Department of Laboratory Medicine and Pathobiology, University of Toronto, Canada.
Best Pract Res Clin Gastroenterol. 2013 Aug;27(4):471-83. doi: 10.1016/j.bpg.2013.08.002. Epub 2013 Aug 29.
The liver may be injured during the course of many systemic diseases. The mechanisms of injury can be broadly divided into four pathways: vascular, toxic, immune, and hormonal. Vascular obstruction may be an early event but is also the late common pathway from all mechanisms. Despite the large number of possible initiating factors, the end results are few, including death of hepatocytes or cholangiocytes, leading to the stereotyped syndromes of acute liver failure, non-cirrhotic portal hypertension, or cirrhosis. This small number of outcomes is a reflection of the few anatomic patterns that can be generated by microvascular obstruction. Vascular obstruction may occur by thrombosis, inflammation, or congestive injury. The innate immunity pathway is activated by endotoxin and other agents, leading to inflammatory infiltration, release of cytokines and reactive oxygen species, and necrosis. The adaptive immune pathway involves the generation of antibodies and antigen-specific cell-mediated attack on hepatic cells. Hormonal effects are principally involved when overnutrition leads to hyperinsulinemia followed by hepatocellular necrosis.
肝脏在许多全身性疾病的发展过程中可能会受到损伤。损伤的机制可大致分为四大途径:血管、毒性、免疫和激素。血管阻塞可能是早期事件,但也是所有机制的晚期共同途径。尽管可能存在大量的起始因素,但最终结果却很少,包括肝细胞或胆管细胞死亡,导致急性肝衰竭、非肝硬化性门静脉高压或肝硬化的典型综合征。这种少数的结果反映了微血管阻塞可以产生的少数解剖模式。血管阻塞可能由血栓形成、炎症或充血性损伤引起。先天免疫途径被内毒素和其他物质激活,导致炎症浸润、细胞因子和活性氧释放以及坏死。适应性免疫途径涉及抗体的产生和针对肝细胞的抗原特异性细胞介导攻击。当营养过剩导致高胰岛素血症继而导致肝细胞坏死时,激素作用主要涉及其中。