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Review
. 2010 Apr;210(4):515-26.
doi: 10.1016/j.jamcollsurg.2010.01.020.

Clinical review of nonalcoholic steatohepatitis in liver surgery and transplantation

Amit D Tevar  1 , Calissia Clarke, Jiang Wang, Steven M Rudich, E Steve Woodle, Alex B Lentsch, Michael L Edwards
Affiliations
Review

Clinical review of nonalcoholic steatohepatitis in liver surgery and transplantation

Amit D Tevar et al. J Am Coll Surg. 2010 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Histologic progression of nonalcoholic fatty liver disease from simple steatosis to cirrhosis.
Figure 2
Figure 2
Progression of nonalcoholic fatty liver disease demonstrating the 2-hit hypothesis. The first hit consists of lipid accumulation resulting in simple benign steatosis. This primes the liver for a second hit, which can be multifactorial. This 2-hit process results in hepatic injury, inflammation, and ultimately fibrosis.
Figure 3
Figure 3
Histology of progression from steatosis to nonalcoholic steatohepatitis (NASH) cirrhosis. (A) Normal liver. Hematoxylin and eosin staining 200×. (B) Diffuse macrocytic steatosis with inflammatory changes. Hematoxylin and eosin staining 200×. (C) Macrocytic steatosis with neutrophil accumulation inflammation (NASH). Hematoxylin and eosin staining 400×. (D) NASH with pericellular fibrosis. Trichrome straining 400×. (E) NASH cirrhosis with bridging fibrosis. Trichrome staining 400×.
Figure 4
Figure 4
Histology of macrocytic and microcytic hepatic steatosis. (A) Macrocytic steatosis. Hematoxylin and eosin staining 400×. Fat vacuoles cause displacement of the hepatocyte nuclei. (B) Microcytic steatosis. Hematoxylin and eosin staining 400×. Small fat vacuoles clustered within hepatocyte with no displacement of nuclei.
See this image and copyright information in PMC

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