The authors have no conflict of interest.
Fibroblast Growth Factor-23 Is Regulated by 1α,25-Dihydroxyvitamin D†
Version of Record online: 18 JUL 2005
Copyright © 2005 ASBMR
Journal of Bone and Mineral Research
Volume 20, Issue 11, pages 1944–1950, November 2005
How to Cite
Collins, M. T., Lindsay, J. R., Jain, A., Kelly, M. H., Cutler, C. M., Weinstein, L. S., Liu, J., Fedarko, N. S. and Winer, K. K. (2005), Fibroblast Growth Factor-23 Is Regulated by 1α,25-Dihydroxyvitamin D. J Bone Miner Res, 20: 1944–1950. doi: 10.1359/JBMR.050718
- Issue online: 4 DEC 2009
- Version of Record online: 18 JUL 2005
- Manuscript Accepted: 13 JUL 2005
- Manuscript Revised: 8 JUN 2005
- Manuscript Received: 8 MAR 2005
- fibroblast growth factor-23;
- fibrous dysplasia;
- McCune-Albright syndrome;
- vitamin D;
Serum FGF-23 regulation was studied in patients with hypoparathyroidism or pseudohypoparathyroidism treated with calcitriol. Serum FGF-23 levels changed in parallel in response to changes in serum 1,25-D, suggesting that FGF-23 may be regulated by 1,25-D. In addition, the phosphaturic effect of FGF-23 may be diminished in the absence of PTH action on the kidney.
Introduction: Fibroblast growth factor (FGF)-23 is a recently described hormone that has been shown to be involved in the regulation of phosphate and vitamin D metabolism. The physiologic role of FGF-23 in mineral metabolism and how serum FGF-23 levels are regulated have yet to be elucidated. Three patients with mineral metabolism defects that allowed for the investigation of the regulation of FGF-23 were studied.
Materials and Methods: Patient 1 had postsurgical hypoparathyroidism and Munchausen's syndrome and consumed a pharmacologic dose of calcitriol. Patient 2 had postsurgical hypoparathyroidism and fibrous dysplasia of bone. She was treated with increasing doses of calcitriol followed by synthetic PTH(1–34). Patient 3 had pseudohypoparathyroidism type 1B and tertiary hyperparathyroidism. She underwent parathyroidectomy, which was followed by the development of hungry bone syndrome and hypocalcemia, requiring treatment with calcitriol. Serum FGF-23 and serum and urine levels of mineral metabolites were measured in all three patients.
Results: Patient 1 had an acute and marked increase in serum FGF-23 (70 to 670 RU/ml; normal range, 18–108 RU/ml) within 24 h in response to high-dose calcitriol administration. Patient 2 showed stepwise increases in serum FGF-23 from 117 to 824 RU/ml in response to increasing serum levels of 1α,25-dihydroxyvitamin D (1,25-D). Finally, before parathyroidectomy, while hypercalcemic, euphosphatemic, with low levels of 1,25-D (10 pg/ml; normal range, 22–67 pg/ml), and with very high serum PTH (863.7 pg/ml; normal range, 6.0–40.0 pg/ml), patient 3 had high serum FGF-23 levels (217 RU/ml). After surgery, while hypocalcemic, euphosphatemic, and with high serum levels of serum 1,25-D (140 pg/ml), FGF-23 levels were higher than preoperative levels (305 RU/ml). It seemed that the phosphaturic effect of FGF-23 was diminished in the absence of PTH or a PTH effect.
Conclusions: Serum FGF-23 may be regulated by serum 1,25-D, and its phosphaturic effect may be less in the absence of PTH.