Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 13 P230

SFEBES2007 Poster Presentations Neuroendocrinology and behaviour (including pituitary) (27 abstracts)

The AVP precursor, Copeptin, predicts the severity of acute and prolonged traumatic brain injury (TBI)

Andrea Kleindienst 1 , Daniel Weigel 1 , Nils Morgenthaler 2 , Joachim Struck 2 , Michael Buchfelder 1 & Georg Brabant 3

1Dept. of Neurosugery, University Erlangen-Nuremberg, Erlangen, Germany; 2Research Dept., BAHMS AG, Henningsdorf/Berlin, Germany; 3Dept. of Endocrinology, Christie Hospital, Manchester, United Kingdom.

Introduction: 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, is stoichiometrically secreted together with mature AVP. Due to his long ex vivo stability, the AVP precursor, copeptin, can be used as a surrogate of AVP readily to be measured in serum or plasma. In the present study we prospectively tested the impact of TBI on copeptin release and on 6 months outcome of these patients.

Materials and methods: Copeptin was measured in 71 consecutive patients admitted for TBI (57 male, 14 female, mean age 53 yrs). Injury severity was assessed by the Glasgow Coma Score (GCS) and an initial CT. Copeptin and pituitary function were examined on day 0, 3 and 7, and in part dynamically 24-36 months post-injury. Recovery was assessed by the Glasgow Outcome Scale (GOS).

Results: 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 was normalized at follow-up in all but one patient (4.2±1.7 pmol/l). The data demonstrate a significant correlation of high copeptin levels on day 3 with the GCS (r=−0.661, P<0.001), midline shift on CT (r=0.349, P=0.019), intracerebral hemorrhage (r=0.325, P=0.026), SAPS (r=0.53, P=0.001), cortisol levels (r=0.437, P<0.001), late somato- and thyreotropic deficiency (r=0.397, P=0.037), as well as with GOS at 6 months (r=−0.302, P=0.031). Copeptin levels on day 7 were significantly decreased in patients with a skullbase fracture (r=−0.357, P=0.016).

Conclusions: Our data support a significant predictive function of copeptin for the severity of TBI. Since AVP/copeptin serves important stimulatory functions for the anterior pituitary copeptin levels may predict pituitary dysfunction in patients following TBI.

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