Buhac I, Jarmolych J
Am J Dig Dis. 1978 May;23(5):417-22. doi: 10.1007/BF01072924.
Portal hypertension and hypoalbuminemia are usually incriminated in the development of ascites in liver cirrhosis, and altered peritoneal permeability is considered only as a hypothetical possibility. Jejunal postmortem specimens were studied in 15 control patients and 16 patients dying with cirrhosis of the liver and ascites. In decompensated cirrhosis a fibrous thickening of the peritoneum was found, 159.0 +/- 96.4 micrometer (mean +/- SD) compared to 24.5 +/- 10.6 micrometer in controls (P less than 0.001). An increase in the size and number of blood vessels, lymphangiectasiae, and mononuclear cell infiltration were invariably present. These histological changes are consistent with a nonspecific chronic peritonitis. The findings indicate there is increased blood perfusion and lymph flow within the intestinal peritoneum in patients with decompensated cirrhosis of the liver and support the existence of an intestinal peritoneal factor in the pathogenesis of cirrhotic ascites.
门静脉高压和低白蛋白血症通常被认为是肝硬化腹水形成的原因,而腹膜通透性改变仅被视为一种假设的可能性。对15例对照患者和16例死于肝硬化腹水的患者的空肠尸检标本进行了研究。在失代偿期肝硬化患者中,发现腹膜有纤维性增厚,厚度为159.0±96.4微米(平均值±标准差),而对照组为24.5±10.6微米(P<0.001)。血管大小和数量增加、淋巴管扩张以及单核细胞浸润总是存在。这些组织学变化与非特异性慢性腹膜炎一致。研究结果表明,失代偿期肝硬化患者肠腹膜内的血液灌注和淋巴流量增加,支持了肠腹膜因素在肝硬化腹水发病机制中的存在。