AI Article Synopsis

  • The study investigates the relationship between serum markers (NFL, GFAP, t-tau) and pituitary dysfunction in adults who experienced traumatic brain injury (TBI).
  • During the acute phase, NFL levels showed significant correlations with patient outcomes like hospital stay length and hormonal changes, while GFAP and t-tau did not correlate with hormone levels.
  • One year after TBI, NFL, GFAP, and t-tau levels decreased significantly, and no hormone deficiencies were observed, indicating potential recovery but highlighting the need for more extensive research on long-term effects.

Article Abstract

Purpose: Traumatic brain injury (TBI), a well-known risk factor for pituitary dysfunction, is associated with increased serum neurofilament light chain (NFL), glial fibrillary acidic protein (GFAP), and total tau (t-tau) levels. We aimed to assess the predictive value of these markers and pituitary dysfunction following TBI in a prospective manner.

Methods: Adult patients following TBI were included. Serum levels of NFL, GFAP, t-tau and pituitary and target hormones were analyzed prospectively during first week and one year after TBI.

Results: Twenty-two patients (17 males, 5 females; mean age 40±15 years) were included in the study. Basal NFL levels correlated positively with length of hospital stay and basal cortisol (r=0.643, p=0.001 and r=0.558, p=0.007, respectively) and negatively with Glasgow Coma Scale (GCS) score and basal IGF-1 levels (r=-0.429, p=0.046 and r=-0.481, p=0.023, respectively), while there was no significant correlation between GFAP, t-tau and hormone levels. NFL, GFAP, and t-tau levels significantly decreased, and none of the patients developed hormone deficiencies one year after TBI. No correlations were detected between basal markers and first year pituitary hormone levels.

Conclusion: Serum NFL levels were correlated with hormonal changes during acute phase of TBI reflecting the physiological response to trauma. Larger studies are needed to analyze the associations during chronic phase.

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Source
http://dx.doi.org/10.1016/j.ando.2024.10.003DOI Listing

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