Evaluation of pituitary function in cases with the diagnosis of pediatric mild traumatic brain injury: Cross-sectional study

TL;DR

In this cross-sectional study of 24 children evaluated 12–44 months after predominantly mild/moderate traumatic brain injury (TBI), no pituitary hormone deficiency was identified, although 9 (37.5%) had IGF-1 Z-scores below −2 SD and 2 had low basal cortisol. The authors conclude that long-term follow-up is still warranted because pituitary dysfunction after TBI may present early or late.

Key findings

• Among 24 children (mean age 9.5 ± 3.1 years; 14 mild, 9 moderate, 1 severe TBI by Glasgow coma scale [GCS]; mean 29.4 ± 9.8 months after trauma), no pituitary hormone deficiency was found; fT3, fT4, TSH, prolactin, serum sodium, urine density, and gonadotropin values were normal/appropriate, and no delayed or early puberty was identified.
• Low basal cortisol was reported in 2 cases in the Results/Discussion (the abstract says 1, 4.2%); one had a low-dose ACTH stimulation test with normal post-stimulation cortisol (18.44 µg/dl), and the other refused testing. Basal cortisol did not correlate with GCS (P = 0.097) and was lower in moderate versus mild TBI without statistical significance (P = 0.1).
• IGF-1 values were within normal limits, but 9/24 (37.5%) had IGF-1 Z-scores below −2 SD (8 pubertal, 1 prepubertal); none had short stature. No significant differences were found between mild and moderate TBI groups for IGF-1, IGF-1 Z-score, height SDS, thyroid hormones, prolactin, sodium, or urine density.

Methods

• Cross-sectional study of 24 pediatric patients aged 5–17 years diagnosed with TBI at Trakya University Pediatric Emergency Department between April 2006 and December 2008; inclusion required GCS ≤13 or GCS 13–15 with pathology on computed brain tomography; exclusions included long-term medication use, syndromes/chromosomal anomalies/CNS developmental defects, previous infection or metabolic disease, or previous head trauma diagnosis.
• After 12 h fasting, morning blood samples measured basal cortisol, fT3, fT4, TSH, prolactin, IGF-1, FSH, LH, estradiol in females, total testosterone in males, and serum sodium; morning urine density was also measured. IGF-1 Z-scores were calculated using a formula for Turkish children.
• Cases were divided into mild versus moderate TBI (the single severe case was included in the moderate group) and compared; Spearman correlation and Mann–Whitney U-test were used, with P < 0.05 considered significant.

Limitations

• Stated: the number of cases was low; the cross-sectional design did not assess the acute period, so the authors cannot comment on whether early hyperprolactinemia or central diabetes insipidus occurred; one severe TBI case was included in the moderate group for comparisons; one case with low basal cortisol refused ACTH stimulation.
• Evident: there was no control group, and no dynamic GH stimulation tests were performed (only planned/monitoring), so GH deficiency could not be definitively excluded; the single-center design may limit generalizability.
• Evident: the abstract reports one low basal cortisol while the Results/Discussion report two, an internal inconsistency in the paper.