Following Brain Trauma, Copeptin, a Stable Peptide Derived from the AVP Precusor, Does Not Reflect Osmoregulation but Co
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 prohormo
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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 145 mmol/l, plasma osmolality > 300 mosmol/kg, ratio osmolality urine/plasma 3.5 l/24 h), and 14% demonstrated symptoms suggestive for an inappropriate antidiuretic hormone (syn. AVP) secretion (SIADH, plasma sodium 40 mM) (1). The diabetes insipidus persisted in 6% of patients while all patients recovered from SIADH. Because of methodological problems, the hypothalamicposterior pituitary function has been poorly investigated, yet. In the study mentioned above, both diabetes insipidus and SIADH have been diagnosed on the basis of water and electrolyte dysbalances alone but were not confirmed by AVP measurements (1). Copeptin, the C-terminal part of the AVP prohormone, is concomitantly secreted together with mature AVP (5). Due to an ex vivo stability lasting several days, copeptin can be readily assayed in serum or plasma. In the present study, we investigated the copeptin release in the acute period following TBI, and after more than 24 months combined with a repetitive neurological examination. In parallel, we performed a comprehensive assessment of different osmoregulatory parameter.
Z. Czernicki et al. (eds.), Brain Edema XIV, Acta Neurochirurgica Supplementum Vol. 106, DOI 10.1007/978-3-211-98811-4_41, © Springer-Verlag/Wien 2010
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Seventy-one consecutive patients (57 male, 14 female, mean age 53 years, range 18–87years), who were admitted to our neurosurgical unit, were studied. According to the Glasgow Coma Score (GCS, 15), 24 patients suffered from mild (GCS 13–15), 32 from moderate (GCS 9–12), and 15 from severe (GCS 3–8) TBI. All patients underwent routinely an initial computerized tomography (CT) scan. The CT demonstrated an open TBI in 19, a skull fracture in 36, a cranio-facial fracture in 6, a skull base fracture in 17, a subdural hematoma in 14, an epidural hematoma in 8, an intracerebral hemorrhagic contusion in 20, a subarachnoid hemor
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