scholarly journals Long-Term Treatment with Recombinant Insulin-Like Growth Factor (IGF)-I in Children with Severe IGF-I Deficiency due to Growth Hormone Insensitivity

2007 ◽  
Vol 92 (3) ◽  
pp. 902-910 ◽  
Author(s):  
Steven D. Chernausek ◽  
Philippe F. Backeljauw ◽  
James Frane ◽  
Joyce Kuntze ◽  
Louis E. Underwood ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Term Treatment ◽  
Insulin Like Growth Factor ◽  
Recombinant Insulin ◽  
Long Term Treatment ◽  
Igf I ◽  
Growth Hormone Insensitivity

Long-term treatment with recombinant insulin-like growth factor 1 (IGF-1) in a child with IGF-1 gene mutation

2009 ◽  
Vol 169 (2) ◽  
pp. 245-247 ◽  
Author(s):  
Daniela Concolino ◽  
Gianluca Muzzi ◽  
Simona Sestito ◽  
Giovanna Vega ◽  
Giuseppe Bonapace ◽  
...  
Keyword(s):  
Growth Factor ◽  
Gene Mutation ◽  
Term Treatment ◽  
Insulin Like Growth Factor ◽  
Recombinant Insulin ◽  
Long Term Treatment

Long-Term Treatment of Growth Hormone Insensitivity Syndrome with IGF-I

1999 ◽  
Vol 51 (3) ◽  
pp. 128-134 ◽  
Author(s):  
M.B. Ranke ◽  
M.O. Savage ◽  
P.G. Chatelain ◽  
M.A. Preece ◽  
R.G. Rosenfeld ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Term Treatment ◽  
Long Term Treatment ◽  
Igf I ◽  
Growth Hormone Insensitivity

Long-term treatment of Laron type dwarfs with insulin-like growth factor-1 increases serum insulin-like growth factor-binding protein-3 in the absence of growth hormone activity

1993 ◽  
Vol 128 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Hannah Kanety ◽  
Avraham Karasik ◽  
Beatrice Klinger ◽  
Aviva Silbergeld ◽  
Zvi Laron
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Binding Protein ◽  
Serum Insulin ◽  
Continuous Treatment ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Long Term Treatment ◽  
Igf I ◽  
Igfbp 3

Insulin-like growth factor binding protein-3 (IGFBP-3) is the major carrier of insulin-like growth factor I (IGF-1) in serum, and its production is growth hormone (GH) dependent. It is unclear whether in humans IGFBP-3 production is directly regulated by GH or mediated via IGF-I. We addressed this question in six patients with Laron-type dwarfism, a syndrome characterized by the absence of GH receptor activity (LTD), who were chronically treated with recombinant IGF-I. Analysis of the electrophoretic profiles of serum IGFBPs in these patients by Western ligand blotting revealed an extremely low IGFBP-3 level. A striking progressive increase in serum IGFBP-3 was observed with continuous treatment, despite the absence of GH action. In LTD children, serum IGFBP-3 increased up to 19-fold after six months of therapy and equalled levels observed in controls, whereas in adult LTD patients the increase was smaller. A rise in serum levels of 34, 30 and 24 kDa BPs (presumably IGFBP-2, -1 and -4, respectively was also noted with chronic IGF-I therapy. This proof of GH-independent induction of IGFBP-3 by IGF-1 may be a major advantage in the therapeutic use of biosynthetic IGF-I in several types of short stature children.

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