title: Nonspecific increase of systemic neuron-specific enolase after trauma: clinical and experimental findings.
abstract: The aim of this clinical and experimental study was to determine whether systemic neuron-specific enolase (NSE) is a useful early marker of traumatic brain injury (TBI) and whether NSE is affected by ischemia/reperfusion damage of abdominal organs. Our study included patients with and without TBI (verified by computerized tomography) admitted within 6 h after trauma and male Sprague-Dawley rats with ischemia and reperfusion of the abdominal organs liver, gut, or kidney. Thirty-eight study patients included 13 with isolated TBI and 18 patients with multiple trauma and TBI. Seven patients had multiple trauma but no TBI. Fifteen rats were anaesthetized and subjected to isolated ischemia of the liver, gut, or kidney (n = 5 each) for 1 h, followed by reperfusion for 3 h. In patients, NSE increased over 2-fold versus the upper normal limit (10 microg/L) within 6 h after trauma, regardless of whether TBI had occurred or not. In rats, NSE increased over 3-fold versus laboratory controls during ischemia of the liver and kidney (both P < 0.0005), but not of the gut. NSE increased over 2-fold after onset of reperfusion of the liver and kidney (both P < 0.05), but not of the gut and increased over 3-fold after 3 h of reperfusion of the liver, gut (both P < 0.005), and kidney (P < 0.0005). Our data show that systemic NSE increases to similar degrees with and without TBI. Therefore, NSE is not a useful early marker of TBI in multiple trauma.
authors.affiliation: Ludwig Boltzmann Institute for Experimental and Clinical Traumatology at the Research Centre of the Allgemeine Unfallversicherungsanstalt, A-1200, Vienna, Austria. lindapel@via.at
authors.forename: Linda E
authors.initials: LE
authors.lastname: Pelinka
authors.forename: Harald
authors.initials: H
authors.lastname: Hertz
authors.forename: Walter
authors.initials: W
authors.lastname: Mauritz
authors.forename: Naoki
authors.initials: N
authors.lastname: Harada
authors.forename: Mohammad
authors.initials: M
authors.lastname: Jafarmadar
authors.forename: Manfred
authors.initials: M
authors.lastname: Albrecht
authors.forename: Heinz
authors.initials: H
authors.lastname: Redl
authors.forename: Soheyl
authors.initials: S
authors.lastname: Bahrami
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001930:Brain Injuries / Q000378:metabolism; D003404:Creatinine / Q000378:metabolism; D005260:Female; D023261:Glasgow Outcome Scale; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010751:Phosphopyruvate Hydratase / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury; D013997:Time Factors; D014018:Tissue Distribution; D014057:Tomography, X-Ray Computed; D014947:Wounds and Injuries / Q000378:metabolism*
chemical_list: D003404:Creatinine; D000410:Alanine Transaminase; D010751:Phosphopyruvate Hydratase