Valla D, Flejou J F, Lebrec D, Bernuau J, Rueff B, Salzmann J L, Benhamou J P
Service d'Hépatologie, Unité de Recherches de Physiopathologie Hépatique (INSERM U 24), Clichy, France.
Hepatology. 1989 Oct;10(4):482-7. doi: 10.1002/hep.1840100414.
We attempted to ascertain the mechanism of portal hypertension and ascites complicating acute hepatitis in 66 patients who underwent transvenous liver biopsy and measurement of hepatic venous pressure gradient. Increase in hepatic venous pressure gradient was related to the severity of acute hepatitis, as indicated by the significant correlation between the values for hepatic venous pressure gradient and serum bilirubin, serum albumin or coagulation factor V, and by its higher value in patients with, than in patients without, encephalopathy. Hepatic venous pressure gradient was higher in patients with, than in patients without, ascites (12.5 +/- 3.4 vs. 8.4 +/- 3.6 mmHg, respectively; p less than 0.001). No ascites was clinically detectable in the patients in whom hepatic venous pressure gradient was below 6 mmHg. We tested the hypothesis that sinusoidal collapse due to liver cell dropout was a major factor in portal hypertension. Semiautomatic determination of the fractional area of sinusoidal collapse on chromotrope-stained sections and automatic measurement of Sirius red-stained collagen fiber density were performed. Hepatic venous pressure gradient significantly correlated with fractional sinusoidal collapse area (r = 0.61, p less than 0.001) and with Sirius red-stained collagen fiber density (r = 0.43, p less than 0.01). We conclude that portal hypertension in the course of acute hepatitis is related to the severity of liver damage and is a major factor in the development of ascites. Portal hypertension is mainly determined by intrahepatic vascular space being reduced by the collapse of sinusoids.
我们对66例接受经静脉肝活检及肝静脉压力梯度测量的患者进行研究，试图确定急性肝炎合并门静脉高压和腹水的机制。肝静脉压力梯度升高与急性肝炎的严重程度相关，这表现为肝静脉压力梯度值与血清胆红素、血清白蛋白或凝血因子V之间存在显著相关性，且肝性脑病患者的肝静脉压力梯度值高于无肝性脑病患者。有腹水患者的肝静脉压力梯度高于无腹水患者（分别为12.5±3.4 mmHg和8.4±3.6 mmHg；p<0.001）。肝静脉压力梯度低于6 mmHg的患者临床上未检测到腹水。我们检验了肝细胞缺失导致肝血窦塌陷是门静脉高压主要因素这一假说。对嗜铬染料染色切片上肝血窦塌陷的部分面积进行半自动测定，并对天狼星红染色的胶原纤维密度进行自动测量。肝静脉压力梯度与肝血窦塌陷部分面积显著相关（r = 0.61，p<0.001），与天狼星红染色的胶原纤维密度也显著相关（r = 0.43，p<0.01）。我们得出结论，急性肝炎病程中的门静脉高压与肝损伤严重程度相关，是腹水形成的主要因素。门静脉高压主要由肝血窦塌陷导致肝内血管间隙减小所决定。
