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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

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Volume 24, Issue 9-10 (Oct 2011)

Issues

Changes in plasma FGF23 in growth hormone deficient children during rhGH therapy

James Gardner
  • Department of Pediatrics, Division of Pediatric Endocrinology, University of Alabama at Birmingham School of Medicine, Birmingham, AL, USA
  • Children’s of Alabama, Birmingham, AL, USA
  • Email
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Ambika Ashraf
  • Department of Pediatrics, Division of Pediatric Endocrinology, University of Alabama at Birmingham School of Medicine, Birmingham, AL, USA
  • Children’s of Alabama, Birmingham, AL, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Zhiying You
  • Department of Medicine, Division of Preventive Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, AL, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Kenneth McCormick
  • Department of Pediatrics, Division of Pediatric Endocrinology, University of Alabama at Birmingham School of Medicine, Birmingham, AL, USA
  • Children’s of Alabama, Birmingham, AL, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2011-08-11 | DOI: https://doi.org/10.1515/JPEM.2011.301

Abstract

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.

Keywords: childhood; fibroblast growth factor 23; GH deficiency; phospho-calcium metabolism; recombinant human growth hormone

About the article

Corresponding author: James Gardner, Jr, MD, FAAP, 1601 4th Avenue South, CPP 230 Birmingham, AL 35209, USA Phone: +1 205 939-9107, Fax: +1 205 939-9821


Received: 2011-06-07

Accepted: 2011-06-18

Published Online: 2011-08-11

Published in Print: 2011-10-01


Citation Information: Journal of Pediatric Endocrinology and Metabolism, ISSN (Online) 2191-0251, ISSN (Print) 0334-018X, DOI: https://doi.org/10.1515/JPEM.2011.301.

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