Shibayama Y, Urano T, Asaka S, Hashimoto K, Nakata K
Department of Pathology, Osaka Medical College, Japan.
J Gastroenterol Hepatol. 1993 Nov-Dec;8(6):530-4. doi: 10.1111/j.1440-1746.1993.tb01647.x.
The exact pathogenesis of centrilobular necrosis following congestion of the liver is still unknown. We reviewed the clinical data related to systemic circulatory disturbance and histopathology of the liver and the gut in 320 autopsy subjects. Congestion of the liver alone was associated only with atrophy and loss of hepatocytes in centrilobular areas, but not with hepatocellular coagulative necrosis. In many patients with coagulative necrosis of centrilobular hepatocytes and congestion of the liver, fibrin thrombi and neutrophil infiltration in the sinusoids, which are the characteristic histopathological features of the liver in endotoxaemia, were found in and around the necrotic area. Congestion, erosion or haemorrhage of the intestinal mucosa, which may allow entrance of endotoxin into the liver through the portal vein, was seen in such patients. Prolonged hypotension or shock, which may lead to portal endotoxaemia, was present in half the patients with centrilobular necrosis and congestion of the liver. These results suggest that not only congestion of the liver but also portal endotoxaemia may be involved in the pathogenesis of centrilobular necrosis in patients with congestion of the liver.
肝脏淤血后小叶中心性坏死的确切发病机制仍不清楚。我们回顾了320例尸检对象中与全身循环障碍以及肝脏和肠道组织病理学相关的临床资料。单纯的肝脏淤血仅与小叶中心区域肝细胞的萎缩和丧失有关，而与肝细胞凝固性坏死无关。在许多伴有小叶中心肝细胞凝固性坏死和肝脏淤血的患者中，在坏死区域及其周围发现了纤维蛋白血栓和窦状隙内的中性粒细胞浸润，这些是内毒素血症时肝脏的特征性组织病理学表现。在这类患者中可见肠黏膜充血、糜烂或出血，这可能使内毒素通过门静脉进入肝脏。在半数伴有小叶中心坏死和肝脏淤血的患者中存在可导致门静脉内毒素血症的长时间低血压或休克。这些结果表明，对于伴有肝脏淤血的患者，小叶中心坏死的发病机制中不仅涉及肝脏淤血，还可能涉及门静脉内毒素血症。
