# Preoperative Burosumab With Delayed FGF23 Recovery and High Postoperative Bone Turnover in Tumor-Induced Osteomalacia

## TL;DR

A patient with tumor-induced osteomalacia received preoperative burosumab, leading to prolonged FGF23 elevation and high bone turnover after surgery.

## Contribution

Highlights the prolonged FGF23 elevation and bone turnover after PMT resection in patients treated with preoperative burosumab.

## Key findings

- Burosumab can cause prolonged FGF23 elevation for months post-surgery.
- Postoperative patients may experience high bone turnover similar to hungry bone syndrome.
- Alternative biochemical markers are needed for monitoring recovery after burosumab use.

## Abstract

Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by the overproduction of fibroblast growth factor 23 (FGF23) from phosphaturic mesenchymal tumors (PMTs). Clinical features include skeletal deformities, bone mineral density (BMD) loss, and debilitating myopathy. Hypophosphatemia and low 1,25(OH)2D levels are hallmark biochemical findings. We report a 46-year-old man with delayed tumor localization who received preoperative burosumab. Postoperatively, he developed transient mild hypocalcemia, persistently elevated alkaline phosphatase and parathyroid hormone, and prolonged FGF23 elevation for 6 months despite normalized serum phosphate and improved BMD. Burosumab can interfere with FGF23 assays and may cause extremely high in vivo FGF23 values for months. Alternative biochemical markers should be pursued postoperatively in patients who received burosumab before surgery. A high bone turnover state resembling hungry bone syndrome may occur after PMT resection. Awareness of these postoperative biochemical changes and the effects of burosumab on FGF23 assays is essential for monitoring TIO recovery.