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Review
. 2014 Nov 14;20(42):15539-48.
doi: 10.3748/wjg.v20.i42.15539.

Histopathology of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

Yoshihisa Takahashi  1 , Toshio Fukusato  1
Affiliations
Review

Histopathology of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis

Yoshihisa Takahashi et al. World J Gastroenterol. .

Abstract

Nonalcoholic fatty liver disease (NAFLD), a hepatic manifestation of metabolic syndrome, is the most common chronic liver disease, and the prevalence is rapidly increasing worldwide. Nonalcoholic steatohepatitis (NASH), the severe form of NAFLD, can progress to liver cirrhosis and hepatocellular carcinoma (HCC). Although noninvasive clinical scores and image-based diagnosis for NAFLD have improved, histopathological evaluation of biopsy specimens remains the gold standard for diagnosing NAFLD/NASH. Steatosis, lobular inflammation, and hepatocellular ballooning are all necessary components for the diagnosis of NASH; fibrosis is also typically observed. Other histopathological abnormalities commonly observed in NASH include hepatocellular glycogenated nuclei, lipogranulomas, and acidophil bodies. The characteristics of pediatric NAFLD/NASH differ from adult NAFLD/NASH. Specifically, steatosis and portal inflammation are more severe in pediatric NAFLD, while intralobular inflammation and perisinusoidal fibrosis are milder. Although interobserver agreement for evaluating the extent of steatosis and fibrosis is high, agreement is low for intralobular and portal inflammation. A recently reported histological variant of HCC, steatohepatitic HCC (SH-HCC), shows features that resemble non-neoplastic steatohepatitis, and is thought to be strongly associated with underlying NASH. In this report, we review the histopathological features of NAFLD/NASH.

Keywords: Histopathology; Interobserver variation; Nonalcoholic fatty liver disease; Nonalcoholic steatohepatitis; Pediatric.

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Figures

Figure 1
Figure 1
Steatosis in nonalcoholic fatty liver disease. Macrovesicular steatosis, predominantly distributed in zone 3, is observed (Masson trichrome staining).
Figure 2
Figure 2
Lobular inflammation in nonalcoholic steatohepatitis. Necroinflammatory foci (arrows) are scattered in the hepatic lobule (hematoxylin and eosin staining).
Figure 3
Figure 3
Ballooning and Mallory-Denk bodies in nonalcoholic steatohepatitis. Ballooned hepatocytes are recognized as swollen hepatocytes with rarefied cytoplasm (black arrows). Mallory-Denk bodies are eosinophilic irregular-shaped aggregates in the cytoplasm of hepatocytes (white arrow) (hematoxylin and eosin staining).
Figure 4
Figure 4
Fibrosis in nonalcoholic steatohepatitis. The characteristic pattern of fibrosis in nonalcoholic steatohepatitis is perisinusoidal/pericellular (chicken wire) fibrosis, which usually begins in zone 3 (reticulin staining).
Figure 5
Figure 5
Histological appearance of alcoholic steatohepatitis. Canalicular cholestasis (black arrow), Mallory-Denk bodies (white arrows), and acute inflammation in the portal tract are observed (hematoxylin and eosin staining).
Figure 6
Figure 6
Histological appearance of steatohepatitic hepatocellular carcinoma. Large droplet steatosis, ballooning of malignant hepatocytes, Mallory-Denk bodies (arrows), inflammation, and fibrosis are observed in tumor tissue (hematoxylin and eosin staining).
See this image and copyright information in PMC

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