disease evaluation. He had osteoporosis along with fatigue, myalgia, muscle weakness requiring a walker for ambulation, and 100 lb unintentional weight loss. Labwork revealed hypophosphatemia 1.6 mg/dL (2.5-4.5 mg/dL), elevated PTH 141 pg/mL (16-77 pg/mL), elevated alkaline phosphatase (ALKP) 197 U/L (36-130 U/L), low 1,25(OH)2 vitamin D 16 pg/mL (18-70 pg/mL), and elevated FGF23 356 RU/mL (<180 RU/mL). Phosphate supplements, calcitriol, and Burosumab were started with partial improvement. FDG-PET CT scan and octreotide scan showed a tumor with uptake in the left lateral 3rd rib. A 2 cm tumor was resected, and the histopathology showed a PMT with positive FGF23 mRNA expression. Postoperative blood tests revealed hypocalcemia 7.7 mg/dL (8.6-10.3 mg/dL), elevated ALKP 266 U/L (36-130 U/L), markedly elevated C-telopeptide 2981 pg/mL (60-700 pg/mL), and persistent elevated PTH 253 pg/mL (16-77 pg/mL) requiring calcium and vitamin D3 supplementation. The FGF23 level was persistently elevated for 6 months after tumor resection despite normalization of phosphorous levels 5.2 mg/dL (2.5-4.5 mg/dL). Discussion: Our patient developed HBS post-operatively as evidenced by post-operative hypocalcemia with persistent secondary HPT and elevated ALKP for 6 months after tumor resection despite aggressive calcium and vitamin D3 supplementation. The mechanism was thought to result from rapid mineralization of the bone from increased phosphate availability due to rapid decline in FGF23 concentrations. Close monitoring for hypocalcemia after PMT resection is warranted in addition to monitoring of ALKP and PTH levels. Our patient also had persistently elevated FGF23 levels for 6 months after tumor resection, thought to be secondary to Burosumab. Burosumab is a monoclonal antibody that binds FGF23 and inhibits FGF23 biological activity. It is known to interfere with the measurement of FGF23 levels leading to anomalously high C-terminal fragment results and has a prolonged elimination half-life of 19 days. Persistent elevation in FGF23 levels should be expected if patients with TIO have received Burosumab preoperatively. Presentation: Sunday, July 13, 2025