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Related Experiment Videos

IGF-I levels rise and GH responses to GHRH decrease during long-term prednisone treatment in man.

M H Borges1, A C Pinto, F B DiNinno

  • 1Division of Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo SP, Brazil.

Journal of Endocrinological Investigation
|March 25, 1999
PubMed
Summary
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Glucocorticoid therapy with prednisone blunts growth hormone (GH) response to GHRH but increases insulin-like growth factor-I (IGF-I) and albumin levels over time. These findings suggest glucocorticoids may influence hepatic synthesis of IGF-I and albumin.

Area of Science:

  • Endocrinology
  • Pharmacology
  • Metabolism

Background:

  • Glucocorticoid excess is linked to altered growth hormone (GH) secretion.
  • Insulin-like growth factor-I (IGF-I) levels in hypercortisolism are variable, with conflicting reports.
  • The longitudinal effects of corticotherapy on GH, IGF-I, and related proteins require further investigation.

Purpose of the Study:

  • To longitudinally assess time-dependent changes in GH response to GHRH, IGF-I, IGF-Binding Protein-3 (IGFBP-3), and albumin during prednisone treatment.
  • To compare these parameters between patients undergoing corticotherapy and healthy controls.

Main Methods:

  • Six patients received GHRH tests before, after one week, and after one month of oral prednisone (20-60 mg/d).
  • IGF-I, IGFBP-3, and albumin levels were measured at each time point.

Related Experiment Videos

  • Ten normal controls were evaluated for comparison.
  • Main Results:

    • Prednisone administration significantly decreased peak GH response to GHRH after one week and one month.
    • Circulating IGF-I levels significantly increased after one week and one month of prednisone.
    • Albumin levels rose significantly during prednisone treatment, while IGFBP-3 showed no significant change.

    Conclusions:

    • Corticotherapy with prednisone markedly reduces GH responsiveness to GHRH.
    • Prednisone administration is associated with increased circulating IGF-I and albumin levels.
    • The exact physiological mechanisms, potentially involving increased hepatic synthesis, require further elucidation.