Zetterman R K
University of Nebraska Medical Center, Omaha 68198-2000.
Alcohol Alcohol Suppl. 1991;1:305-10.
There are many unanswered questions in the possible autoimmune pathogenesis of alcoholic liver disease. Why do only 15-20% of chronic alcoholic patients develop alcoholic hepatitis and cirrhosis? What factors make a patient susceptible to immune events in alcoholism? What initiates immune reactivity in susceptible patients? What permits accumulation of alcoholic hyalin in patients with alcoholic hepatitis? Is alcoholic hyalin central to the pathogenesis of alcoholic hepatitis? If adducts play a role, why don't more alcoholics develop liver disease, as adducts probably form in all patients? Unfortunately, the lack of an appropriate animal model will probably allow these questions to remain unanswered for some time. However, further research into the role of adducts in alcoholic liver disease may be helpful. Isolation of adducts from hepatocytes of patients with alcoholic hepatitis may permit study of their intracellular location, formation and perhaps of their timing in the sequence of liver disease. These studies should provide additional clues to the pathogenesis of alcoholic liver disease.
在酒精性肝病可能的自身免疫发病机制方面,存在许多尚未解答的问题。为什么只有15% - 20%的慢性酒精中毒患者会发展为酒精性肝炎和肝硬化?哪些因素使患者易在酒精中毒时发生免疫反应?是什么引发了易感患者的免疫反应?是什么使得酒精性肝炎患者体内出现酒精性透明小体聚集?酒精性透明小体在酒精性肝炎发病机制中起核心作用吗?如果加合物起作用,为什么不是更多酗酒者患肝病,因为加合物可能在所有患者体内形成?不幸的是,缺乏合适的动物模型可能会使这些问题在一段时间内仍无法得到解答。然而,进一步研究加合物在酒精性肝病中的作用可能会有所帮助。从酒精性肝炎患者的肝细胞中分离加合物,可能有助于研究它们在细胞内的位置、形成过程,或许还能研究它们在肝病发展过程中的出现时间。这些研究应该能为酒精性肝病的发病机制提供更多线索。