Impact of burosumab on kinetics of intact FGF23 values after the removal of a causative tumor in a patient with tumor-induced osteomalacia.

Tumor-induced osteomalacia (TIO) is a paraneoplastic syndrome caused by tumors secreting fibroblast growth factor 23 (FGF23). Burosumab, an anti-FGF23 antibody, is used for the management of TIO. However, burosumab therapy significantly elevates serum intact FGF23 levels, rendering preoperative systemic venous sampling unreliable. This report aims to evaluate the half-life of measured intact FGF23 in a TIO patient treated with burosumab and to elucidate its effect on the kinetics of intact FGF23 levels. A 13-yr-old female who had been receiving burosumab for TIO underwent wide excision of an FGF23-positive phosphaturic mesenchymal tumor located in the right distal femur. Burosumab was discontinued postoperatively, and intact FGF23 levels were measured sequentially at outpatient follow-ups. The half-life was calculated using a single-phase exponential decay model based on postoperative days and measured intact FGF23 levels. Although hypophosphatemia resolved following tumor removal, measured intact FGF23 levels remained high (44 300 pg/mL on postoperative day 1) but gradually declined and normalized (29.5 pg/mL on postoperative day 271). Based on these measurements, the half-life of measured intact FGF23 was calculated to be 20.2 d. This half-life is similar to that of burosumab itself, likely reflecting the presence of biologically inactive FGF23-burosumab complexes. In conclusion, the half-life of measured intact FGF23 following burosumab discontinuation is considerably longer than that reported in TIO patients not receiving burosumab, indicating that measured intact FGF23 levels should be interpreted with caution after discontinuation of burosumab.