Zurborn K H, Gram J, Rohwedder E, Bewig B, Bruhn H D
Med Klin (Munich). 1989 Nov 15;84(11):515-8.
The activation of coagulation and fibrinolysis as well as coagulation inhibitors in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis were studied. Protein C (PC) was decreased in a more pronounced manner than antithrombin III (AT III) in liver cirrhosis. Thereby, PC proved to be a highly sensible indicator of liver cell dysfunction. Decreased levels of PC activity (PC ratio activity/antigen 0.82) in decompensated liver cirrhosis suggest production of dysfunctional, undercarboxylated PC. We observed increased blood concentrations of fibrinopeptide A (FPA) (p less than 0.05) in both groups of patients compared to healthy volunteers (n = 25), while D-Dimer was increased only in patients with decompensated liver cirrhosis (p less than 0.01). Comparing both groups of patients. D-Dimer was significantly different with higher levels in decompensated liver cirrhosis (p less than 0.01). The ratio D-Dimer/FPA was significantly increased in decompensated liver cirrhosis compared to both other groups. These observations indicate that efflux from the extravascular space, e.g. ascitic fluid, contributes to the high contents of fibrin degradation products (D-Dimer) in patients with decompensated liver cirrhosis. In summary we conclude that patients with liver cirrhosis have enhanced activation of both coagulation and fibrinolysis but that the balance is not significantly displaced.
对代偿期(n = 25)和失代偿期(n = 25)肝硬化患者血液中的凝血、纤维蛋白溶解以及凝血抑制剂的激活情况进行了研究。肝硬化患者中蛋白C(PC)的降低比抗凝血酶III(AT III)更为明显。由此证明,PC是肝细胞功能障碍的一个高度敏感指标。失代偿期肝硬化患者PC活性水平降低(PC活性/抗原比值为0.82),提示存在功能失调的、羧化不足的PC。与健康志愿者(n = 25)相比,我们观察到两组患者的纤维蛋白肽A(FPA)血液浓度均升高(p < 0.05),而D - 二聚体仅在失代偿期肝硬化患者中升高(p < 0.01)。比较两组患者,失代偿期肝硬化患者的D - 二聚体水平显著更高(p < 0.01),差异有统计学意义。与其他两组相比,失代偿期肝硬化患者的D - 二聚体/FPA比值显著升高。这些观察结果表明,血管外间隙(如腹水)的流出导致失代偿期肝硬化患者纤维蛋白降解产物(D - 二聚体)含量升高。总之,我们得出结论,肝硬化患者的凝血和纤维蛋白溶解均有增强,但平衡并未显著偏移。