Bron B, Waldram R, Silk D B, Williams R
Gut. 1977 Sep;18(9):692-6. doi: 10.1136/gut.18.9.692.
Bile acid levels were measured in the sera, cerebrospinal fluid (CSF), and brain tissue of 10 patients immediately after death from fulminant hepatic (FHF). Serum bile acids in FHF were predominantly conjugated, and total bile acid levels were higher in all 10 patients than in normal controls (85.9 +/- SE 8.4 compared with 5.7 +/- 0.4 nmol/ml, P less than 0.001). Small but significant amounts could be detected in CSF (range 1.2-5.3 nmol total bile acid/ml) and brain biopsies (1.0-18.8 nmol/g wet weight) of FHF patients, whereas none could be detected in CSF and brain biopsies of patients dying without evidence of liver disease. There was no relationship between serum, CSF, or brain levels and duration of coma, or presence of cerebral oedema found in five FHF patients at necropsy. However, serum bile acid levels were similar in FHF to those found in chronic liver disease without encephalopathy and lower than those found to inhibit brain respiration in vitro. A primary role for these compounds in the pathogenesis of coma in FHF therefore seems unlikely.
在10例暴发性肝衰竭(FHF)患者死亡后立即检测其血清、脑脊液(CSF)和脑组织中的胆汁酸水平。FHF患者血清中的胆汁酸主要是结合型的,10例患者的总胆汁酸水平均高于正常对照组(分别为85.9±标准误8.4与5.7±0.4 nmol/ml,P<0.001)。在FHF患者的脑脊液(总胆汁酸范围为1.2 - 5.3 nmol/ml)和脑活检组织(1.0 - 18.8 nmol/g湿重)中可检测到少量但显著的胆汁酸,而在无肝病证据死亡患者的脑脊液和脑活检组织中未检测到。在5例尸检时有脑水肿的FHF患者中,血清、脑脊液或脑内胆汁酸水平与昏迷持续时间或脑水肿的存在均无关联。然而,FHF患者的血清胆汁酸水平与无肝性脑病的慢性肝病患者相似,且低于体外实验中发现的抑制脑呼吸的水平。因此,这些化合物在FHF昏迷发病机制中的主要作用似乎不太可能。