Acute and chronic hypopituitarism following traumatic brain injury: a systematic review and meta-analysis.
Level 3 - non-randomized controlled study
Systematic review and meta-analysis of observational studies
PubMed 39527353 · doi:10.1007/s10143-024-03088-3
What was done
Authors conducted a systematic review and meta-analysis across multiple databases from January 1, 2000, to March 31, 2024, to determine the prevalence of pituitary axis dysfunction following traumatic brain injury (TBI). Pooled prevalence estimates with 95% confidence intervals were calculated using random-effects models. Subgroup analyses examined temporal patterns across four post-injury intervals (<3 months, 3-6 months, 6-12 months, and >12 months) and evaluated individual endocrine axes.
What was found
Across 52 studies comprising 7,367 participants, the pooled overall prevalence of any post-TBI pituitary axis dysfunction was 33% (95% CI 28% to 37%). By time post-injury, prevalence was 40% at <3 months (95% CI 27% to 53%), 31% at 3-6 months (95% CI 15% to 47%), 26% at 6-12 months (95% CI 19% to 33%), and 32% at >12 months (95% CI 26% to 38%). Multiple axes involvement occurred in 7% (95% CI 6% to 9%). Deficiencies by specific axis were growth hormone at 18% (95% CI 14% to 21%), gonadal axis at 16% (95% CI 12% to 19%), ACTH at 10% (95% CI 8% to 13%), and TSH at 6% (95% CI 5% to 7%).
Why it matters
Pituitary dysfunction affects approximately one in three patients following traumatic brain injury and frequently persists into the chronic phase. Systematic endocrine evaluation and surveillance are warranted in post-TBI care to address treatable hormonal deficits.
Limits
The abstract does not report baseline injury severity breakdowns, diagnostic criteria, or specific hormone testing protocols used across the included studies. Contributing clinical risk factors were not fully delineated, and high between-study variability may exist across differing clinical settings.
Cited by
- supports Head trauma and concussions can damage the anterior pituitary gland, leading to reduced testosterone and growth hormone production.