Journal of Pediatric Endocrinology and Metabolism
Editor-in-Chief: Kiess, Wieland
Ed. by Bereket, Abdullah / Darendeliler, Feyza / Dattani, Mehul / Gustafsson, Jan / Luo, Feihong / Mericq, Veronica / Roth, Christian / Toppari, Jorma
Editorial Board: Battelino, Tadej / Buyukgebiz, Atilla / Cassorla, Fernando / Chrousos, George P. / Cutfield, Wayne / Fideleff, Hugo L. / Hershkovitz, Eli / Hiort, Olaf / LaFranchi, Stephen H. / Lanes M. D., Roberto / Mohn, Angelika / Root, Allen W. / Rosenfeld, Ron G. / Werther, George / Zadik, Zvi
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Changes in plasma FGF23 in growth hormone deficient children during rhGH therapy
Background: Children with growth hormone deficiency (GHD) have increased renal phosphorus reabsorption during rhGH therapy, Fibroblast growth factor 23 (FGF23) is a known regulator of serum phosphorus and may be responsible for this effect.
Methods: Prospective study in GHD children investigating changes in plasma C-terminal FGF23 (C-FGF23), markers of mineral metabolism, and insulin-like growth factor (IGF-1) in the first year of rhGH therapy. Normal stature children served as baseline controls.
Results: The two groups at baseline were similar, except GHD patients had lower baseline TmP/GFR vs. controls (p<0.05). C-FGF23 in GHD patients trended upward at follow-up 1 (p=0.058) and significantly increased at follow-up 2 (p=0.0005) compared to baseline. TmP/GFR also rose at follow-up 1 (p=0.002) and follow-up 2 (p=0.027). The C-FGF23 rise persisted after adjusting for age, gender, sex, total calcium, and phosphorus (p<0.01) but attenuated after adjusting for TmP/GFR or IGF-1.
Conclusions: C-FGF23 rises during rhGH therapy in spite of increased Tmp/GFR, an unanticipated observation given the role of FGF23 as a phosphaturic factor. The C-FGF23 rise may be a secondary response during rhGH therapy.
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