Abstract
While hypopituitarism after traumatic brain injury (TBI) was previously considered rare, it is now thought to be a major cause of treatable morbidity among TBI survivors. Consequently, recommendations for assessment of pituitary function and replacement in TBI were recently introduced. Given the high incidence of TBI with more than 100 pr. 100,000 inhabitants, TBI would be by far the most common cause of hypopituitarism if the recently reported prevalence rates hold true. The disproportion between this proposed incidence and the occasional cases of post-TBI hypopituitarism in clinical practice justifies reflection as to whether hypopituitarism has been unrecognized in TBI patients or whether diagnostic testing designed for high risk populations such as patients with obvious pituitary pathology has overestimated the true risk and thereby the disease burden of hypopituitarism in TBI. The findings on mainly isolated deficiencies in TBI patients, and particularly isolated growth hormone (GH) deficiency, raise the question of the potential impact of methodological confounding, determined by variable test-retest reproducibility, appropriateness of cut-off values, importance of BMI stratified cut-offs, assay heterogeneity, pre-test probability of hypopituitarism and lack of proper individual laboratory controls as reference population. In this review, current recommendations are discussed in light of recent available evidence.
Highlights
Traumatic brain injury (TBI) has until recently been considered a rare cause of hypopituitarism, accounting for less than one per cent of all new cases, i.e., less than one new case in 10 million inhabitants per year
In a cohort of 104 TBI patients hospitalised at a tertiary hospital with neurosurgical facility, we found that when adjusted for confounders such as trauma severity, posttraumatic hypopituitarism remained an independent predictor of worsened quality of life (QoL) [59], which could point to an association
The strength of these KIMS studies was related to the size of the cohorts and the inherent ability to perform direct comparison with non-functioning pituitary adenoma (NFPA) patients, but it is worth mentioning that such registry studies include non-randomised highly selected cohorts which may not be representative for a general cohort of TBI patients
Summary
Traumatic brain injury (TBI) has until recently been considered a rare cause of hypopituitarism, accounting for less than one per cent of all new cases, i.e., less than one new case in 10 million inhabitants per year. Newer studies have indicated that TBI-related chronic anterior pituitary hormone deficiency may be far more frequent, and a recent meta-analysis reported hypopituitarism in over 25% of adults after TBI [1], with similar data found in children. Given the high incidence of TBI with more than 100 cases in 100,000 inhabitants, TBI would be by far the most common cause of hypopituitarism if the reported prevalence rates hold true. The published clinical studies on posttraumatic hypopituitarism are scrutinized, and current recommendations are discussed in light of recent available evidence
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