Mörl M, Schwalbach G, Wannagat L, Bavastro P
Med Klin. 1979 Nov 2;74(44):1629-34.
Alcoholic liver damage is associated with the development of portal hypertension quite early, as a result of increasing fibrosis. By means of laparoscopic transhepatic manometry (LTM) in the branches of the portal and hepatic veins, we measured the pressure levels in 15 patients with early and transitional-stage alcoholic injury extending to cirrhosis of the liver, and compared them with histological and laboratory investigation criteria. We discovered that parenchymal damage with portal and centrolobular fibrosis already gave rise to some portal hypertension which, compared to a group showing histological changes of remodelling or cirrhosis, constantly increased. In completely developed alcoholic cirrhosis (n = 41), the pressure levels reached a peak. Despite this fact, bleeding from oesophageal varices cannot be predicted. Over the period of observation of 33 months, 4 deaths occurred (portal vein pressure between 4.5 to 5 kPa = 34.0 to 38.8 mm Hg), and three variceal bleedings we were able to manage were seen (pressures between 3.6 to 4.3 kPa = 27.0 and 32.0 mm Hg). Compared to hepatitic cirrhosis the prognosis was slightly more favourable.
由于纤维化不断加重,酒精性肝损伤在早期就与门静脉高压的发展相关。通过对门静脉和肝静脉分支进行腹腔镜经肝测压(LTM),我们测量了15例早期和过渡阶段酒精性损伤并发展至肝硬化的患者的压力水平,并将其与组织学和实验室检查标准进行比较。我们发现,伴有门静脉和小叶中心纤维化的实质损伤已经导致了一些门静脉高压,与显示重塑或肝硬化组织学变化的一组相比,门静脉高压持续升高。在完全发展的酒精性肝硬化患者(n = 41)中,压力水平达到峰值。尽管如此,食管静脉曲张出血仍无法预测。在33个月的观察期内,有4例死亡(门静脉压力在4.5至5 kPa = 34.0至38.8 mmHg之间),并观察到3例我们能够处理的静脉曲张出血(压力在3.6至4.3 kPa = 27.0至32.0 mmHg之间)。与肝炎后肝硬化相比,预后略好。