Green G, Poller L, Thomson J M, Dymock I W
Gut. 1977 Nov;18(11):909-12. doi: 10.1136/gut.18.11.909.
The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
最近有报道称，肝病患者中异常纤维蛋白聚合反应频繁发生。为进一步研究这一现象，对68例肝硬化或慢性活动性肝病患者的纤维蛋白聚合反应进行了研究。其中33例患者显示出这一凝血阶段的损害。当对出现这种异常的患者与纤维蛋白聚合反应正常的患者的其他肝功能检查进行比较时，发现前一组患者的白蛋白浓度显著降低（p<0.0002），胆红素和天冬氨酸转氨酶水平升高（分别为p<0.0006和<0.003），与后一组患者相比，一期凝血酶原时间延长更明显（p<0.001），因子VII水平降低更显著（p<0.002）。结论是，肝病患者中发生的纤维蛋白聚合缺陷表明肝细胞功能严重受损。这可能解释了纤维蛋白聚合异常的肝硬化患者伴有胃食管静脉曲张出血时预后不良的原因。
