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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Tumor-induced osteomalacia (TIO) is a rare paraneoplastic disorder caused by excess FGF23 secretion, leading to renal phosphate wasting, hypophosphatemia, and defective bone mineralization. Patients present with bone pain, muscle weakness, and fractures, and the diagnosis is often delayed due to nonspecific symptoms
A 22-year-old male presented with persistent hypophosphatemia and a history of a biopsy-confirmed giant cell tumor of the right femur with secondary aneurysmal bone cyst changes, diagnosed in February 2025. He reported progressive lower back pain radiating to the right leg for two years, initially managed as lumbar sciatica. MRI revealed an L5–S1 disc extrusion, and femoral imaging demonstrated a multiloculated lytic lesion consistent with a giant cell tumor.
Denosumab therapy was initiated in March 2025; however, after the second dose, the patient developed recurrent symptomatic hypophosphatemia, requiring frequent outpatient phosphate replacement and hospitalization. Surgical excision of the tumor was subsequently performed, but hypophosphatemia persisted, with serum phosphorus <2.0 mg/dL, elevated parathyroid hormone, low calcium, and low 25-hydroxyvitamin D levels. He was then referred to nephrology due to persistently low symptomatic phosphate levels.
Further laboratory evaluation revealed elevated FGF23 at 66RU/ml (normal range <22 RU/mL), increased fractional phosphate excretion (19.6%), and low TmP/GFR, indicating renal phosphate wasting and confirming the diagnosis of tumor-induced osteomalacia (TIO). The patient was treated with phosphate, calcium, and vitamin D supplementation. Despite of weekly phosphate infusions , pt was frequently admitted to hospital with symptomatic hypophosphatemia
Burosumab, a monoclonal antibody that binds to and inhibits excess FGF23 activity, thereby restoring renal phosphate reabsorption and normalizing serum phosphate levels, was subsequently initiated to correct the patient’s persistent hypophosphatemia. After the first dose, serum phosphate increased to 4.5 mg/dL within one week, allowing discontinuation of phosphate infusions. Following the second dose, phosphate levels remained stable within the normal range (3.6 mg/dL), eliminating the need for further supplementation.
This case underscores the importance of recognizing tumor-induced osteomalacia (TIO) as a potential cause of persistent hypophosphatemia, even after surgical resection of the tumor. It highlights the diagnostic challenge due to overlapping symptoms with common musculoskeletal conditions and the critical role of biochemical evaluation, particularly FGF23 measurement, in establishing the diagnosis. Burosumab proved to be an effective therapeutic option in correcting the phosphate imbalance and maintaining normal serum phosphate levels, thereby reducing the need for ongoing supplementation. Early recognition and a multidisciplinary approach involving nephrology, oncology, orthopedics, and endocrinology are essential for timely diagnosis, effective management, and improved patient outcomes.
