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Normal FGF23 levels in adult idiopathic phosphate diabetes.
M Laroche1, J F Boyer, H Jahafar
1Service de Rhumatologie, CHU Rangueil, Toulouse, France. laroche.m@chu-toulouse.fr
Calcified Tissue International
|January 17, 2009
Summary
Fibroblast growth factor 23 (FGF23) does not appear to cause idiopathic phosphate diabetes (IPD). However, FGF23 levels are lower in IPD patients with osteopenia or osteoporosis, suggesting a role in bone health.
Area of Science:
- Endocrinology
- Metabolic Bone Disease
- Mineral Metabolism
Background:
- Fibroblast growth factor 23 (FGF23) regulates phosphate metabolism and is implicated in phosphate diabetes.
- Idiopathic phosphate diabetes (IPD) can lead to osteoporosis and diffuse pain.
Purpose of the Study:
- To investigate the role of FGF23 in the pathogenesis of idiopathic phosphate diabetes (IPD).
Main Methods:
- Assessed FGF23, serum phosphate, 1-25(OH)2D3, and parathyroid hormone in 29 IPD patients and 15 controls.
- Measured bone mineral density (BMD) and evaluated phosphate reabsorption.
- Correlated FGF23 levels with phosphate and 1-25(OH)2D3 levels.
Main Results:
- IPD patients had lower serum phosphate than controls, but FGF23 levels were similar.
- FGF23 levels were significantly lower in IPD patients with osteopenia/osteoporosis compared to those with normal bone status.
- Serum phosphate levels were comparable between IPD patients with normal bone status and those with osteopenia/osteoporosis.
- Positive correlation between serum phosphate and FGF23; negative correlation between FGF23 and 1-25(OH)2D3.
Conclusions:
- FGF23 does not appear to be the primary cause of IPD.
- The FGF23/phosphate/1-25(OH)2D3 axis remains functional in IPD patients.
- Decreased FGF23 may be associated with bone loss in IPD.
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