RESUMO
We built the hypothesis that the hypertrophic callus formation is mediated by beta-endorphin that stimulates secretion of GH and increase circulation growth factor activity in head injury patient. We classified 4 groups such as 5 normal person(control), group I;5 patients with only fracture, group II;5 patients with fracture and head injury, group III; 5 patients with only head injury, group IV. We obtained the samples of serum from each group at 0, 2, 4, 6, 8 weeks after trauma and assessed the serum level of GH, GHRH, somatostatin. The serum level of GH was statisticallyu higher in group III, IV than group I, II. There was not significant difference in serum level of GHRH. The serum level of somatostatin was higher in group II, III, IV than group I, but there was no statistical significance in each group. GH has a important role in hypertrophic callus formation in severe head injury patients, but there was no evidence that the mechanism is mediated by beta-EndorphinGHRH & somatostatin-GH-GF-1, beta-FGF axis. There may be a another mechanism in increasing GH that was stimulated by beta-endorphin in thalamus and lateral ventricle, and it should be necessary for further evaluation of it.