论文部分内容阅读
作者对15例肝硬化伴有非感染性腹水的患者作腹膜活检及腹腔镜检查,其中男性12例,女性3例,均有饮酒史。9例腹水为漏出液,1例腹水中蛋白浓度为3.4g％。另5例曾经肝组织学检查证实为肝硬化伴腹水,作经皮腹膜活检。10例腹腔镜检查呈现增厚不透明的壁层腹膜,伴有弥漫性片状充血和弥漫性增多的小血管充盈。光反射较正常情况下减弱。网膜皱缩。腹膜活检呈非特异性慢性炎症,细胞呈立方形,间皮细胞增生。表层有纤维蛋白沉积及机化,深层为纤维组织所替代,浆膜下层有不同程度的单核细胞浸润。作者认为,在肝硬化伴有非感染性腹水患者中产生壁层腹膜炎症的原因很可能是腹水内存在刺激物所致,
The author of 15 cases of cirrhosis with non-infectious ascites in patients with peritoneal biopsy and laparoscopic examination, including 12 males and 3 females, all drinking history. 9 cases of ascites as leakage, 1 case of ascites protein concentration of 3.4g%. The other 5 cases had liver histology confirmed cirrhosis with ascites for peritoneal biopsy. Ten cases of laparoscopic thickened opaque parietal peritoneum with diffuse patchy congestion and diffuse small blood vessels filling. Light reflex is weaker than normal. Retina shrinking. Peritoneal biopsy showed non-specific chronic inflammation, cells were cubic, mesothelial cell proliferation. The surface of fibrin deposition and mechanization, deep fibrous tissue replacement, subserosal different levels of mononuclear cell infiltration. The authors suggest that the cause of parietal peritonitis in cirrhotic patients with non-infectious ascites is likely due to the presence of irritants in the ascites fluid,