SUN-798 - Avascular Necrosis Unmasks Tumor Induced Osteomalacia

Tumor-induced osteomalacia (TIO) is a paraneoplastic syndrome caused by small, benign mesenchymal tumors involving bone or soft tissue that overproduce fibroblast growth factor 23 (FGF23), resulting in renal phosphate wasting, reduced 1α-hydroxylation of vitamin D, hypophosphatemia, and osteomalacia. In this case report, we present a 65-year-old male with avascular necrosis (AVN) as the initial finding leading to the diagnosis of TIO. The patient reported a four-year history of fatigue, generalized weakness, and chronic bilateral leg pain. He presented to the emergency department (ED) with worsening right hip pain. Initial laboratory evaluation revealed low phosphorous at 1.8 mg/dL (normal 2.3-4.4 mg/dL), elevated alkaline phosphatase at 199 U/L (normal 37-136 U/L), elevated PTH at 126 (normal 8.0- 72 pg/dL), normal calcium at 9.3 mg/dL (normal 8.5-10.5 mg/dL) and normal 25-hydroxyvitamin D at 37 ng/mL (normal 30-100 ng/mL). X-ray demonstrated a right femoral neck fracture, and MRI confirmed a chronic right proximal femur fracture and more importantly AVN of the left hip. Due to persistent hypophosphatemia and bone symptoms, FGF23 was measured and markedly elevated at 246 pg/mL (reference range < 59 pg/mL). Whole-body PET/CT imaging did not identify a tumor. The patient was started on burosumab-twza, a FGF-23 blocking antibody. AVN may be misattributed to a primary orthopedic condition, and this case highlights the importance of recognizing TIO, which remains frequently underdiagnosed.

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