Craniopharyngioma: The Role of Insulin in Promoting Postoperative Growth

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 μU/ml after oral glucose and 56.7 ± 8.4 μU/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 < 0.05) than those of idiopathic hypopituitary children. In 2 obese children with craniopharyngioma peak IRI levels were 255 and 107 μU/ml after glucose and 208 and 103 μU/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 < 0.025) and tolbutamide (r = 0.75, P < 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 β-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.