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Dynamics of bone turnover in children with GH deficiency treated with GH until final height
G I Baroncelli1, S Bertelloni, C Ceccarelli
1Endocrine Unit, Division of Pediatrics, Department of Reproductive Medicine and Pediatrics, University of Pisa, Pisa, Italy.
Insights
Children with growth hormone deficiency (GHD) show reduced bone turnover, which is stimulated by long-term growth hormone (GH) treatment. Bone markers do not predict final height in GHD patients.
Area of Science:
- Pediatric Endocrinology
- Bone Metabolism Research
- Growth Hormone Therapy
Background:
- Children with growth hormone deficiency (GHD) exhibit altered bone turnover dynamics.
- Understanding bone metabolism is crucial for optimizing growth hormone (GH) therapy outcomes.
Purpose of the Study:
- To investigate the longitudinal changes in bone turnover markers in children with GHD during extended GH treatment.
- To assess the relationship between bone marker dynamics and growth response in GHD patients.
Main Methods:
- Longitudinal measurement of growth velocity and serum bone markers (osteocalcin, PICP, ICTP) in 24 GHD patients.
- Comparison of bone marker levels at baseline, during treatment, and at final height against controls.
- Statistical analysis to determine correlations between bone marker changes and growth parameters.
Main Results:
- Baseline bone turnover markers (OC, PICP, ICTP) were significantly lower in GHD children compared to controls.
- GH treatment led to a significant increase in bone markers, peaking at 12 months.
- While OC and PICP declined post-year one, ICTP remained stable; all markers stayed elevated above baseline.
- Changes in bone markers did not correlate with growth rate or final height.
Conclusions:
- Children with GHD have diminished bone turnover, which is enhanced by long-term GH therapy.
- Serum markers OC, PICP, and ICTP are not predictive of growth velocity or final height in GHD patients undergoing GH treatment.
Objective:
To examine the dynamics of bone turnover in children with growth hormone deficiency (GHD) during long-term treatment.
Design:
We longitudinally measured growth velocity and serum concentrations of osteocalcin (OC), carboxyterminal propeptide of type I procollagen (PICP), and cross-linked carboxyterminal telopeptide of type I collagen (ICTP) in 24 patients with GHD during long-term GH treatment until final height (age: 7.7+/-0.7 and 16.9+/-0.5 years at baseline and at final height respectively).
Results:
At baseline, OC, PICP, and ICTP levels were significantly (P<0.0001) reduced in comparison with prepubertal bone age-matched controls (10.2+/-2.3 microgram/l and 22.5+/-7.6 microgram/l; 187.8+/-26.2 microgram/l and 328. 4+/-74.3 microgram/l; 7.7+/-2.0 microgram/l and 14.2+/-1.3 microgram/l respectively). During the first year of treatment mean levels of the bone markers increased significantly (P<0.0001) with a peak at 12 months. After the first year of treatment, OC and PICP levels progressively declined, whereas ICTP levels remained stable until the final height; in any case, bone marker levels remained significantly higher (P<0.03-P<0.0001) than baseline. The change in bone marker levels at 6 and 12 months of treatment with respect to the baseline values was not related to growth rate during long-term treatment or final height.
Conclusions:
The results show that children with GHD have reduced bone turnover at baseline, and that long-term GH treatment is associated with a stimulation of bone turnover. OC, PICP, and ICTP do not predict growth rate during long-term treatment or final height in children with GHD.