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Growth retardation in fetal alcohol syndrome. Unresponsiveness to growth-promoting hormones
Insights
Children with fetal alcohol syndrome (FAS) experience growth retardation not from hormone deficiency, but from peripheral unresponsiveness to growth-promoting hormones.
Area of Science:
- Pediatrics
- Endocrinology
- Genetics
Background:
- Fetal alcohol syndrome (FAS) is a leading cause of preventable birth defects.
- Growth retardation is a common feature in children diagnosed with FAS.
- The underlying mechanisms of growth impairment in FAS are not fully understood.
Purpose of the Study:
- To investigate the relationship between growth retardation and metabolic/hormonal parameters in children with FAS.
- To determine if hormonal deficiencies contribute to growth defects in FAS.
- To explore potential peripheral unresponsiveness to growth factors in FAS.
Main Methods:
- Studied 7 children with FAS, assessing fasting hormone levels (TSH, T4, T3, FSH, LH) and prolactin response to chlorpromazine.
- Evaluated oral glucose tolerance tests and insulin response.
- Measured peak growth hormone (GH) response to insulin-induced hypoglycemia and fasting serum somatomedin activity.
Main Results:
- Hormonal levels (TSH, T4, T3, FSH, LH, prolactin) were normal in FAS patients.
- Abnormal glucose tolerance tests with hyperinsulinemia were observed in 3 children.
- Elevated peak GH response to hypoglycemia was noted in 5 patients; somatomedin activity was variable (3 elevated, 3 normal).
Conclusions:
- Growth defects in FAS are unlikely due to deficiencies in growth-promoting hormones.
- Data suggest peripheral unresponsiveness to hormonal signals contributes to growth retardation in FAS.
- Further research into the mechanisms of peripheral resistance is warranted.
Abstract:
The relationships between growth retardation and metabolic and hormonal parameters were studied in 7 children with fetal alcohol syndrome (FAS). Fasting blood concentrations of TSH, T4, T3, FSH and LH were normal. Plasma prolactin concentrations after chlorpromazine stimulation were normal. 3 children had abnormal oral glucose tolerance tests with increased plasma insulin response. Peak plasma growth hormone responses to insulin-induced hypoglycemia were elevated in 5 patients. Fasting bioassayable serum somatomedin activity, determined in 6 patients, was elevated in 3 patients and normal in 3 patients. Administration of hGH to 3 patients with FAS had little effect upon nitrogen retention and did not increase plasma insulin concentrations, although serum somatomedin activity sharply increased in 1 patient evaluated for somatomedin response. The data indicate that the growth defect in FAS is not due to deficiency of growth-promoting hormones, but rather to peripheral unresponsiveness.