Artikel
Activation of the pituitary hypothalamic system correlates with brain damage and outcome following traumatic brain injury
Die Aktivierung des hypophysär-hypothalamischen Systems korreliert mit der Hirnschädigung und dem Outcome nach Schädelhirnverletzungen
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Autoren
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A. Kleindienst
- Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
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D. Weigel
- Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
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N. G. Morgenthaler
- BAHMS AG, Biotechnology Centre, Research Department, Henningsdorf, Deutschland
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G. Brabant
- Christie Hospital, Department of Endocrinology, Manchester, United Kingdom
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M. Buchfelder
- Klinik für Neurochirurgie, Klinikum der Universität Erlangen-Nürnberg, Erlangen, Deutschland
| Veröffentlicht: | 11. April 2007 |
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Gliederung
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Objective: In traumatic brain injury (TBI), a relevant percentage of patients suffer from water and electrolyte disturbances that have been attributed to a dysregulation of the hypothalamic peptide arginine-vasopressin (AVP) system. Furthermore, AVP is involved in hemodynamic control and has been successfully implemented in cardiovascular resuscitation. Since the direct measurement of AVP concentration is difficult due to its instability, we measured copeptin, the C-terminal part of the AVP prohormone. Due to an ex vivo stability which lasts several days, copeptin can be readily assayed in serum or plasma. In this study, we tested the impact of TBI on copeptin release and on the 6-month outcome.
Methods: In 71 consecutive patients admitted for TBI (57 male, 14 female, mean age 53 years), we measured copeptin, a stable derivate of AVP, which has been demonstrated to reflect AVP activity by a sandwich immunoassay. 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 24 to 36 months post-injury. Recovery was assessed by the Glasgow Outcome Score (GOS) at 6 months.
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 between 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), the SAPSII score (r=0.53, p=0.001), as well as with the GOS at 6 months (r=-0.302, p=0.031). Copeptin levels on day 7 were significantly decreased in patients with a skull base fracture (r=-0.357, p=0.016).
Conclusions: Our data reveal a significant predictive function of copeptin for the severity of TBI, for the acute physiological dysregulation as assessed by the SAPSII score, and even more importantly for the outcome of the patients.
