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Published on: January 7, 2016
Changes in plasma FGF23 in growth hormone deficient children during rhGH therapy
James Gardner1, Ambika Ashraf, Zhiying You
1Department of Pediatrics, Division of Pediatric Endocrinology, University of Alabama at Birmingham School of Medicine, Birmingham, AL, USA. jgardner@peds.uab.edu
Insights
Children with growth hormone deficiency (GHD) show increased fibroblast growth factor 23 (FGF23) during therapy, despite higher phosphorus reabsorption. This suggests FGF23 may be a secondary response to growth hormone treatment.
Area of Science:
- Pediatric Endocrinology
- Mineral Metabolism
- Hormone Therapy
Background:
- Children with growth hormone deficiency (GHD) exhibit increased renal phosphorus reabsorption during recombinant human growth hormone (rhGH) therapy.
- Fibroblast growth factor 23 (FGF23) is a key regulator of serum phosphorus and may mediate this effect.
Purpose of the Study:
- To investigate changes in plasma C-terminal FGF23 (C-FGF23), mineral metabolism markers, and insulin-like growth factor 1 (IGF-1) during the first year of rhGH therapy in children with GHD.
- To compare these changes with normal stature children.
Main Methods:
- Prospective study involving children with GHD undergoing rhGH therapy.
- Measurement of plasma C-FGF23, TmP/GFR (renal phosphorus reabsorption), and IGF-1 levels at baseline and during the first year of therapy.
- Inclusion of normal stature children as baseline controls.
Main Results:
- GHD patients showed significantly increased C-FGF23 levels at follow-up points compared to baseline (p = 0.0005).
- Renal phosphorus reabsorption (TmP/GFR) also increased significantly during rhGH therapy (p = 0.002).
- The rise in C-FGF23 persisted after adjusting for several factors but was attenuated when adjusted for TmP/GFR or IGF-1.
Conclusions:
- Plasma C-FGF23 levels rise during rhGH therapy in children with GHD, contrary to expectations given FGF23's phosphaturic role and the observed increase in TmP/GFR.
- The increase in C-FGF23 may represent a secondary response to rhGH therapy rather than a direct cause of altered phosphorus reabsorption.
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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