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Following Brain Trauma, Copeptin, a Stable Peptide Derived from the AVP Precusor, Does Not Reflect Osmoregulation but Correlates with Injury Severity

  • A. KleindienstEmail author
  • G. Brabant
  • N. G. Morgenthaler
  • K. C. Dixit
  • H. Parsch
  • M. Buchfelder
Conference paper
Part of the Acta Neurochirurgica Supplementum book series (NEUROCHIRURGICA, volume 106)

Abstract

The incidence of water and electrolyte disturbances following traumatic brain injury (TBI) is considerable and has been attributed to a dysregulation of the hypothalamic peptide arginine-vasopressin (AVP). Copeptin, the C-terminal part of the AVP prohormone, reflects AVP activity.

In 71 TBI patients we measured copeptin in serum by a sandwich immunoassay. Injury severity was assessed by Glasgow Coma Score (GCS) and computed tomography, and recovery by Glasgow Outcome Score (GOS). Neuroendocrine and osmoregulation regulation were examined on day 0, 3 and 7, and 24 months post-injury.

Copeptin was highest on admission (40.0 ± 72.3 pmol/l), stabilized on day 3 and 7 (21.2 ± 18.3 resp. 20.3 ± 17.1 pmol/l), and normalized at follow-up (4.2 ± 1.7 pmol/l). On admission, there was a correlation between serum sodium and urine excretion (p = 0.003), but the correlation got lost on day 3 and 7. Copeptin did not reflect the individual 24 h urine excretion or serum sodium levels indicating an uncoupling of copeptin/AVP release and renal water excretion. High copeptin level on day 3 were correlated with a low GCS (p < 0.001), midline shift (p = 0.019), intracerebral hemorrhage (p = 0.026), SAPS score (p = 0.001), as well as with a low GOS (p = 0.031). Copeptin was significantly decreased following skullbase fracture (p = 0.016).

Our data reveal a loss of hypothalamic osmoregulation following TBI. The measurement of Copeptin/AVP release reveals a significant predictive function for the severity of TBI.

Keywords

Neuroendocrine function osmoregulation outcome traumatic brain injury 

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Copyright information

© Springer-Verlag/Wien 2010

Authors and Affiliations

  • A. Kleindienst
    • 1
    Email author
  • G. Brabant
    • 2
  • N. G. Morgenthaler
    • 4
  • K. C. Dixit
    • 2
  • H. Parsch
    • 3
  • M. Buchfelder
    • 1
  1. 1.Department of NeurosurgeryFriedrich-Alexander-University Erlangen-NurembergErlangenGermany
  2. 2.Department of EndocrinologyChristie HospitalManchesterUnited Kingdom
  3. 3.University Erlangen-NurembergCentral LaboratoryErlangenGermany
  4. 4.Research DepartmentB.R.A.H.M.S. AG, Biotechnology CentreHennigsdorfGermany

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