[Hypopituitarism following traumatic brain injury: diagnostic and therapeutic issues]

Ann Endocrinol (Paris). 2015 Oct;76(6 Suppl 1):S10-8. doi: 10.1016/S0003-4266(16)30003-8.
[Article in French]


Traumatic Brain Injury (TBI) is a well-known public health problem worldwide and is a leading cause of death and disability, particularly in young adults. Besides neurological and psychiatric issues, pituitary dysfunction can also occur after TBI, in the acute or chronic phase. The exact prevalence of post-traumatic hypopituitarism is difficult to assess due to the wide heterogeneity of published studies and bias in interpretation of hormonal test results in this specific population. Predictive factors for hypopituitarism have been proposed and are helpful for the screening. The pathophysiology of pituitary dysfunction after TBI is not well understood but the vascular hypothesis is privileged. Activation of pituitary stem/progenitor cells is probably involved in the recovery of pituitary functions. Those cells also play a role in the induction of pituitary tumors, highlighting their crucial place in pituitary conditions. This review updates the current data related to anterior pituitary dysfunction after TBI and discusses the bias and difficulties encountered in its diagnosis.

Keywords: Cellule souche; Déficit hypophysaire; Hypopituitarism; Pituitary tumorigenesis; Stem cell; Traumatic brain injury; Traumatisme crânien; Tumorigenèse hypophysaire.

Publication types

  • Review

MeSH terms

  • Acute Disease
  • Brain Injuries / complications*
  • Brain Injuries / epidemiology
  • Chronic Disease
  • Humans
  • Hypopituitarism / diagnosis
  • Hypopituitarism / etiology*
  • Hypopituitarism / therapy
  • Pituitary Gland, Anterior / physiopathology
  • Stem Cells / physiology
  • Subarachnoid Hemorrhage / complications