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Multiple hormone resistance in short children born with intrauterine growth retardation?
P G Chatelain1, M Nicolino, O Claris
1Department of Pediatrics, Université Claude-Bernard and INSERM U 418, Hôpital Debrousse, Lyon.
Insights
Children with intrauterine growth retardation (IUGR) may show partial insulin resistance. This suggests a potential defect in insulin-like growth factor 1 (IGF-1) signaling, impacting their growth response to treatments.
Area of Science:
- Pediatrics
- Endocrinology
- Growth Disorders
Background:
- Intrauterine growth retardation (IUGR) affects 2.5% of newborns, with 8-20% experiencing persistent short stature postnatally.
- Catch-up growth mechanisms in IUGR are heterogeneous, and some may develop growth hormone (GH) insufficiency.
- Understanding GH and IGF-1 dynamics is crucial for managing short stature in IUGR.
Purpose of the Study:
- To analyze the response to GH treatment in persistently short idiopathic IUGR children.
- To compare GH treatment response (plasma IGF-1, GH dose, growth velocity) with GH-deficient (GHD) and familial short stature (FSS) children.
- To investigate the hypothesis of partial IGF-1 resistance in IUGR.
Main Methods:
- Comparative analysis of growth parameters and hormonal responses.
- Treatment response assessment in IUGR, GHD, and FSS cohorts.
- Measurement of plasma IGF-1 levels before and during GH therapy.
Main Results:
- IUGR children require higher basal and GH-induced plasma IGF-1 levels for comparable growth velocity.
- Growth velocity achieved in IUGR children was similar to FSS and GHD children but with different IGF-1 requirements.
- Data suggest a potentially reduced GH sensitivity or partial IGF-1 resistance in idiopathic IUGR.
Conclusions:
- Idiopathic IUGR children may exhibit partial IGF-1 resistance, necessitating higher IGF-1 levels for adequate growth.
- This resistance might involve IGF-1 receptor or post-receptor defects.
- Findings support further investigation into the specific mechanisms of impaired growth in IUGR.
Abstract:
Intrauterine growth retardation (IUGR) is encountered in 2.5% (-2 SD) of newborns. Lack of postnatal catch-up growth is found in 8-20%. If GH secretion is increased early postnatally in IUGR, then some persistently short IUGR children may present with GH insufficiency. However, the mechanism of postnatal catch-up growth is heterogenous. The response to GH treatment with regard to plasma IGF-1, GH dose and growth velocity was analyzed in persistently short idiopathic IUGR children and compared to GH-deficient (GHD) and familial short stature (FSS) children of similar age and degree of short stature. IUGR children require both a greater basal and GH-induced plasma IGF-1 in order to achieve a growth velocity of similar magnitude to that of FSS and GHD children. These data suggest a different sensitivity to GH in IUGR compared to FSS or GHD children, sustaining the hypothesis that these idiopathic IUGR children may be partially IGF-1 resistant. The recent report of partial insulin resistance in IUGR subjects raises the possibility of an IGF-1 receptor- or post-receptor-mediated defect.