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Craniopharyngioma: the role of insulin in promoting postoperative growth
Insights
Children with craniopharyngioma often experience normal growth after surgery despite growth hormone deficiency. Insulin appears crucial for regulating somatomedin and growth in these pediatric patients.
Area of Science:
- Pediatric Endocrinology
- Pediatric Oncology
- Metabolic Research
Background:
- Craniopharyngioma surgery can lead to growth hormone deficiency in children.
- Postoperative growth patterns in these children require further elucidation.
- Understanding hormonal regulation is key to managing growth outcomes.
Purpose of the Study:
- To investigate the mechanism of growth in children post-craniopharyngioma surgery.
- To assess the roles of somatomedin, prolactin, and insulin in postoperative growth.
- To correlate hormonal levels and responses with growth rates in affected children.
Main Methods:
- Measured serum somatomedin and prolactin levels in children after craniopharyngioma removal.
- Assessed plasma insulin (IRI) response to oral glucose and intravenous tolbutamide.
- Correlated hormonal data with postoperative growth rates (cm/year).
Main Results:
- Most children (7/8) exhibited normal postoperative growth despite growth hormone deficiency.
- Normal serum somatomedin levels were observed in children with normal growth.
- Insulin response to stimuli was normal in non-obese patients and correlated with growth rates.
Conclusions:
- Normal growth in children with craniopharyngioma post-surgery is associated with normal somatomedin and insulin response, despite GH deficiency.
- Insulin appears to play a significant role in controlling somatomedin and growth in these children.
- Further research into insulin's role is warranted for optimizing growth outcomes.
Abstract:
To elucidate the mechanism for growth following surgery in children with craniopharyngioma, serum somatomedin and prolactin levels, and plasma insulin (IRI) levels in response to oral glucose and intravenous tolbutamide, were determined in 5 and 8 children, respectively, at variable intervals following removal of the tumor. All patients had growth hormone (GH) deficiency following surgery. Seven of 8 children had normal growth (5 cm per year or greater) postoperatively for varying periods of time; 2 children continued to grow normally 6 and 8 years after surgery. Mean (+/- SE) somatomedin level was 0.78 +/- 0.1 U/ml (normal 0.4-1.5 U/ml). Serum somatomedin was normal in 4 children with normal postoperative growth and was also normal in a child who grew poorly. Mean (+/- SE) prolactin level was 6.9 +/- 3.3 ng/ml (normal 0-20 ng/ml). In 5 non-obese children with craniopharyngioma mean (+/- SE) peak IRI level was 104.4 +/- 24.4 muU/ml after oral glucose and 56.7 +/- 8.4 muU/ml after intravenous tolbutamide. These values are similar to mean (+/- SE) peak IRI levels following glucose and tolbutamide in normal children, and significantly higher (P less than 0.05) than those of idiopathic hypopituitary children. In 2 obese children with craniopharyngioma peak IRI levels were 255 and 107 muU/ml after glucose and 208 and 103 muU/ml after tolbutamide, respectively. The patient with suboptimal growth had low IRI responses to stimuli similar to hypopituitary children. Although there was a significant correlation between peak IRI levels following glucose (r = 0.63, P less than 0.025) and tolbutamide (r = 0.75, P less than 0.01) and the rates of growth of the combined data from obese and non-obese patients, no correlation was found between the growth rates of only the non-obese craniopharyngioma patients and their peak IRI levels. No significant correlation was found between mean somatomedin level and mean rate of growth. Normal postoperative growth in all children with craniopharyngioma was associated with normal serum somatomedin activity and pancreatic beta-cell responsiveness to stimuli despite GH deficiency. The results suggest that insulin may be important in the control of somatomedin and growth in these children.