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S‐100b and neuron‐specific enolase in patients with fulminant hepatic failure
Author(s) -
Strauss Gitte Irene,
Christiansen Michael,
Møller Kirsten,
Clemmesen Jens Otto,
Larsen Fin Stolze,
Knudsen Gitte Moos
Publication year - 2001
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2001.28742
Subject(s) - medicine , fulminant hepatic failure , gastroenterology , hepatic encephalopathy , cerebral edema , enolase , cirrhosis , hyperventilation , encephalopathy , liver transplantation , anesthesia , transplantation , immunohistochemistry
Patients with fulminant hepatic failure (FHF) frequently develop cerebral edema and intracranial hypertension. The aim of this study was to evaluate circulating S‐100b and neuron‐specific enolase (NSE) levels as markers of neurological outcome in patients with FHF. In a subgroup of patients, the cerebral flux of S‐100b and NSE was measured. We included 35 patients with FHF, 6 patients with acute on chronic liver disease (AOCLD), 13 patients with cirrhosis of the liver without hepatic encephalopathy, and 8 healthy subjects. Blood samples were obtained from catheters placed in the radial artery and internal jugular bulb. The net cerebral flux of S‐100b and NSE was measured, and the effect of short‐term hyperventilation, as well as the effect of high‐volume plasmapheresis, on circulating levels of these two biomarkers was determined. Blood levels of S‐100b were greater in patients with FHF and AOCLD than patients with cirrhosis and healthy subjects (median, 0.39 μg/L; range, 0.02 to 10.31 μg/L; and 1.11 μg/L; range, 0.19 to 4.84 μg/L v 0.05 μg/L; range, 0.02 to 0.27 μg/L; and 0.09 μg/L; range, 0.02 to 0.15 μg/L, respectively; P < .05, ANOVA). Among patients with FHF, blood levels of NSE tended to be greater in patients who subsequently developed cerebral herniation than in survivors (median, 10.5 μg/L; range, 5.2 to 15.9 μg/L v 5.1 μg/L; range, 2.8 to 12 μg/L; P = .05). There was no net cerebral flux of S‐100b or NSE. Short‐term hyperventilation had no effect on any of these measures, whereas high‐volume plasmapheresis reduced circulating S‐100b levels from 0.45 μg/L (range, 0.19 to 10.31 μg/L) to 0.42 μg/L (range, 0.11 to 6.35 μg/L; P = .01). In conclusion, blood levels of S‐100b were elevated in almost all patients with FHF and AOCLD, but were unrelated to survival. Conversely, NSE showed a clear tendency toward greater circulating levels in patients with FHF who subsequently developed cerebral herniation than in survivors. This finding encourages further evaluation of NSE as a marker of neurological outcome in FHF.