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Plasma growth hormone concentration in corticosteroid-treated children
Insights
Corticosteroid therapy in children does not appear to affect growth hormone levels. Studies show similar growth hormone concentrations in children on steroids versus controls, suggesting other factors cause steroid-induced dwarfism.
Area of Science:
- Pediatric Endocrinology
- Growth Hormone Research
- Pharmacology
Background:
- Corticosteroids are widely used in pediatric care.
- Corticosteroid therapy is associated with growth retardation (dwarfism) in children.
- The underlying mechanisms of steroid-induced dwarfism require further elucidation.
Purpose of the Study:
- To investigate the impact of corticosteroid therapy on endogenous plasma growth hormone concentrations in children.
- To determine if altered growth hormone secretion contributes to dwarfism observed in corticosteroid-treated children.
Main Methods:
- Measured plasma growth hormone levels in children receiving daily corticosteroid therapy.
- Compared growth hormone concentrations with a control group of asthmatic children not on steroids.
- Assessed growth hormone levels during fasting and after insulin-induced hypoglycemia.
- Evaluated growth hormone changes in children before and after a period of prednisone withdrawal.
Main Results:
- No significant differences in fasting or hypoglycemia-stimulated growth hormone concentrations were observed between children on corticosteroids and controls.
- Growth hormone levels remained unchanged in children before and after a 2-week course of high-dose prednisone withdrawal.
- These findings indicate that corticosteroid therapy does not suppress growth hormone secretion.
Conclusions:
- Deficiency in growth hormone secretion is unlikely to be the primary cause of dwarfism in children treated with corticosteroids.
- Alternative mechanisms should be explored to understand the etiology of growth retardation associated with corticosteroid use.
Abstract:
Endogenous plasma growth hormone concentrations were measured in 23 children who were receiving daily corticosteroid therapy and in 10 control asthmatic children who had not received steroids for at least 8 months. The growth hormone concentrations were similar in the two groups of patients both during the fasting state and after insulin-induced hypoglycemia. 12 children, who were studied while receiving a large dose of prednisone and again 2 wk after steroid withdrawal, also showed no change in growth hormone concentration in relation to corticosteroid therapy. These findings suggest that deficiency of growth hormone is not the major mechanism responsible for the dwarfism of corticosteroid-treated children.
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