title: S-100b and neuron-specific enolase in patients with fulminant hepatic failure.
abstract: 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 microg/L; range, 0.02 to 10.31 microg/L; and 1.11 microg/L; range, 0.19 to 4.84 microg/L v 0.05 microg/L; range, 0.02 to 0.27 microg/L; and 0.09 microg/L; range, 0.02 to 0.15 microg/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 microg/L; range, 5.2 to 15.9 microg/L v 5.1 microg/L; range, 2.8 to 12 microg/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 microg/L (range, 0.19 to 10.31 microg/L) to 0.42 microg/L (range, 0.11 to 6.35 microg/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.
authors.affiliation: Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark. rh07184@rh.dk
authors.forename: G I
authors.initials: GI
authors.lastname: Strauss
authors.forename: M
authors.initials: M
authors.lastname: Christiansen
authors.forename: K
authors.initials: K
authors.lastname: Møller
authors.forename: J O
authors.initials: JO
authors.lastname: Clemmesen
authors.forename: F S
authors.initials: FS
authors.lastname: Larsen
authors.forename: G M
authors.initials: GM
authors.lastname: Knudsen
mesh_terms: D000208:Acute Disease; D000328:Adult; D002560:Cerebrovascular Circulation; D002908:Chronic Disease; D004677:Encephalocele / Q000097:blood / Q000209:etiology; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood; D008107:Liver Diseases / Q000097:blood; D017093:Liver Failure / Q000097:blood* / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009414:Nerve Growth Factors; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D010956:Plasmapheresis; D012016:Reference Values; D012121:Respiration, Artificial / Q000379:methods; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood*
chemical_list: D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase