Strauss G I, Christiansen M, Møller K, Clemmesen J O, Larsen F S, Knudsen G M
Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark.
Liver Transpl. 2001 Nov;7(11):964-70. doi: 10.1053/jlts.2001.28742.
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.
暴发性肝衰竭（FHF）患者常发生脑水肿和颅内高压。本研究旨在评估循环中S-100b和神经元特异性烯醇化酶（NSE）水平作为FHF患者神经功能预后的标志物。在一组患者中，测量了S-100b和NSE的脑通量。我们纳入了35例FHF患者、6例慢性肝病急性发作（AOCLD）患者、13例无肝性脑病的肝硬化患者和8名健康受试者。从置于桡动脉和颈内静脉球部的导管采集血样。测量了S-100b和NSE的脑净通量，并确定了短期过度通气以及大容量血浆置换对这两种生物标志物循环水平的影响。FHF和AOCLD患者的S-100b血水平高于肝硬化患者和健康受试者（中位数分别为0.39μg/L；范围为0.02至10.31μg/L；以及1.11μg/L；范围为0.19至4.84μg/L，而肝硬化患者为0.05μg/L；范围为0.02至0.27μg/L；健康受试者为0.09μg/L；范围为0.02至0.15μg/L；P<0.05，方差分析）。在FHF患者中，随后发生脑疝的患者的NSE血水平往往高于幸存者（中位数分别为10.5μg/L；范围为5.2至15.9μg/L，而幸存者为5.1μg/L；范围为2.8至12μg/L；P = 0.05）。S-100b或NSE均无脑净通量。短期过度通气对这些指标均无影响，而大容量血浆置换使循环中的S-100b水平从0.45μg/L（范围为0.19至10.31μg/L）降至0.42μg/L（范围为0.11至6.35μg/L；P = 0.01）。总之，几乎所有FHF和AOCLD患者的S-100b血水平均升高，但与生存率无关。相反，FHF患者中随后发生脑疝的患者的NSE循环水平明显高于幸存者。这一发现鼓励进一步评估NSE作为FHF患者神经功能预后标志物的价值。
