S-100b and neuron-specific enolase in patients with fulminant hepatic failure

Patients with fulminant hepatic failure (FHF) frequently develop cerebral e dema and intracranial hypertension. The aim of this study was to evaluate c irculating S-100b and neuron-specific enolase (NSE) levels as markers of ne urological outcome in patients with ME In a subgroup of patients, the cereb ral 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 ci rrhosis of the liver without hepatic encephalopathy, and 8 healthy subjects . Blood samples were obtained from catheters placed in the radial artery an d internal jugular bulb. The net cerebral flux of S-100b and NSE was measur ed, 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 an d AOCLD than patients with cirrhosis and healthy subjects (median, 0.39 mug /L; range, 0.02 to 10.31 mug/L; and 1.11 mug/L; range, 0.19 to 4.84 mug/L v 0.05 mug/L; range, 0.02 to 0.27 mug/L; and 0.09 mug/L, range, 0.02 to 0.15 mug/L, respectively; P < .05, ANOVA). Among patients with FHF, blood level s of NSE tended to be greater in patients who subsequently developed cerebr al herniation than in survivors (median, 10.5 mug/L; range, 5.2 to 15.9 mug /L v 5.1 mug/L; range, 2.8 to 12 mug/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-1 00b levels from 0.45 mug/L (range, 0.19 to 10.31 mug/L) to 0.42 mug/L (rang e, 0.11 to 6.35 mug/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 circulatin g levels in patients with FHF who subsequently developed cerebral herniatio n than in survivors. This finding encourages farther evaluation of NSE as a marker of neurological outcome in FHF.