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Updated: Oct 14, 2025
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Analysis of Minerals Produced by hFOB 1.19 and Saos-2 Cells Using Transmission Electron Microscopy with Energy Dispersive X-ray Microanalysis
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FGF23 and Hypophosphatemic Rickets/Osteomalacia
Yuichi Takashi1, Daiji Kawanami1, Seiji Fukumoto2
1Department of Endocrinology and Diabetes Mellitus, Fukuoka University School of Medicine, Fukuoka, Japan.
Current Osteoporosis Reports
|November 10, 2021
Summary
X-linked hypophosphatemia and tumor-induced osteomalacia involve impaired phosphate reabsorption due to excess FGF23. New treatments targeting FGF23 show promise, but long-term effects require further study.
Area of Science:
- Endocrinology
- Nephrology
- Genetics
Background:
- X-linked hypophosphatemia (XLH) and tumor-induced osteomalacia (TIO) are characterized by hypophosphatemia and defective renal phosphate handling.
- Current management for XLH and inoperable TIO involves phosphate and active vitamin D supplementation.
- Surgical tumor resection is the primary treatment for TIO.
Purpose of the Study:
- To review the pathogenesis of XLH and TIO.
- To discuss emerging therapeutic strategies for these conditions.
Main Methods:
- Literature review focusing on pathogenesis and treatment of XLH and TIO.
- Analysis of recent clinical findings on FGF23-targeting therapies.
Main Results:
- Elevated Fibroblast Growth Factor 23 (FGF23) production is a common pathogenic factor in XLH and TIO.
- Burosumab, an anti-FGF23 monoclonal antibody, is approved for certain hypophosphatemic diseases.
- The efficacy and indications for burosumab vary globally.
Conclusions:
- Targeting excessive FGF23 activity represents a novel therapeutic approach for hypophosphatemic disorders.
- Further research is essential to establish the long-term safety and efficacy of burosumab.
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