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Hemoglobin level is linked to growth hormone-dependent proteins in short children

E Vihervuori1, M Virtanen, H Koistinen

  • 1Children's Hospital and the Department of Obstetrics and Gynecology, University of Helsinki, Finland.

Blood
|March 1, 1996
PubMed

Insights

Growth hormone (GH) treatment boosts hemoglobin in children with short stature and skeletal dysplasia. The GH-IGF axis plays a role in childhood hemoglobin elevation.

Area of Science:

  • Pediatric Endocrinology
  • Hematology
  • Growth Factor Research

Background:

  • Erythropoiesis regulation in children with growth disorders is not fully understood.
  • The role of the growth hormone-insulin-like growth factor (GH-IGF) axis in hemoglobin production requires further investigation.

Purpose of the Study:

  • To investigate erythropoiesis in children with short stature and skeletal dysplasia during growth hormone (GH) therapy.
  • To examine the relationship between hemoglobin levels, growth, and serum concentrations of insulin-like growth factor I (IGF-I), IGF binding protein-3 (IGFBP-3), and erythropoietin (EPO).

Main Methods:

  • Studied 32 children with short stature and 8 with skeletal dysplasia over 12 months of recombinant human GH treatment.
  • Monitored blood hemoglobin, serum IGF-I, IGFBP-3, and EPO levels before, during, and after treatment.
  • Analyzed correlations between hemoglobin, growth parameters, and growth factor levels.

Main Results:

  • Hemoglobin positively correlated with height, IGF-I, and IGFBP-3, but not EPO.
  • GH treatment increased hemoglobin, IGF-I, and IGFBP-3, accelerating growth.
  • Children with skeletal dysplasia showed a pronounced hemoglobin increase, with strong correlations between hemoglobin, IGF-I, and IGFBP-3.

Conclusions:

  • The GH-IGF axis is implicated in the physiological elevation of hemoglobin during childhood.
  • GH therapy positively impacts erythropoiesis in children with short stature and skeletal dysplasia.
  • Specific correlations highlight the GH-IGF axis's role in hemoglobin regulation in skeletal dysplasia.

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