Popper H
Leber Magen Darm. 1978 Apr;8(2):65-72.
Hepatic fibrosis may result from collapse after hepatocellular necrosis or from new formation of connective tissue. Fibroplasia, particularly within the lobular parenchyma, is a dynamic process. Newer cellular and biochemical investigations clarified its various steps. The process begins with stimulation of cells to connective tissue formation and can be divided into (1) intracellular synthesis, (2) extracellular maturation, and (3) collagen breakdown. The turnover of the connective tissue in the liver is conspicuously increased in chronic hepatitis of any type, as indicated by an elevation of several cellular and metabolic parameters. They are particularly raised in chronic hepatitis and in alcoholic liver injury. Further development of these parameters in the future should facilitate the analysis of the dynamics of fibroplasia. The strongest stimuli for hepatic fibroplasia are hepatocellular necrosis and inflammation, but ethyl alcohol and steatosis are also stimulating, though to a lesser degree. This explains the particular elevation of the fibroplastic parameters in alcoholic hepatitis. It points, however, also to the possibility that cirrhosis might develop without significant hepatocellular necrosis and inflammation. Perihepatocellular, periductular, and septal fibrosis are the functionally most important localizations leading to additional hepatic injury. The initiation of these types of fibrosis by liver injury points to a vicious circle. Specific anti-fibroplastic therapy is still in infancy.
肝纤维化可能源于肝细胞坏死后的塌陷，也可能源于结缔组织的新生成。成纤维细胞增生，尤其是在小叶实质内，是一个动态过程。更新的细胞和生化研究阐明了其各个步骤。这个过程始于细胞对结缔组织形成的刺激，可分为（1）细胞内合成、（2）细胞外成熟和（3）胶原降解。肝脏中结缔组织的周转在任何类型的慢性肝炎中都显著增加，这由几个细胞和代谢参数的升高所表明。它们在慢性肝炎和酒精性肝损伤中尤其升高。这些参数在未来的进一步发展应有助于分析成纤维细胞增生的动态过程。肝成纤维细胞增生的最强刺激因素是肝细胞坏死和炎症，但乙醇和脂肪变性也有刺激作用，尽管程度较轻。这解释了酒精性肝炎中纤维增生参数的特别升高。然而，这也指出了在没有明显肝细胞坏死和炎症的情况下可能发展为肝硬化的可能性。肝周、胆管周围和间隔纤维化是导致额外肝损伤的功能上最重要的部位。肝损伤引发这些类型的纤维化指向一个恶性循环。特异性抗纤维化治疗仍处于起步阶段。
