van Leeuwen D J, Howe S C, Scheuer P J, Sherlock S
Academic Department of Medicine, Royal Free Hospital, London.
Gut. 1990 Mar;31(3):339-43. doi: 10.1136/gut.31.3.339.
Various anatomical factors were examined which might provide passive resistance to portal venous flow and so cause portal hypertension. Methods included the measurement of portal pressure (WHVPG) in cirrhotic and non-cirrhotic patients, morphological assessment by semiquantitative grading of severity of disease, calculation of hepatocyte size indices, and assessment of volume density of hepatocytes, sinusoids, Disse's space and Disse's space collagen by electron microscopy. The wedged hepatic venous pressure gradient increased with progression of disease and portal hypertension was present before histologically detectable cirrhosis had developed. With increasing progression of disease towards cirrhosis, the relationship between individual and aggregated features and the WHVPG diminished and lost statistical significance. Hepatocyte size increased with progression of histological changes and correlated significantly with increase of WHVPG, both in non-alcoholic and alcoholic patients. Disse's space collagen was increased significantly in non-alcoholic chronic active hepatitis compared with patients with near-normal liver. No significant decrease of sinusoidal space was found. Multiple factors rather than any single feature influence the development of portal hypertension.
研究了各种解剖学因素,这些因素可能对门静脉血流产生被动阻力,从而导致门静脉高压。方法包括测量肝硬化和非肝硬化患者的门静脉压力(WHVPG),通过疾病严重程度的半定量分级进行形态学评估,计算肝细胞大小指数,以及通过电子显微镜评估肝细胞、窦状隙、狄氏间隙和狄氏间隙胶原的体积密度。肝静脉楔压梯度随疾病进展而增加,在组织学上可检测到的肝硬化出现之前就存在门静脉高压。随着疾病向肝硬化的进展,个体特征和综合特征与WHVPG之间的关系减弱并失去统计学意义。肝细胞大小随组织学变化的进展而增加,在非酒精性和酒精性患者中均与WHVPG的增加显著相关。与肝脏接近正常的患者相比,非酒精性慢性活动性肝炎患者的狄氏间隙胶原显著增加。未发现窦状隙空间有明显减少。多种因素而非任何单一特征影响门静脉高压的发展。