Endocrine Abstracts

GH deficiency is recognised as a complication of adult traumatic brain injury (TBI) but there are conflicting data in children possibly due to the influences such as age at TBI, trauma mechanism but also by timing, method and criteria of hormonal evaluation.

Objectives: To assess the long-term impact of TBI on the GH–IGF1 axis following TBI in childhood.

Patients: Longitudinal study of 28 participants with a history of moderate/severe TBI. Age (median (range)) at TBI 10.8 (1–17) years; 9 were prepubertal, 12 peripubertal, 8 postpubertal. Age at study 19 (11–26) years, time post TBI 8.7 (7–10.8) years, 2 were prepubertal. All subjects had clinical review, auxology and pubertal assessment. 24/28 participants had a GH stimulation test (ITT) and a 12-h overnight growth hormone profile (15 min sampling). For comparison a non-TBI control group with normal GH status (n=7, aged 18 (14–20) years) also had an overnight GH profile. There were no differences in age, BMI, gender and fat composition between TBI and control group.

Results: Deconvolution analysis of the overnight profiles showed that the number of secretion events, mean secretory pulse mass and mean secretory pulse interval were significantly different between the TBI and control group (P<0.05). In 6/24 of the TBI group the ITT GH response was abnormal (<3 μg/l in four postpubertal and <5 μg/l in two peripubertal participants). One had a suboptimal cortisol response. All other endocrine baseline blood samples (thyroid function, sex steroids) were normal and there was no clinical evidence of diabetes insipidus. The mechanism of injury was high speed RTA in 12 participants and falls and other type of low speed injury in the remaining.

Conclusions: GH deficiency and neurosecretory dysfunction occurs following moderate/severe TBI in childhood.