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Special Features: Whitney W. Brown, Harald Jüppner, Craig B. Langman, Heather Price, Emily G. Farrow, Kenneth E. White, and Kenneth L. McCormick Hypophosphatemia with Elevations in Serum Fibroblast Growth Factor 23 in a Child with Jansen’s Metaphyseal Chondrodysplasia J Clin Endocrinol Metab 2009; 94: 17-20 [Abstract] [Full text] [PDF]

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FGF-23 and PTH secretion

Yair Liel   (12 March 2009)

FGF-23 and PTH secretion 12 March 2009
Yair Liel, Endocrinologist Soroka University Medical Center, Beer-Sheva, Israel Send letter to journal: Re: FGF-23 and PTH secretion liel{at}bgu.ac.il Yair Liel	In their discussion, the authors suggest that FGF-23 could play a role in PTH suppression in patients with Jansen's metaphyseal chondrodysplasia, and support this hypothesis with observations that FGF-23 was shown to suppress parathyroid activity in rats and to inhibit PTH secretion from bovine parathyroid cells. However, it should be noted that in patients with oncogenic osteomalacia, associated with elevated concentrations of FGF-23, basal PTH levels were observed to be normal, or even elevated, and were further increased upon phosphate treatment (1-3). These clinical observations raise some doubt on the proposed role for FGF-23 in PTH suppression in patients with Jansen’s metaphyseal chondrodysplasia. References 1. Wilkins GE, Granleese S, Hegele RG, Holden J, Anderson DW, Bondy GP. Oncogenic osteomalacia: evidence for a humoral phosphaturic factor. J Clin Endocrinol Metab. 1995;80:1628-1634. 2. Yang IM, Park YK, Hyun YJ et al. Oncogenic osteomalacia caused by a phosphaturic mesenchymal tumor of the oral cavity: a case report. Korean J Intern Med. 1997;12:89-95. 3. Seijas R, Ares O, Sierra J, Perez-Dominguez M. Oncogenic osteomalacia: two case reports with surprisingly different outcomes. Arch Orthop Trauma Surg. [early online publication] 2009.