Endocrine Abstracts (2008) 17 OC3

Pituitary function after childhood traumatic brain injury

S Khadr1, P Crofton2, B Wardhaugh2, J Roach2, P Jones1, A Drake1, R Minns1 & C Kelnar1

1University of Edinburgh, Edinburgh, UK; 2Royal Hospital for Sick Children, Edinburgh, UK.

Objectives: To determine the prevalence and clinical significance of pituitary dysfunction following moderate/severe childhood traumatic brain injury (TBI).

Subjects and methods: We recruited 25 survivors of childhood TBI (19 males). Age at study was 5.4–18.9y (median 13.0y). Median time since TBI: 4.4y (2.3–6.7y). Subjects provided an early morning urine sample for osmolality and underwent basal hormone evaluation at 0800–1000h, followed by a GnRH test and either insulin tolerance test (ITT, n=19) or glucagon test (in those with previous seizures, n=6). Sex-hormone priming was not performed.

Results: Median (range) SDS for height, weight and BMI were +0.56 (−1.57 to +3.0), +0.61 (−1.28 to +2.86) and +0.56 (−1.01 to +2.92). No subject had diabetes insipidus or abnormal thyroid function. IGF-I, oestradiol/testosterone, and baseline and GnRH-stimulated LH/FSH concentrations were all appropriate for age/sex/pubertal stage. One male had isolated prolactin deficiency (<50 mU/l). Peak growth hormone (GH) response to stimulation was 23.8 (7.5–47.3) mU/l. Three male subjects had GH responses <15 mU/l. All were tall (height SDS +0.8, +1.3 and +1.39) and peri-pubertal.

Median basal morning cortisol was 294 (146–722) nmol/l. Peak cortisol response amongst those who underwent an ITT was 528 (367–717) nmol/l. Seven of the 19 had sub-optimal responses based on local age-related cut-offs1, none low enough to warrant routine glucocorticoid replacement. In two, steroid cover was recommended for moderate/severe illness/injury. In four of the remaining five, repeat testing was advised in one/two years; the fifth had high basal levels (624 nmol/l). Five of six subjects had adequate cortisol responses to glucagon; the sixth had high basal levels (722 nmol/l).

Conclusions: Whilst pituitary ‘dysfunction’ was seen in 10/25 (40%) of subjects, no unequivocal clinically significant endocrinopathies were found. Contrary to other paediatric reports, GH deficiency was not observed in this cohort 2.3–6.7 years after TBI however the hypothalamo–pituitary–adrenal axis may be vulnerable. Further work is relating these findings to the degree of primary injury and secondary brain insult in a larger cohort.

1Crofton PM et al. Horm Res 2004 61 92–97.

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