Key result
Growth hormone insensitivity is primarily caused by GH receptor defects, and while IGF-I therapy is used, its limitations highlight the need for alternative therapies.
This review summarizes the evolution of understanding growth hormone insensitivity and highlights the limitations of current IGF-I therapies.
Limitations of IGF-I in GH insensitivity warrant cautious use; leaves open development of alternative therapies.
The concept of growth hormone (GH) insensitivity has evolved since the condition was originally identified in 1966, and we now know that the primary defect involved is in the GH receptor. Cloning of the receptor molecule has led to great progress in our understanding of GH insensitivity (GHI) and its therapy, including the roles of GH and insulin-like growth factor I (IGF-I) in growth and development, and the relationships between height and serum levels of GH, IGF-I and their binding proteins. Despite the success of work on GHI and IGF-I, a number of opportunities have been missed in the past. The differences between the metabolic effects of GH and IGF-I are not fully understood, while measurements of IGF-I and IGF-binding protein 3 are perhaps not the ideal means of diagnosing GHI. Finally, the use of IGF-I to treat GHI has a number of limitations, and work is underway to develop alternative therapies.
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Rosenfeld et al. (2001) conducted a review in Growth Hormone Insensitivity Syndromes. Growth hormone insensitivity is primarily caused by GH receptor defects, and while IGF-I therapy is used, its limitations highlight the need for alternative therapies.
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