Fukui H, Brauner B, Bode J C, Bode C
Abteilung Innere Medizin I (Gastroenterologie), Robert-Bosch-Krankenhaus, Stuttgart, Federal Republic of Germany.
J Hepatol. 1991 Mar;12(2):162-9. doi: 10.1016/0168-8278(91)90933-3.
Plasma endotoxin concentration was measured in 85 patients with alcoholic liver disease (alcoholic cirrhosis (n = 64), alcoholic hepatitis without cirrhosis (n = 11), fatty liver (n = 10), and in patients with non-alcoholic cirrhosis (n = 15]. Endotoxin concentration was determined with an improved chromogenic substrate assay, using individual standard curves for each plasma sample. In patients with alcoholic cirrhosis the mean endotoxin concentration was significantly higher than in patients with non-alcoholic cirrhosis (p less than 0.05). In addition, distinctly higher endotoxin concentrations (greater than 20 pg/ml) were more frequently observed in patients with alcoholic cirrhosis than in non-alcoholic cirrhosis (34.4 vs. 14.3%, p less than 0.05). Mean endotoxin concentration was not significantly higher in cirrhotics with ascites or esophageal varices as compared with the subgroup without ascites or esophageal varices. The endotoxin concentration did not correlate with serum bilirubin, prothrombin concentration or serum enzyme activities. In patients with alcoholic liver disease, however, endotoxin concentration revealed a negative correlation (p less than 0.05) with the concentration of high density lipoprotein cholesterol. On admission endotoxin concentrations in alcoholics with fatty liver were similarly elevated as observed in alcoholic cirrhosis. In six out of 12 patients with fatty liver or alcoholic hepatitis, in whom a second sample of plasma was investigated after 6 to 8 days, endotoxemia was no longer detectable; in the remaining patients, the endotoxin concentration decreased markedly. The results indicate that, irrespective of the stage of liver disease, alcohol abuse favours the development of endotoxemia. They support the hypothesis that gut-derived endotoxins might play a role in the initiation and aggravation of alcohol-induced liver disease.
对85例酒精性肝病患者(酒精性肝硬化64例、无肝硬化的酒精性肝炎11例、脂肪肝10例)以及非酒精性肝硬化患者15例测定了血浆内毒素浓度。采用改良的显色底物法测定内毒素浓度,每个血浆样本均使用各自的标准曲线。酒精性肝硬化患者的平均内毒素浓度显著高于非酒精性肝硬化患者(p<0.05)。此外,酒精性肝硬化患者中内毒素浓度明显升高(>20 pg/ml)的情况比非酒精性肝硬化患者更常见(34.4%对14.3%,p<0.05)。有腹水或食管静脉曲张的肝硬化患者的平均内毒素浓度与无腹水或食管静脉曲张的亚组相比无显著升高。内毒素浓度与血清胆红素、凝血酶原浓度或血清酶活性无相关性。然而,在酒精性肝病患者中,内毒素浓度与高密度脂蛋白胆固醇浓度呈负相关(p<0.05)。入院时,脂肪肝酒精患者的内毒素浓度与酒精性肝硬化患者相似升高。在12例脂肪肝或酒精性肝炎患者中,6至8天后对第二份血浆样本进行检测,其中6例患者不再检测到内毒素血症;其余患者内毒素浓度明显下降。结果表明,无论肝病处于何种阶段,酗酒都有利于内毒素血症的发生。这些结果支持了肠道来源的内毒素可能在酒精性肝病的发生和加重中起作用这一假说。