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. © 2009 Springer-Verlag Vienna.
CITATION STYLE
Kleindienst, A., Brabant, G., Morgenthaler, N. G., Dixit, K. C., Parsch, H., & Buchfelder, M. (2009). Following brain trauma, copeptin, a stable peptide derived from the AVP precusor, does not reflect osmoregulation but correlates with injury severity. In Acta Neurochirurgica, Supplementum (pp. 221–224). Springer-Verlag Wien. https://doi.org/10.1007/978-3-211-98811-4_41
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