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酒精性肝病的组织学发现。

Histologic findings in alcoholic liver disease.

机构信息

Department of Pathology and Laboratory Medicine, Hofstra North Shore-LIJ School of Medicine, Uniondale, NY, USA.

出版信息

Clin Liver Dis. 2012 Nov;16(4):699-716. doi: 10.1016/j.cld.2012.08.004.

DOI:10.1016/j.cld.2012.08.004
PMID:23101978
Abstract

The necessity of the liver being the organ responsible for metabolism of alcohol exposes it to many untoward toxic side effects. In the first instance of hepatic steatosis, fibrosis may occur indolently over years, slowly converting a greasy, steatotic liver into a cirrhotic liver. In the case of alcoholic hepatitis, brisk sinusoidal fibrosis may lead to more rapid development of cirrhosis, with the liver extensively subdivided by sublobular fibrous septa developing in the midst of extensive ongoing inflammation and hepatocellular destruction. Continued destruction of the parenchyma after cirrhosis has developed may produce a densely fibrotic organ with little remaining parenchyma.

摘要

肝脏作为负责酒精代谢的器官,使其容易受到许多不良的毒性副作用的影响。在肝脂肪变性的最初阶段,纤维化可能在数年内缓慢发生,将一个油腻的脂肪性肝脏逐渐转变为肝硬化肝脏。在酒精性肝炎的情况下,活跃的窦状纤维化可能导致更快速地发展为肝硬化,肝小叶纤维性间隔广泛地将广泛进行的炎症和肝细胞破坏分隔开。在肝硬化发展后,实质的持续破坏可能导致一个致密纤维化的器官,剩余的实质很少。

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