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Postprandial hyperglycemia corrected by IGF-I (Increlex®) in Laron syndrome
Hanane Latrech1, Albane Simon, Jacques Beltrand
1Endocrinologie Diabétologie, Hôpital Militaire d'Instruction Mohammed V, Rabat, Maroc.
Hormone Research in Paediatrics
|September 19, 2012
Summary
Laron syndrome, a growth hormone receptor defect, can cause postprandial hyperglycemia. Insulin-like growth factor-I (IGF-I) replacement therapy successfully reversed this hyperglycemia in a patient with Laron syndrome.
Area of Science:
- Endocrinology
- Genetics
- Metabolic Disorders
Background:
- Laron syndrome results from growth hormone receptor mutations, leading to insulin-like growth factor-I (IGF-I) deficiency.
- This deficiency typically causes severe short stature and hypoglycemia.
- A novel presentation of postprandial hyperglycemia in Laron syndrome is reported.
Observation:
- A pediatric patient with Laron syndrome presented with severe short stature, hypoglycemia, and truncal obesity.
- Genetic analysis confirmed a homozygous mutation in the growth hormone receptor gene.
- Continuous glucose monitoring revealed asymptomatic hypoglycemia alongside significant postprandial hyperglycemia.
Findings:
- Serum IGF-I levels were markedly low, with elevated baseline growth hormone.
- Treatment with recombinant human IGF-I (mecasermin) normalized blood glucose profiles.
- Improved glucose control was dose-dependent, with full normalization at 0.12 µg/kg/day.
Implications:
- Postprandial hyperglycemia is identified as a metabolic consequence of chronic IGF-I deficiency.
- IGF-I replacement therapy demonstrates efficacy in managing this specific metabolic abnormality.
- The findings suggest improved postprandial glucose transfer as a mechanism for IGF-I therapy's benefit.
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